Full Supplement - British Cardiovascular Society

97 

Volume 97 Supplement I Pages A1–A104 HEART June 2011 

June 2011 Volume 97 Supplement I 

heart 

British Cardiovascular Society 

Annual Conference 

13–15 June 2011 

Manchester Central 

heart.bmj.com www.bcs.com

Young Research Workers’ Prize 

A 

ENDOTHELIAL CELL NITRIC OXIDE BIOAVAILABILITY AND 

INSULIN SENSITIVITY ARE REGULATED BY IGF-1 AND 

INSULIN RECEPTOR LEVELS 

doi:10.1136/heartjnl-2011-300110.1 

A Abbas, H Viswambharan, H Imrie, A Rajwani, M Kahn, M Gage, R Cubbon, J Surr, 

S Wheatcroft, M Kearney. Leeds Institute of Genetics Health and Therapeutics, Leeds, UK 

Abstract A Figure 2 




Heart June 2011 Vol 97 Suppl 1 

Background In a similar manner to insulin, the growth promoting 

hormone Insulin-like Growth Factor-1 (IGF-1), may be an important 

regulator of endothelial nitric oxide (NO) bioavailability. We have 

previously reported evidence of increased basal NO production in 

the vasculature in two murine models of reduced IGF-1 receptor 

(global hemizygous knockout (IGFRKO) and endothelial cell specific 

IGF-1R knockout (ECIGFRKO)). Augmentation of this increase in 

NO is relative to progressive decrease in IGF-1R number (WT vs 

ECIGFRKO hemizygotes p¼0.01, WT vs ECIGFRKO homozygotes 

p¼0.001). Furthermore, by decreasing IGF-1R numbers in the 

insulin resistant hemizygous insulin receptor knockout (IRKO) 

model (IRKO 3 IGFRKO) we have shown insulin sensitivity in the 

vasculature can be restored. In this study, we have investigated 

further these receptor interactions with the generation of a mouse 

overexpressing the human IGF-1R specifically in the endothelium 

under control of the Tie-2 promoter-enhancer (hIGFREO), and by 

targeted knockdown of the IGF-1R in human umbilical vein endothelial 

cells (HUVECs). 

Methods Metabolic function was assessed in mice by tolerance tests 

using whole-blood micro-sampling after insulin or glucose intraperitoneal 

injection. Cardiovascular function was assessed by 

thoracic aortic vasomotion ex vivo in the organbath. Complimentary 

in vitro studies were conducted by siRNA mediated downregulation 

of the IGF-1 receptor in HUVECs with and wihout insulin stimulation. 

Nitric oxide synthase activity was measured using an assay 

measuring conversion of [14C]-L-arginine to [14 C]-L-citrulline. 

Results Glucose and insulin tolerance testing showed no difference 

between hIGFREO mice and wild-type (WT) littermates. Murine 

thoracic aorta from hIGFREO mice were hypercontractile to 

phenylepherine (PE) compared to WT (Emax hIGFREO¼ 

0.9160.045 g; WT¼0.6260.045 g, p¼0.0036) with decreased 

response to LNMMA (Emax hIGFREO¼47.7069.87 g; 

WT¼106.1630.10 g, p¼0.048). These data indicate reduced endothelial 

NO bioavailability in hIGFREO mice compared to WT. 

HUVECs transfected with IGF1R-siRNA showed increased basal 

and insulin mediated eNOS phosphorylation in the presence of 

insulin (Ins: 16464.9% vs siRNA+Ins: 19260.7%, p




strategy by which to modify vascular NO bioavailability and 

endothelial cell insulin sensitivity. 

intervention (PCI) were prospectively enrolled and underwent full 

3-vessel VH-IVUS pre-PCI. Troponin-I (cTnI), IL-6, IL-18, hsCRP, 

neopterin, MCP-1 and sICAM-1 were measured pre-PCI and 24-h 

post-PCI. LTL was determined by qPCR. The combined primary 

endpoint (MACE) included unplanned revascularisation, myocardial 

infarction (MI) and death, with a secondary endpoint of post-PCI 

MI (MI 4a). 

Results 18 MACE occurred in 16 patients (median follow-up: 625 

(463e990) days). 30 372 mm of VH-IVUS were analysed and 1106 

plaques classified (Abstract B Figure 1) locally and via a core-lab. 

After multivariable regression: 

1. Total number of non-calcified VH-IVUS-identified thin 

capped fibroatheromata (VHTCFA) was the only factor 

independently associated with MACE (HR¼3.16, (95% 

CI¼1.16 to 8.64), p¼0.025). 

2. Total VHTCFA number (OR¼1.26 (1.03 to 1.53) p¼0.021) 

and total stent length (OR¼1.04 (1.01 to 1.08), p¼0.01) were 

the only factors independently associated with MI 4a. 

3. A novel 3-vessel vulnerability index (necrotic core: fibrous 

tissue ratio) and side branch loss were independently associated 

with stenting-related cTnI rise (standardised beta coefficient 

(sb)¼0.29, p¼0.004 and sb¼0.23, p¼0.019 respectively). 

4. Necrotic core area at the minimum luminal area frame was 

the only factor independently associated with ACS presentation 

(OR¼1.59, p¼0.030). 

5. Stented vessel VHTCFA number (OR¼1.75 (1.22 to 2.51), 

p¼0.002) was independently associated with the lower LTL 

tertile (DNA-based cardiovascular risk predictor). 

6. Stenting-related IL-6 rise was the only biomarker independently 

associated with MACE (HR¼1.03 (1.01e1.05), 

p¼0.007). 

Conclusion We present the first report of an association between 

VHTCFA and MACE. This provides novel evidence that VHTCFA 

definitions are important in their own right (rather than as 

analogues of histological TFCA definitions). We also present the first 

report of associations between VHTCFA and MI 4a as well as a 

novel vulnerability index that is association with stenting-related 

troponin rise. Finally, we report a novel association between 

VHTCFA and DNA-based cardiovascular risk prediction (LTL). 

B 

VH-IVUS FINDINGS PREDICT MAJOR ADVERSE 

CARDIOVASCULAR EVENTS. THE VIVA STUDY (VIRTUAL 

HISTOLOGY INTRAVASCULAR ULTRASOUND IN 

VULNERABLE ATHEROSCLEROSIS) 

doi:10.1136/heartjnl-2011-300110.2 

1 P A Calvert, 1 D R Obaid, 2 N E J West, 2 L M Shapiro, 2 D McNab, 2 C G Densem, 

2 P M Schofield, 2 D Braganza, 2 S C Clarke, 2 M O’Sullivan, 3 K K Ray, 1 M R Bennett. 

1 University of Cambridge, Cambridge, UK; 2 Papworth Hospital NHS Foundation Trust, 

Cambridge, UK; 3 St George’s University of London, London, UK 

Background Identification of high-risk atherosclerotic plaques offers 

opportunities for risk stratification and targeted intensive treatment 

of patients with coronary artery disease. Virtual Histology intravascular 

ultrasound (VH-IVUS) has been validated in human atherectomy 

and post-mortem studies and can classify plaques into 

presumed high- and low-risk groups. However, VH-IVUS-defined 

plaques have not been shown to be associated with major adverse 

cardiovascular events (MACE), or biomarkers that confer increased 

cardiovascular risk, such as serum cytokines or shortened leukocyte 

telomere length (LTL). 

Methods 170 patients with stable angina or troponin-positive acute 

coronary syndrome (ACS), referred for percutaneous coronary 

Abstract B Figure 1 

A2 Heart June 2011 Vol 97 Suppl 1


C 

INSULIN RESISTANCE IMPAIRS ANGIOGENIC PROGENITOR 

CELL FUNCTION AND DELAYS ENDOTHELIAL REPAIR 

FOLLOWING VASCULAR INJURY 

doi:10.1136/heartjnl-2011-300110.3 

may be normalised by transfusion of APCs from insulin-sensitive 

animals but not from insulin-resistant animals. These data may 

have important implications for the development of therapeutic 

strategies for insulin-resistance associated cardiovascular disease. 

M B Kahn, N Yuldasheva, R Cubbon, J Surr, S Rashid, H Viswambharan, H Imrie, 

A Abbas, A Rajwani, M Gage, M T Kearney, S Wheatcroft. Leeds University, Leeds, UK 

Introduction Insulin-resistance, the primary metabolic abnormality 

underpinning type-2-diabetes mellitus (T2DM) and obesity, is an 

important risk factor for the development of atherosclerotic cardiovascular 

disease. Circulating-angiogenic-progenitor-cells (APCs) 

participate in endothelial-repair following arterial injury. Type-2 

diabetes is associated with fewer circulating APCs, APC dysfunction 

and impaired endothelial-repair. We set out to determine whether 

insulin-resistance per se adversely affects APCs and endothelialregeneration. 

Research Design and Methods We quantified APCs and assessed 

APC-mobilisation and function in mice hemizygous for knockout of 

the insulin receptor (IRKO) and wild-type (WT) littermate controls. 

Endothelial-regeneration following femoral artery wire-injury was 

also quantified at time intervals after denudation and following APC 

transfusion. 

Results The metabolic phenotype of IRKO mice was consistent 

with compensated insulin resistance, with hyperinsulinaemia after a 

glucose challenge but a normal blood glucose response to a glucose 

tolerance test. IRKO mice had fewer circulating Sca-1+/Flk-1+ 

APCs than WT mice at baseline. Culture of mononuclear-cells 

demonstrated that IRKO mice had fewer APCs in peripheral-blood, 

but not in bone-marrow or spleen, suggestive of a mobilisation 

defect. Defective VEGF-stimulated APC mobilisation was confirmed 

in IRKO mice, consistent with reduced eNOS expression in bone 

marrow and impaired vascular eNOS activity. Paracrine-angiogenicactivity 

of APCs from IRKO mice was impaired compared to those 

from WT animals. Endothelial-regeneration of the femoral artery 

following denuding wire-injury was delayed in IRKO mice 

compared to WT (re-endothelialised area 35.864.8% vs 66.665.2% 

at day 5 following injury and 35.664.8% vs 59.866.6% at day 7; 

P


(Abstract E Figure 2B) and potentially causative sequence variants 

in these 3 candidate genes have been identified. We have translated 

these findings to humans using data from a genome-wide association 

study population. 

Conclusions We have identified a new genomic locus for HR, which 

does not contain genes in pathways already known to determine 

HR. We prioritised three candidate genes at the locus, which may be 

targets for therapeutic modulation of HR in patients with heart 

disease. 

Abstract D Figure 2 

E 

INTEGRATIVE GENOMICS APPROACHES IDENTIFY NEW 

GENES CONTROLLING HEART RATE 

doi:10.1136/heartjnl-2011-300110.5 

1,2 J S Ware, 

3 H Dobrzynski, 

4 M Pravanec, 

1 P J Muckett, 

1 S Wilkinson, 

5 Y Jamshidi, 1 T J Aitma, 6 N S Peters, 1,2 S A Cook. 1 MRC Clinical Sciences Centre, 

Imperial College London, London, UK; 

2 National Heart & Lung Institute, Imperial 

College London, London, UK; 

3 School of Medicine, University of Manchester, 

Manchester, UK; 4 Institute of Physiology, Czech Academy of Science, Prague, UK; 

5 Division of Clinical Developmental Sciences, St. George’s University of 

London, London, UK; 

6 National Heart & Lung Institute, Imperial College London, 

London, UK 

Introduction Heart rate (HR) is a fundamental measure of cardiac 

function, and is of prognostic and therapeutic significance. We 

applied genetic and genomic approaches to identify new loci and 

genes controlling HR in a rat model that has previously been used to 

find human cardiovascular disease genes. 

Methods Telemetric aortic pressure transducers were implanted into 

226 animals from 33 rat strains: the Brown Norway, the Spontaneously 

Hypertensive Rat, and 31 strains from a recombinant inbred 

panel derived from these parental strains and HR was measured over 

several weeks. Statistical analyses were carried out using the R 

package, and quantitative trait loci (QTL) identified by linkage 

mapping using QTL Reaper. Potential covariates of HR were 

analysed in SPSS. The sinus node (SN) and right atria (RA) of 20 rats 

were microdissected (Abstract E Figure 1). Gene expression data 

were generated with the Affymetrix Rat Gene 1.0 ST microarray 

and analysed using Bioconductor. Differentially expressed genes 

were identified using SAM & Limma. Genes in the QTL that were 

expressed in the SN were resequenced to identify potential causative 

sequence variants. 

Results Narrow sense heritability of HR in this population was 

51%, suggesting a large genetic contribution to HR. Linkage 

mapping identified a region on rat chromosome 13 controlling HR, 

with peak LOD score 6.7 (Abstract E Figure 2A). This QTL has not 

previously been identified in human, rat or mouse. Mean nocturnal 

HR in strains carrying the SHR allele was 388, compared with 357 

in BN-like strains; an allelic effect of 31bpm (8.7%, p0.00005). The horizontal line approximates to genomewide 

significance. (B) A volcano plot showing 3 genes significantly enriched in 

SN compared with RA. 


BCS Abstracts 2011 

Abstracts 

1 ROUTE OF ADMISSION IN STEMI: DO PATIENTS WHO 

PRESENT DIRECTLY TO A PCI-CAPABLE HOSPITAL DIFFER 

FROM INTER-HOSPITAL TRANSFERS? 

doi:10.1136/heartjnl-2011-300198.1 

D Austin, Z Adam, J Shome, M Awan, A G C Sutton, J A Hall, R A Wright, D F Muir, 

N M Swanson, J Carter, MA de Belder. James Cook University Hospital, Middlesbrough, 

UK 

Background Rapid delivery of reperfusion therapy with PPCI is the 

gold standard treatment in STEMI. Systems have been developed, 

such as direct admission to a PCI-capable hospital, to minimise the 

time from diagnosis to PPCI. Despite this, a significant minority of 

patients are initially admitted to non-PCI capable hospitals. The aim 

of this study was to determine whether patients differed in their 

characteristics, time to PPCI, and outcome by route of admission. 

Methods The study was performed in a single tertiary centre in 

North England. Data are collected routinely on all patients undergoing 

PPCI and include demographic, clinical and procedural variables. 

In-hospital MACCE (death, re-infarction or CVA) and mortality 

are collected providing relevant outcome measures. Baseline clinical 

variables by route of admission were compared and unadjusted inhospital 

MACCE rates determined. One-year mortality by route of 

admission was calculated using the K-M product limit estimate. Inhospital 

and 1-year outcomes were analysed after adjustment for 

factors known to be predictors of early mortality following STEMI 

(models 1 and 3). To determine the relative importance of delays in 

treatment, call-to-balloon time was added (models 2 and 4). Logistic 

regression was used for the adjusted in-hospital outcomes, and Coxproportional 

regression for adjusted 1-year mortality. 

Results 2268 patients were included in the analysis. 510 patients 

(22.5%) were treated with PPCI following transfer from a non-PCI 

capable centre. Analysis of baseline variables (Abstract 1 table 1) 

showed the transfer group were more likely to have an LAD 

occlusion treated, and previous MI. Despite shorter DTB times, the 

transfer group had a greater median CTB time (52 minutes longer) 

compared with direct admissions. Other baseline variables were 

statistically no different between groups. There were 110 in-hospital 

MACCE events, and 168 deaths within 1-year follow-up. The transfer 

group had significantly higher unadjusted in-hospital MACCE rates 

(2.4% absolute, 58% relative increase (Abstract 1 table 2)). At 1 year, 

the transfer group had significantly higher unadjusted mortality 

(2.7% absolute, 48% relative increase (Abstract 1 table 2)). After 

adjustment for relevant co-variates (models 1 and 3) route of 

admission remained a significant predictor of in-hospital and 1-year 

mortality. With the addition of call-to-balloon time, no significant 

Abstract 1 Table 1 

Direct Transfer p 

Age (years6SD) 64.3 (12.7) 63.9 (12.4) 0.17 

Male 1252 (71.2) 367 (72.0) 0.74 

Diabetes 177 (10.1) 55 (10.8) 0.68 

Previous MI 225 (12.6) 89 (17.3) 0.001 

Treated vessel 0.001 

LMS 24 (1.4) 13 (2.5) 

LAD 630 (36.1) 218 (42.9) 

LCx 249 (14.3) 83 (16.3) 

RCA 812 (46.6) 188 (37.0) 

Graft 28 (1.7) 5 (1.1) 

Cardiogenic shock 28 (1.7) 35 (6.9) 0.61 

Smoking (ex/current) 1331 (75.7) 377 (73.9) 0.42 

Call-to-balloon time 102 (82e135) 154 (107e235)



Inclusion criteria 

Exclusion criteria 

(42.4%) of patients were treated with medical therapy alone. NSTE- 

ACS (encompassing NSTEMI and unstable angina) was the discharge 

diagnosis for 75.4% of HACX patients. 10% of patients had another 

cause for chest pain symptoms (including pericarditis and, myocarditis); 

14.6% had a non-cardiac diagnosis. Mean time from presentation 

to angiography was pre-HAC-X 7349 mins (66836) and post HAC-X 

754 mins (6458) (p


4 A RATIONAL APPROACH TO RAISED TROPONINS ON A 

HYPERACUTE STROKE UNIT: COPING WITH THE IMPACT ON 

CARDIOLOGY SERVICES 

doi:10.1136/heartjnl-2011-300198.4 

S S Nijjer, G Banerjee, J Barker, S Banerjee, S Connolly, K F Fox. Imperial College 

Healthcare NHS Trust, London, UK 

Introduction Troponin is frequently measured on admission to 

hyperacute stroke units (HASUs). Modest elevations in stroke are 

common but whether patient management changes in response to 

the blood test is unclear. Raised troponin without chest pain or 

dynamic ECG changes create diagnostic dilemmas. Management 

strategies were assessed with the introduction of the Imperial HASU 

covering North West London. 

Methods Consecutive HASU admissions over 6 months were 

assessed for measurement of troponin, the result, and the cardiac 

investigations performed. Clinical parameters guided investigations 

lead by two Consultant Cardiologists (KF, SC) rather than strict 

research protocol. 

Results 412 patients were admitted: 245 patients had a total of 435 

troponin-I levels measured, without chest pain or dynamic 

ischaemic ECG changes. 70 (29%) patients had positive levels 

(>0.032 ng/l): 53 (22%) were “low” (0.032e0.3 ng/l), 17 (7%) were 

“high” (>0.3 ng/l). 237 had diagnoses readily available: 170 had 

stroke (ischaemic or haemorrhagic), 67 had non-stroke (eg, seizure). 

Troponin was more likely to be raised if stroke, OR 4.3 (2.0e9.7, 

p¼0.0001). Five patients with “high” troponins had non-invasive 

stress testing (1 perfusion scan and 4 stress echos): all were negative. 

All positive troponins had echocardiography and cardiology review 

with no change in management in 91% of cases. 6 patients had 

invasive coronary angiography: 3 “high” and 3 “low” troponin. Only 

2 patients (3% of those with positive troponin) required percutaneous 

coronary intervention (PCI); both had troponin >0.3 and 

multiple cardiac risk factors. Patients with troponin 0.3 ng/l should be assessed for chest pain and ECG changes 

suggesting true myocardial infarction. Without these, non-invasive 

assessment and optimal medical therapy is sufficient in the 

majority. Minor troponin rise (0.032e0.3 ng/l) represents myocytolysis: 

cerebral insular damage causes sympathoadrenal activation 

and patchy myocyte damage. Without chest pain or ECG changes, 

optimal medical management without further investigation is 

appropriate. Since this does not represent true acute coronary 

syndrome, an early invasive strategy confers no additional benefit 

over medical therapy. In contrast, aspirin and statins benefit 

both stroke and any coronary disease present. The financial and 

medical implications of performing non-indicated tests in a routine 

manner when the result will be disregarded is significant. Therefore, 

we caution against routine measurement of troponin in 

stroke. 

Cardiovascular Science, Edinburgh University, Edinburgh, UK; 2 Edinburgh Heart Centre, 

Royal Infirmary of Edinburgh, Edinburgh, UK; 3 Epidemiology and Statistics Core, Wellcome 

Trust Clinical Research Facility, Edinburgh, UK; 4 Department of Clinical Biochemistry, 

Royal Infirmary of Edinburgh, Edinburgh, UK 

Introduction Although troponin assays have become increasingly 

more sensitive, it is unclear whether further reductions in the 

threshold of detection for plasma troponin concentrations impact 

on clinical outcomes in patients with suspected acute coronary 

syndrome. The aim of this study was to determine whether 

lowering the diagnostic threshold for myocardial infarction with a 

sensitive troponin assay will improve clinical outcomes. 

Methods Consecutive patients admitted with suspected acute 

coronary syndrome before (n¼1038; validation phase) and after 

(n¼1054; implementation phase) lowering the threshold of detection 

for myocardial necrosis from 0.20 to 0.05 ng/ml with a sensitive 

troponin I assay were stratified into three groups:


6 CARDIAC MORBIDITY AND MORTALITY CAN BE 

ACCURATELY PREDICTED IN PATIENTS PRESENTING WITH 

ACS USING MULTIPLE BIOMARKERS MEASURED ON AN 

ADMISSION BLOOD SAMPLE 

doi:10.1136/heartjnl-2011-300198.6 

1 I R Pearson, 1 K Viswanathan, 1 N Kilcullen, 2 A S Hall, 2 C P Gale, 1 U M Sivananthan, 

1 J H Barth, 2 C Morrell. 1 Leeds Teaching Hospitals, Leeds, UK; 2 University of Leeds, 

Leeds, UK 

Background Rapid assessment of patients with suspected acute 

coronary syndrome (ACS) allows the right patients to receive the 

right treatment at the right time. Discrimination of risk permits 

clinical triage into pathways of immediate inpatient or deferred 

outpatient care. It is known that a significant proportion of the 

ACS patients sent home following an “MI screen”, based on a 

negative 12-h troponin level, are misdiagnosed as having noncardiac 

chest pain when in fact they are at high risk of cardiac 

events. It has been shown that the novel biomarker H-FABP can 

detect myocardial ischaemia even in the absence of myocyte 

necrosis. We hypothesise that a multi biomarker blood test incorporating 

troponin I, CK-MB and H-FABP, taken on admission, 

can accurately discriminate those patients with a non-cardiac 

cause of chest pain who are at low risk of cardiac morbidity or 

mortality. 

Methods We studied 519 patients with suspected ACS admitted to 

a single UK Teaching Hospital. A risk scoring model was 

constructed based on tertile values for Randox Cardiac-Array 

measurement of troponin I, H-FABP and CK-MB. These were 

measured on a blood sample taken at the time of hospital admission. 

The lowest two lower tertiles were each given a score of 1 and 

the top tertile a score of 3. The scores were then combined by 

summation resulting in an overall score of between 3 and 9. 

Outcome measures up to 12 months were: (i) death from all causes; 

(ii) repeat acute coronary syndrome (ACS) (iii); readmission for 

heart failure; (iv) readmission for cerebrovascular event (CVA); (v) 

coronary revascularisation. 

Results The distribution of Cardio-Array scores was: 3 (n¼164; 

31.6%); 5 (n¼134; 25.8%); 7 (n¼110; 21.2%); 9 (n¼111; 21.4%). The 

cumulative incidence of events according to the Cardiac-Array score 

is shown in Abstract 6 table 1. 

Abstract 6 Table 1 The cumulative incidence of events according to 

the Cardiac-Array Score 

7 IN ACUTE CORONARY SYNDROMES, HEART-TYPE FATTY 

ACID BINDING PROTEIN IS A MORE ACCURATE PREDICTOR 

OF LONG TERM PROGNOSIS THAN TROPONIN 

doi:10.1136/heartjnl-2011-300198.7 

1 I R Pearson, 2 A S Hall, 2 C P Gale, 1 U M Sivananthan, 1 K Viswanathan, 1 N Kilcullen, 

2 C Morrell, 1 J H Barth. 1 Leeds Teaching Hospitals, Leeds, UK; 2 University of Leeds, 

Leeds, UK 

Introduction We have previously shown that heart-type fatty acid 

binding protein (H-FABP) has a role in predicting all-cause 

mortality after acute coronary syndromes (ACS) and after multivariable 

analysis, provides additional information to that gained 

from the GRACE clinical risk factor score, troponin and highly 

sensitive CRP. H-FABP is released into the circulation during 

myocardial ischaemia and after myocardial necrosis, in contrast to 

troponin which is released after myocardial necrosis only. We 

have also shown that there is a group of ACS patients who are at 

high risk of cardiac events and death despite normal troponin 

levels on admission. This group may benefit from an early invasive 

strategy. 

Hypothesis Plasma H-FABP level, taken between 12 and 24 h after 

admission, can identify troponin negative ACS patients who are at a 

high long term risk of death. 

Methods Six-year mortality data is now available for patients 

enrolled in the FAB 1 study, for which 1-year mortality data was 

published in 2007. In this study, 1448 unselected patients admitted 

to hospital with ACS had serum H-FABP level measured in addition 

to usual care. Mortality was tracked by the UK Office of National 

Statistics. 

Results At 6 years overall all-cause mortality, available for 1421 

patients (98.1%), was 43.5%. If troponin ve/H-FABP ve 

mortality was 20.9%; troponin ve/H-FABP +ve 56.4%; troponin 

+ve/H-FABP ve 20.2%; troponin +ve/H-FABP +ve 49.1%. 

Mortality rate was independent of troponin status but strongly 

related to H-FABP status. 

Conclusion The current system of stratification of ACS patients for 

early invasive management if troponin positive will miss a cohort of 

patients who are at high risk of death despite being troponin 

negative, and who may benefit from invasive investigation. 

Conversely, it is likely that some ACS patients undergo angiography 

based on a false positive troponin level. The addition of H-FABP 

measurement to the management of ACS could avoid this. 

Score Death or ACS or HF or CVA or Revasc 

3 0.61% 3.07% 3.11% 3.11% 4.28% 

5 3.21% 5.77% 5.81% 5.81% 6.41% 

7 11.11% 17.78% 19.05% 20.93% 24.44% 

9 12.98% 16.23% 18.37% 18.92% 22.08% 

Ratio (9/3) 21.28 5.29 5.91 6.08 5.16 

p Value


8 DOES THE ADDITION OF A RADIAL ARTERY GRAFT 

IMPROVE SURVIVAL AFTER HIGHER RISK CORONARY 

SURGERY? A PROPENSITY-SCORE ANALYSIS 

doi:10.1136/heartjnl-2011-300198.8 

1 C H Yap, 

2 P A Hayward, 

2 W Y Shi, 

1 D T Dinh, 

1 C M Reid, 

3,4 G C Shardey, 

3,4 J A Smith. 

1 Department of Epidemiology and Preventative Medicine, Monash 

University, Melbourne, UK; 2 Department of Cardiac Surgery, Austin Hospital, University 

of Melbourne, Melbourne, UK; 3 Department of Cardiothoracic Surgery and Surgery, 

Monash Medical Centre, Monash University, Melbourne, UK; 4 Department of Surgery, 

Monash Medical Centre, Monash University, Melbourne, UK 

Introduction The use of the radial artery as a second arterial graft 

during coronary surgery has become popular due to high patency, 

encouraging clinical outcomes and low harvest site complication 

rates. However it is not clear whether higher risk patients derive 

such benefits. We sought to assess this by examining outcomes in 

higher risk subgroups. 

Methods A multicentre database was analysed. From 2001 to 2009, 

11 388 patients underwent isolated multivessel coronary surgery. We 

identified a higher risk subgroup (n¼3149) according to emergent 

status, coronary instability, low ejection fraction, aortic counterpulsation 

or anticoagulant status. Among these, 2231 (71%) received 

at least 1 radial artery graft in addition to a left internal thoracic 

artery (LITA). The remaining 918 (29%) received LITA and veins 

only. Propensity-score matching and adjustment was performed to 

correct for group differences. 

Results Patients who did not receive a radial artery were more likely to 

be older (mean age, radial: 66610 years vs vein: 71610, p


10 EVALUATING A NURSE LED TRIAGE PROCESS IN TREATING 

PATIENTS WITH LEFT BUNDLE BRANCH BLOCK (LBBB) 

REFERRED FOR PRIMARY PERCUTANEOUS CORONARY 

INTERVENTION (PPCI) 

doi:10.1136/heartjnl-2011-300198.10 

1 N V Joshi, 

2 B R Bawamia, 

2 S Jamieson, 

2 A Zaman, 

2 R Edwards. 

1 Centre for 

Cardiovascular Science, The University of Edinburgh, Edinburgh, UK; 2 The Cardiothoracic 

Centre, Freeman Hospital, Newcastle Upon Tyne, UK 

Background The Freeman Hospital (FRH) performs over 900 pPCI a 

year. Patients with suspected Acute Myocardial Infarction (AMI) are 

referred either by paramedics or networked hospitals for consideration 

of pPCI via a Telmed system, which is triaged by experienced 

CCU nurses. The pPCI Pathway can be activated in patients with 

LBBB suspected of having an AMI. However, there remains 

considerable variation in the clinical utility of new or presumed new 

LBBB as a ST-elevation myocardial infarction (STEMI)-equivalent 

ECG diagnostic criterion. The major discriminators the triage staff 

use in this population are ECG findings and symptoms suggestive of 

AMI. Our aim was to evaluate outcomes in patients with LBBB 

accepted to FRH or referred to local hospitals for assessment. 

Methods Consecutive patients referred to FRH with LBBB and 

suspected AMI from 1st August 2009 to 30th November 2009 were 

analysed by recording: 1) Peak Troponin Level 2) Angiographic 

findings 3) Revascularisation rates. 

Results 1069 patients were referred for consideration of pPCI. 177 

(16.6%) of patients had new or presumed new LBBB. 33 (18.6%) 

patients were accepted by FRH and 144 patients (81.4%) were 

declined and referred to their local hospitals for assessment. Abstract 

10 Table 1 Troponin levels in patients with LBBB referred for 

consideration of pPCI. 26.5% of patients with LBBB referred for 

consideration of pPCI had moderately to highly raised troponin. Of 

the 33 patients admitted to FRH, 13 underwent inpatient angiography 

and 9 patients had significant coronary disease (coronary 

stenosis 70%e100% in at least one coronary artery). Of those, 5 had 

PCI and 1 required urgent CABG. Only one patient had a 100% 

coronary occlusion believed to be an acute occlusion. 4 patients had 

unobstructed coronaries and were managed medically. Of the 132 

patients declined for pPCI only 2 (1.5%) were referred back to FRH 

for PCI. Neither of these patients was found to have a 100% acute 

occlusion of a coronary artery. 


FRH Assessed FRH Declined 

Number of patients 33 144 

Number analysed 33 132 (Biochemistry 

data not found for 

12 patients) 

Troponin levels 

Trop I


Conclusions High plasma copeptin levels indicate a worse outcome 

in NSTEMI patients. We have demonstrated that copeptin fulfils 

AHA criteria by improving risk stratification over established 

markers GRACE score and NT-proBNP. Copeptin is also useful for 

rapid rule-out of MI and the current findings further support clinical 

uptake. 

12 THE RELATIONSHIP BETWEEN PSYCHOLOGICAL FACTORS 

AND IMPAIRED HEALTH-RELATED QUALITY OF LIFE POST 

ST-ELEVATION MYOCARDIAL INFARCTION 

doi:10.1136/heartjnl-2011-300198.12 

1 L McGowan, 2 H Iles-Smith, 1 C Dickens, 1 M Campbell, 1 C Rogers, 2 F Fath-Ordoubadi. 

1 University of Manchester, Manchester, UKI; 2 CMFT, Manchester, UK 

Introduction Evidence suggests that psychological factors, such as 

depression and anxiety, are independent risk factors for increased 

morbidity and mortality post ST-elevation myocardial infarction 

(STEMI). Since improved treatments have increased survival rates 

post STEMI the emphasis has turned to more patient related 

outcome measures such as health-related quality of life (HRQoL). 

The aim of the study was to assess the contribution of anxiety 

and depression to HRQoL in post STEMI patients, after 

controlling for possible confounding factors, including type of 

treatment. 

Methods We conducted a prospective cohort study of 385 post- 

STEMI patients who had undergone either lysis (183) or PPCI (202). 

The mean age was 60.0 years (SD 11.8) and 78% were male. 

Patients were assessed on a range of demographic, clinical and 

psychosocial variables, including measures of cardiac risk, 

cardiac severity and comorbidity (Charlson Comorbidity Indexd 

CCI). Psychosocial assessment included anxiety and depression 

(Hospital Anxiety and Depression Scale), illness perceptions (brief 

IPQ), and health-related quality of life (SF-36). The main outcome 

was the SF-36 Physical Component Score (PCS) at 6 months post- 

STEMI. 

Results Baseline results revealed a small number significant differences 

between groups on a range of clinical variables, including 

higher GRACE scores for PPCI group (p¼0.007) but no differences in 

LV function. Lysis patients had more comorbid illness as measured 

by the CCI (p¼0.037). Regarding psychological variables the total 

HADS score was significantly higher in the PPCI vs lysis group at 

baseline (means 13.2 (SD 7.9) and 11.4 (SD 8.9), p¼0.035), while 

anxiety and depression almost reached significance, with raised 

anxiety and depression scores in the PPCI group. In order to identify 

variables at baseline that may contribute to SF-36 PCS at 6 months, 

we conducted a hierarchical multiple regression with four blocks of 

independent variablesddemographic, comorbidity-related, clinical 

and psychological. Factors which contributed to the final model 

were cholesterol levels (p¼0.031) and depression (p


Abstract 14 Figure 1 


MI, relating these to global and segmental myocardial function at 

6 months. 

