THE JOURNAL OF TEHRAN UNIVERSITY HEART CENTER

Zohair Yousef Al-halees, MD , FRCSC, FACS 

King Faisal Heart Institute, Saudi Arabia 

Yadolah Dodge, PhD 

University of Neuchâtel, Switzerland 

Ali Dodge–Khatami, MD, PhD 

University of Hamburg- Eppendorf School of Medicne, Germany 

Iradj Gandjbakhch, MD 

Hopital Pitie, France 

Omer Isik, MD 

Yeditepe University, School of Medicine, Turkey 

Sami S. Kabbani, MD 

Damascus University Cardiovascular Surgical Center, Syria 

Kayvan Kamalvand, MD, FRCP, FACC 

William Harvey Hospital, United Kingdom 

Jean Marco, MD, FESC 

Centre Cardio- Thoracique de Monaco, France 

Ali Massumi, MD 

Texas Heart Institute, U. S. A 

Carlos-A. Mestres, MD 

University of Barcelona, Spain 

Hossien Ahmadi, MD 

Tehran University of Medical Sciences 

Shahin Akhondzadeh, PhD 


Mohammad Alidoosti, MD 


Mohammad Ali Boroumand, MD 


Gholamreza Davoodi, MD 


Ahmad Reza Dehpour, PhD 


Alimohammad Haji Zeinali, MD 


Abbasali Karimi, MD 


Ali Kazemi Saeed, MD 


Seyed Ebrahim Kassaian, MD 


Davood Kazemi Saleh, MD 

Baghiatallah University of Medical Sciences 

Majid Maleki, MD 


Mehrab Marzban, MD 

Shahid Beheshti University of Medical Sciences 

THE 

JOURNAL OF TEHRAN 

UNIVERSITY HEART 

CENTER 

Editor-in-Chief 

ABBASALI KARIMI, MD 

PROFESSOR OF CARDIAC SURGERY 

TEHRAN UNIVERSITY OF MEDICAL SCIENCES 

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TEHRAN HEART CENTER 

TEHRAN UNIVERSITY OF MEDICAL SCIENCES 

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Fred Morady, MD 

University of Michigan, U. S. A 

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University of Texas, U. S. A 

Ahmand S. Omran, MD, FACC, FASE 

King Abdulaziz Cardiac Center, Saudi Arabia 

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Stanford University, School of Medicine, U. S. A 

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Wisconsin Heart Hospital, U. S. A 

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Indiana University, School of medicine, U. S. A 

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Seyed Mahmood Mirhoseini, MD, DSc, FACC, FAES 


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Mohammad-Hasan Namazi 

Shaheed beheshti University of Medical Sciences 

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Saeed Sadeghian, MD 

Tehran University of Medical Sciences

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Nizal Sarraf –Zadegan, MD 

Isfahan University of Medical Sciences 

Ahmad Yaminisharif, MD 


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Seifollah Abdi, MD 


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Alireza Amirzadegan, MD 


Naser Aslanabadi, MD 


Carlo Briguori, MD 

Clinica Mediterranea Hospital, Naples, Italy 

Alaide Chieffo, MD 

San Raffaele Scientific Institute, Milano, Italy 

Sirous Darabian, MD 

St. John Cardiovascular Reserach Center, USA 

Saeed Davoodi, MD 


Iraj Firoozi, MD 


Seyed Khalil Foroozannia, MD 

Shaheed Sadoghi University of Medical Sciences 

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Content 

Volume: 7 Number: 4 Autumn 2012 

The Journal of Tehran University Heart Center 

Review Article 

Prosthetic Tricuspid Valve Thrombosis: Three Case Reports and Literature Review 

Ahmad Yaminisharif, Mohammad Javad Alemzadeh-Ansari, Seyed Hossein Ahmadi ……………..…........................................................................... 147 

Original Articles 

Increased Carotid Artery Intima-Media Thickness in Pregnant Women with Gestational Diabetes Mellitus 

Gholamreza Yousefzadeh, Hashem Hojat, Ahmad Enhesari, Mostafa Shokoohi, Nahid Eftekhari, Mehrdad Sheikhvatan …………….....………………. 156 

Right Ventricular Myocardial Tissue Velocities, Myocardial Performance Index, and Tricuspid Annular Plane 

Systolic Excursion in Totally Corrected Tetralogy of Fallot Patients 

Asadolah Tanasan, Keyhan Sayadpour Zanjani, Armen Kocharian, Abdolrazagh Kiani, Mohammad Ali Navabi ……………...……............................ 160 

Anatomy of Atrioventricular Node Artery and Pattern of Dominancy in Normal Coronary Subjects: A 

Comparison Between Individuals With and Without Isolated Right Bundle Branch Block 

Ali Kazemisaeid, Marziyeh Pakbaz, Ahmad Yaminisharif, Gholamreza Davoodi, Masoumeh Lotfi Tokaldany, Elham Hakki Kazazi ……..................... 164 

Determinants of Length of Stay in Surgical Ward after Coronary Bypass Surgery: Glycosylated Hemoglobin as 

a Predictor in All Patients, Diabetic or Non-Diabetic 

Mahdi Najafi, Hamidreza Goodarzynejad …………….......………..........................….................................................................................................... 170 

Obvious or Subclinical Right Ventricular Dysfunction in Diabetes Mellitus (Type II): An Echocardiographic 

Tissue Deformation Study 

Mozhgan Parsaee, Parvaneh Bahmanziari, Maryam Ardeshiri, Maryam Esmaeilzadeh ……...........….....................................................................…… 177 

Case Reports 

Surgical Treatment of Amplatzer Embolus in a Secundum Atrial Septal Defect Patient 

Ahmet Baris Durukan, Hasan Alper Gurbuz, Murat Tavlasoglu, Nevriye Salman, Halil Ibrahim Ucar, Cem Yorgancioglu ………….……….............. 182 

Post-Traumatic Chordae Rupture of Tricuspid Valve 

Kyomars Abbasi, Hossein Ahmadi, Arezoo Zoroufian, Mohammad Sahebjam, Naghmeh Moshtaghi, Seyed Hessamedin Abbasi ................................ 185 

Late Diagnosis of Large Left Ventricular Pseudoaneurysm after Mitral Valve Replacement and Coronary Artery 

Bypass Surgery by Real-Time Three-Dimensional Echocardiography 

Mohammad Sahebjam, Abbas Salehiomran, Neda Ghaffari-Marandi, Azam Safir …………….....………..…............................................................... 188 

Letter to the Editor 

A Memorandum of "World Heart Day 2012": Myocardial Infarction Mortality in Women in Birjand, 2008-2009 

Toba Kazemi, Gholam Reza Sharifzadeh …………........................................................................................................................................................... 191 

Photo Clinic 

Ball in Chest 

Mohammad Bagher Rahim, Mohammad Hossein Mandegar, Farideh Roshanali …………............................................................................................. 192 

The Journal of Tehran University Heart Center

TEHRAN HEART CENTER


Volume: 7 Number: 4 

Summary of Contents 

What you will find 

in this Issue 

Autumn 2012 

REVIEW ARTICLE 

147 Prosthetic Tricuspid Valve Thrombosis: 

Three Case Reports and Literature Review 

Ahmad Yaminisharif, MD, Mohammad Javad Alemzadeh- 

Ansari, MD * , Seyed Hossein Ahmadi, MD 

Tehran Heart Center, Tehran University of Medical Sciences, 

Tehran, Iran. 

* 

Mohammad Javad Alemzadeh-Ansari, Department of 

Cardiology, Tehran University of Medical Sciences, Tehran 

Heart Center, Karegar Street, Tehran, Iran. 1411713138. 

Tel: +98 21 88029600. Fax: +98 21 88029731. E-mail: 

aansari@razi.tums.ac.ir. 

common complication of prosthetic heart 

A valves is thrombosis. Although the incidence 

of prosthetic valve thrombosis (PVT) in the tricuspid 

position is high, there are not enough data on the 

management of it, in contrast to left-sided PVT. 

Here, we describe three cases of tricuspid PVT with 

three different management approaches: thrombolytic 

therapy; close observation with oral anticoagulants; 

and surgery. The first case was a woman who suffered 

from recurrent PVT, for which we successfully used 

Tenecteplase for second and third episodes. We 

employed Tenecteplase in this case for the first time in 

the therapy of tricuspid PVT. The second case had fixed 

leaflets in open position while being symptomless. At 

six months' follow-up, with the patient having taken 

oral anticoagulants, the motion of the leaflets was 

restricted and she was symptom-free. The last case 

was a woman who had a large thrombus in the right 

atrium immediately after mitral and tricuspid valvular 

replacement. The patient underwent re-replacement 

surgery and a new biological valve was implanted in 

the tricuspid position. Also, we review the literature 

on the pathology, signs and symptoms, diagnosis, and 

management of tricuspid PVT. 

ORIGINAL ARTICLES 

156 Increased Carotid Artery Intima-Media 

Thickness in Pregnant Women with 

Gestational Diabetes Mellitus 

GholamrezaYousefzadeh, MD 1 , Hashem Hojat, MD 1 , Ahmad 

Enhesari, MD 1 , Mostafa Shokoohi, MSc 2* , Nahid Eftekhari, 

MD 1 , Mehrdad Sheikhvatan, MD 3 

1 

Physiology Research Center, Kerman University of Medical 

Sciences, Kerman, Iran. 

2 

Research Center for Modeling in Health, Kerman University 

of Medical Sciences, Kerman, Iran. 

3 


Tehran, Iran. 

* 

Mostafa Shokoohi, Research Center for Modeling in Health, 

Kerman University of Medical Sciences, Jihad Blvd, Shariati Street, 

Azadi Square, Kerman, Iran. 7619813159. Tel: +98 341 2263983. 

Fax: +98 341 2264079. E-mail: shokouhi.mostafa@gmail.com. 

Background: Pregnant women with previous 

gestational diabetes mellitus are at increased 

risk of progressive carotid artery disorders. The current 

study evaluated carotid intima-media thickness (IMT) 

in pregnant women with gestational diabetes at two 

time points of mid-term and full-term pregnancy to 

determine whether gestational diabetes mellitus causes 

increased IMT. 

Conclusion: In conclusion, an impaired OGCT 

test is proven to be an independent risk factor for 

increased carotid IMT and subsequent coronary artery 

disease. Even with this small study, we were able to 

find an increased IMT after diabetes appearance, which 

might be used as an indicator of a potential increased 

vascular risk. Furthermore, IMT measurements in 

diabetic pregnant women could offer an opportunity 

to identify a high-risk group of women who might


benefit from early screening and preventive measures. 