Methods and Results CMR scans were performed on 30 patients 

with ST elevation MI (STEMI) treated by primary PCI at each of 4 

time points: 12e48 h (TP1); 5e7 days (TP2); 14e17 days (TP3); and 

6 months (TP4). All patients showed oedema at TP1. The mean 

volume of oedema (% LV) was 37616 at TP1 and 39617 at TP2 


14 DYNAMIC CHANGES OF OEDEMA AND LATE GADOLINIUM 

ENHANCEMENT AFTER ACUTE MYOCARDIAL INFARCTION 

AND THEIR RELATIONSHIP TO FUNCTIONAL RECOVERY 

AND SALVAGE INDEX 

doi:10.1136/heartjnl-2011-300198.14 

1 E Dall’Armellina, 1 N Karia, 1 A Lindsay, 1 T D Karamitsos, 1 V Ferreira, 1 M D Robson, 

2 P Kellman, 1 J M Francis, 3 C Forfar, 3 B Prendergast, 3 A P Banning, 1 K Channon, 

3 R J Kharbanda, 1 S Neubauer, 1 R P Choudhury. 1 NIHR Biomedical Research Centre, 

Department of Cardiovascular Medicine, University of Oxford, Oxford, UK; 

2 NIH, 

Bethesda, USA; 3 NIHR Biomedical Research Centre, Department of Cardiology, John 

Radcliffe Hospital, Oxford, UK 

Introduction Changes in myocardial tissue in acute ischaemia are 

dynamic and complex and the characteristics of myocardial tissue 

on cardiovascular magnetic resonance (CMR) in the acute setting 

are not fully defined. We investigated changes in oedema and late 

gadolinium enhancement (LGE) with serial imaging early after acute 




with a reduction to 24613 (p


percutaneous coronary interventions (PCI). The incidence is 

increasing and to date outcomes are not well characterised, though 

there is a suggestion that there is a worse clinical outcome. 

We therefore sought to compare STEMI caused by ST vs de novo 

coronary thrombosis to evaluate procedural risk and clinical outcome. 

Methods Clinical information was analysed from a prospective 

database on 2421 patients who underwent Primary PCI following 

STEMI between October 2003 and May 2010 at a London centre. 

Information was entered at the time of procedure, diagnosis of stent 

thrombosis made at the time by primary operator and outcome 

assessed by all-cause mortality information provided by the Office 

of National Statistics via the BCIS CCAD national audit. 

Results Stent thrombosis (ST) accounted for 7.4% (180/2421) of all 

STEMIs with a frequency that has increased over time (5.4% in 2005 

to 9.8% 2009). ST occurred early (0e30 days) in 36% (65/180), late 

(30 dayse1 year) in 22% (40/180) and very late (>1 year) in 42% (75/ 

180) of pts. Drug-eluting stents (DES) accounted for 48% of SToverall 

and 70% over the past 3 years. Proposed mechanisms included 

premature discontinuation of anti-platelets (11%), under-deployment 

of previous stent insertion (22%) and underlying prothrombotic 

conditions (eg, SLE) (6%). Pts with ST compared to native artery 

occlusion had higher rates of previous MI (53.9% vs 11%, p


slowing dramatically from 2006 to 2008. JoinPoint regression analysis 

of different age groups demonstrates that the slower rate of 

decline from 2006 may be due to stubbornly high numbers of deaths 

in the 35e44 age group. Lastly the National figures on mortality 

from CHD are shown to be misleading as many people are still 

dying from CHD just when they have crossed the 75-year old 

exclusion criteria; as a result a delay in mortality is presented as 

prevention of mortality from CHD. 

Discussion There is a danger that previous successes are being offset 

by high rates in the younger cohorts, and that the overall trend may 

be eventually be reversed. There is still work to be done in reducing 

risk factors and also applying treatments that have had a proven 

positive impact (such as revascularisation) more effectively. Statistically 

significant changes in declining CHD mortality rates. 

Future work This 10 000 word report formed the basis of a funding 

application to the British Heart Foundation for a follow-up to the 

United Kingdom Heart Attack Study. 

figure 1. After adjusting for comorbidities, anaemia remained an 

independent predictor of long-term adverse outcome (OR¼2.4, 95% 

CI¼1.1 to 3.7, p


up to 1-year of follow-up with the lowest rates of events in the SR 

group. However after 3 years MACE rates are significantly increased 

in the COR group (24%) but were similar in the CR (18%) and SR 

(17%) groups. See Abstract figure 1. MACE rates were driven mainly 

by death in the CR with high rates of TVR in the COR and SR 

groups. See Abstract figure 2. 


COR N[638 SR N[100 CR N[263 Significance 

Age 64.77 61.46 64.32 0.144 

Gender (female) 156 (23.7%) 13 (13.0%) 74 (27.9%) 0.0114 

Ethnicity (Caucasian) 441 (67.0%) 79 (79.0%) 185 (69.8%) 0.0511 

Previous MI 109 (16.6%) 11 (11.0%) 36 (13.6%) 0.2414 

Previous CABG 15 (2.3%) 2 (2.0%) 3 (1.1%) 0.5231 

Previous PCI 83 (12.6%) 5 (5.0%) 23 (8.7%) 0.031 

Diabetes Mellitus 129 (19.6%) 16 (16.0%) 55 (20.8%) 0.5932 

Hypertension 312 (48.1%) 40 (40.0%) 91 (41.2%) 0.1205 

Hypercholestrolaemia 269 (41.5%) 37 (37.0%) 92 (41.6%) 0.7751 

GPIIb/IIIa Inhibitor 572 (87.7%) 93 (93.0%) 231 (89.5%) 0.1724 

Cardiogenic Shock 29 (4.7%) 2 (2.0%) 31 (12.26%) p


Setting The cardiac catheterisation laboratory in a regional heart 

centre in the UK. 

Definitions The clinical indication for FFR measurement was the 

presence of an intermediate coronary stenosis (50%e75% of the 

reference vessel diameter) which resulted in diagnostic and treatment 

uncertainty. FFR measurement was used to provide functional 

information on lesion severity and an FFR


predictive of CIN development (p2 cardiologists and 2 

cardiothoracic surgeons with a special interest in mitral valve 

surgery prior to being accepted. 

Results Mitraclip therapy was attempted in 24 patients aged 

71611 years with an average Euroscore of 16%. The indication for 

intervention was functional MR in 10 patients (42%), ischaemic MR 

in 7 patients (29%) and degenerative MR in 7 patients (29%). Twenty 

patients had successful deployment of the Mitraclip device (83%). 

Fifteen patients (75%) had 2 clips deployed. There were no vascular 

complications or strokes. We were unable to grasp the mitral valve 

leaflets in 2 patients due to an excessive coaptation gap. There was 1 

procedural death due to leaflet tear in a patient with end-stage 

ischaemic cardiomyopathy and a grossly dilated left ventricle. All 

patients (100%) treated with the Mitraclip had severe MR (grade 3 

+/4+) prior to intervention. Mitral regurgitation was graded by 

colour Doppler alone following intervention as standard quantitative 

analyses are not validated in the presence of a Mitraclip. At 1-month 

Abstract Figure 1 

Abstract Figure 2 

Change in MR grade post-Mitraclip. 

Change in NYHA class post-Mitraclip. 



25 TAVI OPERATOR RADIATION DOSE COMPARED TO PCI AND 

ICD OPERATORS: DO WE NEED ADDITIONAL RADIATION 

PROTECTION FOR TRANS-CATHETER STRUCTURAL HEART 

INTERVENTIONS 

doi:10.1136/heartjnl-2011-300198.25 

M Drury-Smith, A Maher, C Douglas-Hill, R Singh, M Bhabra, J Cotton, S Khogali. 

Heart and Lung Centre, New Cross Hospital, Wolverhampton, UK 

Introduction Trans-catheter cardiac aortic valve implantation 

(TAVI), implantable cardiac defibrillators (ICD), and percutaneous 

coronary intervention (PCI), are common procedures associated 

with radiation exposure to the operator and the patient. Radiation 

dose exposure is cumulative and if above the recommended annual 

levels may have significant consequences for the operator. The 

radiation dose TAVI operators are exposed to is not widely known, 

but it is an important consideration in view of the increasing 

volume of procedures and the potential risks of over-exposure. Our 

aim was to monitor and compare, radiation exposure time, dose, and 

individual operator dose, in TAVI, PCI and ICD. 

Method Ten TAVIs were performed, 6 via the trans-femoral route and 4 

via the subclavian approach. Radiation protection was employed in all 

cases using standard lead skirts and screens. During each procedure the 

radiation dose exposure was monitored for each operator using ThermoLuscent 

Dosemeters (TLD) on the left finger (LF), right finger (RF) 

and forehead. The six TAVI procedures performed via the transfemoral 

approach used only two operators, while the subclavian approach 

involved three operators. The third operator was a surgeon who was 

nearest to the x-ray images. Radiation exposure doses were also 

collected from ICD and PCI operators during the same period, using the 

same type of TLDs on LFand RF. Operator specific radiation doses were 

obtained from a central RRPPS Approved Dosimetry Service. PCI was 

considered a standard trans-catheter procedure. TAVI and ICD operator 

doses were compared to the mean standardised PCI operator dose. 

Results The mean exposure times and doses for the different types 

of trans-catheter procedures performed are detailed in the tables 

below. Despite the use of standard radiation protection measures, 

the mean dose to operators undertaking TAVI was 6 times higher 

than the trans-femoral PCI operator (p¼0.008). The mean radiation 

exposure time of TAVI was seven times more than PCI. Although 

subclavian TAVI and ICD procedures were expected to be comparable 

with respect to operator dose, subclavian TAVI operators have 

an unexpectedly higher dose (p¼0.03). 

Conclusions Overall TAVI operators are exposed to significantly 

higher radiation doses compared to PCI and ICD operators. Additional 

radiation protection for TAVI operators is strongly advocated. 

We are currently evaluating the impact of using a RADPAD as 

additional protection during TAVI procedures. 


Variable TAVI ICD PCI p Value 

Mean exposure Time (mins) 27.0* 3.26 3.825


Results As expected CwP was higher in patients with NSTEMI 

(46.5 (SD) 18.8) compared with the stable angina patients (Mean 

(SD) 21.1 (9.3) p¼0.01). IMR was also higher in patients with 

NSTEMI (Mean (SD) 27.6 (12.6)) compared with patients with 

stable angina (Mean (SD) 20.7 (5.4) p¼0.2). Total PMAs were nonsignificantly 

higher in patients with NSTEMI (Mean (SD) 14 

(4.8)) compared with stable angina (Mean (SD) 10.9 (4.3) p¼0.07). 

CD62+ PMAs were significantly higher in patients with NSTEMI 

(Mean (SD) 26.9 (12.2)) compared with stable angina (Mean (SD) 

13.7 (5.1) p¼0.02) Abstract 27 figure 1. CwP correlated positively 

with total PMA (p¼0.01) in NSTEMI but not in stable angina 

patients. However, IMR correlated positively with total PMAs in both 

stable angina (p¼0.02) and NSTEMI (p¼0.08) Abstract 27 figure 2. 


study. As yet, the impact of PCI to significant CAD upon outcome 

after TAVI is not known and will be assessed in a prospective, 

randomised controlled trial currently underway. 

27 PLATELET MONOCYTE AGGREGATES ARE DETERMINANTS 

OF MICROVASCULAR DYSFUNCTION DURING 

PERCUTANEOUS CORONARY INTERVENTION FOR STABLE 

ANGINA AND NON-ST SEGMENT ELEVATION MYOCARDIAL 

INFARCTION 


doi:10.1136/heartjnl-2011-300198.27 

1 C A Mavroudis, 1 B Majumder, 2 M Lowdell, 1 R D Rakhit. 1 Cardiology Department, Royal 

Free Hospital, London, UK; 2 Haematology Department, Royal Free Hospital, London, UK 

Background Microvascular dysfunction is associated with adverse 

outcome in patients with acute coronary syndrome (ACS). During 

ACS platelet and monocyte derived chemokines, in conjunction 

with adhesion molecule expression, promote the inflammatory 

process. Activated platelets express p-selectin which binds to the p- 

selectin glycoprotein ligand on the monocyte forming platelet 

monocyte aggregates (PMA). PMA expression is a sensitive marker 

of platelet activation and inflammation. Although platelet monocyte 

interaction is a normal physiological process, in the presence of 

platelet activation, activated (CD62+ PMA) may be directly 

involved in the pathophysiology of intracoronary inflammation and 

microvascular dysfunction in ACS. 

Aim To investigate the relationship between microvascular 

dysfunction and PMA expression in patients with stable angina and 

non-ST elevation myocardial infarction (NSTEMI). 

Methods Six patients with stable angina undergoing elective PCI and 

six patients with NSTEMI undergoing non-elective PCI were recruited. 

Microvascular dysfunction was assessed by measuring the coronary 

wedge pressure (CwP) and the index of Microvascular resistance (IMR) 

using a single pressure-temperature sensor-tipped coronary wire from 

the simultaneous measurement of distal coronary pressure and thermodilution 

derived mean transit time (Tmn) of a bolus of saline 

injected at room temperature into the coronary artery during 

maximum hyperaemia. Blood samples were taken from the coronary 

artery (distal to the culprit lesion), aorta and the right atrium for PMA 

estimation. PMAs were assessed using fluorescent monoclonal antibodies 

and flow cytometry. Total PMAs were calculated and expressed 

as a percentage of the total monocyte count. Activated CD62+ PMAs 

were expressed as a percentage of total PMAs. 


Conclusions PMAs are elevated in stable coronary disease and ACS 

with elevated activated CD62+ PMA a hallmark of ACS. PMAs 

correlate with measured microvascular dysfunction during PCI in 

stable angina and NSTEMI. This study supports the hypothesis that 

PMA formation may be important determinants of platelet activation, 

inflammation and microvascular dysfunction in coronary disease. 

28 LOW FRAME RATE SCREENING DURING PERCUTANEOUS 

CORONARY ANGIOPLASTY SIGNIFICANTLY REDUCES 

RADIATION EXPOSURE, GIVES GOOD IMAGE QUALITY 

WITHOUT AFFECTING PATIENT OUTCOME 

doi:10.1136/heartjnl-2011-300198.28 

1 S J Wilson, 1 P Venables, 2 O Gosling, 1 V Suresh. 1 South West Cardiothoracic Centre, 

Plymouth, UK; 2 Royal Devon and Exeter Hospital, Exeter, UK 

Introduction Minimisation of radiation exposure during cardiac 

procedures is required by statute (IRMER 2000). During coronary 

angioplasty 47% of radiation dose is related to screening at standard 




Screening 

DAP (mGycm 2 ) 

Total DAP 

(mGycm 2 ) 

Fluoro time 

(seconds) 

Standard (15 fps) 28564.5 60746.9 770 26.7 

Low (7.5 fps) 19248.5 50953.4 800 26.8 

Mean DAP reduction 33% 16% e e 

Significance p


patients who suffered acute ST was 20%, compared to 80% 

following subacute ST. There was no difference in outcomes 

between bivalirudin treated patients who also received heparin 

compared to those who didn 9 t (death 7.0% vs 5.0%, p value: 0.80; 

MACE 14.0% vs 10.8%, p value: 0.32; acute ST 0% vs 1.2%, p: 0.61). 


Outcomes at 30 days 

All patients Bivalirudin GPI + heparin p value 

No. of patients 968 882 85 

Death 52 (5.4%) 46 (5.2%) 6 (7.1%) 0.450 

Cardiac death 45 (4.7%) 39 (4.4%) 6 (7.1%) 0.277 

Re-infarction 16 (1.7%) 14 (1.6%) 2 (2.4%) 0.645 

Unplanned TVR 12 (1.2%) 10 (1.1%) 2 (2.4%) 0.286 

Stroke 56 (5.8%) 54 (6.1%) 2 (2.4%) 0.222 

Death, re-infarction, stroke or TVR 110 (11.4%) 100 (11.3%) 10 (11.8%) 0.906 

Acute stent thrombosis 10 (1.0%) 9 (1.0%) 1 (1.2%) 0.604 

Subacute stent thrombosis 15 (1.6%) 13 (1.5%) 2 (2.4%) 0.386 

Conclusion Routine use of bivalirudin in a large UK all-comers 

primary PCI population was associated with excellent 30-day 

outcomes, including all-cause and cardiac mortality. Acute stent 

thrombosis was infrequent, despite the absence of routine additional 

heparin. 

p¼1.0 respectively). Even though the bleeding risk was higher in the 

abciximab group when compared with bivalirudin, this was not 

significant (5.8% vs 3.1%, p¼0.27). There was also no difference in 

the outcomes between the bivalirudin and “UFH only” groups for 

mortality, stent thromboses (acute and 30-day) and major bleeding. 

The abciximab group had significantly higher major bleeding rates 

than the “UFH only” group (5.8% vs 2.4%, p¼0.04); all other 

outcomes were similar. 


Abciximab + 

UFH (n[346) 

Age in yrs (range) 64614.1 

(25e99) 

Bivalirudin + 

UFH (n[162) 

65613.0 

(31e94) 

UFH only 

(n[253) 

67613.2 

(30e96) 

Male (%) 77.7 72.2 66.8 

Diabetes (%) 12.4 6.2 11.5 

Pre-procedure cardiogenic shock (%) 7.8 6.2 4.7 

Drug eluting stent (at least one) (%) 56.1 56.8 53.8 

No of stents 1.460.9 1.460.8 1.460.9 

Single vessel PCI (%) 91.3 87 89.3 

Three vessel PCI (%) 1.4 1.9 2 

Radial procedure (%) 28 26.5 31.2 


30 COMPARISON OF BIVALIRUDIN VS ABCIXIMAB VS 

“UNFRACTIONATED HEPARIN ONLY” FOR PRIMARY 

PERCUTANEOUS CORONARY INTERVENTION IN A HIGH- 

VOLUME CENTRE 

doi:10.1136/heartjnl-2011-300198.30 

R Showkathali, J Davies, N Malik, W Taggu, J Sayer, R Aggarwal, P Kelly. The Essex 

Cardiothoracic Centre, Basildon, UK 

Introduction Primary percutaneous coronary intervention (PPCI) has 

been established as a standard therapy for ST elevation myocardial 

infarction (STEMI). In addition to thrombectomy and unfractionated 

heparin (UFH), thrombus burden in STEMI may require use 

of more potent antithrombotic agents. Bivalirudin is shown to be 

superior to abciximab in reducing the net adverse clinical events and 

major bleeding in STEMI in the HORIZONS-AMI trial (Stone et al 

NEJM, 2008). We aimed to carry out a “real world” comparison of 

different anti-thrombotic regimes in patients undergoing PPCI in 

our unit. 

Methods Our PPCI service started in September 2009 and we 

included all patients undergoing PPCI between September 2009 and 

September 2010. Prospectively entered data were obtained from our 

dedicated cardiac service database system (Philips CVIS). Mortality 

data were obtained from the summary care record (SCR) database. 

We used Fisher 9 s exact test to compare clinical outcomes between 

the groups. 

Results Of the 998 patients admitted with suspected STEMI to our 

unit during the study period, 776 (77.8%) underwent PPCI. After 

excluding patients who had both bivalirudin and abciximab during 

their procedure (n¼15), we divided the others (n¼761) into 3 groups 

according to the anti-thrombotic regime used (Grp 1- Abciximab 

+UFH, Grp 2- Bivairudin+UFH and Grp 3- “UFH only”). Patient 

demographics and procedural information are given in Abstract 30 

table 1. Continuous data are presented as mean6 SD. Clinical 

outcomes are shown in Abstract 30 table 2. In-hospital and 30-day 

mortality did not differ between patients who had bivalirudin vs 

abciximab (5.6% vs 3.8%, p¼0.35 and 6.8% vs 5.2% p¼0.53 

respectively). Both acute and 30 day stent thrombosis rates were 

also similar in the two groups (0.6% vs none, p¼0.3, 0.6% vs 0.9%, 

% 

Abciximab + 

UFH (n[346) 

Bivalirudin + 

UFH (n[162) 

UFH only 

(n[253) 

In-hospital Mortality (including 

3.8 5.6 5.1 

cardiogenic shock) 

30 day Mortality (including cardiogenic 5.2 6.8 7.1 

shock) 

30 day Mortality (excluding cardiogenic 3.5 4.9 5.5 

shock) 

Stent Thrombosis (within 30 days) 0.9 0.6 1.2 

Acute stent Thrombosis (24 h) # 0 0.6 0.4 

Major bleed requiring blood transfusion 5.8 3.1 2.4 

(non CABG related) 

Access related bleed requiring 

transfusion (includes IABP related) 

3.8 1.9 1.2 

Conclusion These “real-world” data do not show any significant 

difference in the clinical outcome for patients who had bivalirudin 

or abciximab. There was no advantage seen with the more expensive 

agent (abciximab) in keeping with previous trial data. Therefore 

bivalirudin should be considered as a non-inferior alternative to 

abciximab. This would have considerable economic benefits in the 

present situation. The “UFH only” group had similar outcomes to 

both bivalirudin and abciximab, which suggests that this may be a 

viable alternative in its own right. However, our study is clearly 

limited by not being randomised and those patients treated with 

UFH alone may have been a lower risk group. 

31 ASSESSMENT OF LEFT VENTRICULAR FUNCTION WITH 

CARDIAC MRI AFTER PERCUTANEOUS CORONARY 

INTERVENTION FOR CHRONIC TOTAL OCCLUSION 

doi:10.1136/heartjnl-2011-300198.31 

1 G A Paul, 2 K Connelly, 1 A J Dick, 1 B H Strauss, 3 G A Wright. 1 Sunnybrook Health 

Sciences Centre, Toronto, Ontorio, Canada; 2 St Michaels Hospital, Toronto, Ontorio, 

Canada; 3 University of Toronto, Toronto, Ontorio, Canada 

Objective To assess the role of CMR in the treatment of true chronic 

total occlusions (CTO) with percutaneous coronary intervention 

(PCI) and drug eluting stent implantation. 



Introduction Successful PCI for CTO may confer an improved 

prognosis and a reduction in major adverse cardiac events (MACE). 

However most trials have included occlusions of short duration (less 

than 4 weeks). In this study we assessed the impact of PCI on LV 

function in patients with true CTOs (TIMI flow grade 0 and greater 

than 12 weeks duration) using serial CMR imaging as well as the 

predictive value of late gadolinium enhancement when performed 

prior to revascularisation. 

Methods Thirty patients referred for PCI to a single vessel CTO 

underwent CMR examination prior to and 6 months after PCI. 

Technical success was defined as recanalisation of the occluded 

vessel and DES implantation with a final residual diameter stenosis 


dysfunction. Over a follow-up period of 2.661.1 years there were 42 

deaths. All-cause mortality was inversely related to baseline BCIS-1 

JS (HR 2.20 (1.34 to 3.62), p¼0.002) and to post-PCI BCIS-1 JS (HR 

3.98 (2.33 to 6.78), p¼0.0001). Increasing degrees of revascularisation 

were associated with improved survival (Abstract 33 figure 1); a 

revascularisation index of $ 0.67 was associated with a survival 

advantage compared to a RI #0.66 (HR 0.39 (0.24 to 0.54), p¼0.0001) 

(Abstract 33 table 2). A multiple regression model, incorporating age, 

acuity of presentation, LV function and renal failure, demonstrated 

that RI¼0.67e1 continued to be an independent predictor of survival 

(HR 0.51 95% CI 0.35 to 0.81, p¼0.004) (Abstract 33 figure 1). 


33 COMPLETENESS OF REVASCULARISATION PREDICTS 

MORTALITY FOLLOWING PERCUTANEOUS CORONARY 

INTERVENTION: UTILITY OF THE BCIS-1 JEOPARDY SCORE 

doi:10.1136/heartjnl-2011-300198.33 

K De Silva, G Morton, P Sicard, E Chong, A Indermeuhle, B Clapp, M Thomas, 

S Redwood, D Perera. St. Thomas’ Hospital, King’s College London, London, UK 

Introduction Many coronary-scoring systems are complicated to use 

on a day-to-day basis, have varying degrees of reproducibility and 

exclude important subsets of patients such as those with previous 

coronary artery bypass grafts (CABG) or left main stem (LMS) 

disease (Abstract 33 table 1). The recently described BCIS-1 

Myocardial Jeopardy score (BCIS-1 JS), a modification of the Duke 

Jeopardy score to include LMS and CABG, is simple to use and 

overcomes many of these limitations. We assessed the prognostic 

relevance of the BCIS-1 JS in patients undergoing percutaneous 

coronary intervention (PCI). 


Left Main 

Stem Disease 

classified 

Duke Jeopardy 

Score (Original) 

Patients 

with CABG 

classified 

Ease 

of use 

Relevance to 

contemporary PCI 

x x O x O 

Syntax Score O x x O O 

BCIS-1 JS O O O O x 

Prognostic 

validation 

Methods Consecutive patients undergoing PCI between 2005 and 

2009 a single cardiac centre were screened. Patients were eligible if 

they had undergone assessment of left ventricular function before 

PCI and the sample was enriched for coronary artery bypass graft 

(CABG) cases by using the following weightingd1 CABG: 3 non- 

CABG. Clinicians (who were blinded to clinical or outcome data) 

scored diagnostic and procedural coronary angiograms. The BCISd1 

JS was recorded before and after PCI (range: 0 to 12) and a Revascularisation 

Index (RI) calculated as RI¼(JS PRE dJS POST )/JS PRE . 

RI¼1.0 indicates full revascularisation and 0 indicates no revascularisation. 

The primary end-point was all-cause mortality. Mortality 

data was captured by tracking the database of the UK Office of 

National statistics. Predictors of outcome were assessed by 

univariate and multivariate analyses. 

Results 660 patients were included (6869 years). 44% presented as 

acute coronary syndromes with 41% having left ventricular 

Cumulative survival according to Revascularisa- 


tion Index (RI). 


Variables 

Univariate analysis 

HR (95% CI) p value 

Multivariate 

analysis HR (95% CI) p value 

Revascularisation 0.36 (0.24 to 0.54) 0.0001 0.51 (0.33 to 0.81) 0.004 

Index (0.67e1) 

BCIS-1 JS pre PCI 1.26 (1.14 to 1.39) 0.0001 1.14 (0.65 to 2.02) 0.65 

BCIS-1 JS post PCI 1.35 (1.23 to 1.48) 0.0001 1.78 (0.93 to 3.39) 0.08 

LV impairment 3.76 (2.53 to 5.58) 0.0001 1.97 (1.21 to 3.20) 0.007 

Age 1.04 (1.01 to 1.08) 0.01 1.04 (1.00 to 1.08) 0.05 

Renal dysfunction 5.82 (2.77 to 12.24) 0.0001 3.74 (1.60 to 7.37) 0.002 

Acute coronary 2.31 (1.24 to 4.30) 0.008 1.30 (0.63 to 2.66) 0.47 

syndrome 

Cardiogenic shock 14.56 (6.45 to 32.88) 0.0001 2.83 (0.69 to 11.54) 0.15 

Previous CABG 3.35 (1.80 to 6.25) 0.0001 1.83 (0.88 to 3.82) 0.10 

Conclusion The BCIS-1 Jeopardy Score predicts mortality following 

PCI. Furthermore, it can be used to assess the degree of revascularisation, 

with more complete revascularisation (RI$0.67) conferring 

a survival advantage in the medium term. 

34 COMPARISON OF PCI VS CABG IN INSULIN TREATED AND 

NON-INSULIN TREATED DIABETIC PATIENTS IN THE 

CARDIA TRIAL 

doi:10.1136/heartjnl-2011-300198.34 

1 A Baumbach, 2 S Kesavan, 3 K Beatt, 4 E Cruddas, 4 M Flather, 2 G Angelini, 5 R Hall, 

6 A Kapur. 

1 Bristol Heart Institute, Bristol, UK; 

2 Bristol Heart Institute, Bristol, UK; 



3 Mayday University Hospital, London, UK; 4 Royal Brompton, London, UK; 5 Imperial 

College, London, UK; 6 London Chest Hospital, London, UK 

Aims The CARDia trial randomised diabetic patients to coronary 

artery bypass grafting (CABG) or percutaneous coronary intervention 

(PCI) and concluded that PCI is a potentially safe and feasible alternative 

to CABG in selected patients with diabetes mellitus (DM) and 

multivessel coronary artery disease. The impact of insulin treatment 

on clinical outcomes after revascularisation is unclear. The present 

study is a sub group analysis of the CARDia trial comparing the 

cardiovascular outcomes at 12 months following revascularisation 

between the insulin treated (IT) and non-insulin treated (NIT) group. 

Methods 508 patients with an established diagnosis of DM and de 

novo coronary artery disease were identified and randomised to 

CABG or PCI. Of those, 316 patients were treated with oral antidiabetic 

medication and the rest were treated with additional 

subcutaneous insulin injections. Demographics, clinical presentation, 

history, haemodynamic parameters, anti diabetic therapy, concomitant 

medications, duration of DM and HBA1C were documented. 

Death, stroke and myocardial infarction were classified as the primary 

outcome events. The secondary outcome events included death, MI, 

Stroke, repeat revascularisation and TIMI major bleed. The clinical 

results of patients in the ITand NIT groups were compared. 

Results There were 192 patients in the IT group (37.8%). Asian 

patients constituted one fifth of the total population with a slightly 

higher representation (24.5% vs 21.6%) in the NIT. The clinical 

severity of dyspnoea, heart rate, systolic and diastolic BP, body mass 

index, risk factors for coronary artery disease appeared similar in the IT 

and NIT groups, but more patients in the IT group had a prior MI 

(30.7% vs 19.6%, p¼0.004) and duration of diabetes was longer in the 

IT group (14 vs 6 yrs, p


event, more recent studies suggested that a reasonable amount of 

patients with ISR many develop ACS as the first manifestation of this 

adverse event. The aim of this study was to determine the different 

clinical presentations of ISR in a large cohort of consecutive, nonselected 

patients and compare with native coronary disease. 

Methods 14 445 consecutive patients underwent PCI at a single centre 

(October 2003eMay 2010), we identified 922 (6.4%) cases presenting 

with restenosis after previous PCI. All patients with restenosis 

presented with new or recurrent symptoms. Demographic and procedural 

data were collected at the time of intervention (Abstract 36 

table 1). In-hospital MACE (myocardial infarction, urgent revascularisation, 

stroke or death) was documented at discharge. All cause 

mortality data was obtained from the Office of National Statistics via 

the BCIS/CCAD national audit out to 3.2 years (mean 3.161.8 years). 


Restenosis Native disease Sig 

Total 

n[922 n[13 523 e 

Age 63.09 63.76 0.0868 

Ethnicity (cau) 683 (74.2%) 9160 (97.8%) p


illustrated that use of BMS was independently associated with 

increased risk of MACE (HR 1.54; 95% CI 1.05 to 2.25, p¼0.03), 

driven through an increase in revascularisation. 

Conclusion In conclusion, in one of the largest analyses of its kind, 

use of DES in patients with diabetes in a real world setting undergoing 

PCI in large diameter coronary vessels ($3 mm) is safe and is 

independently associated with a reduction in MACE events. This is 

in contrast to that of non-diabetic patients where the benefits of 

DES in large diameter coronary vessels are less evident. 

38 FALSE ACTIVATION FOR PRIMARY PERCUTANEOUS 

CORONARY INTERVENTION IS NOT A BENIGN 

PHENOMENON 

doi:10.1136/heartjnl-2011-300198.38 

U Chaudhry, C Mavroudis, R D Rakhit. Cardiology Department, Royal Free Hospital, 

London, UK 

Introduction Primary percutaneous coronary angioplasty (PPCI) is 

the preferred reperfusion strategy following an acute ST elevation 

myocardial infarction (STEMI). Since 2005 24/7 primary PCI has 

been the first line treatment for an acute STEMI in our centre. 93% 

of patients are direct access admissions by London Ambulance but a 

significant proportion (up to 20%) do not fulfil the diagnostic 

criteria for STEMI and are termed “false activations”. Data on the 

outcome of this cohort of patients is limited. 

Aim To review the clinical outcome of patients presenting to our 

heart attack centre with false activation PPCI. 

Method From January 2008 until October 2010, we identified 209 

false PPCI activations defined as patients with incomplete diagnostic 

criteria for acute STEMI: absence of chest pain and/or typical 

ECG features (ST elevation or new LBBB). Data was collected via a 

“false activation” database together with retrospective review of case 

records. 

Results Complete data was available in 165 cases. 71% were male 

and 29% were female (mean age 67). The mean length of stay was 

4 days (range 1e33). 71% presented with chest pains and 29% had 

no chest pains, but presented with breathlessness, palpitations or 

syncope. The ECG abnormality was non-specific ST-T changes in 

22%, LBBB in 19%, left ventricular hypertrophy in 15%, fixed ST 

elevation or Q waves in 14%, early repolarisation changes in 10%, 

RBBB in 8% and other ECG abnormalities in 12%. The final diagnosis 

was non-STelevation acute coronary syndrome (NSTEACS) in 

19%, sepsis in 19% and congestive heart failure (CHF) in 15%. Stable 

angina was observed in 8% and syncope in 7%. Musculoskeletal or 

non-cardiac chest pains were noted in 8% and 7% of the patients 

respectively. 2% of the patients had pulmonary embolism and in 5%, 

a gastric cause for presentation was diagnosed. 14% had other 

cardiac problems, including arrhythmia, dilated cardiomyopathy, 

hypertension, pericarditis, pericardial effusion and late presentation 

STEMI. 15% had other diagnoses. The mean follow-up period was 

18.7 months, during which 21.5% of false PPCI activation admissions 

died (n¼45). 25% (n¼11) died during the index admission and 

33% (n¼15) died within 30 days of admission. The overall 30-day 

mortality for false activations was 7.2%, which is higher than the 

overall PPCI mortality of 6.0% (including cardiogenic shock) 

(p¼0.008) and 3.3% (excluding shock) (p


particular the differences between physician and patient reported 

outcomes has not been analysed. High quality data from the Stent 

or Surgery (SOS) trial allows such an analysis. 

Methods The SoS trial was a large RCT (n¼988) comparing stentassisted 

percutaneous coronary intervention (PCI) with coronary 

artery bypass grafting (CABG) in patients with multivessel CAD. 

Participation in the SoS trial included an appraisal of angina symptoms 

by both patient and physician according to the Canadian Cardiovascular 

Society (CCS) Classification System prior to, and subsequently 

at 6 and 12 months following coronary intervention. In this study 

patient and doctor reported outcomes were compared systematically. 

Results Paired CCS scores at baseline, 6 months and 12 months were 

available for 919, 886 and 888 cases respectively. At baseline the overall 

level of agreement was good with >75% paired data sets demonstrating 

a difference of #61 CCS class. Patterns of discordance change however 

between baseline and follow-up time points. Abstract 40 figure 1 shows 

the paired scores at baseline, charting the patient score and, for each 

CCS grade, the observed differenceddoctor (D) minus patient (P). 

Doctors are reluctant to record scores of 0 or 4, preferring CCS grades 2 

and 3. Thus there is little overall difference in mean CCS score (P 2.2 vs 

D2.5,p


London, UK; 2 Clinical Pharmacology, St Thomas Hospital, KCL, London, UK; 3 Department 

of Bio-Engineering, University of Amsterdam, AMC, Amsterdam, The Netherlands 

Background The mechanisms of the clinically observed phenomenon 

of reduced angina on second exertion, or warm-up angina, are 

poorly understood. This study compared changes in central 

haemodynamics, peripheral wave reflection and patterns of coronary 

blood flow during serial exercise that may contribute. 

Methods and Results 16 patients (15 male, 6164.3 yrs) with a positive 

exercise stress test and exertional angina completed the protocol. 

During cardiac catheterisation via radial access they performed 2 

consecutive exertions (Ex1, Ex2) using a supine cycle ergometer. 

Throughout exertions, distal coronary pressure (P d ) and flow velocity 

(V) were recorded in the culprit vessel using a dual sensor coronary 

guide wire while aortic pressure was recorded using a second wire. 

Time to 1 mm ST depression was longer in Ex2 (p¼0.003) and rate 

pressure product (RPP) was higher (p¼0.025) confirming warm-up. A 

33% decline in aortic wave reflection (p33) 

43 PROGNOSIS AFTER PRIMARY PERCUTANEOUS CORONARY 

INTERVENTION FOR STEMI: CAN THE SYNTAX SCORE HELP? 

doi:10.1136/heartjnl-2011-300198.43 

A J Brown, L M McCormick, N E J West. Papworth Hospital, Cambridge, UK 

Background Factors affecting prognosis after primary percutaneous 

coronary intervention (PPCI) for ST-elevation myocardial infarction 

(STEMI) include age at presentation, the presence of diabetes mellitus, 

left ventricular function and/or cardiogenic shock. Although the 

debate continues over a strategy of complete revascularisation 

(immediate or staged) vs culprit-only, little is known about the impact 

of the extent of coronary disease at presentation on prognosis after 

PPCI. The SYNTAX score, designed to stratify outcomes in multivessel 

PCI and CABG, has been validated in unselected populations undergoing 

elective PCI; to date, no studies have assessed its utility in PPCI. 

Methods Consecutive patients attending a single UK tertiary centre 

for PPCI between September 2008 and June 2010 (n¼695) were 

included. SYNTAX scoring was performed by a single trained 

operator blinded to patient details and outcome. Scoring was validated 

by analysis of 3 separate cohorts by 2 other experienced 

operators. Patients were split into 3 subgroups as in the SYNTAX 

trial (score #22 (low, L), 22.5e32 (intermediate, IM) and $32.5 

(high, H)), and patient data and outcome measures obtained by 

interrogation of local and national databases. 

Results 671 of 695 patients were included in the analysis with 24 

being excluded owing to inability to score (previous CABG, images 


A29


unavailable). The ability to allocate a SYNTAX tertile was reproducible 

between observers (r¼0.94). Median scores in the 3 groups were: 

L 14, IM 26, H 36 (Abstract 43 figure 1A). Although there was no 

correlation between SYNTAX score and patient sex or diabetic status, 

there was a linear relationship with patient age (r 2 ¼0.03; p


at PPCI in elderly patients such as SENIOR PAMI (Grines, 2005) and 

TRIANA (Bueno, 2009) the minimum age for inclusion was 70 yrs 

and 75 yrs respectively. With an ageing population in the western 

world, about 20% of patients admitted for suspected STEMI are 

$80 yrs. We evaluated the outcome of PPCI in patients $80 yrs 

who were admitted to our unit with STEMI. 

Methods Our PPCI service was started in September 2009 and we 

analysed all the patients who were $80 yrs presenting to the PPCI 

service between September 2009 and September 2010 (13 months). 

Prospectively entered data were obtained from our dedicated cardiac 

service database system (Philips CVIS). Mortality data were 

obtained from the summary care record (SCR) database. Follow-up 

data were obtained from patients’ respective district general hospitals 

and general practitioners medical records. 

Results Of the 998 patients who were admitted to our unit for 

primary PCI for suspected STEMI during the study period, 183 

(18.3%) were $80 yrs of age. After excluding 51 patients (27.9%) 

who did not undergo PPCI, we included 132 (70.1%) patients for 

analysis. Of those who were included in the study (n¼132, 63 

female), the mean age was 8563.95 yrs (range 80e99 yrs, median 

85 yrs). There were 20 diabetics (15.2%) and 39 (29.5%) had 

previous myocardial infarction. Ten patients (7.6%) were in cardiogenic 

shock on arrival of which 9 (90%) had an Intra aortic balloon 

pump (IABP). The infarct related vessel was the right coronary in 

42.4% and left anterior descending in 37.1%. Drug eluting stents 

were used in 40.2% of patients. In-hospital and 30-day mortality 

was 14.4% and 19.7% respectively. There was a significant difference 

in the mortality between patients age


reduction in mortality from cardiomyopathies and cardiac conduction 

disorders. Although PPCE is endorsed by large medical and 

sporting organisations, including the European Society of Sports 

Cardiology, the International Olympic Committee and FIFA, the 

state health system in the UK (and many other Western countries) 

does not support cardiovascular evaluation of athletes. Certain elite 

sporting organisations in the UK mandate PPCE in all athletes prior 

to competition. In 2010 the English Premier Rugby league introduced 

formal PPCE in all competing players. 

Methods Athletes participating in the English Premiership Rugby 

underwent PPCE with a structured clinical questionnaire and 12- 

lead ECG. Trans-thoracic echocardiogram (TTE) and additional 

investigations were performed where indicated. 

Results A total of 606 players were assessed (mean age 22.9 years; 

range 15e37). Of these, 45 (7.4%) required TTE (35 (5.7%) due to 

ECG abnormalities; 5 (0.08%) due to family history of sudden death; 

5 (0.08%) due to symptoms). ECG abnormalities warranting TTE 

included right axis deviation (n¼4), left axis deviation (n¼17), right 

bundle branch block (n¼3), right ventricular hypertrophy (n¼1), 

abnormal T wave inversion (n¼5) and prolonged QT (n¼1). Six of 

the 45 subjects demonstrated mild changes on TTE (markedly 

dilated LV cavity (n¼3), mitral regurgitation (n¼1), pulmonary 

stenosis (n¼1), dilated aortic root (n¼1)), requiring serial surveillance. 

Five demonstrated abnormalities on TTE and/or ECG that 

warranted referral for further evaluation including exercise stress 

test (n¼5), 24-h ECG (n¼5) and cardiac MRI (n¼3). The reasons for 

these tests included possible arrhythmogenic right ventricular 

cardiomyopathy (n¼3), suspicion of hypertrophic cardiomyopathy 

(n¼1) and QT prolongation on ECG (n¼1). None of the players 

exhibited a cardiac disorder that warranted disqualification from 

sport. Overall 7.4% of athletes required further investigation 

following initial ECG, and 1.8% required further tests following 

TTE. False positive rate was 5.6%. 

Conclusion Cardiovascular evaluation of British rugby players with a 

structured questionnaire and ECG resulted in clearance of 92.6% 

following initial tests, and 5.6% were reassured after TTE. Only 1% 

players required surveillance echocardiograms and 0.8% were 

referred for further diagnostic evaluation. False positive rate was 

5.6%. The results indicate that PPCE carried out in an expert setting 

results in a relatively small number of athletes requiring further 

tests, and a low false positive rate. 

enhanced by ischaemia; whether they are present in humans is 

unknown. We examined whether the erythropoietin analogue 

darbepoetin improves flow mediated dilatation (FMD), a measure of 

endothelium-derived NO, and whether this is influenced by 

preceding ischaemia-reperfusion. 

Methods 36 patients (50e75 years) with stable coronary artery 

disease were randomised to receive a single dose of darbepoetin 300 mg 

or saline placebo. Immunoreactive erythropoietin was measured by 

an enzyme linked immunospecific assay. FMD was measured at the 

brachial artery using high resolution ultrasound. CD34+/VEGFR2 

+/133+ circulating EPC were enumerated by flow cytometry. 

Measurements were made immediately before darbepoetin/placebo 

and at 24 h, 72 h and 7 days. At 24 h FMD was repeated after 20 min 

ischaemia-reperfusion of the upper limb. A further group of 11 

patients were studied according to the same protocol, all receiving 

darbepoetin, with omission of forearm ischaemia-reperfusion at 24 h. 

Results Immunoreactive erythropoietin peaked at 24 h in the 

darbepoetin group (median value of 724 U/l (IQR 576e733 U/l), 

compared to 12 U/l (IQR 9e21 U/l) in the placebo group) and 

remained elevated at approximately 500 fold baseline at 72 h. FMD 

did not differ significantly between groups at 24 h (before ischaemiareperfusion). 

At 72 h, (48 h after ischaemia-reperfusion) FMD 

increased from baseline in the darbepoetin group but not in the 

placebo group so that FMD (and change in FMD from baseline) was 

significantly greater in the darbepoetin group (change from baseline 

1.760.3% and 0.660.4% in darbepoetin and placebo groups 

respectively, p


49 ETHNIC VARIATION IN QT INTERVAL AMONG HIGHLY 

TRAINED ATHLETES 

doi:10.1136/heartjnl-2011-300198.49 

1 H Raju, 

1 M Papadakis, 

2 V Panoulas, 

2 J Rawlins, 

2 S Basavarajaiah, 

1 N Chandra, 

1 E R Behr, 1 S Sharma. 1 St George’s University of London, London, UK; 2 University 

Hospital Lewisham, London, UK 

Background Studies in Caucasian (white) athletes indicate that a 

significant proportion exhibit an isolated prolonged corrected QT 

interval (QTc), raising concerns for potentially false diagnoses and 

disqualification from competitive sport. The prevalence of prolonged 

QTc interval in athletes of African/Afro-Caribbean (black) descent is 

unknown. However, this ethnic group generally exhibits a high 

proportion of ECG repolarisation changes and increased left 

ventricular wall thickness, that may impact on QTc. 

Aim We aimed to assess the impact of ethnicity on QTc in young 

elite athletes. 

Methods We assessed 3035 elite athletes, aged 14e35 years, who 

were participating at national and international level in a variety of 

sporting disciplines. Athletes were evaluated with ECG and 2D 

echocardiography. Athletes diagnosed with structural heart disease 

or hypertension were excluded from analysis. 

Results Demographic and cardiological results are summarised in 

Abstract 49 table 1. Black male athletes exhibited shorter QTc than 

white male athletes, but QTc was similar among black and white 

female athletes. Bivariate analysis revealed that none of T wave 

inversions, ST segment elevation, or left ventricular wall thickness 

were associated with QTc. No ethnic difference was observed in 

prevalence of QT prolongation, as defined by ESC Sports Consensus 

criteria (male >440 ms; female >460 ms). 

Aim We determined the diagnostic yield of exercise tolerance testing 

(ETT) in investigation of inherited cardiac conditions following 

familial premature SCD. 

Methods Between 2006 and 2010, we evaluated 308 blood relatives 

of 148 SCD victims, who completed at least 3 min of the Bruce 

protocol. ETTs were analysed for: QT prolongation; Brugada type 1 

pattern; ST depression: blood pressure (BP) response; multiple 

ventricular ectopics or arrhythmia. Individual pathological phenotypes 

were determined by a combination of 12-lead ECG, echocardiogram, 

24-h holter monitor, with additional MRI, CT coronary 

angiography and genetic mutation analysis, as appropriate. 

Results Thirty (9.8%) patients had an abnormality during ETT, 

details of which are summarised in Abstract 50 figure 1. All ETTs 

with abnormal QT prolongation and dynamic Brugada pattern were 

associated with diagnoses of long QT syndrome and Brugada 

syndrome respectively. An example of dynamic Brugada phenotype 

is given in Abstract 50 figure 2. Ventricular ectopy was seen in 15 

patients, of whom 5 demonstrated phenotypic cardiomyopathy or 

channelopathy on further investigations. No patients with significant 

ST depression had evidence of coronary abnormalities on 

imaging. No hypotensive BP response was seen, but exertional 

hypertension was associated with systemic hypertension. 


Characteristics of athletes evaluated 

Black Male 

(n[901) 

White Male 

(n[1652) 

Black Female 

(n[122) 

White Female 

(n[360) 


familial evaluation. 

ETT abnormalities and associated diagnoses at 

Mean Age, years 2265 1764 2165 1864 

Mean Heart Rate, bpm 61612 56610 63610 5969 

Mean QRS duration, ms 88614 96610 84610 8869 

Mean LV wall thickness, mm 10.661.6 9.4*61.2 9.261.2 7.9*62.9 

ST segment elevation, n (%) 570 (63.3%) 406 (24.6%) 20 (16.3%) 64 (17.8%) 

T wave inversions, n (%) 204 (22.6%) 66* (4.0%) 18 (14.6%) 15* (4.2%) 

Mean QTc (Bazett’s), ms 393626 404*620 407625 412627 

QTc >440 ms, n (%) 20 (2.2%) 49 (3.0%) 13 (10.6%) 39 (10.9%) 

QTc >460 ms, n (%) 4 (0.4%) 7 (0.4%) 1 (0.8%) 5 (1.4%) 

Means presented as mean 6 SD. 

*p


pattern. Ventricular ectopy is non-specific, but is associated with 

both cardiomyopathic and channelopathic processes in a significant 

minority. ST segment depression, however, is unhelpful and should 

be viewed in the context of the patient’s cardiovascular risk profile. 

51 LOW-DOSE SODIUM NITRITE RELIEVES MYOCARDIAL 

ISCHAEMIA IN PATIENTS WITH CORONARY ARTERY 

DISEASE: A TARGETED NO-DONOR EFFECT 

of DPSV/DHR were different in the saline/ischaemia group compared 

to the three other groups (ie, saline/ischaemia ¼3.760.6 cm/s/s, 

NO 2 - /ischaemia ¼8.261.0 cm/s/s, saline/control ¼10.561.1 cm/s/s, 

NO 2 - /control ¼8.460.7 cm/s/s; p


53 B-TYPE NATRIURETIC PEPTIDE PERFORMS BETTER THAN 

CURRENT CARDIOVASCULAR RISK SCORES IN IDENTIFYING 

SILENT “PANCARDIAC” TARGET ORGAN DAMAGE IN 

ALREADY TREATED PRIMARY PREVENTION PATIENTS 

doi:10.1136/heartjnl-2011-300198.53 

1 A Nadir, 1 S Rekhraj, 2 J Davidson, 1 T M MacDonald, 1 C C Lang, 1 A D Struthers. 

1 University of Dundee, Dundee, UK; 2 Ninewells Hospital, Dundee 

Background Primary prevention needs to be improved because up to 

70% of cardiovascular (CV) events occur outwith those classified as high 

risk by CV risk scores currently used in clinical practice (eg, 

Framingham). One possible way to improve primary prevention of CV 

disease is to identify those patients who may already harbour silent 

pancardiac target organ damage in the form of left ventricular hypertrophy 

(LVH), systolic dysfunction (LVSD), diastolic dysfunction 

(LVDD), left atrial enlargement (LAE) or silent myocardial ischaemia. 

This could be achieved by reapplying traditional CV risk scores to 

primary prevention patients after they have been treated or by screening 

with a simple biomarker like B-type natriuretic peptide (BNP). 

Methods We prospectively recruited 300 asymptomatic individuals 

without known cardiovascular disease already on primary prevention 

therapy. Patients with valvular heart disease, atrial fibrillation and 

renal impairment were excluded. We measured BNPand calculated 10- 

year global CV risk scores (based on Framingham, QRISK and 

ASSIGN) in each participant. Transthoracic echocardiography was 

used to assess LV mass, LV systolic and diastolic function, and left 

atrial volume while the presence of inducible ischaemia was assessed 

by dobutamine stress echocardiography or dipyridamole myocardial 

perfusion imaging. Patients were divided into low, intermediate and 

high risk groups based on 10-year global CV risk. The prevalence of 

various cardiac TOD in each group was compared and ROC curves 

were constructed for BNP and for 10-year global CV risk scores to 

assess their ability to detect presence of silent cardiac TOD. 

Results One hundred and two (34%) patients (Mean age 

6466.0 years, 58% males) had evidence of silent cardiac TOD 

(29.7% LVH, 18% LAE, 17.3% LVDD, 7.3% LVSD and 6.3% 

Ischaemia). The prevalence of cardiac TOD ranged from 19 to 28% 

in the low risk, 26%e33% in the intermediate risk and 36%e41% in 

the high risk groups based on three commonly used CV risk equations. 

BNP levels were significantly higher (median (IQR); 21.6 

(13.6e40.0) vs 11.4 (6.3e20.0) pg/ml, p


between rs727139 (KCNH8) on chromosome 3 and rs11167496 

(PDGFRB) on chromosome 5 (p¼2.45310 8 ). Analysis of subsets 

of SNPs pre-selected based on their nominal association with CAD 

(p60%, invasive 

coronary angiography (ICA) is recommended as the first-line diagnostic 

investigation. If estimated likelihood is 30%e60%, functional 

imaging is recommended. If estimated likelihood is


(CrCl) was calculated using Cockcroft-Gault formula. Patients were 

subgrouped into 5 grades based on preoperative CrCl; Group I 

CrCl$90 ml/min; II 60e89; III 30e59; IV 15e29; V


magnetic resonance. Detailed lifestyle information and anthropometric 

measurements were collected during childhood and 

adolescence. Metabolic parameters were measured multiple times 

per week for the first 9 weeks of life and again at follow-up visits. 

Results Individuals that received IV lipids achieved significantly 

higher maximum cholesterol levels during the first 9 weeks of life 

than those that did not (mean6SD¼4.3861.65 vs 3.1260.78 mmol/ 

l, p¼0.006). Dose given and number of days on IV lipids also associated 

with maximum cholesterol level during this period (r¼0.557, 

p


single-vessel CAD 212 (396) and more severe disease 170 (327) ms 2 ; 

p-value for trend¼0.003. There was a similar reduction in LF power 

regardless of the anatomical location of coronary stenoses (see 

Abstract 61 figure 1). Comparing patients with LF


64 DIAGNOSTIC ACCURACY OF EXERCISE STRESS TESTING IN 

INDIVIDUALS WITHOUT KNOWN CORONARY ARTERY 

DISEASE: A SYSTEMATIC REVIEW AND META-ANALYSIS 

doi:10.1136/heartjnl-2011-300198.64 

1 A Banerjee, 2 D Newman, 2 A Van den Bruel, 2 C Heneghan. 1 West Midlands Deanery, 

Birmingham, UK; 2 Department of Primary Care, University of Oxford, Oxford, UK 

Background Exercise stress testing offers a non-invasive, less 

expensive way of risk stratification prior to coronary angiography, 

and a negative stress test may actually avoid angiography. 

However, previous meta-analyses have not included all exercise 

test modalities, or patients without known coronary artery 

disease. 

Objectives To systematically review the literature to determine the 

diagnostic accuracy of exercise stress testing for coronary artery 

disease on angiography. 

Search methods MEDLINE (January 1966eNovember 2009) and 

EMBASE (1980e2009) databases were searched for articles on 

diagnostic accuracy of exercise stress testing. 

Selection criteria We included prospective studies comparing exercise 

stress testing with a reference standard of coronary angiography 

in patients without known coronary artery disease. Results From 

6055 records, we included 34 studies with 3352 participants. 

Overall, we found published studies regarding five different exercise 

testing modalities: treadmill ECG, treadmill echo, bicycle ECG, 

bicycle echo and myocardial perfusion imaging. The prevalence of 

CAD ranged from 12% to 83%. Positive and negative likelihood 

ratios of stress testing increased in low prevalence settings. Treadmill 

echo testing (LR+ ¼7.94) performed better than treadmill ECG 

testing (LR+ 3.57) for ruling in CAD and ruling out CAD (echo LR 

¼0.19 vs ECG LR ¼0.38). Bicycle echo testing (LR+ ¼11.34) 

performed better than treadmill echo testing (LR+ ¼7.94), which 

outperformed both treadmill ECG and bicycle ECG. A positive 

exercise test is more helpful in younger patients (LR+ ¼4.74) than 

in older patients (LR+ ¼2.8). 

Conclusions The diagnostic accuracy of exercise testing varies, 

depending upon the age, sex and clinical characteristics of the 

patient, prevalence of CAD, and modality of test used. Exercise 

testing, whether by echocardiography or ECG, is more useful 

at excluding CAD than confirming it. Clinicians have concentrated 

on individualising the treatment of CAD, but there is great 

scope for individualising the diagnosis of CAD using exercise 

testing. 




Probability of coronary artery disease. 

65 OUTCOMES AFTER CARDIAC SURGERY: ARE WOMEN OF 

SOUTH ASIAN ORIGIN AT INCREASED RISK? 

doi:10.1136/heartjnl-2011-300198.65 

1 D A George, 1 D Morrice, 2 A M Nevill, 1 M Bhabra. 1 New Cross Hospital, 

Wolverhampton, UK; 2 University of Wolverhampton, Wolverhampton, UK 

Objectives The population served by our centre has a relatively high 

proportion of people originating from the Indian subcontinent 

(“South Asians”) compared to the national average (14.3% vs 4.6%). 

We observed that the mortality rate in South Asian women undergoing 

cardiac surgery in our unit appeared to be relatively high. We 

investigated this observation further to determine whether ethnic 

origin was an independent risk factor for postoperative death in 

females. 

Methods Data for all patients undergoing cardiac surgery were 

collected prospectively in a registry. Retrospective analysis was 

carried using SPSS on data for 4901 patients operated on in the 6- 

year period April 2004 to March 2010. Categorical data associated 

with mortality were analysed using c 2 tests. Risk factors for inhospital 

mortality were subjected to univariate analysis, and those 

found to be significant were tested for independence using multivariate 

logistic regression. 

Results During the study period, 1160 female patients underwent 

surgery with a mortality rate of 4.7%. Mortality in 113 South Asians 

was 8.9% vs 4.3% in non-Asians (p¼0.03). Of 20 risk factors tested 

with univariate analysis, 16 were significantly associated with 

mortality. Logistic regression showed the following to be independent 

predictors of postoperative mortality: urgency of operation 

(OR 32.0; p


66 ETHNIC DIFFERENCES IN CAROTID INTIMAL MEDIAL 

THICKNESS AND CAROTID-FEMORAL PULSE WAVE 

VELOCITY ARE PRESENT IN UK CHILDREN 

doi:10.1136/heartjnl-2011-300198.66 

1 P H Whincup, 1 C M Nightingale, 2 A Rapala, 2 D Joysurry, 2 M Prescott, 2 A E Donald, 

2 E Ellins, 1 A Donin, 2 S Masi, 1 C G Owen, 1 A R Rudnicka, 1 D G Cook, 2 J E Deanfield. 

1 Division of Population Health Sciences, St George’s, University of London, London, UK; 

2 Vascular Physiology Unit, Institute of Child Health, UCL, London, UK 

Introduction There are marked ethnic differences in cardiovascular 

disease risks in UK adults; South Asians have high risks of coronary 

heart disease and stroke while black African-Caribbeans have high 

risks of stroke and slightly low risks of coronary heart disease when 

compared with white Europeans. Ethnic differences in cardiovascular 

risk factors are apparent in childhood, but little is known abut 

ethnic differences in vascular structure and function during childhood. 

We set out to measure two vascular markers of cardiovascular 

risk, common carotid intimal-medial thickness (cIMT) and carotidfemoral 

pulse wave velocity (PWV) in UK children from different 

ethnic groups. 

Methods We conducted a school-based study examining the cardiovascular 

risk profiles of 9e10 year-old UK children, including 

similar numbers of South Asian, black African-Caribbean and white 

European participants. Following a baseline cardiovascular risk 

survey with measurements of body build, blood pressure, fasting 

blood lipids, insulin and HbA1c, 1400 children were invited to have 

measurements of cIMT (bilateral measurements were made with a 

Zonare ultrasound scanner). A subgroup of these children (n¼900) 

was also invited for PWV measurements, made with a Vicorder 

device. All analyses were adjusted for age, gender and allowed for 

clustering at school level. 

Results In all, 939 children (67% response) had measurements of 

cIMT and 631 children (70% response) had measurements of PWV. 

Mean cIMTwas 0.475 mm (SD 0.035 mm); mean PWV was 5.2 m/s 

(SD 0.7 m/s). Compared with white European children, black 

African-Caribbeans had higher cIMT (mean difference 0.014 mm, 

95%CI 0.008 to 0.021 mm) and PWV (% difference 3.3, 95%CI 0.4 to 

6.2); South Asian children had similar cIMT to white Europeans but 

slightly higher PWV (% difference 2.7, 95%CI 0.1 to 5.5%). cIMT 

was positively associated with systolic and diastolic blood pressure 

but not with other cardiovascular risk markers. In contrast, PWV 

was positively associated with adiposity, diastolic blood pressure 

and insulin resistance. Black African-Caribbean children had lower 

LDL-cholesterol levels and higher insulin and HbA1c levels than 

white Europeans; South Asian children had higher insulin, HbA1c 

and triglyceride levels. However, adjustment for these risk factors 

had little effect on the ethnic differences in cIMTand PWVobserved. 

Conclusions Ethnic differences in cIMT and PWV, markers of longterm 

cardiovascular risk, are apparent in childhood. These differences 

are not fully explained by the ethnic differences in established cardiovascular 

risk markers observed. The results suggest that there may be 

important opportunities for prevention of cardiovascular disease 

before adult life, particularly in high-risk ethnic minority groups. 

67 SPONTANEOUS CARDIAC HYPERTROPHY AND ADVERSE LV 

REMODELLING IN A NOVEL HUMAN RELEVANT MOUSE 

MODEL OF DIABETES; A MECHANISTIC INSIGHT 

doi:10.1136/heartjnl-2011-300198.67 

1 S M Gibbons, 

1 Z Hegab, 

1 M Zi, 

1 S Prehar, 

1 T M A Mohammed, 

2 R D Cox, 

1 E J Cartwright, 1 L Neyses, 1 M A Mamas. 1 University of Manchester, Manchester, UK; 

2 MRC mammalian genetics unit, oxford, UK 

Heart failure (HF) is one of the commonest cardiovascular complications 

of Diabetes Mellitus (DM) with the prevalence of DM 


reported at around 30% in many pivotal heart failure studies. DM is 

an independent predictor of mortality in patients with HF, however 

molecular mechanisms that contribute to HF development in the 

diabetic population are poorly understood. Using a novel human 

relevant mouse model of DM (GENA348), identified through the 

MRC mouse mutagenesis programme with a point mutation in the 

pancreatic glucokinase (GLK) gene we investigate the molecular 

mechanisms that contribute to the HF phenotype in DM. GLK is 

the glucose sensor which regulates insulin secretion and GLK 

activity is reduced by 90% by the GENA348 point mutation 

resulting in severe hyperglycaemia. Similar mutations underlie 

Maturity Onset Diabetes of the Young Type 2 (MODY 2) in 

humans. Mean random blood glucose was found to be increased in 

the GENA348 mutant (HO) mice compared to wild type (WT) 

littermates (WT 6.960.3 mmol/l vs HO 20.660.8 mmol/l, 

p


(MAF


71 A GENOME-WIDE ASSOCIATION STUDY IN INDIAN ASIANS 

IDENTIFIES FOUR SUSCEPTIBILITY LOCI FOR TYPE-2 

DIABETES 

doi:10.1136/heartjnl-2011-300198.71 

1,2 J Sehmi, 3 D Salaheen, 4 Y Yeo, 5 W Zhang, 1,2 D Das, 6 M I McCarthy, 4 E S Tai, 

3 J Danesh, 1,2 J Kooner, 2,7 J Chambers. 1 National Heart and Lung Institute, Imperial 

College, London, UK; 2 Ealing Hospital NHS Trust, London, UK; 3 Department of Public 

Health and Primary care, Cambridge University, Cambridge, UK; 

4 Department of 

Medicine, National University of Singapore, Singapore; 5 Department of Epidemiology 

and biostatistics, Imperial College London, London, UK; 6 Wellcome Trust for human 

Genetics, Oxford University, Oxford, UK; 7 Department of Epidemiology and biostatistics, 

Imperial College London, London, UK 

Background Type-2 diabetes (T2D) is a major risk factor for cardiovascular 

disease, and a leading causing of mortality worldwide. 

T2D is 2e4 fold more common among Indian Asians than Europeans, 

and contributes to higher cardiovascular disease mortality in 

Asians. Little is known of the genetic basis of T2D in Indian Asians. 

Methods We carried out a genome-wide association (GWA) study of 

T2D in 5561 Indian Asian cases and 14 458 controls from LOLIPOP, 

PROMIS and SINDI cohorts. Whole genome scans were performed 

using the Illumina 317 k or 610 k arrays. Further testing of suggestive 

SNPs was carried out in independent cohorts of Indian Asian 

(12 K T2D cases and 25 K controls) and European ancestry 

(DIAGRAM+, 8 K T2D cases and 39 K controls). 

Results There were two novel loci associated with T2D at p


coronary flow and is an important predictor of coronary microvascular 

function. A variety of environmental stimuli have been 

shown to affect CFR but little is known about the genetic 

component of CFR. To characterise the genetics of CFR we initially 

measured in vivo blood pressure (BP) and ex vivo cardiac phenotypes 

including CFR in two inbred rat strains, Brown Norway 

(BN) and Spontaneously Hypertensive Rat (SHR) which is a 

genetic model for hypertension and microvascular dysfunction. We 

then studied BP and coronary flow (CF) phenotypes in F 1 and F 2 

crosses derived from BN and SHR to estimate the heritability of 

CFR and its relationship with BP. 

Methods Animals were anaesthetized using a mixture of Oxygen and 

Isoflurane. BP was measured invasively by cannulation of carotid 

artery. Following BP measurement hearts were excised and rapidly 

transferred to the ex vivo perfusion apparatus where retrograde 

perfusion was established using the Langendorff technique. Hearts 

were perfused with Carbogen buffered Kreb 9 s solution and paced 

constantly at 360 bpm. A fluid filled balloon was placed in the left 

ventricular (LV) cavity to measure the pressure indices. CF, LV 

developed pressure, myocardial contractility (LV dP/dt max ) and 

myocardial relaxation (LV dP/dt min ) were recorded at baseline, during 

peak hyperaemia, regional ischaemia (induced by ligation of the 

proximal left anterior descending artery) and reperfusion. 

Results 1) CFR differs significantly between the two inbred parental 

rat strains. (BN¼2.1 6 0.32, SHR¼1.5 6 0.18, p¼2.6310 7 ,n¼16 

each). 2) Heritability of CFR: Broad sense heritability (the proportion 

of total phenotypic variance attributable to total genetic 

variance) for CFR is 62% indicating a large and previously unrecognised 

genetic component of CFR. 3) Relationship between CFR 

and BP: We did not find statistically significant correlation between 

CFR and BP in the F 2 intercross (r¼0.11, p¼0.11, n¼176). 4) Relationship 

between CF and myocardial relaxation (LV dP/dt min ): LV 

dP/dt min correlated strongly with CF during all stages of the 

experiment (baseline CF, r¼ 0.36, p


of ROS and NO favours the production of peroxynitrite that is 

capable of nitrosylation of key cellular proteins such as the 

Ryanodine receptor that has a crucial role in cardiac excitationcontraction 

coupling. This study provides novel insights into the 

mechanisms of cardiac damage in diabetes that occur independent of 

vascular disease through AGEs. 

75 OPTIMISATION OF MEDICAL THERAPY AFTER CARDIAC 

RESYNCHRONISATION: A NURSING OPPORTUNITY NOT TO 

BE MISSED 

doi:10.1136/heartjnl-2011-300198.75 

1 S J Russell, 2 J Bell, 3 L Edmunds, 4 J Davies, 3 H Rose, 3 Z R Yousef. 1 Wales Heart 

Research Institute, Cardiff, UK; 2 Cardiff University, Cardiff, UK; 3 University Hospital of 

Wales, Cardiff, UK; 4 University Hospital Llandough, Cardiff, UK 

Introduction Cardiac resynchronisation therapy (CRT) is indicated in 

patients with left ventricular dysfunction (EF#35%), electromechanical 

dyssynchrony, and limiting heart failure (HF) symptoms 

despite optimal medical therapy. In many cases target doses of HF 

medications prior to CRTare not achieved due to bradycardia and/or 

limiting hypotension. CRT however provides bradycardia backup 

and improved haemodynamics, thus providing an opportunity to 

further optimise HF medical therapies known to confer substantial 

morbidity and mortality benefits. We conducted the present study 

to evaluate the potential to further optimise medical treatments in 

patients receiving CRT within the framework of nurse-led pre and 

post CRT clinics. 

Methods Our unit operates an integrated CRT service with preassessment, 

implantation, and follow-up components. Pre-assessment 

and follow-up incorporate dedicated HF nurse clinics to 

support protocol-driven optimisation of medical therapies. We 

therefore conducted a retrospective analysis of our CRT database 

over a 9-month period to quantify the frequency of use, and dose of 

HF medications (bblockers; bB, angiotensin converting enzyme 

inhibitors: ACE-I or angiotensin receptor blockers: ARB, aldosterone 

antagonists, digoxin, and loop diuretics) before and 6 months after 

CRT. Total daily dose equivalences within each class of medication 

(bisoprolol for bB, lisinopril for ACE-I/ARB, spironolactone for 

aldosterone antagonists, and frusemide for loop diuretics) and 

titration protocols were based on National Institute of Clinical 

Excellence guidelines for HF (guideline 5). 

Results Between October 2009 and Jun 2010, 74 patients (age: 

67611 yrs, 86% male) underwent implantation of a CRT device. All 

Abstract 75 Table 1 Heart Failure nurse supervised use of medications 

before and 6 months After CRT 

Pre-CRT Post-CRT p Value 

b-Blocker: exemplar bisoprolol 

Frequency of use 78% 88%


Results Following the implementation of the direct entry pathway 

in May 2010 the CTBT for all patients admitted direct to our 

hospital have reduced. This is statistically significant when looking 

at Quarter 2 results from baseline. Patient safety has not been 

compromised. Patients who were admitted directly have been asked 

about their experience and if anything could be done differently 

from their perspective. They have said: 

< The process is quick which is good from their perspective 

< They are fully informed 

< The ambulance crews deal with them competently 

< The lab staff are waiting for their arrival. 