These measures could include lifestyle interventions 

such as improving diet and physical activity as well as 

increased surveillance of blood pressure, serum lipids, 

and particularly blood glucose. 

160 Right Ventricular Myocardial Tissue 

Velocities, Myocardial Performance 

Index, and Tricuspid Annular Plane 

Systolic Excursion in Totally Corrected 

Tetralogy of Fallot Patients 

Asadolah Tanasan, MD 1 , Keyhan Sayadpour Zanjani, 

MD 2* , Armen Kocharian, MD 2 , Abdolrazagh Kiani, MD 2 , 

Mohammad Ali Navabi, MD 2 

1 

Besat Hospital, Hamadan University of Medical Sciences, 

Hamadan, Iran. 

2 

Children’s Medical Center, Tehran University of Medical 

Sciences, Tehran, Iran. 

* 

Keyhan Sayadpour Zanjani, Assistant Professor of Pediatric 

Cardiology, Tehran University of Medical Sciences, Children’s 

Medical Center, No.62, Dr Gharib Street, Tehran, Iran. 1419733151. 

Tel: +98 21 66911029. Fax: +98 21 66930024. E-mail: sayadpour@ 

tums.ac.ir. 

Background: Longer survival after the total 

repair of the Tetralogy of Fallot increases 

the importance of late complications such as right 

ventricular dysfunction. This is a prospective study 

of the right ventricular function in totally corrected 

Tetralogy of Fallot patients versus healthy children. 

Conclusion: RVMPI was significantly correlated 

with PR severity without the presence of a significant 

correlation between RVMPI (obtained by pulsed wave 

Doppler) and the RV function indices obtained by tissue 

Doppler imaging (EA, Aa, Ea/Aa, and Sa). We suggest 

that these indices, RVMPI by tissue Doppler and PRi, 

be measured basically at postoperative and follow-up 

evaluations. In addition, as TAPSE was significantly 

decreased in the totally corrected TOF patients and 

there was a significant correlation between TAPSE and 

Sa, we suggest that TAPSE be also measured as the 

global RV systolic function index. 

164 Anatomy of Atrioventricular Node Artery 

and Pattern of Dominancy in Normal 

Coronary Subjects: A Comparison between 

Individuals with and without Isolated 

Right Bundle Branch Block 

Ali Kazemisaeid, MD, Marziyeh Pakbaz, MD * , Ahmad 

Yaminisharif, MD, Gholamreza Davoodi, MD, Masoumeh 

Lotfi Tokaldany, MD, Elham Hakki Kazazi, MD 


Tehran, Iran. 

* 

Marziyeh Pakbaz, Department of Cardiology, Tehran University 

of Medical Sciences, Tehran Heart Center, North Kargar Street, 

Tehran, Iran.1411713138. Tel: +98 21 88029256. Fax: +98 21 

88029256. E-Mail: marzi.pakbaz@gmail.com. 

Background: Isolated right bundle branch block 

(RBBB) is a common finding in the general 

population. The atrioventricular node (AVN) artery 

contributes to the blood supply of the right bundle 

branch. Our hypothesis was that the anatomy of 

the AVN artery and the pattern of dominancy differ 

between subjects with and without RBBB. 

Conclusion: According to our observations, there 

was no relationship between the dominancy of the 

epicardial arteries and the presence of RBBB in 

subjects with normal coronary arteries. There was 

a great variation of the AVN artery origin. Non-crux 

origination of the AVN artery was more common than 

the crux origination in both groups, and the prevalence 

of non-crux origination of the AVN artery was 

significantly higher in the cases than in the controls. 

Origination of the AVN artery from the right circulatory 

system was more common in both groups and the 

prevalence of the right origin of the AVN artery was 

significantly higher in the cases than in the controls. 

The AVN artery most commonly originated from the 

dominant artery but not necessarily from the crux. 

170 Determinants of Length of Stay in Surgical 

Ward after Coronary Bypass Surgery: 

Glycosylated Hemoglobin as a Predictor in 

All Patients, Diabetic or Non-Diabetic 

Mahdi Najafi, MD * , Hamidreza Goodarzynejad, MD

1 


Tehran, Iran. 

* 

Mahdi Najafi, Assistant Professor of Anesthesiology, Tehran 

Heart Center, Tehran University of Medical Sciences, Tehran Heart 

Center, North Karegar Street, Tehran, Iran. 1411713138. Tel: +98 21 

88029600. Fax: +98 21 88029731. E-mail: najafik@sina.tums.ac.ir. 

Background: Reports on the determinants of 

morbidity in coronary artery bypass graft surgery 

(CABG) have focused on outcome measures such as 

length of postoperative stay in the Intensive Care Unit 

(ICU). We proposed that major comorbidities in the 

ICU hampered the prognostic effect of other weaker 

but important preventable risk factors with effect on 

patients’ length of hospitalization. So we aimed at 

evaluating postoperative length of stay in the ICU and 

surgical ward separately. 

Conclusion: Among the five predictors of the LOS 

in the surgical ward, three were the indices of glycemic 

control. HbA1c is the most reliable marker of outcome 

because its level is not influenced by perioperative 

events. Taking these findings into consideration, 

the prognostic role of HbA1c for the LOS following 

CABG is promising. We would, therefore, recommend 

its use as a simple predictor of outcome after cardiac 

surgery in daily practice. 