Conclusions The CCU nurses have embraced this development and 

expansion of their nursing practice, allowing major changes to be 

made to the Primary Angioplasty pathway within the existing 

infrastructure, despite the challenges of working within the 

complex nature of traditional geographical referral patterns. Along 

with the work of all members of the multi disciplinary team this has 

significantly reduced times to treatment for patients. 

77 SCREENING FIRST DEGREE RELATIVES FOR HYPERTROPHIC 

CARDIOMYOPATHY: 12-MONTH EXPERIENCE OF A CARDIO- 

GENETICS NURSE SERVICE 

doi:10.1136/heartjnl-2011-300198.77 

Abstract 77 Table 1 Screening outcomes of 221 at risk subjects 

identified from 64 index cases of hypertrophic cardiomyopathy 

Number of Patients 

New screening initiated (local heart muscle clinic) 52 

New screening initiated (local paediatric clinic) 19 

New screening initiated (out of area service) 6 

Pre-existing screening in place 63 

Personal preference (declined screening) 28 

Awaiting response from subject (literature delivered) 19 

Complex family relationships (unable to deliver literature) 14 

Geographical/Logistical constraints 10 

Subject deceased (non-hypertrophic cardiomyopathy) 3 

Subject deceased (hypertrophic cardiomyopathy) 7 

Conclusions Proactive screening for HCM can be effectively facilitated 

by cardio-genetic nurse services. Each new index case generates 

3e4 at risk relatives who require long-term surveillance. Of 71 

asymptomatic at risk subjects screened in our unit, we diagnosed 15 

new cases of HCM, and 3 patients at high risk of sudden cardiac 

death who subsequently received primary prevention defibrillator 

implantation. 

1 S Finch, 2 S Russell, 1 D Kumar, 1 Z R Yousef. 1 University Hospital of Wales, Cardiff, UK; 

2 Wales Heart Research Institute, Cardiff, UK 

Introduction Hypertrophic cardiomyopathy (HCM) is an autosomally 

transmitted cardiomyopathy with an estimated gene prevalence 

of 1:500, and an important cause of sudden cardiac death. 

Screening to identify at risk first degree relatives is therefore 

recommended. The British Heart Foundation (BHF) recently funded 

nine Nationwide cardio-genetic nurses to support local initiatives. 

Our application for a nurse was successful and we present our 

12-month experience of HCM screening. 

Methods We mapped the course of patients with suspected HCM 

referred to our tertiary heart muscle clinic which serves a population 

of 1.4million. Following phenotype confirmation, a family tree and 

contact details from the index case were recorded by the cardiogenetic 

nurse. The index case was given literature to pass onto at 

risk relatives. The information pack included an open invitation 

(referral via primary care) to attend for screening. For relatives 

residing outside our catchment area screening was arranged via links 

with the BHF cardio-genetic network and other health care 

providers. Relatives domiciled outside UK were given our details 

with offers to support screening. Throughout, strict adherence to 

patient confidentiality was maintained. 

Results Over 12 months, 64 index HCM cases presented to our 

heart muscle clinic. Pedigree analysis identified 221 first degree 

relatives at risk of carrying the HCM gene; mean index-to-at RR: 

1-to-3.4 (range 0e14 subjects). Of the 221 at risk subjects, 71 

(19 through paediatrics) have undergone screening through 

clinical assessment at our unit with plans for long-term 2e5 yearly 

follow-up in view of variable gene penetrance. Of the 71 screened 

subjects, 15 were newly diagnosed with HCM. Newly diagnosed 

HCM patients underwent further risk stratification for sudden 

cardiac death; where we identified 3 patients at high risk ($2 

conventional high sudden death risk factors). After appropriate 

counselling, these 3 patients have received primary prevention 

defibrillators. Despite our approach, 52 subjects remain unscreened 

(Abstract 77 table 1), either due to complex family relationships 

(n¼14), personal preference (n¼28) and/or geographical/logistical 

reasons (n¼10). 


78 FIRST YEAR EXPERIENCE OF A DEDICATED “RADIAL 

LOUNGE” FOR PATIENTS UNDERGOING ELECTIVE 

PERCUTANEOUS CORONARY PROCEDURES 

doi:10.1136/heartjnl-2011-300198.78 

S Brewster, R Weerackody, K Khimdas, A Little, N Cleary, A Penswick, M Rothman, 

A Archbold. London Chest Hospital, London, UK 

Introduction The potential to achieve safe early mobilisation and 

same day discharge on a consistent basis after radial artery access 

has provided us with the opportunity to make a step change in the 

way we deliver elective care to patients undergoing percutaneous 

coronary procedures. We designed a dedicated “radial lounge” to 

accommodate patients before and after their procedure with the aim 

of minimising the feeling of “hospitalisation” that accompanies 

most encounters with health services. The lounge is a day case unit 

that has no beds, only chairs, and televisions but no cardiac monitors. 

Patients remain in their clothes throughout their hospital visit. 

Here we report our first year 9 s experience of this facility. Methods: 

The study population comprised all patients who attended the 

radial lounge between July 2009eJune 2010 for coronary angiography 

or percutaneous coronary intervention (PCI). Patients were 

suitable for the radial lounge if they were elective cases who had a 

satisfactory radial pulse and no pre-procedure contraindication to 



same day discharge. Patients were excluded if they had any of the 

following: an unsuitable radial pulse, planned femoral access, prior 

coronary artery bypass surgery, or the requirement for an overnight 

hospital stay for planned complex/high risk PCI, renal impairment, 

or social reasons. The final decision regarding route of arterial access 

was left to the operator. 

Results In the one year study period, 1548 patients were managed in 

the radial lounge. 1109 patients underwent coronary angiography, 

114 (10.2%) of whom also had a pressure wire or intravascular 

ultrasound, and 439 underwent PCI. This represented approximately 

88% of our unit 9 s elective angiograms and 60% of our 

elective PCIs. Among the patients who underwent angiography, 938 

(84.5%) were performed radially and 1076 (97.0%) were discharged 

from the radial lounge on the same day as their procedure. Among 

the PCI patients, 359 (81.8%) were performed radially and 372 

(84.7%) were discharged the same day. The PCI group included 326 

(74.3%) patients who had a single vessel treated, 105 (23.9%) who 

had two vessels or a bifurcation with a significant side branch 

treated, and 8 (1.8%) patients who had three vessels treated. There 

were no deaths or arrhythmias in the radial lounge. Requirement for 

overnight admission was significantly more common after femoral 

access compared with radial access for both angiography (4.1% vs 

2.8%; p


PPCI NURSE LED DISCHARGE PROTOCOL 

PPCI -REPERFUSION 

TIME 0 

CCU 

12HRS 

PATIENT STABLE* 

(SYSTOLIC BP> 100 mmHg - NO NEW ECG CHANGES - PAIN FREE - SaO2>93%) 

REG/SENIOR NURSE TO 

BOOK ECHO & TRANSFER 

TO WARD (IF APPLICABLE) 

Results As previously described apical rotation was reduced at rest 

and on exercise Basal rotation was comparable at rest but significantly 

reduced on exercise in patients. The SD for four different 

systolic peak motions (basal and apical rotation, longitudinal and 

radial displacement) was comparable at rest but on exercise controls 

showed a significantly reduced SD compared to patients showing a 

greater ability to synchronise motions. Furthermore a ratio of 

untwist during IVRT and longitudinal extension (Ratio Untwist 

/Extension in IVRT) showed a significant deeper slope on exercise 

for patients indicating a loss of synchrony in diastole, too. All results 

are presented in Abstract 81 table 1. 

24 HRS 

PATIENT STABLE * (AS ABOVE) 


DEMONITOR + 

ECHOCARDIOGRAM+ 

REHAB REFERRAL 

ECHO PERFORMED? 

Patients 

Rest 

Controls 

Rest 

p value 

Patients 

Exercise 

Controls 

Exercise 

p value 

EF≤ 39% 

DR R/V 

SCREEN FOR 

ICD 

36 HRS 

PATIENT STABLE* (AS ABOVE) 

EF≥ 40% & KILLIP I 

TTA’S, D/C LETTER, 

MINAP, REHAB TO SEE 

48 HRS 

PATIENT STABLE* (AS ABOVE) 

Y 

N 

ARRANGE 

ASAP 

Apical Rotation (8) 9.964.4 13.464.0


choice has changed in favour of rotary pumps; 19%, 69% and 96% 

for E1, E2 and E3 respectively. Median duration of VAD support 

increased from 84 days (IQR 20e209) in E1 to 280 days (IQR 

86e661) in E3 (p


dyssynchrony and remodelling response in contrast to EMRCTs 

(p


and therefore simply using peak velocity might give a less reliable 

optimum? Surely the time saved by using peak would have a price 

to pay in poorer reproducibility of the optimum? In this study, we 

evaluate whether peak velocity is a suitable alternative to VTI, 

having regard to both time consumed and reproducibility. We also 

examine whether averaging multiple replicate measurements 

improves optimisation. 

Methods & Results VV optimisation was performed on 40 subjects 

with biventricular pacemakers using LVOT velocity (VTI or peak) as 

the echocardiographic marker being maximised. Importantly, 6 

successive replicate optimisations were performed per patient at a 

single session. Scatter of apparent VV optimum between repeat 

optimisations was threefold smaller for peak than VTI (p


The correlations of optimal AV delays by non-invasive (Finometer) 

systolic blood pressure (SBP) vs invasive measures were as 

follows; aortic SBP, r 2 ¼0.96, p


decreased from 186668 ml to 157668 ml (p


identified 119/138 (86%) patients that met the minimum requirement 

for palliative care input. However, the SHF model predicted 

that only 6/138 patients (4.3%) had a predicted life expectancy of 

less than 1 year. Patients who met GSF criteria for palliative care had 

significantly more hospital admissions (p¼0.001) and had significantly 

lower predicted survival rates at 1 year (p¼0.038) than those 

patients that did not meet GSF criteria. At follow-up, 43/138 

patients had died (31%). Of these, 58% (25/43) died in hospital, 

following an acute admission. The sensitivity and specificity for the 

GSF and SHF model were 22%/83% and 98%/12% respectively. 

Overall, the patients renal function (eGFR35% vs ejection fraction#35%), functional limitation 

(New York Heart Association; NYHA class), and cause (ischaemic vs 

non-ischaemic) were recorded. In addition, we collected data on 

patient’s resting pulse (absolute value and rhythm: sinus vs atrial 

fibrillation), and blood pressure at the first and last clinic visits. 

Between the two clinic visits, patients underwent protocol-guided 

forced up-titration of standard neurohormonal HF therapies. We 

also collected data on the maximal tolerated doses of beta blocker 

(bB), ACE inhibitor (ACE-I) or angiotensin receptor blocker (ARB), 

and the reasons for the inability to achieve target doses of bB. 

Results Of 172 consecutive patients referred for optimisation of HF 

therapies (age 71613 yrs, 67% male), 71 (41%) were in atrial fibrillation. 

Of the patients in sinus rhythm, 78% had severe LV systolic 

dysfunction (Abstract 93 figure 1). Overall, 145 of 172 patients 

(83%) tolerated bB therapy; of these, 39% achieved the target 

maximal dose, 57% at least half target dose, and 4% less than half of 

the target dose of bB. Reasons for failure to initiate bB (n¼27, 17%) 

included; severe and limiting hypotension (48%), intractable lethargy 

(26%), and hospitalisation with worsening airways disease 

(26%). ACE-I/ARB, aldosterone antagonists, and digoxin were 

Abstract 93 Figure 1 Heart Failure Patients Potentially Suitable for 

Additional Heart Rate Reduction After Optimisation of Standard Medical 

Therapy. 


Patient Characteristics (n¼172) 

NYHA Class (%) 

I 10.5 

II 62.2 

III 26.2 

IV 1.1 

HF aetiology (%) 

Ischaemic 57 

Non-ischaemic 43 

LV function (%) 

Ejection Fraction #35% 92.4 

Ejection Fraction >35% 7.6 

Cardiac rhythm (%) 

Sinus 58.7 

Atrial Fibrillation 41.3 

Medication use (%) 

b-blockers 83 

ACE-I/ARBs 92 

Aldosterone antagonists 30 

Digoxin 18 

Abstract 93 Table 2 Haemodynamic profiles before and after 

optimisation of medication 

First Clinic Visit 

(pre-optimisation) 

Final Clinic Visit 

(post-optimisation) 

p value 

Resting Heart Rate (beats/min) 73.8614.8 67.369.5


94 A COMPARISON OF FUNCTIONAL AND 

ECHOCARDIOGRAPHIC OUTCOMES IN NICE COMPLIANT 

AND NON-COMPLIANT PATIENTS UNDERGOING CRT IN THE 

REAL WORLD 

doi:10.1136/heartjnl-2011-300198.94 

1 S J Russell, 1 I Rees, 2 P O’Callaghan, 2 Z R Yousef. 1 Wales Heart Research Institute, 

Cardiff, UK; 2 University Hospital of Wales, Cardiff, UK 

Characteristics of NICE compliant and non- 


compliant patients 

NICE:+ve 

NICE:Lve 

Age: years (SD) 65 (11) 66 (11) 

Male: % 83 90 

Ejection fraction: % (SD) 22 (7.1) 24 (7.2) 

QRS duration: mS (SD) 164 (26) 158 (37) 

CRT-Defibrillator: % 57 46 


patients 

Outcomes in NICE compliant and noncompliant 

NICE:+ve 

(n[89) 

p value 

(baseline v 

6 months) 

NICE:Lve 

(n[50) 

p value 

(baseline v 

6 months) 

QOL (score): baseline (SD) 58.2 (23.6) 63.5 (31.7) 

QOL (score): 6 months (SD) 40.1 (25.0)



(1.1260.06). The single-visit RISE95 test incorporating incrementaland 

step- exercise phases, each to the volitional limit, was well 

tolerated by CHF patients: The SE phase was contraindicated in only 

3 of the 47 tests. The RISE95 detected VO 2max in 14 of 21 patients 

with a sensitivity of w10% (ie, similar to healthy subjects), and 

without the need for secondary criteria or incidence of false-positive. 

In contrast, the end-exercise RER was sensitive to both modality and 

ramp rate and provided a false-positive for VO 2max attainment in 

every incidence. Therefore, the RISE95 protocol provides a robust 

measure of VO 2max in CHF patients, to within an individuallydefined 

CI without dependence on secondary criteria. 

97 INCREASING SKELETAL MUSCLE OXYGENATION BY PRIOR 

MODERATE-INTENSITY EXERCISE INCREASES AEROBIC 

ENERGY PROVISION IN CHRONIC HEART FAILURE 

doi:10.1136/heartjnl-2011-300198.97 


96 A TEST TO CONFIRM MAXIMAL OXYGEN UPTAKE IN 

CHRONIC HEART FAILURE PATIENTS WITHOUT THE NEED 

FOR SECONDARY CRITERIA 

doi:10.1136/heartjnl-2011-300198.96 

T S Bowen, D T Cannon, G Begg, V Baliga, K K Witte, H B Rossiter. University of 

Leeds, Leeds, UK 

Cardiopulmonary exercise testing for peak oxygen uptake (VO 2peak ) 

is widely used to evaluate severity, pathophysiology and prognosis in 

patients with chronic heart failure (CHF). A VO 2peak #14 (or 12 with 

b-blocker) ml/kg/min is associated with increased mortality and is a 

key criterion for cardiac transplant listing. A symptom-limited 

exercise test, however, may elicit a VO 2peak lower than the maximum 

physiological limit (VO 2max ); the latter commonly “confirmed” using 

the secondary criterion of respiratory exchange ratio (RER) >1.05. 

RER, however, is sensitive to the test format. We, therefore, determined 

if a ramp-incremental (RI) step-exercise (SE) (or RISE) test 

could determine VO 2max in CHF patients without using RER, by 

satisfying the criterion that two different work rates are terminated 

at the same VO 2peak . Twenty-one male CHF patients (NYHA class I: 

n¼3, II: n¼16, and III: n¼1) initially performed a modified Bruce 

treadmill test. Patients then completed a symptom-limited RISE95 

cycle ergometer test in the format: RI (4e18 W/min; w10 min); 

5-min recovery (10 W); SE (95% of peak RI work rate). Thirteen of 

these patients also performed RISE95 tests using slow (RI 3e8W/ 

min; w15 min) and fast (RI 10e30 W/min; w6 min) ramp rates. 

VO 2 and RER were measured breath-by-breath by a mass spectrometer 

and turbine (MSX, NSpire, UK). Peak VO 2 and RER were 

compared within-subjects, between RI and SE, by unpaired t test of 

the final 12 breaths of exercise. This approach allowed VO 2max and its 

associated 95% confidence limits to be estimated. VO 2peak was 

similar (p>0.05) in treadmill and cycle exercise (mean6SD: 16.262.7 

vs 15.063.2 ml/kg/min, n¼20, respectively), despite RER being 

greater in cycling (1.0860.12 vs 1.1560.09; p0.05) between RI and SE (mean6SD: 

14.663.2 vs 14.963.2 ml/kg/min, n¼21). A within-subject comparison, 

however, revealed that the VO 2max criterion was met in 14 of 21 

patients (measurement sensitivity range 0.6e3.8 ml/kg/min), 

despite RER being >1.05 in the remaining 7 (1.1660.09). There was 

no effect of ramp rate on VO 2peak (p>0.05), however RER was greater 

(p


98 HIGH PREVALENCE OF UNDIAGNOSED CARDIAC 

DYSFUNCTION IN THE OLDEST OLD: FINDINGS FROM THE 

NEWCASTLE 85+ STUDY 

doi:10.1136/heartjnl-2011-300198.98 

1 F Yousaf, 1 J Collerton, 2 A Kenny, 1 T Kirkwood, 1 C Jagger, 1 A Kingston, 3 B Keavney. 

1 Institute of Ageing and Health, Newcastle University, Newcastle upon Tyne, UK; 

2 Freeman Hospital, Newcastle upon Tyne, UK; 

3 Institute of Human Genetics, 

Newcastle University, Newcastle upon Tyne, UK 

Background Heart failure prevalence increases sharply at older ages. 

The section of the population aged 85 and over represents the most 

rapidly increasing demographic worldwide. Previous epidemiological 

studies of ventricular dysfunction and heart failure have included 

only small numbers of the “oldest old”, and have generally been 

conducted in hospital-based settings, potentially introducing ascertainment 

biases. We conducted a community-based study of the 

oldest old using domiciliary echocardiography to estimate the 

prevalence of cardiac dysfunction and heart failure. Since in elderly 

people with multiple comorbidities, heart failure may more 

frequently be incorrectly diagnosed, we cross-referenced our findings 

to preceding diagnoses present in general practice records. 

Methods Four hundred and twenty-seven individuals aged 

86e89 years (mean age 87.9 years; 39.1% (n¼167) men, 60.9% 

(n¼260) women) were visited in their usual place of residence. A full 

cardiovascular and medical history, including current medication, 

was taken; symptoms were graded using the NYHA classification. 

Previous diagnoses of heart failure (HF) were abstracted from the GP 

record. Participants underwent 2-D and Doppler echocardiography, 

including tissue Doppler measurements of LV long axis velocities, 

using a portable instrument (Vivid-I, GE Healthcare). LV systolic 

and diastolic dysfunction were graded according to American 

Society of Echocardiography guidelines. 

Results LV systolic function could be quantified in 93.2% (n¼398) 

participants and diastolic function (classified as normal, mild, moderate 

or severe dysfunction) in 88.1% (n¼376). 37.2% of participants 

(n¼140/376) had normal cardiac function or isolated mild diastolic 

dysfunction; 19.6% (n¼78/398) had moderate or severe LV systolic 

dysfunction, which was commoner in men (27.4%) than women 

(14.5%); and 14.4% (n¼54/376) had isolated moderate or severe 

diastolic dysfunction. 65.1% (278/427) of participants had valid data on 

previous diagnosis of HF, NYHA class and echocardiographic assessment 

of cardiac dysfunction. Of these, 37.4% (104/278) had clinical 

evidence of HF, which was defined as NYHA class II, III, or IV symptoms 

with underlying systolic dysfunction (29.5% (82/278)) or isolated 

moderate or severe diastolic dysfunction (7.9% (22/278)) on echo. Only 

7.6% (21/278) had a previous diagnosis of HF. 33.1% (n¼92/278) had no 

previous diagnosis of HF but had clinical evidence of HF and an additional 

21.6% (n¼60/278) had no previous diagnosis but evidence of 

pre-clinical HF (NYHA class I with systolic or moderate/severe 

diastolic dysfunction). Of those with a previous diagnosis of HF, 23.5% 

(n¼5/21) had no echocardiographic evidence of cardiac dysfunction. 

Conclusions Systolic and diastolic dysfunction and HF were 

commoner in our population than previous studies in the “younger 

old” have suggested. There are significant levels of both undiagnosed 

and misdiagnosed HF in this age group. 

warranting consideration for transplantation (Circulation 2010; 

122:173). We examined whether this variable is a good indicator of 

cardiac function in overweight heart failure (HF) patients. 

Methods We compared the cardiopulmonary exercise performance 

and non-invasive haemodynamics of overweight (BMI >34 kg/m 2 ) 

and non-overweight (BMI #30) male heart failure patients in 

NYHA Classes II and III, with those of healthy male volunteers 

with no known cardiovascular diseases (n¼101, age 43.2618.1 

(SD) years, BMI 26.063.1) as controls. Their physical and cardiac 

functional reserves were measured during treadmill exercise testing 

with standard respiratory gas analyses and rebreathing method of 

non-invasively measuring cardiac outputs during peak exercise. 

Results Consecutive overweight HF were screened and 24 patients (age 

4968(SD) years, BMI 44.966.8, NYHA 2.5060.50) managed to 

exercise to acceptable cardiopulmonary limits (peak RER¼1.0160.12), 

and achieved Vo 2max of 16.864.6 mls/kg/min which was significantly 

lower than controls (37.0610.7 mls/kg/min, p


Conclusion These results indicate that in principle Vo 2max in ml/kg/min 

as an indirect indicator of cardiac function or for cardiac transplantation 

selection is unreliable when applied to overweight heart 

failure patients. Extending this concept to the entire spectrum of 

body weights, the practice of correcting Vo 2max by body weight in 

cardiological practice would also require urgent reconsideration. 

100 PRESSURE VS FLOW AS A GUIDE FOR PACEMAKER 

OPTIMISATION? THE ACUTE HAEMODYNAMIC EFFECTS OF 

CHANGES TO ATRIOVENTRICULAR DELAY 

doi:10.1136/heartjnl-2011-300198.100 

C H Manisty, B Unsworth, R Baruah, P Pabari, Z I Whinnett, J Mayet, D P Francis. 

Imperial College, St. Marys Hospital, London, UK 

Background Non-invasive blood pressure monitoring by continuous 

finger photoplethysmography (Finometer) may have value in pacemaker 

optimisation. However, the immediate increment in blood pressure 

seems to diminish somewhat in the initial minute: it is unclear 

whether this is due to an (undesirable) fall in stroke volume or a 

(desirable) compensatory reduction in peripheral resistance. 

Methods and Results We studied this question by measuring beat-bybeat 

stroke volume (flow) using Doppler echocardiography, and 

blood pressure using continuous finger photoplethysmography, 

during and after atrioventricular delay adjustment from 40 to 

120 ms in 19 subjects with cardiac pacemakers. Quintuplicate 

experimental runs were performed. Blood pressure and stroke 

volume (flow) both increased immediately (p


glyceryltrinitrate- and sodium nitroprusside-mediated (endothelialindependent) 

response was observed between study groups. In 

south Asian subjects, parameters of pulse wave velocity and 

augmentation index did not differ between those with HF and those 

in control groups. No ethnic differences were detected in pulse wave 

velocity. Conclusion: South Asian patients with HF have impaired 

micro- and macro-vascular endothelial function, but preserved 

arterial elastic properties. Significant ethnic differences in endothelial 

function are present in patients with HF. 

103 SENILE SYSTEMIC AMYLOIDOSIS: A COMMON CAUSE OF 

HEART FAILURE IN THE ELDERLY? 

doi:10.1136/heartjnl-2011-300198.103 


Survival of RVSP quartile. 

Conclusion An RVSP of greater than 42 mm Hg is predictive of 

increased mortality in heart failure. This is finding is independent of 

LVSD and COPD. 

102 ETHNIC DIFFERENCES IN ENDOTHELIAL FUNCTION IN 

CHRONIC HEART FAILURE 

doi:10.1136/heartjnl-2011-300198.102 

1 E Shantsila, 2 P S Gill, 3 G Y H Lip. 1 University of Birmingham Centre for Cardiovascular 

Sciences, City Hospital, Birmingham, UK; 2 University of Birmingham, Primary Care and 

Populational Sciences, Birmingham, UK; 3 University of Birmingham Centre for Cardiovascular 

Science, Birmingham, UK 

Background Endothelial dysfunction is characteristic of patients 

with heart failure (HF) and is associated with an increased risk of 

future cardiovascular events. However, data on ethnic differences in 

endothelial function in HF are scarce. In this study we aimed to 

compare parameters of macro- and micro-vascular endothelial 

function and arterial elasticity in HF age- and sex-matched patients 

of different ethnic origin: (i) white European, (ii) south Asian and 

(iii) African-Caribbean. Additionally, SA patients with systolic HF 

were compared to two matched control groups: (i) south Asian 

patients with coronary artery disease without HF(disease controls) 

and (ii) south Asian “healthy controls”. 

Methods We recruited 186 age/sex-matched patients with HF (ejection 

fraction


can be seen on echocardiogram. A positive troponin is a common 

finding with a subsequent normal coronary angiogram. Incidental 

paraproteins are prevalent in up to 8% of this population and it is 

important to obtain a tissue diagnosis to rule out AL amyloidosis. 

With supportive management medium term outcomes are good. 

104 PROGNOSTIC UTILITY OF CALCULATED PLASMA VOLUME 

STATUS IN CHRONIC HEART FAILURE 

doi:10.1136/heartjnl-2011-300198.104 

1 H Z Ling, 1 N Aung, 1,2 J Flint, 1,2 S Aggarwal, 1,2 S Weissert, 1,2 A Cheng, 3 D P Francis, 

3 J Mayet, 1,2 M Thomas, 1,2 S Woldman, 1,2,4 D O Okonko. 1 University College London 

Hospital, London, UK; 

2 The Heart Hospital, London, UK; 

3 International Center for 

Circulatory Health, NHLI, Imperial College London, London, UK; 4 NHLI Imperial College 

London, London, UK 

Background Plasma volume (PV) expansion is a hallmark feature of 

worsening heart failure that is notoriously underestimated by clinical 

examination. While radioisotope assays optimally quantify PV 

status, numerous haemodialysis-based equations also exist for its 

estimation. The prognostic utility of such formulas in chronic heart 

failure (CHF) is unknown. 

Methods We analysed the relation between estimated PV status and 

mortality in 246 outpatients with CHF (mean (6SD) age 67613 years, 

NYHA class 261, LVEF 2868%). PV status was calculated (Hakim 

RM, et al) by subtracting the patients actual PV ((1-haematocrit) 3 

(a + (b 3 weight)); a and b are gender-specific constants) from their 

ideal PV ((c 3 weight); c¼gender-specific constant). 

Results Median (6IQR) PV status wasd2616550 ml with 78% and 

21% of patients having PV contraction and expansion, respectively. 

Patients with PV excess had significantly higher creatinine and lower 

albumin levels. Over a median follow-up of 13616 months, 36 (15%) 

patients died. PV status predicted mortality (HR 1.001, 95% CI 1.001 

to 1.002, p¼0.001) in a graded fashion (Abstract 104 figure 1A) and did 

so independently of NYHA class, LVEF, weight, haematocrit and 

creatinine. A PV status # 178 ml optimally predicted survival (ROC 

AUC 0.68, p¼0.0007) and conferred a 75% reduced hazard for death 

(HR 0.16, 95% CI 0.07 to 0.37, p


heart disease in 63% and 23% had diabetes mellitus. Patients were 

optimally treated (84% on b-blockers, 88% on ACE inhibitors, and 

46% on spironolactone). The mean daily dose of furosemide was 60 

(3) mg. Very few patients (5%) were sufficient in vitamin D. Patients 

with worse symptoms as measured by NYHA status had lower 

vitamin D levels and higher PTH levels (Abstract 106 figures 1 and 

2). There was also a negative relationship between furosemide dose 

and vitamin D (Abstract 106 figure 3) and, in an unselected subset of 

160 patients (mean peak oxygen uptake (pVo 2 ) 16.6 (0.5) ml/kg/ 

min), there was a positive relationship between pVo 2 and vitamin D 

(Abstract 106 figure 4). Patients with diabetes had lower vitamin D 

levels than non-diabetics (p



Conclusions An expanding RDW and evolving iron deficiency over 

time predict an amplified risk of death in CHF and could be utilised 

for risk stratification or therapeutically targeted to improve 

outcomes. 

108 4D-FLOW CMR DEMONSTRATES THE REGIONAL 

DISTRIBUTION OF AORTIC FLOW DISTURBANCE IN 

MARFAN SYNDROME 

doi:10.1136/heartjnl-2011-300198.108 

Results Significant vortical flow in any segment (defined as flow 

disturbance occupying more than one half of the aortic lumen) was 

present in all patients with MFS, but in only 7/18 controls 

(p


Hypothesis 3T MRI of the carotid artery can identify atherosclerotic 

plaque rupture in patients presenting with TIA or minor stroke. 

Methods 81 patients with carotid artery disease were recruited; 41 

presented acutely with TIA or minor stroke and 40 asymptomatic 

patients acted as the control group. Median time from symptom 

onset to MRI in the symptomatic group was 2.1 days (range 

0.17e7.0). All patients underwent T1, T2 and proton densityweighted 

turbo spin echo MRI to 10 mm either side of the carotid. 

As part of a combined scan protocol, study participants then 

underwent diffusion-weighted imaging (DWI) and Fluid-Attenuated 

Inversion Recovery (FLAIR) imaging of the brain to assess acute and 

chronic injury, respectively. If physically able, patients underwent 

follow-up scanning a minimum of six weeks later. Plaques were 

graded according to the MRI modified American Heart Association 

(AHA) system by two independent reviewers blinded to the clinical 

status of the patient. Statistical analysis was performed using the 

Wilcoxon sign rank test and Fisher 9 s exact test to compare plaques, 

in addition to the Mann Whitney U test to compare cerebral injury. 

Results AHA type VI (ruptured) plaque was seen in 22/41(54%) in the 

symptomatic group vs 8/41(20%) in the asymptomatic group 

(p


cardiac CT that are summarised in Abstract 111 table 1. These incidental 

findings resulted in further investigations, documented in 

Abstract 111 table 2. The mean radiation dose (6 SEM) for CAC 

scoring was 0.6160.03 mSv. The mean radiation dose (6 SEM) for 

subsequent CTCA was 2.66 6 0.32 mSv in high pitch “flash” mode 

(n¼27), 5.8660.50 mSv in prospective mode (n¼64) and 

17.1561.68 mSv in the retrospective mode (n¼25). 


Incidental findings on cardiac CT 

Area Structure Incidental Finding n 

Chest (n¼27) Lung parenchyma Nodule 50% luminal stenosis) using a fifteen 

coronary segments model by an independent investigator blinded to 

the results of ICA. 

Results CS ranged from 0 to 1681 (Mean¼91.76275). Out of 77 

patients with absent CS, 3 had significant CAV on ICA. Despite a 

mean resting heart rate of 82 bpm SD613 and body mass index of 

27 kg/m 2 SD 65, 81% of the CTA images were graded as excellent or 

satisfactory. For all the 1755 segments assessed by CTA irrespective 

of the image quality, CTA had sensitivity, specificity, positive and 

negative predictive values of 71%, 79%, 72% and 78% respectively for 

the detection of any CAV found by ICA. On a patient basis, CTA best 

performed in diagnosing CAV of more than 25% with sensitivity, 

specificity, positive and negative predictive values of 74%, 94%, 79%, 

and 92% respectively. None of the 61 patients with completely 

normal CTA had CAV on ICA. 83 (92%) out of 90 patients who 

responded to a patient survey preferred CTA to ICA as a screening 

test for CAV. Non-coronary cardiac and non-cardiac abnormalities 

were identified in 18% and 14% patients respectively. 

Conclusion The study shows that CTA compares favourably with 

ICA in detecting CAV in heart transplant recipients, and may be a 

preferable screening technique because of its non-invasive nature, 

patient preference and yield of additional information. One has to 

exercise caution in just using CS in these patients as significant CAV 

can be missed out. 

113 DUAL ENERGY CT IMPROVES DIFFERENTIATION OF 

CORONARY ATHEROSCLEROTIC PLAQUE COMPONENTS 

COMPARED TO CONVENTIONAL SINGLE ENERGY CT 

doi:10.1136/heartjnl-2011-300198.113 

1 D R Obaid, 1 P A Calvert, 1 J H F Rudd, 2 D Gopalan, 1 M R Bennett. 1 University of 

Cambridge, Cambridge, UK; 2 Papworth Hospital NHS Trust, Cambridge, UK 

Introduction Vulnerable plaques have a relatively high necrotic core 

area and low fibrous tissue content. Although CT can identify 

plaque components on the basis of their x-ray attenuation, there is 



significant overlap between their attenuation ranges, most crucially 

between necrotic core and fibrous plaque. Recently introduced dual 

energy CT (DECT) permits acquisition of 2 different energy data 

sets simultaneously, with the change in attenuation of plaque 

components to different energies depending upon their material 

composition. We therefore examined whether DECT was better 

than single energy CT in determining plaque components defined by 

virtual histology IVUS. 

Methods 20 patients underwent DECT and 3-vessel VH-IVUS. CT 

data was obtained at peak voltages of 100 kV and 140 kV. 52 plaques 

were chosen with either homogenous fibrous plaque or confluent 

areas of calcified plaque or necrotic core as defined by VH-IVUS. VH- 

IVUS images were co-registered and orientated with the corresponding 

CT images using distance from coronary ostia and fiduciary 

markers (Abstract 113 figure 1). Multiple regions of interest 

(ROI) were placed within the plaque components or in lumen on 

cross sectional CT images pre-classified by VH-IVUS (Abstract 113 

figure 1). ROI densities were measured (in Hounsfield Units) and 

assigned to the plaque component. A dual energy index (DEI) was 

created for each component, defined as the ratio of the difference in 

attenuation at 2 different energies / sum of attenuation with 1000 

added to each attenuation value to avoid negatives. 

data sets permitted resolution of necrotic core and fibrous plaque 

without overlap (Abstract 113 figure 2B). 

Abstract 113 Figure 2 (A) Defined CT attenuation spectra of 

plaque components using a single energy (140kV), calcified plaque 

is distinguishable from all others but necrotic core and fibrous 

plaque overlap. (B) The use of dual energy index from the attenuation 

data at 2 energies (100/140kV) allows significant separation of 

necrotic core and fibrous plaque (p


between September 2007 and August 2010 was included; the total 

dose for the whole examination is used including the scout and nonenhanced 

scan (calcium score). Scans were performed on a Lightspeed 

VCT or HD750 (GE Healthcare). To calculate the effective 

dose a conversion factor was applied to the dose length product of 

each examination. The DLP is the radiation dose in one CT slice 

multiplied by the length of the scan. A cardiac specific conversion 

factor was used rather than a chest conversion factor (0.014) which 

significantly underestimates the effective dose from CTCA. Data 

was transformed and expressed as a geometric mean with 99% CI. 

For each analysis period all scans were included; retrospective, 

prospective, low kV and zero padding. 

Results In the 3-year period 1736 scans were performed. The mean 

radiation dose in the first 6 months of the study (retrospective 

gating) was 29.6 mSv; using the accepted conversion factor at the 

time the mean dose was 14.9 mSv. In March 2008 prospective ECG 

gating was installed; this resulted in a halving of the mean radiation 

dose to 13.6 mSv. In March 2009 the scanner parameters was set to 

zero padding and 100 KV reducing the dose to 7.4 mSv. For the final 

6 months the mean radiation dose for a cardiac scan was 5.9 mSv; 

this Abstract 114 figure 1 incorporates scans performed with 

standard filtered back projection, iterative reconstruction, high 

definition scanning and retrospective ECG gating for a variety of 

differing clinical scenarios. 

115 ATRIAL HIGH RATE EPISODES AND ATRIAL FIBRILLATION 

BURDEN: DO THEY HAVE SIMILAR ASSOCIATION WITH 

CARDIAC REMODELLING? 

doi:10.1136/heartjnl-2011-300198.115 

C W Khoo, S Krishnamoorthy, G Dwivedi, B Balakrishnan, H S Lim, G Y H Lip. 

University Department of Medicine Centre for Cardiovascular Sciences, City Hospital, 

Birmingham, UK 

Background and Objectives Contemporary pacemaker devices allow 

quantification of atrial high-rate episodes (AHREs) and atrial fibrillation 

burden (AFB) accurately. Cumulative ventricular pacing (Vp) 

is associated with development of atrial fibrillation, but it is not 

clear if AHREs and AFB share similar pathophysiologic associations 

with left atrium (LA) and ventricle (LV) function and remodelling. 

Methods In total, 87 patients with dual-chamber pacemaker 

underwent two-dimension (2D) and tissue Doppler imaging (TDI) 

echocardiography. LA volume (LAV) was evaluated by area-length 

method and indexed to body surface area. Septal A 9 was used to 

measured regional LA function. LV systolic and diastolic parameters 

were evaluated by mitral inflow velocity (E, A, E/A), LV ejection 

fraction (biplane Simpson’s) and septal TDI velocity. The presence 

of AHREs (defined by atrial-rate $220 beats/min and $5 minutes) 

and AFB were derived from pacemaker diagnostics. Plasma markers 

of remodelling, matrix metalloproteinases-1 (MMP1) and tissue 

inhibitors of metalloproteinases-1 (TIMP1), were analysed by ELISA. 

Results Baseline characteristics and comorbidities were comparable 

between groups (Abstract 115 table 1). Patients with AHREs had 

significantly larger indexed LAV (p¼0.011) and higher cumulative 

Vp (p¼0.012), but this was not associated with elevation of MMP1 

and TIMP1. Plasma markers, LV systolic and diastolic parameters 

were comparable between groups. In patients with AHREs, the AFB 

ranged from 0 to 99% and correlated with E/A (r¼0.966, p


variation on echocardiographic measurements. This can be quantified 

most clearly in the optimisation process, in which genuine small 

changes in cardiac function (signal) must be detected among 

potentially large beat-to-beat variation (noise). 

Methods and Results In this large study of biological variability, we 

performed over 2000 echocardigraphic measurements in 12 patients. 

We performed separate, replicate measurements at a series of interventricular 

delays of each potential optimisation modality at rest. 

This included (i) 3D systolic dyssynchrony index, (ii) aortic preejection 

time, (iii) interventricular mechanical delay, (iv) LVOT VTI 

and (v) QRS width. The equivalent of 31 optimisations per patient 

were performed. For single measurements at each setting, agreement 

between successive optimisations was low, at 39% for SDI, 41% for 

aortic pre-ejection time, 32% for IVMD, 54% for LVOT VTI and 

58% for QRS width. Agreement between one method and another, 

using single replicates, was similarly low, with the average agreement 

between optima by two methods being only 18% similar to 

pure guesswork. The intraclass correlation coefficient was low for all 

methods at 0.11, 0.51, 0.30, 0.50 and 0.55 respectively. The intraclass 

correlation coefficients improved to 0.19, 0.63, 0.42, 0.54 and 0.66 

(p¼0.001) when averages of paired measurements were used. To 

optimise within 20 ms or 10 ms of the true optimum, requires a 

greater number of measurements, as seen in Abstract 116 figure 1, 

dependant on the intraclass correlation coefficient. The scatter of 

optima obtained reduced (improved) significantly when using 

averaged pairs of measurements compared to single measurements 

from 23 ms to 18 ms (3D SDI), 14 ms to 10 ms (aortic pre-ejection 

time), 28 ms to 22 ms (IVMD), 21 ms to 16 ms (LVOT VTI) and 

14 ms to 10 ms QRS duration (p¼0.0002). 

117 TRICUSPID VALVE ANNULAR DYNAMICS IN NORMAL VS 

DILATED RIGHT HEARTS; A 3D TOE STUDY 

doi:10.1136/heartjnl-2011-300198.117 

L Ring, B Rana, R A Rusk. Papworth Hospital NHS Foundation Trust, Cambridge, UK 

Background The tricuspid valve annulus (TVA) is a complex three 

dimensional structure that is non-planar, and is incompletely 

understood. The dynamics of the normal TVA has not been 

described in any significant detail, nor has the impact of abnormal 

right hearts on the TVA been described. This study was designed to 

assess the feasibility of assessing the TVA throughout the cardiac 

cycle using 3D transoesophageal echo (TOE). 

Methods 20 patients were included, divided into 2 groups: normal 

right hearts (n¼10), and dilated right hearts (n¼10). 3D zoom 

images of the TVA were acquired using an iE33 imaging platform 

and X7-2t transducer (Phillips, Andover, Massachusetts, USA). 

Antero-posterior (AP) diameter, septo-lateral (SL) diameter, area and 

height were measured at 6 points of the cardiac cycle adapting 

commercially available software designed for assessing the mitral 

valve (MVQ, Phillips). The eccentricity ratio was calculated as 

AP/SL. 

Results TVA area decreases during systole in both groups, and is 

greatest in mid-diastole. The area is significantly larger in the 

abnormal group (mean 1795 mm 2 abnormal vs 1204 mm 2 normal; 

p


118 HIGH-RESOLUTION CARDIAC MAGNETIC RESONANCE 

PERFUSION IMAGING VS POSITRON EMISSION 

TOMOGRAPHY FOR THE DETECTION AND LOCALISATION OF 

CORONARY ARTERY DISEASE 

doi:10.1136/heartjnl-2011-300198.118 

G D J Morton, M Ishida, A Chiribiri, A Schuster, S Baker, S Hussain, D Perera, 

M O’Doherty, S Barrington, E Nagel. King’s College London, London, UK 

Background Non-invasive imaging has a key role in the detection of 

coronary artery disease (CAD). Its importance has been affirmed by 

recent National Institute of Clinical Excellence (NICE) guidelines. 

Localisation of ischaemia to a coronary territory is also important in 

patient management. Cardiac Magnetic Resonance (CMR) perfusion 

imaging is a well-established and radiation-free test for these 

purposes. However, there are few data comparing perfusion CMR 

with Positron Emission Tomography (PET), which is widely 

regarded as the non-invasive gold standard. Furthermore novel CMR 

methods, including those based on k-t acceleration techniques, allow 

myocardial perfusion imaging with unprecedented spatial resolution. 

Methods 31 patients with known or suspected CAD referred for 

diagnostic x-ray coronary angiography (XCA) underwent both CMR 

and PET examinations. Both PET and CMR protocols included 

adenosine stress and rest perfusion imaging. CMR perfusion 

imaging was performed at 1.5T with a k-t-accelerated steady-state 

free-precession sequence. PET imaging was performed with 13 N- 

Ammonia. The Abstract 118 figure 1 shows an example. Experts 

blinded to the clinical data analysed the imaging data and experts 

blinded to the imaging results visually analysed the XCA data. A 

significant coronary artery stenosis was defined as $70% reduction 

in diameter or a fractional flow reserve 13 mm) 

(9%), arrhythmogenic right ventricular cardiomyopathy (ARVC) 

(6%) and Ebstein anomaly (3%). Two patients (6%) had mid wall 

late gadolinium enhancement. In the remaining 20 (59%) patients, 

no abnormalities on CMR were detected. 




All patients 

(n[34) 

Normal CMR 

(n[20) 

Abnormal CMR 

(n[14) 

p value 

Age (years (median, IQR)) 54.368.9* 57.5 (19.7) 48.5 (17.0) 0.6 

Male gender (no, %) 19 (55.8%) 11 (55.0%) 8 (57.1%) 0.59 

BMI (mean, kg/m2) 28.365.6 27.664.9 29.366.5 0.37 

LVEDV (ml (median, IQR)) 155.0 (58.0) 133.0 (41.5) 182.5 (60.5) 0.012 

LVESV (ml (median, IQR)) 51.0 (26.0) 48.0 (12.5) 71.5 (39.5) 0.005 

LVEF (ml (mean, SD)) 60.6613.9 66.165.5 55.7613.6 0.004 

LV thickness (mm (median, IQR)) 11.0 (7.4) 9.0 (6.1) 12.5 (9.4) 0.059 

LVMI (g/m 2 (median, IQR)) 72.5618.1* 64.0 (15.0) 83.0 (14.5) 0.001 

*mean, SD. IQR. 

Conclusions There is a high rate of sub-clinical cardiomyopathy 

(41%) detected by CMR in asymptomatic patients with LBBB despite 

normal echocardiograms. These findings support the claim that CMR 

is a valuable adjunct to conventional investigations in asymptomatic 

LBBB. Further studies are needed to evaluate the prognostic implications 

of CMR abnormalities in this cohort of patients. 

Abstract 119 Figure 1 CMR findings in asymptomatic patients with 

LBBB and normal echocardiogram. 

120 COMPARISON AND REPRODUCIBILITY OF STANDARD AND 

HIGH TEMPORAL RESOLUTION MYOCARDIAL TISSUE 

TAGGING IN PATIENTS WITH SEVERE AORTIC STENOSIS 

doi:10.1136/heartjnl-2011-300198.120 

The MBH SR curves were filtered with a moving average (MA) to 

reduce noise sensitivity, results from a sample width of three and 

five were examined. Differences between SBH and MBH were 

assessed using Wilcoxon signed-rank test as not all measures were 

normally distributed. Reproducibility assessments were carried out 

on all techniques. 

Results PeakEcc was significantly higher with MBH vs SBH, but 

reproducibility was slightly worse. Results are summarised in 

Abstract 120 table 1. Systolic SR was approximately equal with all 

techniques although MBH using MA of five led to a borderline 

significant reduction. Diastolic SR was higher when measured with 

MBH although only significant using MA of three. Systolic and 

diastolic SR measures were more reproducible with MBH compared 

with SBH, except for the diastolic SR using MA of three, which was 

substantially worse. Strain and SR curves for the same patient are 

shown in Abstract 120 figure 1. 


Peak systolic 

strain (%) 

Peak systolic 

strain rate (1/s) 

Peak diastolic 

strain rate (1/s) 

SBH e13.762.4 e0.7460.15 0.7560.27 

MBH (MA of three) e15.163.1 e0.7360.11 

1.1260.54 

(p¼0.023 vs SBH) (p¼0.877 vs SBH) (p¼0.017 vs SBH) 

MBH (MA of five) 

SBH reproducibility 

(MD6SD; CoV; B-A) 

MBH reproducibility 

(MA of three) 


MBH reproducibility 

(MA of five) 


MD6SD¼mean 

difference 6 SD 

e15.163.1 

(p¼0.023 vs SBH) 

0.5061.52; 11.1%; 

e2.5 to 3.5 

1.1362.23; 14.7%; 

e3.3 to 5.6 

1.1362.23; 14.7%; 

e3.3 to 5.6 

CoV¼coefficient 

of variation 

e0.6960.10 

(p¼0.049 vs SBH) 

e0.0160.13; 18.1%; 

e0.26 to 0.28 

0.0660.04; 5.3%; 

e0.02 to 0.14 

0.0460.05; 7.8%; 

e0.07 to 0.15 

BeA¼BlandeAltman 

95% limits of agreement 

0.9160.36 

(p¼0.535 vs SBH) 

e0.0460.16; 21.0%; 

e0.36 to 0.27 

e0.1360.44; 39.0%; 

e1.00 to 0.75 

0.0960.15; 16.9%; 

e0.39 to 0.22 

1 C D Steadman, 

2 N A Razvi, 

1 K I E Snell, 

3 J P A Kuijer, 

3 A C van Rossum, 

4 G P McCann. 

1 Leicester Cardiovascular Biomedical Research Unit, Leicester, UK; 

2 Department of Cardiovascular Sciences, University Hospitals of Leicester, Leicester, 

UK; 3 Department of Physics and Medical Technology, ICaR-VU, VU University Medical 

Center, Amsterdam, The Netherlands; 4 University Hospitals of Leicester, Leicester, UK 

Objectives The aim of this study was to compare and assess the 

reproducibility of left ventricular (LV) circumferential peak systolic 

strain (PeakEcc) and strain rate (SR) measurements using standard 

and high temporal resolution myocardial tissue tagging in patients 

with severe aortic stenosis (AS). 

Background Myocardial tissue tagging with cardiac magnetic resonance 

(CMR) can be used to quantify strain and SR, however, there 

are little data on the reproducibility. Diastolic SR may be of 

particular interest as it may be the most sensitive marker of diastolic 

dysfunction often occurring early in the course of disease. 

Methods Eight patients with isolated severe AS without obstructive 

coronary artery disease were prospectively enrolled. They underwent 

CMR in a 1.5T scanner (Siemens Avanto) on two separate 

occasions, median interval 12 days. Complementary tagged 

(CSPAMM) images were acquired with both a single breath-hold 

(SBH: temporal resolution 42 ms), and a multiple brief expiration 

breath-hold (MBH: high temporal resolution 17 ms) sequence. Midwall 

PeakEcc was measured in the LV at mid-ventricular level with 

HARP Version 2.7 (Diagnosoft, USA). SR was calculated from the 

strain data; SR¼Ecc2-Ecc1/Time2-Time1. PeakEcc, peak systolic and 

diastolic SR were read from curves of strain and SR against time. 



Conclusions It is likely than SBH may be adequate or even superior to 

MBH for assessment of PeakEcc. The increased temporal resolution of 

MBH may be advantageous for examining systolic and diastolic SR; a 

MA of five for diastolic SR may be the preferred method for quantification 

given the improved reproducibility of this measure. 

A69


121 INCIDENTAL EXTRA-CARDIAC FINDINGS ON CLINICAL 

CMR; A COMPARISON OF 3 HASTE TECHNIQUES 

doi:10.1136/heartjnl-2011-300198.121 

1 R B Irwin, 

2 T Newton, 

3 C Peebles, 

4 A Borg, 

5 D Clark, 

4 C Miller, 

6 N Abidin, 

4 M Greaves, 4 M Schmitt. 1 Wythenshawe Hospital, Manchester, UK; 2 Royal Blackburn 

Infirmary, Blackburn, UK; 

3 Southampton General Hospital, Southampton, UK; 

4 Wythenshawe Hospital, University Hospitals of South Manchester NHS Trust, 

Manchester, UK; 5 Alliance Medical, Wythenshawe Hospital CME unit, Manchester, 

UK; 6 Salford Royal Hospital, Salford, UK 

Introduction Cardiac magnetic resonance (CMR) is an increasingly 

important imaging modality, which by necessity incorporates a 

large field of view. Both “localiser” and multiple slice half-fourier 

spin echo (eg, HASTE) sequences provide coverage of the thorax and 

upper abdomen. Such imaging may reveal hitherto unexpected 

incidental extra-cardiac findings (IEF). First we sought to assess the 

frequency of IEF found on clinically indicated CMR scans. Second 

we compared the 3 clinically used HASTE acquisition protocols in 

this context. Lastly we determined the impact of the 3 different 

protocols on acquisition time and image quality. 

Methods Three subsequent groups of 238 patients (714 patients in 

total), all referred for clinically indicated CMR, were scanned with 

either breath-hold (BH) HASTE (Group 1), free breathing (FB) 

HASTE (Group 2) or diaphragmatic navigated (NAV) HASTE 

(Group 3). Additionally “localiser” sequences performed in 3 orthogonal 

planes were analysed. All 714 clinical reports were reviewed 

regarding the presence of IEF. These were categorised as either minor, 

or major if recommendations for further investigation, follow-up, 

and/or clinical correlation were made. Finally, to determine the 

impact of each HASTE protocol on acquisition time and image 

quality, an additional cohort of 15 patients underwent 3 protocols 

back to back in a random fashion. The length of each acquisition was 

timed and image quality was reviewed and scored externally. 

Results A total of 180 IEF were found in 162 (22.7%) out of 714 

patients. There was no significant difference in frequency of IEF 

between the 3 HASTE groups. Out of 180 IEF, 88 were considered 

minor and 92 major findings. Of the latter, 8 (1.1%) were considered 

highly significant. These included one bronchoalveolar carcinoma 

stage 1B requiring lobectomy, 2 cases of florid sarcoidosis in patients 

presenting with VT and “structurally normal hearts” on echocardiography, 

one case of pulmonary aspergillosis, 2 cases of 

advanced pulmonary fibrosis, one ascending thoracic aortic 

aneurysm and a case of iatrogenic liver haemorrhage following 

placement of a pericardial drain. FB HASTE acquisition (6962.5 s) 

was significantly faster than BH (10563.8 s) and NAV (12162.7 s), 

p


pre-transplant assessment. The median age was 45 yrs (range 

26e63), with 41% female and a median time between scans of 

1.4 yrs (range 0.6e3.0). 59 patients (60%) had two consecutive 

normal scans. The remaining 40 patients had at least one abnormal 

scan. 16% of patients with a normal 1st scan developed an abnormal 

2nd scan within a median period of 1.4 years. 28 (70%) of the 

patients with an abnormal MPS underwent angiography, of these 12 

required revascularisation (either PCI or CABG). Of the remaining 

16 patients; 1 died before angiography and the other 15 patients 

were treated with medical therapy. Of the 59 patients with two 

normal scans; 3 underwent angiography during the study period (for 

new symptoms), 1 of these patients required revascularisation after 

presenting with an ACS. 2 had minor plaque disease. 

Conclusions 40% of SPK patients on the waiting list have an 

abnormal MPS. Of the patients with normal scans 5% required an 

angiogram because of new symptoms with only 2% requiring 

revascularisation. Of the patients undergoing angiography driven by 

MPS 43% subsequently underwent revascularisation. The current 

screening interval is successfully monitoring changes in the patients’ 

cardiovascular status with only one patient requiring an intervention 

which was not predicted by MPS. Therefore a near annual 

MPS is a useful, non-invasive means by which to monitor patients 

at very high risk of asymptomatic cardiovascular disease while 

awaiting a SPK transplant. 

124 VALIDATION OF THE BCIS-1 MYOCARDIAL JEOPARDY 

SCORE USING CARDIAC MRI 

doi:10.1136/heartjnl-2011-300198.124 

1 G D J Morton, 2 K De Silva, 1 M Ishida, 1 A Chiribiri, 1 A Indermuhle, 1 A Schuster, 

2 S Redwood, 1 E Nagel, 1 D Perera. 1 King’s College London, London, UK; 2 Guy’s and St 

Thomas’ NHS Foundation Trust, London, UK 

Introduction The recently described angiographic BCIS-1 Myocardial 

Jeopardy Score (BCIS JS) was designed to classify the extent of 

coronary artery disease (CAD). It provides a semi quantitative 

estimate of the amount of myocardium at risk as a result of severe 

coronary stenoses (0¼no jeopardy; 12¼maximum jeopardy). 

Advantages include ease of use and universal applicability including 

classification of left main stem disease and CABG. However 

anatomic tests, including the BCIS JS, do not incorporate myocardial 

ischaemia and scar, which are important for management and 

prognosis. Cardiac magnetic resonance (CMR) imaging allows reliable 

assessments of myocardial ischaemia and scar in a single 

examination and was used to examine the functional relevance of 

the BCIS JS. 

Methods 60 consecutive patients with angina and known or 

suspected CAD referred for diagnostic x-ray coronary angiography 

underwent CMR examination at a single UK centre. CMR included 

standard functional and scar imaging and also high-resolution k-t 

accelerated adenosine stress and rest perfusion imaging at 1.5T (40 

patients) or 3T (20 patients). Expert observers blinded to the clinical 

data analysed the angiographic and CMR data. The BCIS JS was 

calculated from visual analysis of the coronary angiogram. CMR 

perfusion and scar data were segmented according to the standard 

17-segment model excluding the apex. Segments were subdivided 

into equal endo- and epicardial sub-segments, each assigned 3% of 

the total myocardial volume and classified as normal, ischaemia or 

scar. Myocardial ischaemia and scar burden were calculated and 

correlated with the BCIS JS individually and as a combined score 

(Abstract 124 figure 1). 


Results Patient characteristics are summarised in the Abstract 124 

table 1. 2 patients were excluded (1 claustrophobia; 1 incomplete 

imaging data). Mean interval 6 SD between CMR and coronary 

angiography was 40647 days. 13 patients (22%) with no history of 

myocardial infarction had CMR evidence of prior infarction. There 

was a strong correlation between the BCIS JS and myocardial 

ischaemic burden: Pearson’s r¼0.75, p



Characteristic 

Number of patients 

Age (mean6SD) 65610 

Left ventricular ejection fraction (mean6standard deviation) 59614% 

Male 48 (83%) 

Diabetes 17 (29%) 

Previous CABG 13 (22%) 

Previous percutaneous coronary intervention 22 (38%) 

Previous MI 10 (17%) 

Hypertension 38 (66%) 

125 ASSESSING PATIENT BENEFIT FROM THE 

REVASCULARISATION OF CHRONICALLY OCCLUDED 

CORONARY ARTERIES BY ADVANCED CARDIOVASCULAR 

MRI TECHNIQUES 

doi:10.1136/heartjnl-2011-300198.125 

1 N J Artis, 2 A Crean, 1 A Zaman, 1 S Sorbron, 1 A N Mather, 1 S G Ball, 1 S Plein, 

1 J P Greenwood. 1 University of Leeds, Leeds, UK; 2 Toronto General Hospital, Toronto, 

Canada 

Background Cardiovascular magnetic resonance (CMR) imaging can 

provide an array of information about cardiac function and anatomy. 

The utility of CMR in the setting of coronary artery chronic total 

occlusion (CTO) has not been fully investigated. We set out to 

examine the ability of CMR to show regional improvements in left 

ventricular (LV) function and perfusion and to investigate if any 

features were able to predict those that benefit from revascularisation. 

Methods Twenty-seven patients with single vessel CTO were 

recruited from clinical waiting lists and underwent a comprehensive 

CMR assessment prior to and 6 months following attempted CTO 

revascularisation. A multi-parametric CMR protocol was performed 

which included cine imaging to assess regional wall thickness/ 

thickening and global LV function, rest and adenosine stress perfusion 

imaging (Fermi model), low dose dobutamine stress to assess 

inotropic reserve, and late gadolinium enhancement (LGE) imaging 

to determine scar location and extent. Using the AHA 16 segment 

model only segments supplied by the CTO artery were studied for 

functional improvement. Data are presented as mean (SD). 

Results Procedural success in terms of revascularisation of the 

occluded artery was achieved in 23 of the 27 patients (85%, 20 with 

PCI and 3 with CABG). In those with successful revascularisation 

by PCI LV volumes reduced (EDV 185 (54) vs 174 (50) p


Introduction The National Institute for Health and Clinical Excellence 

(NICE) have released guidelines for the investigation of chest pain of 

recent onset (1). There is concern that the guidelines will increase 

the burden on cardiac imaging, requiring service reconfiguration and 

investment (2, 3). This study was performed to assess the impact of 

the guidelines on outpatient cardiology services in the UK. 

Methods 595 consecutive patients attending chest pain clinics at 

two hospitals over six months preceding release of the NICE 

guidelines (51% male; median age 55 yrs (range 22e94 yrs)) were 

risk stratified using NICE criteria. Preliminary cardiac investigations 

recommended by NICE were compared with existing clinical practice 

and the relative costs calculated. 

Results NICE would have recommended 443 patients (74%) for 

discharge without cardiac investigation, 10 (2%) for cardiac 

computed tomography (CCT), 69 (12%) for functional cardiac 

imaging and 73 (12%) for invasive coronary angiography (ICA). 

Relative to existing practice there would have been a trend towards 

reduced functional cardiac imaging ( 24%; p¼0.06) and increased 

CCT (+43%; p¼0.436) but a significant increase in ICA (+508%; 

p


Background IMR is a simple invasive measure of microvascular 

function available at the time of pPCI. T2-weighted non-contrast 

CMR can reveal myocardial oedema, and in the post-infarct population 

this represents the ischaemic area at risk (AAR). Contrastenhanced 

CMR delineates the area of myocardial infarction. The 

volume of myocardium within the AAR, but not contained within 

the infarct area is salvaged myocardium. 

Methods 108 patients with STEMI underwent invasive coronary 

physiology measurements during pPCI and had a subsequent CMR 

scan at a median of 19 h post pPCI. Short axis non-contrast T2- 

weighted images were acquired and delayed enhancement imaging 

was performed following administration of intravenous gadolinium 

(0.1 mmol/kg). AAR was determined and myocardial salvage was 

calculated as AARdinfarct area. 

Results IMR was 29 (21), AAR 32% (13%) and myocardial salvage 

6% (9%)dall mean (SD). Spearman rank correlation between IMR 

and AAR was 0.27 (p 0.02) and between IMR and salvage was 0.31 

(p 0.01). IMR was also a multivariate predictor of AAR (p 0.01) and 

a negative multivariate predictor of myocardial salvage (p 0.02). 

Conclusions IMR measured acutely correlates with AAR and correlates 

negatively with myocardial salvage as determined by MRI. 

repeatability co-efficient (RC) 2.14; intra-observer R¼0.99, RC 1.49). 

Reproducibility of global e cc measurements by HARP was somewhat 

lower, but still high (inter-observer R¼0.89, RC 4.80; intraobserver 

R¼0.98, RC 2.73). There was much greater variability in 

segmental e cc measurements using both methods, particularly with 

HARP (Abstract 130 figure 2). 

130 COMPARISON OF HARMONIC PHASE IMAGING WITH 

LOCAL SINE WAVE MODELLING FOR THE ASSESSMENT OF 

CIRCUMFERENTIAL MYOCARDIAL STRAIN USING TAGGED 

CARDIOVASCULAR MAGNETIC RESONANCE IMAGES 

doi:10.1136/heartjnl-2011-300198.130 

1 A N Borg, 1 C A Miller, 2 C D Steadman, 2 G P McCann, 1 M Schmitt. 1 University 

Hospital of South Manchester, Manchester; 2 NIHR Leicester Cardiovascular Biomedical 

Research Unit, Leicester, UK 

Introduction Assessment of myocardial strain promises to become an 

important quantitative tool in early diagnosis of cardiac disease and 

treatment monitoring. Advances in image processing software have 

facilitated rapid and clinically feasible analysis of strain from tagged 

cardiac magnetic resonance (CMR) images. Harmonic Phase Analysis 

(HARP) or Local Sine Wave Modelling (SinMod) can be used for 

automated derivation of strain. We obtained tagged CMR images to 

compare measurements of left ventricular (LV) circumferential 

strain obtained using a HARP with a SinMod method. 

Methods Ten normal controls, 10 hypertrophic and 10 dilated 

cardiomyopathy patients (mean age 46.6614.8 years) were 

included. Spatial modulation of magnetisation using short-axis LV 

slices at mid-ventricular level, with a temporal resolution of 

30e50 mS, were obtained using a 1.5 Tesla scanner (Siemens 

Avanto) with a 32-channel coil. Global and segmental transmural 

peak circumferential strains (e cc ) were measured using HARP 

(Diagnosoft, USA, version 2.7) and SinMod (InTag, University of 

Lyons, France, version 3.6.1). Prior to running the algorithm, both 

methods involve manual tracing of the endocardial and epicardial 

borders, and localisation of right ventricle-to-septum insertion 

points, in one frame. Agreement between HARP and SinMod was 

assessed by Spearman’s correlation co-efficient R and Bland Altman 

methods. Repeated measurements were carried out on 10 randomly 

selected scans to assess reproducibility. 

Results There was a high level of agreement between HARP and 

SinMod for global e cc (HARPdSinMod mean difference: 0.12%, 

95% limits of agreement: 5.69% to 5.45%, R¼0.83, p


Conclusions HARP and SinMod methods show a high level of 

agreement for assessment of global mid-ventricular transmural 

circumferential strain, with good reproducibility for both individual 

methods. Agreement is much lower for segmental measurements; 

poor reproducibility for segmental measurements using both techniques 

probably reflect user variability in identification of right 

ventricular septal insertion points and contour tracing. 

131 AETIOLOGICAL ROLE OF FOLATE DEFICIENCY IN 

CONGENITAL HEART DISEASE: EVIDENCE FROM 

MENDELIAN RANDOMISATION AND META-ANALYSIS 

doi:10.1136/heartjnl-2011-300198.131 

V Mamasoula, T Pierscionek, D Hall, J Palomino-Doza, A Topf, T Rahman, J Goodship, 

B Keavney. Institute of Human Genetics, Newcastle upon Tyne, UK 

Background The existence of a causal relationship between lower 

levels of plasma folate and congenital heart disease (CHD) remains 

contentious. Randomised trials of this question are not possible, in 

view of the known protective effect of folate against neural tube 

defects (NTDs). Folate fortification of flour is known to reduce the 

incidence of NTDs, but it is not known whether there is any effect 

on CHD. Clarity regarding the relationship between folate and 

CHD could potentially inform the practice of folate fortification. We 

present a genetic approach using “Mendelian randomisation” to 

determining the causality of folate in CHD risk. 

Methods We compared genotype frequencies at the methylene 

tetrahydrofolate reductase (MTHFR) C677T single nucleotide 

polymorphism (SNP) in 1186 CHD cases and 4168 controls. The TT 

genotype at MTHFR C677T is known to be associated with lower 

activity of MTHFR and plasma folate, and higher levels of plasma 

homocysteine. The effect of TT genotype on plasma folate levels is 

greater in conditions of folate deficiency. Thus, if lower plasma 

folate had a causal effect on CHD risk, a higher frequency of TT 

genotype among CHD cases than among healthy controls would 

be anticipated, and this would be expected to be more marked 

in conditions of folate deficiency. We placed our results in the 

context of a meta-analysis of all previously published studies of this 

question (to September 2010), which together included 1883 cases 

and 3069 controls in 25 studies. Thus, the combined analyses 

included 3069 CHD cases and 7271 controls. We used randomeffects 

models to combine the data. We conducted sensitivity 

analyses to examine folate fortification of flour as a potential source 

of heterogeneity. 

Results The primary genotyping data in 1186 cases and 4168 

controls revealed a trend towards increased risk with the TT 

genotype, but this did not reach statistical significance (OR 1.15 

(95% CI 0.94 to 1.40)). Combination of our primary data with 

previous studies, however, revealed association in the larger dataset 

(OR 1.45 (95% CI 1.12 to 1.89); p¼0.005). The population attributable 

fraction for the TT genotype was 3% of CHD. There was no 

evidence of publication bias among the contributing studies. We 

discovered folate fortification status to be a significant source of 

heterogeneity. Studies conducted in countries with mandatory 

folate fortification showed no effect of C677T genotype on CHD 

risk (OR 0.96 (95% CI 0.64 to 1.44)), whereas studies conducted in 

countries without mandatory fortification showed a significant 

effect of genotype (OR 1.63 (95% CI 1.19 to 2.25)). These ORs were 

significantly different from each other (p¼0.032). 

Conclusions We demonstrate genetic evidence in favour of a causal 

relationship between plasma folate and CHD. The absence of a 

genetic association in countries practicing folate fortification 

suggests that fortification largely abrogates the risk of CHD 

attributable to folate deficiency. 


132 NON-SYNONYMOUS SMAD6 MUTATIONS IMPAIRED 

INHIBITION OF BMP SIGNALLING IN PATIENTS WITH 

CONGENITAL CARDIOVASCULAR MALFORMATION 

doi:10.1136/heartjnl-2011-300198.132 

1 H L Tan, 1 E A Glen, 1 A L Topf, 1 D H Hall, 2 J J O’Sullivan, 2 L Sneddon, 2 C Wren, 

3 P Avery, 4 R J Lewis, 5 P ten Dijke, 1 H M Arthur, 1 J A Goodship, 1 B D Keavney. 

1 Institute of Human Genetics, Newcastle University, Newcastle upon Tyne, UK; 

2 Freeman Hospital, Newcastle upon Tyne, UK; 3 School of Mathematics & Statistics, 

Newcastle University, Newcastle upon Tyne, UK; 4 Institute for Cell and Molecular 

Biosciences, Newcastle University, Newcastle upon Tyne, UK; 

5 Department of 

Molecular Cell Biology and Center for Biomedical Genetics, Leiden University, Leiden, UK 

Introduction Congenital cardiovascular malformation (CVM) 

exhibits familial predisposition but the specific genetic factors 

involved are unknown. Bone morphogenetic proteins (BMPs) regulate 

many processes during development, including cardiac development. 