Background: Diabetes mellitus is capable of 

impairing the myocardial function. Several 

studies have documented the influential impact of 

diabetes mellitus on the left ventricular function. The 

right ventricular function plays a significant role in the 

overall myocardial contractility; hence, this study was 

undertaken to evaluate the effect of diabetes mellitus 

type II on the right ventricular function. 

Conclusion: Whether the RV diastolic abnormalities 

have prognostic implications in the clinical course of 

patients with DM type II remains to be investigated. We 

believe that serial echocardiography measurements are 

warranted in this diabetic population if the progression 

from subclinical RV involvement to symptomatic RV 

dysfunction is to be followed. In addition, subclinical 

RV systolic and diastolic abnormalities should be 

considered when planning pharmacotherapy to prevent 

the development of symptomatic RV dysfunction. 

CASE REPORTS 

182 Surgical Treatment of Amplatzer Embolus 

in a Secundum Atrial Septal Defect Patient 

Ahmet Baris Durukan, MD 1* , Hasan Alper Gurbuz, MD 1 , 

Murat Tavlasoglu, MD 2 , Nevriye Salman, MD 1 , Halil Ibrahim 

Ucar, MD 1 , Cem Yorgancioglu, MD 1 

1 

Medicana International Ankara Hospital, Ankara, Turkey. 

2 

Diyarbakir Military Hospital, Diyarbakir, Turkey. 

177 Obvious or Subclinical Right Ventricular 

Dysfunction in Diabetes Mellitus (Type II): 

An Echocardiographic Tissue Deformation 

Study 

Mozhgan Parsaee, MD * , Parvaneh Bahmanziari, MD, 

Maryam Ardeshiri, MD, Maryam Esmaeilzadeh, MD 

Rajaei Cardiovascular, Medical and Research Center, Tehran 

University of Medical Sciences, Tehran, Iran. 

* 

Mozhgan Parsaee, Assistant Professor of Cardiology, 

Department of Echocardiography, Rajaei Cardiovascular, Medical 

and Research Center, Vali-Asr Ave. Adjacent to Mellat Park, Tehran, 

Iran. 1996911151. Tel: +98 21 23922930. Fax: +98 21 2055594. 

E-mail: parsaeemozhgan@yahoo.com. 

* 

Ahmet Baris Durukan, Medicana International Ankara 

Hospital, Umit Mahallesi 2463.sokak 4/18, 06810, Yenimahalle, 

Ankara, Turkey. Tel: +90 532 2273814. Fax: +90 312 2203170. 

E-mail: barisdurukan@yahoo.com. 

Transcatheter device closure of the ASD can lead 

to serious complications despite its advantages 

over surgical closure. But it should be kept in mind 

that even if most cases are successful, not only early, 

but also late complications may occur regardless 

of the size or type of the current devices. Surgical 

treatment of the complications may be mandatory 

and should be performed immediately, especially 

in cases of embolization. Surgery is quite effective 

in treatment, but it is a fact that operative mortality 

rises when surgery is performed for the treatment of 

complications. Operative mortality is much lower for 

primary surgical repair.


185 Post-Traumatic Chordae Rupture of 

Tricuspid Valve 

Kyomars Abbasi, MD, Hossein Ahmadi, MD, Arezoo 

Zoroufian, MD, Mohammad Sahebjam, MD, Naghmeh 

Moshtaghi, MD, Seyed Hessamedin Abbasi, MD * 


Tehran, Iran. 

* 

Seyed-Hesameddin Abbasi, Tehran University of 

Medical Sciences, Tehran Heart Center, North Kargar Street, 

Tehran, Iran. 1411713138. Tel: +98 21 88029720. Fax: +98 21 

88029702. E-mail: abbasi@tehranheartcenter.org. 

The two cases presented herein demonstrate 

that the rupture of the chordae tendineae of the 

tricuspid valve could be another cause of TR following 

blunt chest trauma. This is, however, a condition that 

can be repaired surgically without the need for valve 

replacement. Advances in echocardiography have 

enabled earlier diagnosis and ergo more effective 

treatment. 

We recommend that physicians working at 

emergency departments be on the alert for this 

potential complication of non-penetrating chest trauma 

and subject all patients admitted to the emergency 

department due to blunt chest trauma to TTE or TEE 

for accurate diagnosis. 

The LV pseudoaneurysm is an important 

complication that may occur late after MVR and 

thus necessitates due heed on the part of cardiologists 

and cardiac surgeons. 

LETTER TO THE EDITOR 

191 A Memorandum of "World Heart Day 

2012": Myocardial Infarction Mortality in 

Women in Birjand, 2008-2009 

Toba Kazemi, MD, Gholam Reza Sharifzadeh, MSc 

Valiassr Hospital, Birjand University of Medical Sciences 

(BUMS), Birjand, Iran. 

* 

Toba Kazemi, Associate Professor of Cardiology, Birjand 

University of Medical Sciences (BUMS), Valiassr Hospital, Ghafari 

Avenue, Birjand, Iran. 9717964151. Tel: +98 56 14443001-9. Fax: 

+98 56 14433004. E-mail: drtooba.kazemi@gmail.com. 

192 Ball in Chest 

PHOTO CLININC 

Mohammad Bagher Rahim, MD, Mohammad Hossein 

Mandegar, MD, Farideh Roshanali, MD * 

Shariati General Hospital, Tehran University of Medical 

Sciences, Tehran, Iran. 