Five genes of the BMP signalling were surveyed for novel 

variants predisposing to CVM risk. One of the genes, SMAD6, 

functions as an inhibitory SMAD which preferentially inhibits BMP 

signalling. The SMAD6 knockout mouse is characterised by cardiac 

valve and outflow tract defects, including aortic ossification. We 

hypothesised that rare functional variation in SMAD6 could 

predispose to congenital cardiovascular malformation (CVM). 

Methods The coding regions of BMP2, BMP4, BMPR1A, BMPR2 and 

SMAD6 were sequenced in 90 unrelated Caucasian cases of CVM. 

The MH2 domain of SMAD6 were further sequenced in additional 

346 CVM patients. Functional effects of the wild-type and variant 

SMAD6 proteins were expressed in C2C12 cells and their capacity to 

inhibit ALK3 activated expression of a BMP-responsive reporter, or 

to inhibit osteogenic differentiation (using an alkaline phosphatase 

assay) was assessed. 

Results We identified two novel non-synonymous variants, P415L 

and C484F, that were not present in 1000 ethnically-matched 

controls. P415L was identified in a patient with congenital aortic 

stenosis and C484F was identified in a patient with coarctation and 

calcification of the aorta. Both mutations are in evolutionarily 

conserved amino acid residues and are predicted to be damaging by 

in silico analysis. This was confirmed in functional assays as both 

SMAD6 variants failed to inhibit BMP signalling compared with 

wild-type SMAD6. The P415L mutant appeared to be hypomorphic 

whereas C484F appeared to be a null allele in the luciferase assay. 

The C484F mutant had a significantly (p


subgroups. Participants completed validated, age-appropriate questionnaires 

examining standard psychological parameters. Participants 

also underwent an evaluation of exercise, including formal 

exercise stress testing and measurement of free-living activity using 

an ActiGraph accelerometer. Results were analysed using parametric 

methods. 143 patients (mean age 15.6 years) consented to participate, 

86 were male (60%) and 105 had major CHD (73%). Diagnostic 

subgroups included 39 acyanotic (27.3%), 61 acyanotic 

corrected (42.7%), 30 cyanotic corrected (21.0%) and 13 (9%) 

cyanotic palliated patients. Beck Youth Inventory demonstrated 

that individuals with major CHD, particularly cyanotic palliated 

patients, had higher anxiety scores (p value 0.01 ( 8.42, 1.13)). 

There were no significant differences across study groups for selfesteem 

or other psychological parameters. 134 participants (93.7%) 

took part in regular exercise each week. There was no significant 

difference in activity score between study groups. On formal exercise 

testing, more complex patients performed worse at peak exercise. 

Exercise time for acyanotic group 11.73 mins (sd 3.74) 

compared to 8.26 mins (sd 4.08) in cyanotic palliated group, p value 

0.002 (1.32, 5.61)). However, patients with major CHD had significantly 

higher activity counts. Correlation analysis showed that selfesteem 

and health locus of control were important predictor variables 

for activity. Self-esteem and mood seem well preserved in 

adolescents with CHD as a whole. The majority of young people 

with CHD, in this group, take part in regular exercise. Surprisingly, 

complex patients rate themselves to be as active as those with minor 

CHD. While accelerometer data indicate that the group may be 

more active day to day, they are limited in terms of peak exercise 

duration. The experience of growing up with a chronic condition 

may therefore have a positive effect on psychological health and 

interventions targeted around this area may influence activity. 

134 MUTATIONS IN THE SARCOMERE PROTEIN GENE MYH7 IN 

EBSTEIN’S ANOMALY 

doi:10.1136/heartjnl-2011-300198.134 

1 T Rahman, 1 J Goodship, 2 A Postma, 2 K Engelen, 2 B Mulder, 3 S Klaassen, 4 B Keavney. 

1 Institute of Human Genetics, Newcastle upon Tyne, UK; 2 Academic Medical Centre, 

Amsterdam, The Netherlands; 3 Max-Delbrueck-Center for Molecular Medicine, Berlin, 

Germany; 4 Institute of Human Genetics, Newcastle upon Tyne, UK 

Background Ebstein’s anomaly is a rare congenital heart malformation 

characterised by adherence of the septal and posterior leaflets of 

the tricuspid valve to the underlying myocardium. As there have 

been reports of abnormal left ventricular morphology and function 

in patients with Ebstein’s anomaly we hypothesised that mutations 

in the b-myosin heavy chain (MYH7) may be associated with 

Ebstein’s anomaly. 

Methods MYH7 mutation analysis was undertaken in 141 unrelated 

affected individuals with Ebstein’s anomaly using next-generation 

sequencing on the 454 platform. 64 probands had no associated 

cardiac anomalies. The most common associated cardiac malformation 

were atrial septal defect (48 probands) and left ventricular 

non-compaction (LVNC) (7 probands). Where mutations were 

discovered, family studies were undertaken and the segregation of 

the mutation with disease was investigated. 

Results Heterozygous mutations were identified in eight of the 

probands including six of the seven with LVNC. Two patients had 

the same mutation; of the seven distinct mutations, five were novel 

(four missense changes and an in-frame deletion) and two have been 

previously reported in patients with hypertrophic cardiomyopathy. 

Family studies revealed additional members with LVNC for three of 

the probands, one of whom also had a relative with Ebstein’s anomaly. 

In these three pedigrees the mutation segregated with disease. 

Conclusions Mutations in MYH7 occur relatively frequently in 

Ebstein’s anomaly accompanied by LVNC. This study is another 

example of mutations in a sarcomere protein causing congenital 

heart malformation. 

135 GENE SCREENING OF THE SECONDARY HEART FIELD 

NETWORK IN TETRALOGY OF FALLOT PATIENTS 

doi:10.1136/heartjnl-2011-300198.135 

ATöpf, H R Griffin, D H Hall, E Glen, B D Keavney, J A Goodship; The Change Study 

Collaborators. Institute of Human Genetics, Newcastle upon Tyne, UK 

Background Tetralogy of Fallot (TOF) is the most common cyanotic 

heart defect, affecting 3e6 infants for every 10 000 births. TOF is 

phenotypically well defined; it consists of four heart abnormalities: a 

VSD, an over-riding aorta, a narrowed pulmonary valve and right 

ventricular hypertrophy. During heart development two heart fields 

can be distinguished. The first one gives origin to the left ventricle 

and contributes to the right and left atria. The secondary heart field 

gives origin to the right ventricle and the outflow tract. Each of 

these fields can be identified by the expression of specific markers. As 

TOF is a malformation of the outflow tract, we hypothesised genes 

involved in the regulatory network of the secondary heart field were 

particularly good candidates for TOF susceptibility. 

Methods We examined by standard Sanger method the full exonic 

and intron boundary regions of 14 secondary heart field genes, 

namely NKX2-5, GATA4, TBX20, MEF2C, BOP, HAND2, FOXC1, 

FOXC2, TBX1, FOXA2, FGF10, FGF8, ISL1 and FOXH1, in a panel of 

93 TOF patients. All newly discovered rare variants were checked in 

a panel of 1000 control chromosomes by multiplex Sequenom 

assays. When available, parents of cases were screened to assess 

inheritance of the rare variant. 

Results We re-sequenced a total of 80 exons and w30 Kb. Among 

the 14 genes studied we found a total of 50 new variants, of which 

23 were exclusive to the patient population, ie, were absent from 

1000 normal chromosomes. Nine of these variants cause change in 

the aminoacid sequence. We found a functional 19aa deletion of a 

highly conserved region of TBX1. InFOXC1 we found a contraction 

of both alanine and glycine tracts. An alanine expansion, usually 

known to be deleterious, was found in HAND2. Four non-synonymous 

changes were found in FOXA2. Most patients presented just 

one variant, however 3 patients presented two, and one patient 

presented up to 3 variants. All patients were heterozygotes for the 

variants, and had inherited them from one of their phenotypically 

normal parents (when parental information was available). In 

addition, 75% of the variants were inherited from the mother. 

Conclusions Although genes of the secondary heart field seemed 

good candidates for TOF susceptibility, thus far we have not found 

any strong indication of unique causal effect, as all variation found 

in probands was also present in their unaffected parents. However, 

the presence of multiple variants in the same proband may result in 

the disruption of gene-gene interactions in the secondary heart field 

pathway, which in turn may lead to outflow tract defects. Based on 

our results, it would seem more likely that susceptibility to TOF be 

determined by a larger number of small genetic contributions which 

are also modified by environmental factors. It is evident that larger 

scale analysis of significant numbers of whole genomes/exomes will 

be necessary to better understand the molecular aetiology of TOF. 

136 SHOULD FAMILIAL SCREENING BE ROUTINELY OFFERED TO 

PATIENTS WITH BICUSPID AORTIC VALVE DISEASE? 

doi:10.1136/heartjnl-2011-300198.136 

R Panayotova, S Hosmane, A Macnab, P Waterworth. University Hospital of South 

Manchester, Manchester, UK 

Background Bicuspid aortic valve (BAV) disease is one of the most 

common congenital cardiac abnormalities with prevalence in the 



general population of up to 2%. There has been growing evidence 

supporting its familial predisposition with an autosomal dominant 

pattern of inheritance. It is often associated with ascending aortic 

dilatation and dissection, occurring at a younger age than in patients 

with idiopathic aortic aneurysms. BAV disease carries a 6% lifetime 

risk of aortic dissection, 9 times higher than that of the general 

population. Thus, the presence of BAV and dilatation of the 

ascending aorta requires regular monitoring with a view to timely 

pre-emptive surgery. Current ACC/AHA guidelines state that 

echocardiographic screening of first degree relatives of patients with 

BAV is recommended. This, however, to our knowledge, is not 

routinely done within the UK. 

Methodology and Results We set out to explore the practicalities of 

running a routine echocardiographic screening programme for first 

degree relatives of patients with BAV disease. We identified a total of 

47 patients who had undergone aortic valve surgery performed by 

the same Consultant Cardiothoracic Surgeon in the context of BAV 

disease in the period May 2007eSeptember 2009. Screening of first 

degree relatives was offered to these patients. 24 patients (51%) gave 

us information regarding family members who would like to attend 

for an echocardiogram. A total of 75 first degree relatives were 

referredean approximate average of 3 per patient. Out of these, 52 

relatives (70%) actually attended for an appointment. The 

remainder did not undergo testing with us as they either lived in a 

different geographic region or expressed a personal preference not to 

be scanned at this time. The incidence of newly diagnosed bicuspid 

aortic valve disease in our cohort of first degree relatives was 8% (4 

out of 52 relatives). One of these asymptomatic individuals had a 

significant ascending aortic aneurysm, which required prompt 

surgery. Among the relatives of the 24 index patients, there were a 

total of 8 cases (3: 1 ratio) of bicuspid aortic valve diseasedeither 

known or newly diagnosed via screening. 

Conclusions There is a relatively high prevalence and incidence of 

bicuspid aortic valve disease among first degree relatives of patients 

with this common congenital cardiac abnormality. Routine echocardiographic 

screening should be offered to these families. Implementing 

such a programme is limited by adequate motivation to 

attend for a screening test if well, and by varying clinical practice in 

different geographic regions. Patients with bicuspid aortic valve 

disease should be made aware of its familial pattern of inheritance 

and screening of their first degree relatives should be actively 

pursued in order to reduce the potential morbidity and mortality 

associated with this condition and its related aortopathy. 

137 A CITED2->VEGFA PATHWAY COUPLES MYOCARDIAL AND 

CORONARY VASCULAR GROWTH IN THE DEVELOPING 

MOUSE HEART 

doi:10.1136/heartjnl-2011-300198.137 

1 S D Bamforth, 

1 S T MacDonald, 

1 J Braganca, 

1 C-M Chen, 

1 C Broadbent, 

1 J E Schneider, 2 R Schwartz, 1 S Bhattacharya. 1 University of Oxford, Oxford, UK; 

2 Texas A&M Health Science Centre, Houston, Texas, USA 

Introduction Myocardial development is dependent on the concomitant 

growth of cardiomyocytes and a supporting vascular network. 

The coupling of myocardial and coronary vascular development is 

mediated in part by VEGFA signalling. Cited2 is a transcriptional cofactor 

that can inhibit hypoxia-activated transcription and also acts 

as a co-activator for transcription factors such as TFAP2. Genetic 

evidence indicates that Cited2 is essential for cardiac left-right 

patterning via regulation of the Nodal-Pitx2c left-right patterning 

pathway. Zygotic and epiblastic deletion of Cited2 results in atrioventricular 

septation, outflow tract and aortic arch abnormalities, as 

well as left-right patterning defects such as right-isomerism. Cited2 

is also essential for adrenal, neural crest, liver, lung, lens and 

placental development. However, the early requirement of Cited2 in 


left-right patterning and placental development makes it difficult to 

identify a later specific role for Cited2 in myocardial development. To 

overcome this problem we therefore investigated the role of Cited2 

in the myocardium by conditional deletion in cardiomyocyte precursors. 

Methods Cited2 was selectively deleted from cardiomyocytes by 

intercrossing mice transgenic for Cited2 and Nkx2-5Cre. Embryos 

were collected and processed for analysis by histology, MRI, X-Gal 

staining, quantitative reverse transcriptase PCR (Q-RTPCR), chromatin 

immunoprecipitation and transient transfection assays. 

Results The cardiomyocyte specific knockout of Cited2 results in 

abnormal myocardial compact zone growth and ventricular septal 

defects. This is associated with a decreased ratio in the number of 

small vessels to large vessels, and a reduction in Vegfa expression. We 

also show that CITED2 is present at the Vegfa promoter in mouse 

embryonic hearts, and that it stimulates human VEGFA promoter 

activity in cooperation with TFAP2 transcription factors in transient 

transfection assays. However, we observed no change in the 

myocardial expression of the left-right patterning gene Pitx2c, a 

known target of Cited2. 

Conclusions The myocardial and capillary defects observed in 

myocardial loss of Cited2 are not associated with Pitx2c deficiency 

and suggests that Cited2 can cause myocardial and vascular defects 

via a mechanism that is distinct from its effect on the left-right 

patterning pathway. Our results delineate a novel mechanism of 

Vegfa regulation by CITED2 and TFAP2 transcription factors, and 

indicate that coupling of myocardial and coronary vascular growth 

in the developing mouse heart occurs, at least in part, through a 

Cited2->Vegfa pathway. This pathway may be targeted for the 

treatment of heart failure resulting from ischaemic heart disease. 

138 CELL-SPECIFIC ROLE OF NOX2 NADPH OXIDASE IN 

DEVELOPMENT OF ANGIOTENSIN II-INDUCED CARDIAC 

FIBROSIS IN VIVO 

doi:10.1136/heartjnl-2011-300198.138 

1 S Chaubey, 1 C E Murdoch, 1 A Ivetic, 1 B Yu, 2 D Vanhoutte, 2 S Heymans, 1 A Brewer, 

1 A M Shah. 1 Kings College London BHF Centre of Excellence, London, UK; 2 University 

Hospital Maastricht, Maastricht, The Netherlands 

Introduction Mice globally deficient in Nox2 are protected against 

cardiac fibrosis in response to chronic AngII infusion even though 

the degree of hypertrophy was unaltered. The selective effect of 

Nox2 on fibrosis may reflect its activation in a non-cardiomyocyte 

cell type. We hypothesised that Nox2, which is expressed in endothelial 

cells and inflammatory cells, may be important for cardiac 

fibrosis in these cell types. 

Methods To investigate the role of Nox2 in inflammatory cells, we 

generated chimeric mice by irradiation (10Gy, 15 min) to deplete 

resident bone marrow cells, followed by bone marrow (BM) transplantation, 

using the following permutations: wild-type (WT) 

recipient with either KO or WT BM, and KO recipients with WT 

BM. To assess the role of endothelial Nox2, we used transgenic mice 

with endothelial-specific overexpression of Nox2 (TG) utilising the 

tie2 promoter construct. 

Result AngII (1.1 mg/kg/day, 14-day) infusion caused similar 

increase in systolic hypertension and cardiac hypertrophy in all 3 

chimeric groups. However, cardiac fibrosis assessed by Sirius red 

staining was significantly lower in KO mice receiving WT BM 

(0.560.1%) compared to the WT:WT group (2.760.7%) or in WT 

receiving KO BM (2.360.6%). These data suggested that resident 

Nox2-expressing cells are responsible for the protective effect 

observed in global Nox2 KO mice. TG mice developed the same level 

of systolic hypertension and hypertrophy as WT littermates after 

AngII infusion. However, the extent of cardiac fibrosis was significantly 

greater in TG than WT by w2-fold (p


inflammatory cells (w1.8-fold, p


2EFHIK&L) were seen by 48hpf. TFPI MO induced coagulopathy (a 

spontaneous clot or bleed; white arrows Abstract 141 figure 2GJMP) 

in 25.262.3% (p


superoxide release in atrial samples of patients with post-operative 

AF but had no effect in patients with permanent AF. Similarly, 

atorvastatin did not induce a mevalonate-reversible changes in the 

atrial BH4 concentration and NOS uncoupling in neither group. 

Conclusions Together, these findings indicate that upregulation of 

NOX2-NADPH oxidases is an early but transient event in the 

natural history of AF, as mitochondrial oxidases and uncoupled NOS 

account for the statin-resistant increase in atrial superoxide 

production in permanent AF. Variation in atrial sources of reactive 

oxygen species with the duration and substrate of AF may explain 

the reported variability in the effectiveness of statins in the 

prevention and management of AF. 


143 TISSUE FACTOR PATHWAY INHIBITOR REGULATES 

ANGIOGENESIS INDEPENDENTLY OF TISSUE FACTOR VIA 

INHIBITION OF VASCULAR ENDOTHELIAL GROWTH FACTOR 

SIGNALLING 

doi:10.1136/heartjnl-2011-300198.143 

1 E W Holroyd, 2 K Larsen, 2 R G Vile, 2 D Mukhopadhyay, 2 R D Simari. 1 Queen Elizabeth 

Hospital, Birmingham, UK; 2 Mayo Clinic, Rochester, Minnesota, USA 

Introduction The biological systems of coagulation and angiogenesis 

show considerable interdependence. Proteases and inhibitors within 

the tissue factor (TF) pathway of coagulation have emerged as 

potential regulators of angiogenesis. Tissue factor pathway inhibitor 

(TFPI), as the primary physiological inhibitor of tissue factor (TF)- 

mediated coagulation, is ideally situated to modulate the proangiogenic 

effects of TF. However, TFPI may also have effects on 

angiogenesis independent of its anti-TF ability. 

Methods We determined the effects of altered TFPI expression on 

the regulation of angiogenesis in vivo using genetically-modified 

murine models of vascular overexpression (SM22áTFPI strain) and 

endothelial-specific deletion of the TF-binding domain of TPFI 

(Tie2TFPI). We then defined the mechanism of these effects in vitro 

using Human Umbilical Vein Endothelial Cells (HUVECs) overexpressing 

TFPI or via exogenous addition of TFPI-derived peptides 

in assays of angiogenesis. 

Results Vascular-directed over-expression of TFPI (SM22áTFPI 

strain) inhibited angiogenesis in vivo (Abstract 143 figure 1). 

SM22áTFPI showed significantly impaired recovery from ischaemia 

in the hindlimb ischaemia model after 3 days (p


mice showed a significant reduction in the cardiomyocyte cross 

sectional area (sham, 26763.4 mm 2 , vehicle treated TAC mice, 

48065.8 mm 2 , AP2 treated TAC mice, 31963.9 mm 2 ). A significant 

reduction in the expression of the hypertrophic marker ANP and BNP 

and in the percentage of fibrosis was also observed in these mice 

compared with vehicle treated TAC mice. AP2 treatment led to a 

significant reduction in the expression of the bona fide calcineurin 

target RCAN1.4 and a reduction in the NFAT phosphorylation level in 

vivo and the NFAT transcriptional activity in vitro. In conclusion, we 

have identified AP2 as a novel PMCA4 specific inhibitor and shown its 

potential to modify the development of cardiac hypertrophy likely 

through inhibition of calcineurin/NFAT signalling. This compound 

has drug-like properties and thus lays the basis for a novel approach for 

treating cardiac hypertrophy and failure through PMCA4 inhibition. 

145 CHARACTERISATION OF FRACTIONATED ATRIAL 

ELECTROGRAMS CRITICAL FOR MAINTENANCE OF AF: A 

RANDOMISED CONTROLLED TRIAL OF ABLATION 

STRATEGIES (THE CFAE AF TRIAL) 

doi:10.1136/heartjnl-2011-300198.145 

R J Hunter, I Diab, M Tayebjee, L Richmond, S Sporton, M J Earley, R J Schilling. Barts 

and The London NHS Trust, London 

Introduction Targeting complex fractionated atrial electrograms 

(CFAE) in the ablation of atrial fibrillation (AF) may improve 

outcomes, although whether this is by eliminating focal drivers or 

simply de-bulking atrial tissue is unclear. It is also uncertain what 

electrogram morphology should be ablated. This randomised study 

aimed to determine the impact of ablating different CFAE 

morphologies compared to normal electrograms (ie, de-bulking 

normal tissue) on the cycle length of persistent AF (AFCL). 

Methods After pulmonary vein isolation CFAE were targeted 

systematically throughout the left then right atrium, until termination 

of AF or abolition of CFAE prior to DC cardioversion. 10 s 

electrograms were classified by visual inspection according to a validated 

scale, with Grade 1 being most fractionated and grade 5 normal. 

Patients were randomised to have CFAE grades eliminated sequentially, 

from grade 1 to 5 (group 1) or grade 5 to 1 (group 2). Because grade 5 

electrograms were considered normal, only 5 were ablated. Mean 

AFCL was determined manually over 30 cycles from bipolar electrograms 

recorded at the left and right atrial appendages before and after 

each CFAE was targeted. Lesions were regarded as individual observations, 

and a resultant increase in mean AFCL $5mswasregardedas 

significant. The randomised strategy first controlled for any cumulative 

effect of ablation on AFCL, and second allowed assessment of 

the order of ablation on the number of CFAE lesions required. 

Results 20 patients were randomised. The CFAE grade determined by 

rapid visual inspection for the 968 electrograms targeted agreed with 

that at off-line manual measurement in 92.7% (l¼0.91). AFCL 

increased after targeting 49.5% of grade 1 CFAE, 33.6% of grade 2, 

12.8% of grade 3, 33.0% of grade 4, and 8.2% of grade 5 CFAE 

(p


Conclusion AFB is independently associated with increased indices 

of P-sel and D-dimer which indicate platelet activation and thrombosis 

respectively. 

147 THROMBOEMBOLIC RISK STRATIFICATION, ANTI- 

THROMBOTIC AND ANTICOAGULATION USE FOR PATIENTS 

WITH ATRIAL FIBRILLATION, A CLINICAL AUDIT 


CHADS2 Score None (%) Aspirin (%) Aspirin or Warfarin (%) Warfarin (%) 

Zero 27.0 70.3 1.3 1.3 

One 4.7 45.1 43.2 7.0 

Two 0.0 7.8 32.2 60.0 

Three 0.0 0.8 11.5 87.7 

Four 0.0 0.0 5.3 94.7 

Five 0.0 0.0 2.9 97.1 

Six 0.0 0.0 2.9 97.1 

doi:10.1136/heartjnl-2011-300198.147 

R A Veasey, R Kulanthaivelu, P Patel, D W Harrington. Kent and Sussex Hospital, 

Tunbridge Wells, UK 

Introduction Atrial fibrillation (AF) is the most prevalent arrhythmia 

in primary and secondary healthcare settings. Thromboembolic (TE) 

risk assessment and initiation of anti-thrombotic or anticoagulation 

(AT/AC) therapy, according to level of risk, is recommended in both 

national and international guidelines. NICE guidance stratifies 

patients with AF in to low, moderate or high risk categories and 

recommends “aspirin”, “aspirin or warfarin” or “warfarin” therapy 

respectively. ACC/ESC guidance endorses use of the CHADS 2 

scoring system and for scores of 0, 1, or $2 recommends “aspirin”, 

“aspirin or warfarin” or “warfarin” therapy respectively. In addition, 

it is recommended that AF episode frequency or subtype (paroxysmal 

(PAF), persistent (PersAF) or chronic (CAF)) does not influence 

TE risk assessment. We audited UK cardiologists and general 

practitioners (GPs) to assess adherence to these guidelines. 

Methods We designed an audit questionnaire assessing: (1) use of 

risk stratification tools, (2) choice of AT/AC for increasing levels of 

risk, and (3) choice of therapy for a number of hypothetical patients 

with variable TE risk and variable AF subtype. The questionnaire 

was distributed by electronic or postal mail to 1176 cardiologists and 

621 randomly selected GPs. 

Results In total, 421 responses were received (306 cardiologists, 115 

GPs). Overall, 91.4% of responders reported use of TE risk stratification 

tools (97.1% cardiologists, 76.5% GPs, p


profile was reported in only 37%. Only 47% (n¼78) of records 

described a witness account. Within the witness accounts that were 

recorded, key elements remained un-reported for example skin 

complexion was only reported in 35% of the 78. The duration of the 

TLOC was recorded in only 44%, Tongue biting in 27% and the 

presence or absence of abnormal movements was recorded in only 

12% of this 78 patients. The presence or absence of a family history 

of sudden cardiac death was only reported in 2% cases. The family 

history of a cardiomyopathy was only recorded in 1% and a family 

history of TLOC was recorded in 1%. A patient past history of 

cardiac disease was asked about in 40% of cases while a past history 

of TLOC was only asked about in 35%. In this majority elderly 

study population, a recent change in drug therapy was only asked 

about in 2% of cases. This study highlights that in a DGH environment, 

the initial assessment of patients with TLOC is undertaken 

by junior medical staff who often do not document key 

diagnostically differentiating elements of the history and examination 

indicating an ongoing lack of adequate training regarding the 

most appropriate and accurate techniques for differentiating the 

causes of TLOC. 

Abstract 149 Figure 1 Comparison of pre-ablation and post-ablation % 

scar using fixed threshold. 

149 AUTOMATED ANALYSIS OF ATRIAL ABLATION-SCAR USING 

DELAYED-ENHANCED CARDIAC MRI 

doi:10.1136/heartjnl-2011-300198.149 

1 L Malcolme-Lawes, 

1 R Karim, 

2 C Juli, 

2 P B Lim, 

2 T V Salukhe, 

2 D W Davies, 

1 D Rueckert, 1 N S Peters, 2 P Kanagaratnam. 1 Imperial College London, London, UK; 

2 Imperial College Healthcare, London, UK 

Introduction Visualisation of the ablation-related atrial scar using 

delayed-enhanced MRI (DE-MRI) may reveal important underlying 

causes for atrial fibrillation (AF) recurrence following ablation. In 

order to develop and objective method for delineating ablation-scar 

we compared pre and post DE-MRI after Cryo-balloon lesion on the 

basis that a more predictable lesion set would be created for 

validation. 

Methods and Results 12 patients undergoing cryoablation for PAF 

were enrolled in the study, and underwent pre-ablation DE-MRI 

scans. Pulmonary vein isolation (PVI) was confirmed in all patients 

at the end of the cryoablation procedure using a circular mapping 

catheter. Additional ablation by RF or Freezer Max was required to 

achieve PVI in 59%. No ablation was performed in any region other 

than the PV ostia. Post-ablation DE-MRI was performed at 

3 months. An automatic segmentation of the LA was produced with 

custom software from the MRA sequence. The preablation and 

postablation free breathing late gadolinium enhanced sequence was 

registered to the MRA and the maximum intensity within the LA 

wall was projected onto the post ablation LA surface. The blood 

pool was identified automatically using custom software as the 

region 1 cm inside the wall of the LA, and its mean (BPM) and SD 

used as a baseline. To identify a universal threshold for scar, regions 

of brightest myocardium were initially selected in pre and post 

ablation MRIs. The brightest regions were 1.961.2 vs 8.763.1 SDs 

above the BPM in pre-and post-ablation MRIs respectively 

(p¼0.001). A threshold of 5 SDs above the BPM was therefore 

programmed into our custom software to identify regions of scar for 

all patients. The ostial regions were defined as extending 1 cm both 

proximal and distal to the PVeLA junction, and selected manually 

for left and right sided veins prior to scar projection. (See Abstract 

149 figure 1). The scar proportion within these regions was calculated 

using commercially available software ITK-SNAP. Total LA 

scar proportion was 0.260.02% vs 6.360.75% in pre and post 

ablation scans respectively. The increase in scar seen in the PV ostia 

was 24.661.38% compared with 2.661.28% in the rest of the LA 

(p¼0.01) (See Abstract 149 figure 2). 


Conclusion We have demonstrated the feasibility an objective, 

automated method of DE-MRI analysis of left atrial ablation-scar. 

This technique will now need to be validated against clinical 

outcomes. 

150 IMPLANTABLE CARDIOVERTER-DEFIBRILLATOR 

LEAD COMPLICATIONS AND CLINICAL EFFECTIVENESS 

IN PATIENTS WITH INHERITED CARDIAC 

CONDITIONS 

doi:10.1136/heartjnl-2011-300198.150 

1,2 R Bastiaenen, 1 S Ben-Nathan, 2 S Jones, 2 D Ward, 2 M Gallagher, 1,2 S Sharma, 

1,2 E R Behr. 1 St George’s University of London, London, UK; 2 St George’s Hospital, 

London, UK 

Background Implantable cardioverter-defibrillator (ICD) therapy can 

reduce sudden death due to ventricular arrhythmia (VT/VF) but is 

not without complication, particularly in young patients who live 

for many years with a device in situ. We aimed to determine the 

ICD complication rate in our inherited cardiac condition (ICC) 

population compared with international reports. Particular importance 

was given to inappropriate shock therapy due to lead failure as 

there are new ICD technologies available. 

Methods Patients with ICCs who had ICD implantation or box 

change between January 2006 and September 2009 were included. 

Data on clinical characteristics, complications and ICD therapies 

were obtained from pacing and hospital records. We compared our 

data with several ICD studies of patients with specific ICCs 

(Abstract 150 table 1). 


A83



SGH ICC 

patients 

(n[101) 

Long QT 

Syndrome 

patients 

(n[51) 

HCM 

patients 

(n[506) 

ARVC 

patients 

(n[106) 

Brugada 

Syndrome 

patients 

(n[220) 

Follow-up (months; mean6SD) 74653 87 44633 58635 38627 

Appropriate therapy (%) 26 24 20 24 8 

Inappropriate therapy (%) 18 29 27 19 20 

Lead failure (%) 21 25 7 2 9 

Complication rate excluding 

lead failure (%) 

26 31 n/a 34 20 

Results 101 patients (mean age 44.1614.8 years; 59 male) were 

included (idiopathic VF 15%; DCM 17%; ARVC 22%; HCM 21%; 

long QT syndrome 17%; Brugada syndrome 6%; others 2%). During 

a mean follow-up of 74.0653.2 months 2 patients died (1 inappropriate 

shocks; 1 stroke). Indications were secondary prevention in 

71.3% of patients. ICD types were 56.4% single chamber; 39.6% 

dual chamber; 4.0% biventricular. Appropriate therapy successfully 

terminated VT/VF in 27 (26.7%) patients 34.7% of secondary and 

6.9% of primary prevention patients received appropriate therapy. 

Inappropriate therapy occurred in 18 (17.8%) patients and lead 

failure (noise/wear/fracture) in 22 (20.8%) patients (Abstract 150 

table 2). 12 out of 18 inappropriate shocks were due to lead failure, 5 

sensing errors (1 T-wave oversensing; 4 AF), 1 generator fault. 10/22 

leads that failed were Medtronic Sprint Fidelis and these were 

responsible for 8/12 patients receiving inappropriate shocks 

including one death due to lead fracture. Comparison with other 

studies indicates a high lead failure rate due to the long follow-up 

period, similar to the LQT Study which reports 25% lead failure over 

87 months (Abstract 150 table 1). With lead failure excluded the 

complication rate is comparable to shorter follow-up studies. Inappropriate 

and appropriate therapy rates are similar among all studies. 


Complication Number of patients % of patients 

Lead failure 21 20.8 

Inappropriate shock 18 17.8 

Lead displacement 5 4.9 

Infection 5 4.9 

Pneumothorax/Haemothorax 5 4.9 

Box/Wound/Other revision procedure 7 6.9 

Thrombosis (venous/lead) 2 1.9 

Haematoma 5 4.9 

Chronic abdominal cavity postexplant 

1 0.9 

Conclusions There is a significant rate of ICD lead failure in patients 

with ICCs, which may be expected given the high frequency of 

Sprint Fidelis leads implanted during this period and the long followup. 

Our results compare favourably to other similar studies. The 

high rate of appropriate therapy highlights the clinical effectiveness 

of ICD intervention in secondary prevention. Lead complications 

may be lower with the use of new ICD technology in selected patients. 

151 RISK OF RECURRENCE FOLLOWING EXTRACTION OF CARDIAC 

IMPLANTABLE ELECTRONIC DEVICES FOR INFECTION: WHEN 

SHOULD A NEW DEVICE BE RE-IMPLANTED? 

doi:10.1136/heartjnl-2011-300198.151 

H E Thomas, M Das, D Twomey, C J Plummer, E J Shepherd. Freeman Hospital, 

Newcastle upon Tyne, UK 

Background The recommended management of cardiac implantable 

electronic device (CIED) infection is complete system 

extraction. There are limited clinical data on the optimal time for 

device re-implantation. A small series reported good results with 

simultaneous contralateral implantation. We evaluated this 

approach in our institution for patients without signs of systemic 

sepsis. We present clinical outcomes and completeness of extraction. 

Methods The clinical records of all patients undergoing lead 

extraction in our institution since January 2008 were reviewed. 