188 Late Diagnosis of Large Left Ventricular 

Pseudoaneurysm after Mitral Valve 

Replacement and Coronary Artery Bypass 

Surgery by Real-Time Three-Dimensional 

Echocardiography 

* 

Farideh Roshanali, Shriati Hospital, North Kargar Street, 

Tehran, Iran. Tel: +98 912 3093151. Fax: +98 21 88797353. E-mail: 

farideh_roshanali@yahoo.com. 

Mohammad Sahebjam, MD * , Abbas Salehiomran, MD, Neda 

Ghaffari-Marandi, MD, Azam Safir, MD 


Tehran, Iran. 

* 

Mohammad Sahebjam, Assistant Professor of Cardiology, 

Echocardiography Department, Tehran Heart Center, Jalal Al Ahmad 

and North Kargar Intersection, Tehran, Iran. 1411713138. Tel: +98 21 

88029600. Fax: +98 21 88029731. E-mail: msahebjam@yahoo.com.



Prosthetic Tricuspid Valve Thrombosis: Three Case Reports 

and Literature Review 

Ahmad Yaminisharif, MD, Mohammad Javad Alemzadeh-Ansari, MD * , 

Seyed Hossein Ahmadi, MD 

Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran. 

Received 24 January 2012; Accepted 17 June 2012 

Abstract 

A common complication of prosthetic heart valves is thrombosis. Although the incidence of prosthetic valve thrombosis 

(PVT) in the tricuspid position is high, there are not enough data on the management of it, in contrast to left-sided PVT. 

Here, we describe three cases of tricuspid PVT with three different management approaches: thrombolytic therapy; close 

observation with oral anticoagulants; and surgery. The first case was a woman who suffered from recurrent PVT, for which 

we successfully used Tenecteplase for second and third episodes. We employed Tenecteplase in this case for the first time in 

the therapy of tricuspid PVT. The second case had fixed leaflets in open position while being symptomless. At six months' 

follow-up, with the patient having taken oral anticoagulants, the motion of the leaflets was restricted and she was symptomfree. 

The last case was a woman who had a large thrombus in the right atrium immediately after mitral and tricuspid valvular 

replacement. The patient underwent re-replacement surgery and a new biological valve was implanted in the tricuspid 

position. Also, we review the literature on the pathology, signs and symptoms, diagnosis, and management of tricuspid PVT. 

J Teh Univ Heart Ctr 2012;7(4):147-155 

This paper should be cited as: Yaminisharif A, Alemzadeh-Ansari MJ, Ahmadi SH. Prosthetic Tricuspid Valve Thrombosis: Three 

Case Reports and Literature Review. J Teh Univ Heart Ctr 2012;7(4):147-155. 

Keywords: Tricuspid valve • Thrombosis • Thrombolytic therapy • Anticoagulants • Surgical procedures, operative 

Introduction 

Since the 1950s, more than 80 models of the prosthetic 

heart valve have been developed and used. 1 Prosthetic valve 

thrombosis (PVT), however, remains a serious complication 

and can even prove lethal. Overall, the incidence of 

thrombosis is reported to be between 0.1% and 5.7% per 

patient-year. 2 The incidence is 0.5% to 6% in the aortic and/ 

or mitral positions and up to 20% in the tricuspid position, 

whereas the risk of thrombosis in spite of adequate oral 

anticoagulation has been estimated at between 1% and 

4% per year. 3 Although inadequate anticoagulant therapy 

remains the main cause of this complication, it seems that 

lower pressures on the right side of the heart with a slower 

blood flow across the tricuspid valve is the most important 

cause of higher risk of thrombus formation in prosthetic 

tricuspid valves. 4, 5 In contrast to left-sided PVT, there is a 

paucity of data on the various aspects of tricuspid PVT. We 

herein present three cases of tricuspid PVT with different 

management approaches, namely thrombolytic therapy, 

conservative management, and re-replacement surgery, and 

then review the relevant literature. 

* 

Corresponding Author: Mohammad Javad Alemzadeh-Ansari, Department of Cardiology, Tehran University of Medical Sciences, Tehran Heart 

Center, Karegar Street, Tehran, Iran. 1411713138. Tel: +98 21 88029600. Fax: +98 21 88029731. Email: aansari@razi.tums.ac.ir. 

The Journal of Tehran University Heart Center 147


Case Reports 

Case # 1 

A 32-year-old woman was admitted to our hospital with 

the complaint of dyspnea (The New York Heart Association 

[NYHA] factional class III) in January, 2004. Transthoracic 

echocardiography (TTE) showed left ventricular ejection 

fraction of 55%, severe mitral stenosis, mild mitral 

regurgitation, severe aortic regurgitation with moderate to 

severe aortic stenosis, and severe tricuspid regurgitation 

with moderate to severe tricuspid stenosis. In April 2004, 

the patient underwent three valves replacement surgery, 

during which she received a 24-mm St. Jude Valve (St. Jude 

Medical, Inc., St. Paul, MN, USA) in the mitral position, 

a 31-mm St. Jude Valve (St. Jude Medical, Inc., St. Paul, 

MN, USA) in the tricuspid position, and a 19-mm Regent 

Mechanical Prosthesis (St. Jude Medical, Inc., St. Paul, MN, 

USA) in the aortic position. Also, due to persistent atrial 

fibrillation with a slow ventricular response, she underwent 

permanent transvenous epicardial pacemaker placement 

during hospitalization. Twenty-one days after valvular 

surgery, TTE revealed that the function and gradients of the 

three prosthetic valves were within the acceptable range and 

the peak and mean gradients in the prosthetic tricuspid valve 

were 5 mm Hg and 3 mm Hg, respectively. At the time of 

discharge, the patient’s international normalized ratio (INR) 

was 3.9. She was discharged from the hospital with the 

recommendation to use Warfarin (with goal INR 2.5 - 3.5) 

plus 80 mg Aspirin daily. 

In February, 2006, the patient was re-admitted with the 

complaint of fatigue and palpitation. The pacemaker had a 

normal function. At the time of presentation, her INR was 

2.5. TTE revealed that the prosthetic aortic and mitral vales 

had normal functions and gradients, whereas the prosthetic 

tricuspid valve had malfunction with high gradients. 

Fluoroscopic evaluation revealed that there was no motion 

in both leaflets of the prosthetic tricuspid valve, while the 

motion of both other prosthetic valves was complete and 

within the normal range. With the diagnosis of tricuspid 

PVT, the patient was prescribed 250,000 U of Streptokinase 

via a peripheral vein over thirty minutes, followed by an 

intravenous infusion of 100,000 U per hour of Streptokinase 

for forty-eight hours. On the next day, fluoroscopic 

evaluation showed no evidence of prosthetic tricuspid valve 

malfunction, and the mobility of both leaflets was completely 

restored. At discharge, the patient’s INR was 2.6. She was 

discharged from the hospital with the recommendation to use 

Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of Aspirin 

daily. 

In November, 2006, the patient was re-admitted to our 

hospital with the complaint of atypical chest pain. At 

presentation, her INR was 1.8 and her other laboratory 

data and also electrocardiogram were unremarkable. TTE 

Ahmad Yaminisharif et al. 

revealed that the prosthetic aortic and mitral vales had 

normal functions and gradients, whereas the prosthetic 

tricuspid valve had malfunction with high gradients. 

Fluoroscopic evaluation revealed that both leaflets of the 

prosthetic tricuspid valve were fixed without any motion, 

whereas the motion of both other prosthetic valves was 

complete and within the normal range. With the diagnosis 

of recurrent tricuspid PVT, the patient was administered a 

total of 35 mg of Tenecteplase: 15 mg bolus, followed by 

20 mg for four hours (the patient’s weight was 64 kg). On 

the next day, fluoroscopic evaluation showed no evidence 

of prosthetic tricuspid valve malfunction, and the mobility 

of both leaflets was completely restored. Twelve days after 

the administration of Tenecteplase, TTE demonstrated that 

a significant reduction had occurred in the gradient across 

the prosthetic tricuspid valve (9.5 mm Hg peak gradient, 

4.9 mm Hg mean gradient). At discharge, the patient’s INR 

was 3.5. She was discharged from the hospital with the 

recommendation to use Warfarin (with goal INR 3.0 - 3.5) 

plus 80 mg of Aspirin daily. 

Because of the battery depletion of the pacemaker, the 

patient was re-admitted for generator replacement on October 

30, 2011. She had discontinued Aspirin two years previously 

due to gastrointestinal problems. She complained of atypical 

chest pain of two months’ duration, but her myocardial 

perfusion scan was normal. TTE showed left ventricular 

ejection fraction of 55%, severe increased gradient in the 

prosthetic tricuspid valve with no paravalvular leakage, and 

normal function of the mitral and aortic prosthetic valves. 

Fluoroscopic evaluation of the prosthetic tricuspid valve 

revealed a severe drop in the motion of both leaflets. The 

patient was candidated for thrombolytic therapy with the 

diagnosis of recurrent tricuspid PVT. A single dose of 35 

mg of Tenecteplase was administrated via a peripheral vein, 

according to the dosing regimen used for acute myocardial 

infarction (the patient’s weight was 65 kg). Fluoroscopic 

evaluation exhibited no evidence of prosthetic tricuspid 

valve malfunction, and the mobility of both leaflets was 

completely restored. Seven days later, TTE demonstrated that 

a significant reduction had occurred in the gradients across 

the prosthetic tricuspid valve (9 mm Hg peak gradient, 4 mm 

Hg mean gradient). She was discharged from the hospital 

with the recommendation to use Warfarin (with goal INR 

3.0 - 3.5) plus 80 mg of Aspirin daily. Table 1 illustrates the 

three episodes of tricuspid PVT in our patient and the three 

successful methods for thrombolytic therapy. 

Case # 2 

A 49-year-old woman was admitted to our hospital for the 

replacement of the generator of a pacemaker in May 2011. 

Thirteen years previously in another center, because of severe 

aortic regurgitation and severe tricuspid regurgitation, she 

148



Table 1. Three episodes of tricuspid PVT in case 1 and successful thrombolytic therapy 

Episode 

Time from valve 

replacement 

TTE findings in prosthetic tricuspid valve 

(before thrombolytic therapy) Thrombolytic drug Dosage 

Peak gradient 

Mean gradient 

1 22 months 14 mm Hg 11 mm Hg Streptokinase 

2 31 months 22 mm Hg 10 mm Hg Tenecteplase 

250,000 U loading dose followed 

by 100,000 U/h for 48 hours 

15 mg bolus, followed by 20 mg 

for 4 hours 

3 93 months 17 mm Hg 8.5 mm Hg Tenecteplase 35 mg bolus 

PVT, Prosthetic valve thrombosis; TTE, Transthoracic echocardiogram 

had undergone two valves replacement surgery, during which 

she received a 31-mm St. Jude Valve (St. Jude Medical, Inc., 

St. Paul, MN, USA) in the tricuspid position and a 21-mm St. 