Results 68 patients underwent CIED extraction for infection during 

this time period (see Abstract 151 table 1). In 34 cases, the device 

was removed with simple traction, 9 with locking stylet, 22 with 

locking stylet and laser sheath, 1 with locking stylet and mechanical 

sheath and 2 with femoral snare. There was complete hardware 

removal in 64 cases (94%). One patient with lead related endocarditis 

required a subsequent surgical procedure to remove a lead 

fragment and in 4 other patients who had erosion, pocket infection 

or threatened erosion, a small fragment of lead remained. 18/68 

patients were re-implanted with a new device on the contralateral 

side on the same day as the extraction. 28/68 patients received a 

new device between 1 and 227 days later and 22/68 have not 

undergone reimplantation. An active fixation bipolar TPW 

(temporary pacing wire) was used in 6 patients for a mean 

7.862.7 days. 3 patients had a further device related procedure 

during a mean follow-up of 4456304 days: 1 lead reposition, 1 

pocket washout and 1 extraction. Of the 2 procedures carried out for 

recurrent infection, 1 was managed with a TPW for 7 days prior to 

reimplantation and 1 underwent reimplantation at 14 days without 

TPW. In addition, the patient requiring pocket washout had a 

fragment of lead remaining following their initial extraction. 


Indication for device extraction Number of patients, n[80 (%) 

Erosion 31 (39) 

Pocket infection 25 (31) 

Lead infection 7 (9) 

Threatened erosion 4 (5) 

Pain 1 (1) 

Conclusion We report low rates of recurrent infections following 

CIED extraction. None of the 18 individuals simultaneously reimplanted 

with a new device on the contralateral side needed any 

further procedures during the follow-up period. This approach may be 

appropriate, particularly in pacing dependant patients who would 

otherwise require a TPW with its associated risks. In those individuals 

who required a TPW, the risk of recurrent infection in our series was 

17% despite our use of an active fixation pacing lead and externalised 

pulse generator which has a lower reported complication rate. Only 

one of the 4 patients with a residual lead fragment required reintervention 

for recurrent infection. This provides some supportive 

evidence that in patients with high surgical risk and pocket abnormalities, 

if fragments of lead may remain, the patient may be treated 

conservatively and monitored for signs of recurrent CIED infection. 

152 REAL-TIME CARDIAC MR ANATOMY AND DYSSYNCHRONY 

OVERLAY TO GUIDE LEFT VENTRICULAR LEAD PLACEMENT 

IN CRT 

doi:10.1136/heartjnl-2011-300198.152 

1,2 A Shetty, 1,2 S Duckett, 1,2 M Ginks, 1,2 Y Ma, 1,2 M Sohal, 1,2 P Mehta, 1,2 S Hamid, 

1,2 JBostock, 1,2 GCarr-White, 1,2 K Rhode, 1,2 RRazavi, 1,2 CARinaldi. 1 Guys and St 

Thomas’ Hospital NHS Foundation Trust, London, UK; 2 King’s College London, London, UK 

Introduction Optimal left ventricular (LV) lead placement via the 

coronary sinus (CS) is a critical factor in defining response to cardiac 

resynchronisation therapy (CRT). Using novel semi-automated 

image acquisition, segmentation, overlay and registration software 



we set out to guide lead placement by avoiding scar and targeting 

the region of the LV with the latest mechanical activation. 

Methods 17 patients underwent cardiac magnetic resonance (CMR) 

scans. 3D whole heart images were segmented to produce high fidelity 

anatomical models of the cardiac chambers and coronary veins. 2, 3, 4 

chamber and short axis cine images were processed using Tomtec 

software to give a 16 segment time volume-dyssynchrony map. In 

patients with myocardial scar the late gadolinium enhancement 

images were manually segmented and registered to the anatomical 

model along with the dyssynchrony map. The 3 latest mechanically 

activated segments with


bipole but was found with another. Furthermore, differences in 

whether phrenic nerve stimulation (PNS) occurred were seen when 

using different LV lead bipoles within the same branch of the CS. 

Conclusion Our data suggest that only a small difference in AHR is 

seen when pacing along the same branch of the CS compared to 

pacing within different branches of the CS within the same patient. 

This means that although the site of LV lead placement is important, 

a proximal or distal position within a CS branch is much less 

important than choosing the right branch in terms of acute 

haemodynamic response. A choice of bipoles on the LV lead may 

mean, however, that problems with capture thresholds or PNS can 

be overcome without the need to reposition the LV lead. 

154 PATIENTS RECEIVING STANDARD PACEMAKER 

GENERATOR REPLACEMENTS FREQUENTLY HAVE 

IMPAIRED LEFT VENTRICULAR FUNCTION AND EXERCISE 

INTOLERANCE, RELATED TO THE PERCENTAGE OF RIGHT 

VENTRICULAR PACING 

doi:10.1136/heartjnl-2011-300198.154 

1 G A Begg, 1 J Gierula, 1 Z L Waldron, 2 K K Witte. 1 Leeds General Infirmary, Leeds, UK; 

2 University of Leeds, Leeds, UK 

Background Right ventricular (RV) pacing is an accepted treatment 

for symptomatic bradycardia. However, long-term RV pacing is 

increasingly recognised to be detrimental to left ventricular (LV) 

systolic function. We wanted to establish the prevalence, associated 

features and predictors of LV systolic dysfunction (LVSD) and 

outcome in a contemporary group of patients with longeterm RV 

pacemakers. 

Methods We prospectively recruited consecutive patients listed for 

PGR between 2008 and 2010 at Leeds General Infirmary. We 

performed echocardiography, exercise testing and recorded indications 

for pacing, pacing variables and duration of pacing, comorbidities, 

current medication and renal function. 

Results Of 399 PGR procedures 342 subjects (86%), 184 men, 

attended. Non-attendees had similar pacing variables and were of 

similar age as attendees. Mean age (SE) was 76 (1), and mean 

duration of pacing was 10 (0.3) years. Comorbidites were common: 

diabetes mellitus in 11%, previous myocardial infarction in 15%, 

previous cardiac surgery in 26% and atrial fibrillation (AF) in 26%. 

Medical therapy included b-blockers in 60% and ACE inhibitors in 

70%. Dual chamber devices were implanted in 77% (45% of all 

patients had rate responsive (RR) pacing programmed). Mean 

percentage of ventricular pacing (%VP) was 61 (2)%. Mean left 

ventricular ejection fraction (LVEF) was 49 (1)%, (44% had an LVEF 


Results 326 STEMI patients were identified. Of these 12(3.7%) 

declined investigation. 25(7.8%) died during the investigation period 

(22 died during their initial acute event, 3 died of non cardiac causes 

following discharge). 10(3.1%) requested follow-up in another 

geographical area. 26(8%) patients were identified as LVEF


consent is an essential part of the implant process. Our aim was to 

get an insight into implanters’ (Imp) practices prior to an ICD 

implantation. 

Methods A questionnaire survey was sent to UK ICD Imp to test 

their knowledge of the risk and benefits of an ICD in patients who 

satisfy trial and national guideline criteria and the incidence of 

implant complications. Information of the style and language of 

consent was requested. This questionnaire was specifically aimed at 

Imp and was part of the larger questionnaire looking at knowledge, 

attitudes and factors influencing ICD prescription in the UK. 

Results Replies were received from 23 implanters. 35% of the 

responders were between the age of 30e39 years and 39% were 

between 40 and 49 years. 83% of the responders were Consultants 

and 96% were working in an implantating centre. 83% of Imp were 

fully aware of Primary Prevention (PP) NICE guidelines while 78% 

were fully aware of Secondary Prevention (SP) NICE guidelines. 

There was widespread use of information leaflets (87%) and 

specialist ICD nurses (83%) to disseminate information to patients. 

All responders said they would personally discuss the therapy with 

the patient prior to the implantation regardless of the referral 

source. A discussion regarding the prevention of SCD, inappropriate 

shocks and driving restrictions were performed by 96% of 

responders and device infections and lead failures discussed by 91%. 

Use of absolute risk reduction in percentages and number needed to 

treat while explaining the risks and benefits gained from ICDs were 

used by 22% and 26% respectively. There was widespread use of 

phrases like “small risk” or “moderate risk” (61%) and life prolongation 

(eg, lets you live longer by an average of 3 months) (30%). 

Replies also indicated that Imp under-estimate overall mortality in 

medicallytreated and ICD-treated patients, lead dislodgement 

requiring re-positioning and major haematoma requiring reoperation. 

Imp overestimate infections leading to device removal and the incidence 

of pneumothorax when compared to published trial or study data. 

Conclusion The majority of implanters are aware of UK ICD 

guidelines. The patient consent process is not universal. Guidelines 

and awareness about end-of-life care in ICD patients is needed and 

should be part of the initial consent process. Evidence based use of 

risk and benefit terminologies like ARR and NNT are needed to 

better inform the patient rather than abstract phrases. Increasing 

awareness of ICD complication rates can help patients and physicians 

balance risk against benefit which could lead to improved 

patient satisfaction with their therapy. 


Estimate of ICD 

complications Mean % Published/Trial data % 

Death as a complication of 

device implant 

Lead dislodgement requiring 

lead repositioning 

Lead failure requiring extraction 

or additional lead insertion 

Major haematoma requiring 

reoperation 

Device infection requiring 

removal/extraction 

0.3760.48 0.77% (Circulation.1998;98:663e670); 

2.08% (Br Heart J.1995:73:20e24) 

3.562.08 5% (PACE.2005; 28:926e932); 

10% (Circulation.1998;98:663e670) 

5.467.28 4.3% (PACE.2005;28:926e932) 

2.7263.07 5.8% (JAMA.2006:295:1901e1911) 

2.2762.4 0.5% (PACE.2005:28:926e932); 0.77% 

(Circulation.1998;98:663e670);0.7% 

(MADIT2 trial) 

Cardiac tamponade 0.761.07 0.2% (PACE.2005;28:926e932); 

0.64% (Circulation.1998;98:663e670) 

Pneumothorax 1.6861.17 1.1% (PACE.2005; 28:926e932); 

0.89% (Circulation.1998;98:663e670) 

Inappropriate shocks 14.8610.92 12% (PACE.2005; 28:926e932); 14.91% 

(Circulation.1998;98:663e670); 

18% (Z Kardiol.1996;85:809e819) 

Psychological problems 

associated with the device 

22.6626.68 13e38% (Clin Cardiol 1999;22:481e9) 

158 IS IT COST EFFECTIVE TO USE A PLUGGED LV PORT? 

doi:10.1136/heartjnl-2011-300198.158 

M A Jones, T R Betts, K Rajappan, Y Bashir, K C K Wong, N Qureshi. John Radcliffe 

Hospital, Oxford, UK 

Background Many patients receiving ICD implants do not meet 

criteria for CRT therapy, yet are often felt likely to benefit from CRT 

in the future. The reasons for this include less severe NYHA class of 

HF symptoms at the time of implant, narrow QRS, and (progressive) 

atrio-ventricular conduction delay. Management options 

include only implanting DDD / VVI devices, and then upgrading to 

CRT if required; implanting CRT-D devices but without an LV lead, 

with the LV port “plugged”, such that if an upgrade were to become 

necessary, only a new LV lead (and implant kit) would be required; 

and finally, implanting CRT-D devices with LV leads in all patients 

in the first instance, as has been suggested by the recent Madit-CRT 

and RAFT studies. It is not clear which of these strategies is superior 

in terms of the cost-benefit ratio. 

Purpose This study analyses a retrospective cohort of patients who 

received CRT-D devices but without LV leads, to examine the cost 

implications of this approach, and to compare this cost to that of merely 

implanting a DDD device, or implanting a full CRT-D system initially. 

Method A retrospective analysis of all patients receiving CRT-ICDs 

with plugged LV ports between September 2004 and June 2009 at 

our institution. Patient characteristics, indication for a plugged LV 

port, subsequent addition of a LV lead and reasons for doing so were 

taken from patient records. The total cost (surgery and hardware) 

was compared with the estimated cost of initially implanting single 

or dual chamber ICDs and upgrading the entire system, and to the 

cost of implanting full CRT-D systems up front. 

Results 35 patients (27 male) were identified. Mean (SD) age was 

6768 years. 26 had ischaemic heart disease and 9 non-ischaemic 

dilated cardiomyopathy. All had LV EF


159 PILOT STUDY EXPLORING THE REGIONAL REPOLARISATION 

INSTABILITY INDEX IN RELATION TO MYOCARDIAL 

HETEROGENEITY AND PREDICTION OF VENTRICULAR 

ARRHYTHMIA AND DEATH 

doi:10.1136/heartjnl-2011-300198.159 

1 W B Nicolson, 

1 C D Steadman, 

1 P Brown, 

2 M Jeilan, 

2 S Yusuf, 

2 S Kundu, 

2 A J Sandilands, 2 P J Stafford, 1 F S Schlindwein, 2 G P McCann, 1 G A Ng. 1 University 

of Leicester, Leicester, UK; 2 University Hospitals of Leicester NHS Trust, Leicester, UK 

Introduction There is a need for better sudden cardiac death (SCD) 

risk markers. Mounting evidence suggests that the mechanism 

underlying risk of ventricular arrhythmia (VA) is increased heterogeneity 

of electrical restitution. We investigated a novel measure of 

action potential duration (APD) restitution heterogeneity: the 

Regional Repolarisation Instability Index (R2I2) and correlated it 

with peri-infarct zone (PIZ) a cardiac magnetic resonance (CMR) 

anatomic marker of VA risk. 

Methods Blinded retrospective study of 30 patients with ischaemic 

cardiomyopathy assessed for an implantable cardioverter defibrillator. 

The R2I2 was derived from high resolution 12 lead ECG 

recorded during programmed electrical stimulation (PES). ECG 

surrogates were used to plot APD as a function of diastolic interval; 

the R2I2 was the maximal value of the mean squared residuals of 

the mean points for anterior, inferior and lateral leads normalised to 

the mean value for the total population. PIZ was measured from late 

gadolinium enhanced CMR images using the full width half 

maximum technique. 

Results Seven patients reached the endpoint of VA/death (median 

follow-up 24 months). R2I2 > median was found to be predictive of 

VA/death independent of PES result, left ventricular ejection fraction 

and QRS duration (6/14 vs 1/15 p¼0.031). Modest correlation 

was seen between the R2I2 and PIZ (r¼0.41 p¼0.057) (Abstract 159 

figure 1). 


Conclusions In this pilot study of ischaemic cardiomyopathy 

patients, the R2I2 was shown to be an electrical measure of VA/ 

death risk with a moderately strong correlation with an anatomic 

measure of arrhythmic substrate, the extent of PIZ. The R2I2 may 

add value to existing markers of VA/death and merits further 

investigation. 


Variable 

Whole Group 

(n[30) 

No VA/death 

(n[23) 

VA/death 

(n[7) p 

Age (years) 6769 6569 7268 0.055 

Sex (% male) 97 96 100 

QRSD(ms) 107620 107621 106615 0.95 

EF(%) 31614 32.4615 2767.5 0.34 

PES result (positive/total) 12/30 7/23 5/7 0.068 

R2I2>median 14/29 8/22 6/7 0.031 

EDV index (ml/cm) 1.4860.41 1.4960.41 1.4560.45 0.84 

SV index (ml/cm) 0.4260.14 0.4360.14 0.3960.15 0.47 

Follow-up (months) 24 (18) 24 (16) 16 (16) 0.088 

PIZ % 7.8 (10.7) 7.5 (8.4) 13.6 (8.5) 0.093 

Scar % 10.9 (16.5) 9.67 (13.5) 21.9 (17.8) 0.16 

160 HIGH DOSE OCTREOTIDE; A NOVEL THERAPY FOR THE 

TREATMENT OF DRUG REFRACTORY POSTURAL 

ORTHOSTATIC TACHYCARDIA SYNDROME IN PATIENTS 

WITH JOINT HYPERMOBILITY SYNDROME 

doi:10.1136/heartjnl-2011-300198.160 

A E French, C Shepherd, A Horne, C Parker, J Tagney, J Pitts-Crick, T Johnson, 

G Thomas. Bristol Heart Institute, Bristol, UK 

Introduction Postural orthostatic tachycardia syndrome (POTS) is 

defined as symptomatic orthostatic intolerance with an increase in 

heart rate of 30 beats per minute within 10 min of head up tilt 

(HUT). This dysautonomia causes wide-ranging symptoms 

including palpitations, presyncope, chronic fatigue, headache and 

cognitive difficulties. When POTS occurs in patients with preexisting 

Joint Hypermobility Syndrome (JHS), symptoms begin 

approximately a decade earlier than non-JHS patients with a 

preponderance of neurological features, secondary to cerebral hypoperfusion. 

Vascular laxity with splanchnic venous pooling has been 

implicated as a causative factor thus measures to expand plasma 

volume (thereby increasing mean arterial pressure and restoring 

cerebral perfusion) form the mainstay of therapy. Symptomatic 

improvements have been previously reported in POTS patients with 

the somatostatin analogue Octreotide, a powerful splanchnic vasoconstrictor. 

We report the first UK series of JHS patients with drug 

refractory POTS treated with high-dose octreotide. 

Methods Six patients (female, aged 21e52) were referred to our 

institution. All had known JHS (4 requiring a wheelchair), neurological 

symptoms (headache and cognitive impairment) and diagnostic 

tilt-table testing with a mean increase in heart rate of 

64 beats/min (range 47e73) with head-up tilt (HUT). All patients 

had remained symptomatic despite pre-treatment with a mean of 5 

POTS medications (range 5e7) including fludrocortisone, midodrine, 

propranolol, ivabradine, selective serotonin reuptake inhibitors, 

gabapentin and erythropoietin. Octreotide was commenced 

using a short-acting preparation given 3 times daily (dosage 

50e250 mg according to body mass) in conjunction with a longacting 

(monthly), intramuscular injection (dosage 10e30 mg). The 

short-acting preparation was weaned following the second monthly 

injection. 

Results During follow-up of 3 months (range 1e8), 3 (50%) patients 

reported a complete resolution of all postural and neurological 

symptoms which corresponded with a normalised response to HUT. 

The remaining patients reported a dramatic improvement but 

ongoing postural symptoms. No patients developed supine hypertension. 

Side effects including mild abdominal discomfort and 

transient diarrhoea were reported in 3 (50%) patients. 

Conclusion Octreotide is increasingly recognised as an effective 

therapy in POTS patients. Both short-acting, subcutaneous (0.9 mg/ 

Kg) and long-acting, intramuscular (10e20 mg) preparations have 


A89


previously been reported. We conclude that higher dosages of both 

preparations when administered together are effective and well 

tolerated in JHS patients with drug refractory POTS. 

161 CATHETER ABLATION OF ATRIAL FIBRILLATION ON 

UNINTERRUPTED WARFARIN USING STANDARD AND DUTY 

CYCLED RADIOFREQUENCY ENERGY: SAFE AND EFFECTIVE 

doi:10.1136/heartjnl-2011-300198.161 

J R J Foley, N C Davidson, B D Brown, D J Fox. University Hospital of South 

Manchester, Manchester, UK 

Introduction Catheter ablation (CA) for atrial fibrillation (AF) is 

growing exponentially. Although ablation for paroxysmal AF (PAF) 

is associated with shorter procedure times and less extensive left 

atrial ablation vs persistent AF thromboembolic complications can 

occur in both sub-groups. Inadequate anticoagulation leads to 

thrombotic complications and excessive anticoagulation can lead to 

bleeding risks. Many centres adopt a policy of discontinuing 

warfarin in the immediate run-up to the procedure, covering the 

procedure with unfractionated heparin and “bridging” postoperative 

patients with low molecular weight heparins (LMWH) back onto 

warfarin. We wished to determine the safety of CA for AF with a 

therapeutic INR using both the single transseptal approach and 

duty cycled radiofrequency energy (RF) with non irrigated PVAC 

catheters and the double transseptal puncture technique using irrigated 

RF catheters and either CARTO or NAVX electroanatomical 

mapping. 

Methods A retrospective analysis of 173 patients who underwent 

CA for AF while taking uninterrupted warfarin. Procedural target 

International Normalised Ratio (INR) was 2e3 with a peri-procedural 

target ACT of 300e350 s. In sub therapeutic INR patients 

weight adjusted LMWH was used post procedure with warfarin 

until INR was >2. Standard technique employed was large area 

circumferential ablation using conventional RF energy or pulmonary 

vein isolation using duty cycled RF energy. Data was gathered for 

demographics, procedural INR, total dose of unfractionated heparin, 

fluoroscopy time, and type of radiofrequency energy used. 

Endpoints were minor bleeding, major bleeding (requiring transfusion), 

vascular complications, pericardial tamponade and stroke/ 

TIA within 28 days of the procedure. 

Results There were 128/173 male patients, age range between 21 

and 73 years (mean 57 years). 122 underwent ablation for PAF and 

51 for persistent AF. Mean procedural INR was 2.4 (range 1.7e3.9). 

Mean unfractionated heparin dose was 6000 units (range 

1000e14 500). Mean fluoroscopy time for the PVAC group was 

23.4 mins (range 8.3e50.1 mins). Mean fluoroscopy time for 

CARTO/NAVX group was 31mins (range 14.10e58.44 mins). There 

were no major bleeding complications. There was 1 minor bleeding 

complication with a groin pseudoaneurysm. There were 2 cases of 

pericardial tamponade (2/173%e1.2%) both managed with percutaneous 

pericardial drainage. There were no stroke/TIAs. 

Conclusion These data demonstrate that CA for AF by both single 

and double transseptal technique using both standard RF and duty 

cycled RF while maintaining a therapeutic INR is a safe procedure. 

Maintaining a therapeutic INR reduces the risk of embolic events 

associated with “bridging” heparin without an increase in bleeding 

complications. This technique is convenient for patients and avoids 

switching between LMWH and warfarin and ensures patient safety 

by maintaining therapeutic anticoagulation before, during and after 

the procedure. 

162 THE CLINICAL MANAGEMENT OF RELATIVES OF YOUNG 

SUDDEN ARRHYTHMIC DEATH VICTIMS; ICDS ARE RARELY 

INDICATED 

doi:10.1136/heartjnl-2011-300198.162 

1 J C Caldwell, 

1 Z Borbas, 

2 N Moreton, 

2 N Khan, 

2 L Kerzin-Storrar, 

2 K Metcalfe, 

2 W Newman, 1 C J Garratt. 1 Manchester Heart Centre, Central Manchester University 

NHS Foundation Trust, Manchester, UK; 2 Department of Clinical Genetics, St Mary 9 s 

Hospital, Central Manchester University NHS Foundation Trust, Manchester, UK 

Introduction Following National Service Framework guidance on the 

management of sudden cardiac death (SCD), regional inherited 

cardiac conditions clinics were established to identify and treat those 

at increased risk of dying from an arrhythmic condition. Studies have 

examined the yield of different diagnostic strategies but the outcome 

of management in these patients has not been reported. 

Methods We present data on 193 consecutive patients (108 families) 

referred to a regional inherited cardiac conditions clinic because of 

SCD/aborted cardiac arrest of a relative. The mean age on referral 

was 38617 yrs and mean duration of follow-up was 15 months 

(range 1 day to 56 months). All individuals underwent clinical 

assessment by history, examination, ECG and echo. If treadmill 

exercise test had not previously been performed this was undertaken. 

Further imaging by CMR or contrast echo was performed in 

those with structurally abnormal hearts or with Twave inversion in 

V 2 /V 3 . Ajmaline provocative testing was performed in those with a 

history and/or ECG suggestive of Brugada syndrome. 

Results Of the 193 patients, 43 individuals (22%) from 36 families 

(33%) were diagnosed with an inheritable cause of SCD and 145 

patients were clinically normal (see Abstract 162 table 1). Five 

patients were found to have other conditions (LV non-compaction, 

AVNRT, skeletal myopathy, mild AS and congenital sub-aortic 

membrane). Of the 43 patients diagnosed with an inheritable 

condition, 21 had medication commenced by the clinic (b-blockers 

(21), ACEi/ARB(2), Spironolactone[1]). ICDs were implanted as per 

HRUK guidelines, resulting in 4 patients having an ICD inserted on 

clinic recommendation (2 HCM, 1 DCM, 1 ARVC). To date no 

appropriate therapies have been administered (follow-up 8e29 

months) but there was 1 inappropriate shock from a fractured lead. 

Three individuals had b-blockade withdrawn after negative genetic 

testing for an established familial mutations (2 CPVT, 1 LQT), one 

ICD was removed and one deactivated (both negative for CPVT). Of 

the 145 patients thought to be clinically normal, 85 were reassured 

and discharged, 13 failed to return to clinic and 47 are regular 

reviewed as the risk of developing an inheritable condition cannot be 

excluded; this includes those with family histories of HCM (7), 

ARVC (12), DCM (9), CPVT (5), Brugada (4) and LQT(1). To date 

no deaths have occurred in those diagnosed with inherited causes of 

SCD (follow-up mean 20, 1e52 range) or those clinically normal 

with ongoing review (follow-up mean 22 months, 1e56 range). 


Diagnosis of patient 

Numbers 

Clinically normal 145 

LQTS 12 

Brugada 2 

CPVT 5 

ARVC 7 

DCM 7 

HCM 10 

Conclusion A diagnosis of an inheritable cause of SCD was obtained 

in 22% of individuals and 33% families with a history of SCD/ 

aborted cardiac arrest in a relative. The number of ICDs inserted was 

very small (2%) and there have been no appropriate therapies in this 



group. Two ICDs have been removed/deactivated after exclusion of 

a known familial mutation. 

163 THE UNITED KINGDOM TRANSCATHETER AORTIC VALVE 

REGISTRY - OUTCOMES TO DECEMBER 2009 AND UPDATE 

doi:10.1136/heartjnl-2011-300198.163 

P F Ludman. On Behalf of the UK TAVI Steering Group, Birmingham, UK 

Introduction The United Kingdom Transcatheter Aortic Valve (TAVI) 

Registry was established to define the clinical and procedural details 

of all patients being treated by TAVI, regardless of access route or 

technology used, and to assess their outcomes. The registry has 

captured all cases in England and Wales. 

Methods For every TAVI performed, all centres complete an agreed 

dataset. The data are encrypted and sent electronically to servers at 

the Central Cardiac Audit Database (CCAD) for analysis. A unique 

patient identifier (the NHS number) is used to link with the NHS 

Central Register to track mortality. This analysis is based on all 

procedures performed up to 31st December 2009. 

Results 25 centres in England and Wales performed a total of 877 

procedures in 870 patients; 66 in 2007, 273 in 2008 and 538 in 2009. 

Median number of cases per centre was 24. Median (IQR) age was 

82 (78e87) yrs. 52% were male, and mean logistic Euroscore (LES) 

was 22.2%. 68% were transfemoral, the remainder being mainly 

transapical. 90% of CoreValve implants and 46% of Edwards used a 

transfemoral approach. Patients needing a transapical route had 

more comorbid conditions than those treated by a transfemoral 

route (LES 25.2% vs 20.9%). Mortality tracking was successful in 

100% of patients. Survival at 30 days was 93.1%, 78.9% at 1 year 

(443 at risk) and 72.3% at 2 years (114 at risk). Survival was 

significantly poorer in those needing non-transfemoral approaches 

(1 year survival 73.5% vs 81.4%). Survival was also poorer in those 

with poorer LV ejection fraction, with moderate or severe post 

procedural aortic regurgitation and with a LES>40. Survival was not 

associated with age, NYHA class, or the presence of concomitant 

coronary artery disease, and not different between those with a 

LES


These were taken at multiple time points (baseline, 6 and 24 hours 

post procedure). Calculated volumetric parameters included 3D enddiastolic 

volume (EDV) and end-systolic volume (ESV), stroke 

volume (SV) and 3D LA volume (LAV). Diastolic function was 

monitored using the indices mean E:E 9 and systolic function/ 

contractility was measured with dP/dt max and early peak systolic 

velocity (S 9 ). The FloTrac system (consisting of the Vigileo monitor 

and sensor), uses a clinically validated algorithm to provide 

continuous cardiac output (CO), stroke volume (SV) and systemic 

vascular resistance in real-time. 

Results TAVI resulted in an immediate increase in cardiac output 

(3.7 (baseline), 4.6 (6 h) 4.5 l/min (24 h), p


aortic velocity 3.160.6/ms, LV mass 172648 g; SBP 127 614 mm 

Hg DBP 76 610 mm Hg) and 18 patients with velocity-matched 

TAV (age 74 66 years, female 28%, velocity 3.160.6/ ms, LV mass 

147627 g; SBP 136617 mm Hg; DBP 7967 mm Hg; Abstract 166 

table 1). Patients were scanned using a 1.5 T Avanto scanner (Siemens 

Healthcare, Erlangen, Germany) and basal, mid-ventricular and apical 

short axis tagging images were acquired. Peak systolic global 

circumferential strain was calculated at each ventricular level using 

CimTag2D software v.7 (Auckland MRI Research Group, New Zealand). 


Bicuspid vs tricuspid aortic valve disease 

Bicuspid 

Morphology 

aortic valve 

(BAV) 

Tricuspid aortic 

valve (TAV) p Value 

Age (yrs) 55615 7466 88 mls (AUC 0.78). Regurgitant fraction and volume were 

the only independent outcome predictors on multiple logistic 

regression analysis. The predictive ability of CMR applied to 

patients with both moderate and severe aortic regurgitation on 

echocardiography. Supporting data also comes from a comparison 

Abstract 166 Figure 1 Velocity matched tricuspid and bicuspid aortic 

valves showing valve morphology, tagging and cine imaging. 


Abstract 167 Figure 1 Kaplan-Meier survival curve showing survival 

without surgery for conventional indications. 

A93


with patients already planning to undergo surgery at the time of 

CMR scanning, which showed similar regurgitant fractions in the 

surgical group (mean 6SD: 45.4%612.1%) compared to the initially 

asymptomatic patients who developed symptoms or other indications 

for surgery (42.8%610.4%); p¼0.32. Subjects who remained 

asymptomatic had a significantly lower regurgitant fraction: 

25.368.6% (p110 000 scans). Patients with a diagnosis of 

moderate or severe MR from 1993 to 2008 were identified. Cox 

regression model (adjusted for age, gender, left ventricular dimensions 

and function, left atrial diameter, cardiovascular (CV) history 

and concurrent CV medications) was used to assess the impact of 

BB therapy on all-cause mortality and cardiovascular events (CV 

death or hospitalisations). 

Results A total of 4437 patients with moderate to severe MR (mean 

age 74 Â611 years, 46% males) were identified. MR was categorised 

as functional in 2523 (57%) and organic in 1894 (43%) while 1324 

(30%) were on BBs. Over a mean follow-up of 3.9 years there were 

2287 (51%) all-cause deaths and 2333 (52%) CV events. Those 

treated with BBs had a significantly lower all-cause mortality with 

an adjusted HR of 0.65 (95% CI 0.56 to 0.75, p


170 ETHNIC DIFFERENCES IN PHENOTYPIC EXPRESSION OF 

HYPERTROPHIC CARDIOMYOPATHY 

doi:10.1136/heartjnl-2011-300198.170 

N Sheikh, M Papadakis, N Chandra, H Raju, A Zaidi, S Ghani, M Muggenthaler, S Gati, 

S Sharma. St. George’s University of London, London, UK 

Purpose Hypertrophic Cardiomyopathy is a heterogeneous condition 

with variable phenotypic expression. Current studies are based 

on predominantly Caucasian cohorts (white patients; WP), therefore 

the phenotypic manifestations of HCM in individuals of 

African/Afro-Caribbean origin (black patients; BP) are not fully 

realised. Data in athletes and hypertensive patients indicate that 

black ethnicity is associated with a greater prevalence of repolarisation 

abnormalities on the ECG as well as a greater magnitude of 

left ventricular hypertrophy (LVH), highlighting the importance of 

defining the HCM phenotype in this ethnic group. 

Methods Between 2001 and 2010, 155 consecutive patients with 

HCM (52 BP, 103 WP) were assessed in 3 specialist cardiomyopathy 

clinics in South London. All individuals underwent comprehensive 


Black HCM 

(n[52) 

white HCM 

(n[103) 

p Value 

Demographics 

Age of diagnosis (years) 48.1617.1 50.5616.5 0.552 

Gender (males) 61.5% 62.1% 0.942 

FH of HCM/SCD 34.6% 32.0% 0.747 

NYHA functional class III or IV 7.7% 7.8% 0.987 

Patients on treatment 55.8% 46.6% 0.281 

B-blockers 28.8% 39.1% 0.445 

Calcium antagonists 26.9% 12.6% 0.026 

Amiodarone 7.7% 1.9% 0.080 

Diuretics 13.5% 9.7% 0.480 

Disopyramide 3.8% 9.7% 0.197 

Intracardiac defibrillator in situ 5.8% 5.8% 0.989 

Echocanliographic characteristics 

Ao (mm) 31.363.7 33.265.8 0.123 

LA (mm) 40.967.3 39.967.3 0.593 

LVED (mm) 44.066.1 44.466.1 0.787 

mLVWTd (mm) 17.364.9 18.864.1 0.069 

LV mass (g) 279.66106.5 287.66112.7 0.767 

FS (%) 40.469.1 39.868.3 0.641 

E wave (m/s) 0.7060.18 0.7460.20 0.443 

A wave (m/s) 0.6760.18 0.6660.27 0.851 

E/A 1.1160.44 1.2260.58 0.422 

SAM 23.1% 37.9% 0.064 

LVOT gradient ¼ 30 mm Hg 23.1% 34.0% 0.163 

LVH pattern 

ASH 25% 57.3% 0.004 

Concentric 44.2% 30.1% 

Apical 28.8% 11.7% 

No hypertrophy 1.9% 1.0% 

Echocanliographic characteristics 

LVH (Sokolow & Lyon) 53.8% 35.9% 0.033 

Left atrial enlargement 44.2% 49.5% 0.534 

Pathological Q waves 9.6% 23.3% 0.039 

Left axis deviation 11.5% 17.2% 0.270 

Inverted T-waves 82.7% 69.9% 0.086 

T-wave inversions in V1eV4 3.8% 3.9% 0.991 

T-wave inversions in inferior leads 1.9% 5.8% 0.269 

T-wave inversions in lateral leads 76.9% 60.2% 0.038 

Deep T-wave inversions 69.2% 51.5% 0.035 

ST-segment elevation 9.6% 9.7% 0.985 

ST-segment depression 50% 35.0% 0.071 


cardiac evaluation including 12-lead ECG and echocardiography. 