Jude Valve (St. Jude Medical, Inc., St. Paul, MN, USA) in the 

aortic position. After surgery, due to the presence of complete 

heart block, she underwent permanent epicardial pacemaker 

placement during hospitalization. But during this period, she 

was admitted frequently because of infection at the site of the 

pacemaker. At the time of recent presentation, her INR was 

1.9. TTE revealed that the prosthetic aortic valve had normal 

function and gradients, whereas the prosthetic tricuspid 

valve had malfunction with high gradients (15 mm Hg peak 

gradient, 10 mm Hg mean gradient). Fluoroscopic evaluation 

revealed that the motion of one leaflet of the prosthetic 

tricuspid valve was very restricted, while the other leaflet 

was fixed in an open position. The patient was symptomless. 

On physical examination, except for a holosystolic murmur 

at the left lower sternal border, there were no signs of heart 

failure. With the diagnosis of tricuspid PVT, the patient was 

administered 250,000 U of Streptokinase via a peripheral 

vein over thirty minutes, followed by an intravenous infusion 

of 100,000 U per hour of Streptokinase for forty-eight 

hours. Fluoroscopic evaluation showed no improvement 

in the motion of the leaflets. The patient was candidated 

for tricuspid valve replacement, but because of fungal 

infection in the pacemaker pocket and lead, replacement of 

the prosthetic valve or the generator was not performed. She 

was discharged from the hospital with the recommendation 

to use antibiotics with Warfarin (with goal INR 3.0 - 3.5) 

plus 80 mg of Aspirin daily. Six months later, she referred 

to our clinic; she had no signs or symptoms of heart failure. 

She was re-admitted for the replacement of the generator of 

the pacemaker. Before replacement, fluoroscopic evaluation 

showed no evidence of improvement in the motion of the 

prosthetic tricuspid valve leaflets. Because the patient was 

symptom-free, did not respond to thrombolytic therapy, and 

had a high risk for infection after valve replacement, surgery 

for valve replacement was not performed. After generator 

replacement, she was discharged with the recommendation 

to use Warfarin (with goal INR 3.0 - 3.5) plus 80 mg of 

Aspirin daily. 

Case # 3 

A 28-year-old woman was admitted to our hospital with the 

complaint of orthopnea and dyspnea (NYHA factional class 

III) in September, 2008. The electrocardiogram revealed 

atrial fibrillation. TTE showed left ventricular ejection 

fraction of 40%, severe mitral stenosis, severe tricuspid 

regurgitation, and a large mobile clot in the left atrium (2.7 

× 2.0 cm). She underwent two valves replacement surgery, 

during which she received a 31-mm St. Jude Valve (St. 

Jude Medical, Inc., St. Paul, MN, USA) in the tricuspid 

position and a 29-mm St. Jude Valve (St. Jude Medical, 

Inc., St. Paul, MN, USA) in the mitral position. Also in the 

same section of surgery, TEE revealed a large mobile clot 

in the left atrium without any lesion in the other chambers; 

the large clot was removed. After surgery, she received an 

intravenous bolus dose of 5000 U of heparin, followed by 

intravenous heparin (20000 U per day in divided doses). 

Because of persistent atrial fibrillation with a low ventricular 

response after surgery, eleven days later, she underwent 

permanent transvenous epicardial pacemaker placement. 

However, during implantation, fluoroscopy revealed that 

the motion of one leaflet of the prosthetic tricuspid valve 

was very restricted. With the diagnosis of the malfunction 

of the prosthetic tricuspid valve, she was transferred to the 

operating room again. During the removal of the previous 

prosthetic tricuspid valve, a large clot was seen in the 

right atrium which was attached to the leaflet. Thus, all of 

the thrombus was removed and a new 29-mm Hancock II 

bioprosthesis (Medtronic Inc., Minneapolis, Minn.) was 

placed in the tricuspid position. Because of the displacement 

of the transvenous epicardial lead during surgery, a new 

epicardial lead was placed. After surgery, TEE demonstrated 

an acceptable gradient across the tricuspid valve (5 mm Hg 

peak gradient, 2 mm Hg mean gradient). She was discharged 

with the recommendation to use Warfarin (with goal INR 3.0 

- 3.5) plus 80 mg of Aspirin daily. 

The Journal of Tehran University Heart Center149


Discussion 

Pathogenesis 

Many studies have demonstrated that the leading cause 

of PVT is subtherapeutic anticoagulation, which chimes 

in with the findings in our two cases. 6-10 This is most often 

due to either patient noncompliance or iatrogenic cessation 

of anticoagulants in preparation for another procedure. 