Patients subject to therapeutic interventions potentially affecting 

repolarisation patterns were excluded. 

Results Black patients revealed significantly different echocardiographic 

patterns of LVH, with more concentric (44.2% vs 30.1%) 

and apical (28.8% vs 11.7%) hypertrophy compared to WP who 

exhibited more asymmetric septal hypertrophy (57.3% vs 25.0%) 

(p¼0.004). Black patients exhibited a similar magnitude of LVH 

compared to WP (17.364.9 vs 18.864.1 mm, p¼0.069). Relating to 

ECG repolarisation abnormalities, BP exhibited more T wave inversions 

in the lateral leads (76.9% vs 60.2%, p¼0.038) and deep 

($ 0.2 mV) T-wave inversions (69.2% vs 51.5%, p¼0.035). Black 

patients also tended to display more ST segment depression (50.0% 

vs 35.0%, p¼0.071), although this was not statistically significant. 

In contrast, WP had significantly more pathological Q waves (23.3% 

vs 9.6%, p¼0.039). 

Conclusions Ethnicity appears to exert a significant effect on ECG 

and echocardiographic patterns in patients with HCM. A significant 

proportion of black patients exhibit concentric LVH, highlighting 

the diagnostic challenges in distinguishing HCM from hypertensive 

heart disease and physiological adaptation to exercise in black 

individuals. The greater prevalence of deep T wave inversions and T 

wave inversions in the lateral leads underscores the importance of 

further evaluation of black individuals with such ECG repolarisation 

abnormalities, which may represent the initial expression of HCM. 

171 THE RIGHT VENTRICLE OF THE ENDURANCE ATHLETE: THE 

RELATIONSHIP BETWEEN MORPHOLOGY AND 

DEFORMATION 

doi:10.1136/heartjnl-2011-300198.171 

1 D Oxborough, 

2 R Shave, 

3 G Whyte, 

1 K Birch, 

4 N Artis, 

3 K George, 

5 S Sharma. 

1 University of Leeds, Leeds, UK; 

2 UWIC, Cardiff, UK; 

3 Liverpool John Moores 

University, Liverpool, UK; 

4 Leeds Teaching Hospitals NHS Trust, Leeds, UK; 

5 St 

Georges University Hospital, London, UK 

Introduction It is well established that endurance exercise results in 

cardiac adaptation including eccentric hypertrophy of the left 

ventricle which can complicate the differential diagnosis of the 

athletic heart from some cardiac pathologies that may pre-dispose to 

sudden cardiac death. The impact of physiological conditioning on 

RV structure and function, and a similar diagnostic challenge with 

arrhythmogenic right ventricular cardiomyopathy (ARVC), has 

received less attention. A recent guideline paper from the American 

Society of Echocardiography (ASE) has provided a range for normal 

RV dimensions and functional deformation. These guidelines 

suggest the RV inflow (RVI) should be


ranged from 30 to 55 mm with 57% of the population having values 

greater than the normal range. Proximal RVOT ranged from 26 to 

49 mm with 40% of the population above the normal range. 28% of 

the population had RVOT values greater than the proposed “major 

criteria” for ARVC. RV length ranged from 70 to 110 mm and 

RVDarea from 13 to 38 cm 2 with values falling above ASE cut-offs 

in 69% and 59% of the population, respectively. When indexed (ratio 

scaling) for BSA proximal RVOT ranged from 13 to 25 mm/m 2 with 

6% of the population meeting the major criteria for ARVC. Peak RV3 

ranged from 18 to 41% and peak RV SRS 9 from 0.75 to 2.65 l/s, 

consistent with normal ranges proposed by the ASE. RV diastolic 

deformation indices displayed marked individual variability with a 

dominant SRE 9 (mean 6 SD¼2.060.61 l/s) and smaller SRA 9 

(1.2560.56 l/s). 

Conclusion RV dimensions in endurance athletes are higher than 

those proposed as “normal” and likewise may be consistent with the 

criteria for ARVC. Despite this enlargement, RV function in 

endurance athletes is preserved and therefore the role of RV strain 

imaging may provide additional diagnostic value in differentiating 

physiological from pathological adaptation. 


ASE Normal Indexed (ratio 

Parameter Mean ± SD (range) Values scaling) for BSA 

RVOT (mm) 3465 (26 to 49)


experimental models. The observed effects are partly due to iron IImediated 

oxidative damage. This was confirmed by the presence of a 

ROS scavenger delaying the onset of the effects of iron II, and 

crucially rendering the effects reversible upon iron-washout. These 

effects of tempol suggest a novel therapeutic target for the treatment 

of IOCM patients. 

173 A GENERIC METHOD TO ASSESS THE ADEQUACY OF 

INDIVIDUAL MATERNAL CARDIAC RESERVE TO TOLERATE 

THE DEMANDS OF PREGNANCY AND LABOUR 

doi:10.1136/heartjnl-2011-300198.173 

1 D Barker, 

2 N Lewis, 

2 G Mason, 

2 L B Tan. 

1 Liverpool Heart and Chest Hospital, 

Liverpool, UK; 2 Leeds General Infirmary, Leeds, UK 

Introduction Clinicians often feel apprehensive when managing 

pregnant patients with heart disease. To complement current evaluation, 

we have developed a new method of directly assessing the 

individual patient’s cardiac functional reserve through stress testing. 

Pregnant mothers with and without heart disease were studied to 

test the hypothesis that pregnant cardiac patients who possess 

cardiac reserve equivalent to that of controls can tolerate the usual 

demands of pregnancy, labour and puerperium. 

Methods Fifty-one pregnant women with heart disease (mean age 

30.766.5 (range 21e42), mean gestation 25.668.6 weeks) and 102 

healthy pregnant women (mean age 31.465.0, (range 19e41), mean 

gestation 25.169.2 weeks) underwent maximal symptom-limited 

treadmill cardiopulmonary exercise testing. Fifty-nine non-pregnant 

women (mean age 32.765.1 (range 20e41) years) were similarly 

tested and used as a control group. Cardiac output (CO) was 

measured at peak exercise using the CO 2 re-breathing method. 

Cardiac power output (CPO) was calculated as the product of CO 

and mean arterial pressure. A composite endpoint including 

maternal death, fetal death, emergency caesarean section for 

maternal distress and significant morbidities was determined. 

Results All tests were performed without significant complications. 

Employing data from a previous study of haemodynamics during 

labour in healthy women, the mean CPO required during peak 

labour is 2.6 W. This value was adopted for investigation as the 

minimum required for an average woman to cope with the circulatory 

demands of normal labour. The healthy controls had a mean 

peak CPO (PkCPO) of 3.7960.6 W and all non-pregnant women had 

PkCPO exceeding 2.6 W. The majority of heart disease patients were 

able to achieve PkCPO values overlapping their healthy counterparts. 

Only a small proportion of the cardiac patients had PkCPO 

values lower than the 2.6 W cutoff. Women were significantly more 

likely to have uncomplicated pregnancy, labour and puerperium if 

able to achieve PkCPO>2.6 W (OR 8.1, 95% CI 1.8 to 37.0, 

p¼0.023). Pregnant women in NYHA class I had PkCPO values 

indistinguishable from controls (mean 3.9860.77 W, NS); whereas 

symptomatic pregnant women had significantly lower values (mean 

3.1560.71W, p

Author index 

The number next to the author indicates the page number, not the abstract number. 

Abbas A, A1, A3 

Abidin N, A70 

Abozguia K, A55 

Abu-Own H, A25 

Adam Z, A5 

Adams PC, A39 

Aggarwal R, A22, A30 

Aggarwal S, A60, A61 

Ahmed R, A43 

Ahsan AJ, A86 

Aitma TJ, A4 

Akhtar M, A9 

Al Fakih K, A36 

Ala L, A82 

Alahmar A, A27 

Alamgir MF, A23 

Alp NJ, A79 

Alpendurada F, A53 

Alpendurado F, A94 

Amersey R, A15 

Anand A, A7 

Angelini G, A24 

Anroniades C, A79 

Antoniou S, A5 

Appleby C, A27 

Archbold A, A46 

Archbold RA, A5 

Arthur H, A78 

Arthur HM, A75 

Artis N, A95 

Artis NJ, A72, A73 

Arujuna A, A85 

Augustine D, A63 

Aung N, A60, A61 

Austin D, A5 

Avery P, A75 

Awan M, A5 

Ayers L, A50 

Aziz A, A78 

Babar J, A63 

Baker CSR, A18 

Baker S, A68 

Balakrishnan B, A66, A81 

Baliga V, A56 

Ball SG, A35, A41, A72 

Balmforth AJ, A35, A41 

Bamforth SD, A77 

Banerjee A, A40 

Banerjee G, A7 

Banerjee R, A63 

Banerjee S, A7 

Banner NR, A48, A49, A64 

Banning AP, A12, A93 

Banypersad SM, A59 

Bapat V, A19 

Baptista-Hon DT, A96 

Barker D, A57, A97 

Barker J, A7 

Barmby D, A21 

Barnes S, A60 

Barrington S, A68 

Barsan A, A49 

Barth J, A60 

Barth JH, A8, A17 

Baruah R, A51, A58 

Basavarajaiah S, A33 

Bashir Y, A87, A88 

Bastiaenen R, A33, A38, A83 

Baudoin F, A80 

Baumbach A, A24 

Bawamia BR, A10 

Beadle RM, A55 

Beatt K, A24 

Bechar I, A70 

Bedell VM, A78 

Begg G, A56 

Begg GA, A60, A86 

Begley D, A50 

Behan M, A16 

Behar J, A15 

Behar JM, A25 

Behr E, A38 

Behr ER, A33, A83 

Bell D, A72 

Bell J, A45 

Bellamy MF, A18 

Ben-Nathan S, A83 

Bennett MR, A2, A64 

Berry C, A16, A73 

Berry EL, A86 

Betts TR, A87, A88 

Bewick AE, A82 

Bhabra M, A19, A40 

Bhan A, A91 

Bhattacharya S, A77 

Biasiolli L, A62 

Bijnens BH, A52 

Birch K, A95 

Blackman DJ, A21 

Blair E, A62 

Blake J, A11 

Blamire A, A78 

Bland MB, A37 

Blaxill JM, A21 

Bleasdale RA, A34, A82 

Bloomer LDS, A41 

Blundell N, A92 

Bonser RS, A36, A48 

Borbas Z, A90 

Borg A, A70 

Borg AN, A74 

Bostock J, A52, A84, A85 

Boston-Griffiths E, A30 

Bowater S, A55 

Bowen TS, A56 

Braganca J, A77 

Braganza D, A2 

Braund PS, A41, A42 

Brewer A, A77 

Brewster S, A46 

Brickham B, A91 

Broadbent C, A77 

Brown AJ, A29 

Brown BD, A90 

Brown P, A89 

Bryan L, A72 

Buchanan L, A23 

Bull S, A92 

Byrom R, A60 

Caldwell JC, A90 

Calver A, A16 

Calvert PA, A2, A64 

Camara O, A52 

Campbell M, A11 

Cannon DT, A56 

Caplin JL, A23 

Carr-White G, A52, A84 

Carre F, A38 

Carrick D, A16 

Carter J, A5 

Cartwright EJ, A41, A80 

Casadei B, A79 

Casey FA, A75 

Casey M, A73 

Cassar TE, A62 

Chalmers RTA, A3 

Chambers J, A43 

Chandra N, A33, A38, A95 

Channon K, A12 

Channon KM, A79 

Chaubey S, A77 

Chaudhry U, A27 

Chen C-M, A77 

Cheng A, A60, A61 

Chico TJA, A43 

Chinchapatnam P, A52 

Chinnappa S, A57 

Chiribiri A, A68, A71 

Chong E, A24 

Choudhury RP, A12, A62, A70 

Chowienczyk P, A28, A32 

Choy AM, A94 

Choy AMJ, A58 

Christiansen JP, A93 

Christie J, A16 

Christofidou P, A41 

Churchhouse AMD, A7 

Clack L, A19 

Clapp B, A24, A32 

Claridge S, A36 

Clark C, A73 

Clark D, A70 

Clarke B, A26 

Clarke SC, A2 

Cleary N, A46 

Clesham G, A30 

Codd V, A42 

Collerton J, A57 

Connelly K, A22 

Connolly S, A7 

Cook DG, A41 

Cook S, A43 

Cook SA, A4 

Corbett S, A16 

Cotton J, A19 

Cowie MR, A53 

Cox RD, A41 

Craig BG, A75 

Crean A, A72 

Crossman D, A13 

Cruddas E, A24 

Cubbon R, A1, A3, A60, A78 

Cunliffe E, A52 

Curzen N, A16 

D’Arcy J, A92, A93 

d’Arcy JL, A92 

Díaz ME, A96 

Dall’Armellina E, A12 

Damm E, A30 

Danesh J, A43 

Das D, A43 


Author index 

Das M, A84 

Davidson C, A14 

Davidson J, A35 

Davidson NC, A90 

Davies DW, A51, A83 

Davies J, A22, A30, A45, A54 

Davies JE, A10 

Davies MJ, A6 

Davis E, A37, A63 

Davison BJ, A78 

Dawson A, A34 

de Belder A, A45 

de Belder MA, A5 

De Silva K, A24, A28, A71 

Deanfield JE, A41 

Deaton C, A26 

Debiec R, A41 

Densem CG, A2 

Dent H, A16 

Denvir MA, A7, A53 

Dhillon OS, A10 

Diab I, A81 

Dick AJ, A22 

Dick KJ, A42 

Dickens C, A11 

Diesch J, A37, A63 

Digby J, A70 

Dinh DT, A9 

Dixit A, A26 

Dixon G, A45 

Dobrzynski H, A4 

Doherty PD, A37 

Donald A, A32 

Donald AE, A41 

Donin A, A41 

Doolin O, A73 

Douglas-Hill C, A19 

Drury-Smith M, A19 

Duckett S, A84, A85 

Duckett SG, A52 

Dungu J, A18, A59 

Durham N, A60 

Dutka DP, A50 

Dweck M, A3 

Dweck MR, A94 

Dwivedi G, A66, A81 

Dworakowski R, A91 

Earley MJ, A81 

Ebbs D, A92 

Eccleston D, A38 

Edmunds L, A45 

Edwards R, A10, A29 

Eftychiou C, A21 

Ekker SC, A78 

El-Omar M, A26 

Elder DH, A94 

Elder DHJ, A34, A58 

Ellins E, A41 

Emin A, A48 

Engelen K, A76 

Englyst N, A16 

Eve S, A47 

Fairbairn TA, A73 

Farmer AJ, A92 

Fath-Ordoubadi F, A11 

Ferguson E, A5 

Ferreira V, A12 

Finch S, A46 

Flather M, A13, A24, A38 


Flint J, A60, A61 

Foley C, A13 

Foley JRJ, A90 

Foo F, A16 

Ford I, A73 

Forfar C, A12 

Forfar JC, A62 

Fox DJ, A90 

Fox K, A13 

Fox KAA, A7 

Fox KF, A7 

Frampton C, A11 

Francis DP, A49, A50, A51, A58, A60, A61, A66 

Francis J, A37, A63 

Francis JM, A12, A62, A68, A92, A93 

Frangi AF, A52 

Fraser AG, A34 

Fraser D, A26 

Freemantle N, A49 

French AE, A89 

Frenneaux MP, A55 

Gage M, A1, A3 

Gage MC, A78 

Gale CP, A8, A17, A60 

Gale CPG, A37 

Gallagher M, A83 

Gallagher S, A15, A31 

Gallagher SM, A5 

Galloway S, A78 

Gamble D, A7 

Garden OJ, A3 

Garratt CJ, A90 

Gasson A, A82 

Gati S, A31, A95 

George DA, A40 

George K, A95 

Ghani S, A31, A95 

Gholap NN, A6 

Gibbins A, A45 

Gibbons SM, A41 

Gibbs SDJ, A59 

Gierula J, A60, A86 

Gilchrist J, A73 

Gill JS, A52 

Gill PS, A59 

Gillivray TJMac, A3 

Gillmore JD, A59 

Ginks M, A52, A84, A85 

Glen E, A76 

Glen EA, A75 

Goodall AH, A42 

Goodship J, A75, A76 

Goodship JA, A75, A76 

Gopalan D, A63, A64 

Gordon B, A49 

Gordon J, A75 

Gosling O, A20 

Gosling OE, A65 

Graham A, A13, A15 

Graham C, A7 

Graham TR, A36 

Gray C, A3, A43 

Gray H, A16 

Greaves M, A70 

Greenwood JP, A13, A21, A72, A73, A93 

Griffin HR, A76 

Grimwade P, A92 

Guha K, A53 

Guilcher A, A28 

Gulati A, A94 

Gunn J, A13 

Guttmann O, A9 

Guttmann OP, A31 

Haga KK, A53 

Hall A, A13 

Hall AS, A8, A17, A35, A41 

Hall ASH, A37 

Hall D, A75 

Hall DH, A75, A76 

Hall JA, A5 

Hall R, A24 

Hamid S, A84, A85 

Hamid SG, A52 

Hancock J, A19 

Handa A, A62 

Haq IU, A39 

Haran H, A19 

Hards R, A49 

Harrington DW, A82 

Harwood SM, A17 

Hawkins NM, A30 

Hawkins PN, A59 

Hayward PA, A9 

Hedger M, A49 

Hegab Z, A41, A44 

Heneghan C, A40 

Heymans S, A77 

Hobson A, A16 

Hodson J, A36 

Holbrook I, A60 

Holroyd EW, A78, A80 

Horne A, A89 

Hosmane S, A76 

Hoye A, A23 

Hughes A, A49 

Hughes AD, A50, A66 

Hunt J, A32 

Hunter A, A60 

Hunter RJ, A81 

Hussain S, A68 

Iles-Smith H, A11 

Imrie H, A1, A3, A78 

Indermeuhle A, A24 

Indermuhle A, A71 

Ingram TE, A34 

Irwin RB, A70 

Ishida M, A68, A71 

Ivetic A, A77 

Iyengar S, A65 

Jackson C, A78 

Jagger C, A57 

Jain A, A13, A15, A25, A31 

Jain AK, A5, A9, A15 

James PE, A34 

Jamieson S, A10 

Jamshidi Y, A4 

Jayaram R, A79 

Jeilan M, A89 

Johnson T, A89 

Jones D, A5 

Jones DA, A9, A13, A15, A25, A31 

Jones JD, A30 

Jones MA, A88 

Jones S, A83 

Joshi NV, A10 

Joshi S, A94 

Joysurry D, A41 

Juli C, A83 

Kahn M, A1, A78 

A99

Author index 

Kahn MB, A3 

Kaier T, A39 

Kanagaratnam P, A51, A83 

Kapetanakis S, A52 

Kapur A, A17, A24, A31 

Kapur AK, A25 

Karamitsos TD, A12, A68, A92, A93 

Karia N, A12 

Karim R, A83 

Kearney L, A60 

Kearney M, A1, A78 

Kearney MT, A3, A60 

Keavney B, A57, A75, A76, A78 

Keavney BD, A75, A76 

Kellman P, A12 

Kelly B, A37 

Kelly P, A22, A30 

Kemp I, A27 

Kemp S, A31 

Kennedy J, A62 

Kenny A, A57 

Kervio G, A38 

Kerzin-Storrar L, A90 

Kesavan S, A24 

Kettle AJ, A11 

Khan FZ, A50 

Khan MF, A23 

Khan N, A90 

Khan S, A39 

Kharbanda RJ, A12 

Khattar R, A26 

Khawaja MZ, A19 

Khimdas K, A46 

Khogali S, A19 

Khoo CW, A66, A81 

Khunti K, A6 

Kilcullen N, A8 

Kingston A, A57 

Kirkwood T, A57 

Klaassen S, A76 

Knight C, A5, A9, A13, A15, A25, A31 

Knight CJ, A25 

Kooner J, A43 

Kotecha D, A38 

Krishnamoorthy S, A66, A81 

Krum H, A38 

Kuehl M, A55 

Kuijer JPA, A69 

Kuker W, A62 

Kulanthaivelu R, A82 

Kumar D, A46 

Kundu S, A89 

Kylintireas I, A62, A70 

Kyriacou A, A50, A51, A66 

Lachmann HJ, A59 

Lang CC, A35, A58, A94 

Langrish JP, A3 

Larsen K, A80 

Lazdam M, A37, A63 

Leadbeater P, A16 

Lee JM, A62, A70 

Lee KK, A7 

Lees B, A13 

Leeson P, A37, A62, A63 

Leisa RA, A80 

Leon FL, A55 

Lewandowski AJ, A37, A63 

Lewin BL, A37 

Lewinter CL, A37 

Lewis N, A57, A97 

Lewis RJ, A75 

Leyva F, A48 

Lim HS, A66, A81 

Lim PB, A83 

Lindsay A, A12 

Lindsay AC, A62 

Ling HZ, A60, A61 

Lip GYH, A59, A66, A81 

Little A, A46 

Liu A, A21 

Llewellyn-Griffiths H, A54 

Loader R, A65 

Lockie TPE, A28 

Loh PH, A23 

Lovell MJ, A5 

Lowdell M, A20 

Lucas A, A37 

Ludman A, A9 

Ludman PF, A91 

Lundmark P, A42 

Ma Y, A84, A85 

MacArtney MG, A94 

MacCarthy P, A91 

MacDonald ST, A77 

MacDonald TM, A35 

Macgillivray K, A19 

Macgilivray TJ, A3 

MacGowan G, A48, A49 

MacLeod M, A7 

Macnab A, A76 

Mahadevan V, A26 

Maher A, A19 

Mahmod M, A68 

Majumder B, A20 

Makri L, A21 

Malcolme-Lawes L, A83 

Malik N, A22 

Mamas M, A26, A44 

Mamas MA, A41 

Mamasoula V, A75 

Manisty C, A50 

Manisty CH, A58 

Mant D, A92 

Marber M, A28 

Margulescu A, A34 

Markl M, A62 

Marshall CJ, A11 

Mascaro J, A36 

Masi S, A41 

Mason G, A97 

Mather AN, A72, A73 

Mathur A, A5, A9, A13, A15, A25, A31 

Mavroudis C, A27 

Mavroudis CA, A20 

May S, A13 

Mayet J, A50, A51, A58, A60, A61, A66 

McCann GP, A69, A74, A89 

McCarthy CA, A59 

McCarthy MI, A43 

Mcclean DR, A11 

McClure J, A73 

McCormick LM, A29 

McCusker CG, A75 

McDiarmid A, A49 

McDonagh T, A53 

McEntegart MB, A73 

McGeoch R, A73 

McGill LA, A15, A25 

McGowan L, A11 

Mckenzie JL, A11 

McKeown PP, A75 

McKillop G, A3 

McLenachan JM, A21 

McMahon M, A75 

McNab D, A2 

Mehta P, A84, A85 

Mehta RL, A6 

Menon A, A36 

Metcalfe K, A90 

Millar FR, A96 

Miller C, A70 

Miller CA, A74 

Mills NL, A7 

Mitchell AG, A64 

Mittal TK, A64 

Moccata T, A11 

Mohamed TMA, A80 

Mohammed TMA, A41, A44 

Mohiaddin R, A93, A94 

Mohiddin S, A5, A9, A13 

Mole G, A14 

Monaghan M, A91 

Moraldo M, A50, A66 

Moreton N, A90 

Morgan-Hughes G, A65 

Morrell C, A8 

Morrice D, A40 

Morrison ML, A75 

Morton AC, A13 

Morton G, A24 

Morton GDJ, A68, A71 

Muckett P, A43 

Muckett PJ, A4 

Muggenthaler M, A33, A95 

Muir DF, A5 

Mukhopadhyay D, A80 

Mulder B, A76 

Mullen LJ, A29 

Murdoch CE, A77 

Murgatroyd SR, A56 

Murigu T, A94 

Murphy A, A73 

Murray SA, A53 

Musameh MD, A35 

Myerson SG, A68, A92, A93 

Nadir A, A35, A94 

Nadra I, A19 

Nagel E, A68, A71 

Nair S, A26 

Nallaratnam M, A11 

Narayan HK, A10 

Nayar V, A50 

Nelson CP, A41, A42 

Ness A, A53 

Neubauer S, A12, A37, A62, 

A63, A68, A92, A93 

Neubauer SN, A62 

Neubuer S, A70 

Nevill AM, A40 

New G, A38 

Newby D, A94 

Newby DE, A3, A7 

Newman D, A40 

Newman W, A90 

Newton T, A70 

Neyses L, A26, A41, A44, A80 

Ng GA, A89 


Author index 

Ng LL, A10 

Nicol E, A72 

Nicolson WB, A89 

Nightingale CM, A41 

Nijjar M, A30 

Nijjer SS, A7, A49 

Norrie J, A16 

Nyawo B, A29 

O’Callaghan P, A55 

O’Doherty M, A68 

O’Donnell M, A53 

O’Sullivan JJ, A75 

O’Sullivan M, A2 

O 9 Neill SC, A96 

Obaid DR, A2, A63, A64 

Oceandy D, A80 

Okonko DO, A60, A61 

Oldroyd K, A16 

Oldroyd KG, A73 

Oliver M, A54 

Oliver RM, A23 

Ordoubadi F, A26 

Oriolo V, A47 

Ormerod OO, A70 

Owen CG, A41 

Owen J, A60 

Oxborough D, A95 

Pabari P, A49, A51, A58 

Pabari PA, A50, A66 

Padgett HC, A86 

Padley S, A72 

Pagano D, A36 

Palmieri V, A49 

Palomino-Doza J, A75 

Panayotova R, A76 

Panicker MG, A64 

Panoulas V, A33, A38 

Papadakis M, A33, A38, A95 

Parameshwar J, A48 

Parker C, A89 

Parry G, A49 

Pashaei A, A52 

Patel P, A82 

Paterson E, A7 

Patterson C, A72 

Paul GA, A22 

Payne AR, A73 

Pearson IR, A8, A17, A60 

Peebles C, A70 

Pennell D, A94 

Penswick A, A46 

Pepper J, A94 

Perera D, A24, A28, A68, A71 

Perry R, A30 

Perry RA, A27 

Peters NS, A4, A51, A83 

Petersen SE, A62 

Petrie MC, A73 

Pettit S, A30 

Pierret CK, A78 

Pierscionek T, A75 

Pinney JH, A59 

Pitcher A, A62, A92 

Pitts-Crick J, A89 

Plein S, A72, A73 

Plummer CJ, A84 

Poole R, A37, A63 

Popov AF, A49 

Postma A, A76 


Prasad S, A53, A94 

Pravanec M, A4 

Prehar S, A41, A80 

Prendergast B, A12, A92 

Prendergast BD, A92 

Prescott M, A41 

Pretsell G, A45 

Pringle SD, A58, A94 

Pugh PJ, A50 

Pye M, A60 

Quinn PA, A10 

Qureshi AC, A17 

Qureshi N, A88 

Rahman T, A75, A76 

Rajappan K, A87, A88 

Raju H, A31, A33, A38, A95 

Rajwani A, A1, A3 

Rakhit RD, A20, A27 

Rampat R, A17 

Rana B, A67 

Rapala A, A41 

Rashid S, A3 

Rathod B, A15, A31 

Rathod K, A13, A25, A31 

Rathod KR, A15 

Rathod KS, A9, A15 

Rathod VS, A15 

Rawling A, A50 

Rawlins J, A33, A38 

Ray KK, A2 

Raybould A, A54 

Razavi R, A84, A85 

Razavi RS, A52 

Razvi NA, A69 

Redgrave R, A78 

Redwood S, A19, A24, A28, A71 

Rees I, A55 

Reid CM, A9 

Reid J, A53 

Reilly S, A79 

Rekhraj S, A35 

Rhode K, A84, A85 

Richards JMJ, A3 

Richards M, A11 

Richards T, A61 

Richmond L, A81 

Rider O, A70 

Rinaldi CA, A52, A84, A85 

Ring L, A67 

Robb SD, A73 

Robinson N, A49 

Robson MD, A12, A62, A70 

Rogers C, A11 

Rogers CA, A48 

Rogers T, A36 

Rolandi C, A28 

Roobottom C, A65 

Rooney SJ, A36 

Rose H, A45, A54 

Rossiter HB, A56 

Rothman A, A13 

Rothman M, A46 

Roughton M, A17 

Rudd JHF, A63, A64 

Rudnicka AR, A41 

Rueckert D, A83 

Rusk RA, A67 

Russell S, A46, A54 

Russell SJ, A45, A55 

Sabharwal NS, A70 

Sadarmin PP, A87 

Salaheen D, A43 

Salukhe TV, A83 

Samani NJ, A35, A41, A42 

Sambu N, A16 

Sammut E, A15, A25 

Sammut EC, A13 

Sanderson JE, A48 

Sandilands AJ, A89 

Sands AJ, A75 

Sattianayagam P, A59 

Saul A, A73 

Sayan S, A51 

Sayer J, A22, A30 

Schilling RJ, A81 

Schlindwein FS, A89 

Schmitt M, A70, A74 

Schneider JE, A77 

Schofield PM, A2 

Schotten U, A79 

Schueler S, A48, A49 

Schuster A, A68, A71 

Schwartz R, A77 

Sehmi J, A43 

Semple SI, A3 

Sermesant M, A52 

Shah A, A7 

Shah AJ, A63 

Shah AM, A77, A91 

Shah NH, A23 

Shantsila E, A59 

Shapiro LM, A2 

Shardey GC, A9 

Sharma R, A53 

Sharma S, A31, A33, A38, A83, A95 

Shave R, A95 

Sheikh N, A31, A38, A95 

Shelton RJ, A21 

Shepherd C, A89 

Shepherd EJ, A84 

Shetty A, A52, A84 

Shetty AK, A85 

Shi WY, A9 

Shirodaria C, A70 

Shome J, A5 

Showkathali R, A22, A30 

Sicard P, A24 

Siebes M, A28 

Sim V, A54 

Simari RD, A78, A80 

Simon A, A48 

Simon AR, A49 

Simpson I, A16 

Singh R, A19 

Singhal A, A37 

Sinha M, A47 

Sivananthan UM, A8, A17 

Skinner JS, A39 

Smith EJ, A25 

Smith J, A78 

Smith JA, A9 

Sneddon L, A75 

Snell KIE, A69 

Sohal M, A84, A85 

Somauroo J, A31 

Somers K, A21 

Sorbron S, A72 

Spath N, A33 

A101

Author index 

Sporton S, A81 

Squire IB, A6, A10 

Stables RH, A27 

Stafford PJ, A89 

Staniforth AD, A86 

Steadman CD, A69, A74, A89 

Stegemann B, A49 

Stoll VMS, A70 

Strain WD, A65 

Strauss BH, A22 

Struck J, A10 

Struthers AD, A34, A35, A58, A94 

Sukumar P, A78 

Suresh V, A20 

Surr J, A1, A3 

Sutaria N, A66 

Suttie J, A62, A63, A92 

Suttie JJ, A68 

Sutton AGC, A5 

Swanson NM, A5 

Syvänen AC, A42 

Szwejkowski BR, A34, A58 

Töpf A, A76 

Taggu W, A22 

Tagney J, A47, A89 

Tai ES, A43 

Tan HL, A75 

Tan LB, A57, A97 

Tan YT, A48 

Tayebjee M, A81 

Taylor R, A29 

Templeton C, A34 

ten Dijke P, A75 

Thackray S, A23 

Thomas G, A89 

Thomas HE, A84 

Thomas HL, A48 

Thomas M, A19, A24, A60, A61 

Thompson CA, A25 

Tilling LM, A32 

Tomaszewski M, A35, A41 

Tooze P, A21 

Topf A, A75 

Topf AL, A75 

Townend J, A78 

Tsui S, A48 

Twomey D, A84 

Tzemos N, A73 

Ungvari T, A23 

Unsworth B, A58, A66 

Van den Bruel A, A40 

van Eeden FJ, A43 

van Rossum AC, A69 

Vanhoutte D, A77 

Veasey RA, A82 

Venables P, A20 

Verheule S, A79 

Vile RG, A80 

Virdee MS, A50 

Viswambharan H, A1, A3, A78 

Viswanathan K, A8 

Waldron ZL, A86 

Walker S, A7 

Wallace W, A3 

Wang WYS, A35 

Ward D, A83 

Ware JS, A4 

Warner T, A16 

Wassef N, A59 

Waterworth P, A76 

Watson D, A14 

Watson J, A60 

Watson OJ, A43 

Watt H, A62 

Wechalekar A, A59 

Weerackody R, A15, A25, A46 

Weissert S, A60, A61 

Wells TA, A47 

Wendler O, A91 

Wenzelburger FWG, A48 

West NEJ, A2, A29 

Westwood M, A5 

Wheatcroft AC, A60 

Wheatcroft S, A1, A3, A78 

Wheatcroft SB, A21 

Whelan CJ, A59 

Whincup PH, A41 

Whinnett Z, A51 

Whinnett ZI, A58 

White J, A60 

Whyte G, A95 

Wicks E, A31 

Wilkinson S, A4 

Williams C, A34 

Williams LK, A55 

Williams M, A3 

Williams P, A26 

Williams R, A28, A39 

Willson K, A51 

Wilson IC, A36 

Wilson K, A19 

Wilson SJ, A20 

Wiper A, A26 

Witte KK, A56, A60, A86 

Woldman S, A60 

Wong KCK, A87, A88 

Woodcock T, A72 

Woodward R, A73 

Wordsworth BP, A62 

Wragg A, A9, A13, A15, A25, A31 

Wren C, A75 

Wright GA, A22 

Wright RA, A5 

Wrightson N, A49 

Yap CH, A9 

Yaqoob MM, A17 

Yellowlees D, A53 

Yeo Y, A43 

Young C, A19 

Young S, A45 

Yousaf F, A57 

Yousef ZR, A45, A46, A54, A55 

Yu B, A77 

Yuldasheva N, A3, A78 

Yusuf S, A89 

Zaidi A, A31, A33, A95 

Zaman A, A10, A72 

Zhang W, A43 

Zi M, A41, A80 

Zych B, A49

Full Supplement - British Cardiovascular Society

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