Furthermore, valve design and materials influence the 

incidence of thrombotic complications. Some mechanisms 

have a role in PVT formation such as molecular interactions 

and influence of transprosthetic blood flow. Molecular 

interaction occurs between corpuscular blood components, 

plasma, and artificial surfaces. The initial adsorption of 

plasma proteins (fibrinogen, fibronectin, von Willebrand 

factor, vitronectin, and thrombospondin) on the artificial 

surface is generally followed by platelet adhesion. The 

passage of blood through the prosthetic valve creates a 

turbulent flow with shear stress, which gives rise to a 

structurally and metabolically damaged endocardium and 

thus reduces its resistance to thrombosis. Also, subclinical 

hemolysis with the release of adenosine diphosphatase, 

platelet factor 4, beta-thromboglobulin, and other proteins 

triggers the activation of the plasma coagulation system. 

Other intrinsic factors can progress to thrombus formation; 

these factors include loss of active atrial contractions (atrial 

fibrillation), presence of some systemic diseases (e.g. 

systemic lupus erythematosus) or malignant tumors, and 

incomplete endothelization of the sewing ring. Use of some 

drugs such as contraceptives leads to hypercoagulability 

state 3, 11-14 Recently, Ricome et al. reported two cases of PVT 

secondary to heparin-induced thrombocytopenia. 15 

Type and position of the prosthetic valve and time from 

1, 13, 16, 17 

surgery can influence thrombus formation (Table 2). 

Additionally, some studies have indicated that season can be 

correlated with an increased risk for thrombotic events. 18-20 

Piper et al. reported that PVT during winter months occurred 

more frequently than in the other seasons. 13 

Signs and Symptoms 

In contrast to the acute presentation of left-sided PVT, the 

onset of the symptoms of tricuspid PVT is usually insidious, 

and its diagnosis is often delayed. Sometimes symptoms 

are so slight that the patient is likely to have suffered from 

them for months or even a year without feeling the need for 

referral to the hospital. 4 Sometimes, the patient even may 

have no symptoms related to the tricuspid vale thrombosis, 

and the thrombosis is detected only during routine clinical 

examination. 4, 6 However, the involvement of both leaflets is 

usually required to produce symptoms. 6 The most frequent 

symptoms related to tricuspid valve malfunction include 

4, 6, 

dyspnea, ascites, peripheral edema, and systemic emboli. 

21, 22 

Also, sometimes the disappearance or attenuation of the 

prosthetic valve noise may be reported by the patient and/ 

or relatives. Moreover, in some cases where an interatrial 

communication is present, a pulmonary embolus or a leftsided 

embolic event may be the presenting manifestation of 

23, 24 

tricuspid PVT. 

It seems that physical examination may provide important 

clues for the diagnosis of tricuspid PVT, compared to the 

thrombosis of the left side, which normally has more severe 

symptoms. 25 Absence or muffling of prosthetic sounds 

in the tricuspid position might be noted. Other findings 

include auscultation of a new holosystolic murmur located 

at the left lower sternal border or in the subxiphoid region 

that may increase with inspiration or maneuvers that 

increase venous return (denoting the presence of tricuspid 

regurgitation), auscultation of a new murmur that is low in 

frequency, diastolic, located at the lower left sternal border 

or infraxiphoid area, and increases with inspiration and other 

maneuvers that increase tricuspid flow velocity (denoting 

tricuspid stenosis), or auscultation of a combination 

of murmurs that characterize both of these conditions. 

Sometimes mid-diastolic and/or pan-systolic murmurs can 

be heard in the tricuspid area (Zhang DY, Lozier J, Chang R, 

Sachdev V, Chen MY, Audibert JL, Horvath KA, Rosing DR. 

Case study and review: Treatment of tricuspid prosthetic 

valve thrombosis. Int J Cardiol 2011 Oct 14. [Epub ahead 

of print]). 

Diagnosis 


The onset of the symptoms of tricuspid PVT is usually 

insidious and sometimes the patient has nonspecific 

symptoms or is even symptomless; therefore, suspicion of 

tricuspid PVT may be raised by physical findings, symptoms 

of heart failure, or rarely the diagnosis of embolization, 

especially in patients with poor anticoagulation therapy 8, 

17, 25 

NYHA has classified PVT in functional classes I to 

IV. The non-obstructive forms of PVT (NYHA functional 

Table 2. Thrombogenicity of mechanical prosthetic valve based on type, position, and time from surgery 

Lower 

Higher 

Valve type Bileaflet-tilting-disk Caged-ball single-tilting-disk 

Position Mitral or aortic Tricuspid 

Time from replacement After 3 months First 3 months 

150



classes I or II) are usually incidental echocardiographic 

findings in patients with symptomless, nonspecific 

symptoms, or thromboembolic events. The obstructive 

forms (NYHA functional classes III or IV) correspond to 

obvious hemodynamic repercussions, sometimes including 

cardiogenic shock, and are often associated with cerebral or 

3, 11, 26 

peripheral embolism. 

Imaging modalities in patients with suspected PVT are 

aimed to evaluate leaflet immobilization, cause of leaflet 

immobilization (thrombus versus pannus or both), and 

whether thrombolytic therapy attempt in the patient would 

be successful. Usually the first modality for detecting 

prosthetic tricuspid valve dysfunction is TTE. Montorsi 

et al. reported that sensitivity, specificity, and positive and 

negative predictive values for the diagnosis of PVT in the 

mitral or aortic position by TTE were 75%, 64%, 57%, and 

78%, respectively. TTE, especially in experienced hands, can 

detect increased transvalvular gradients (mean of 6 mm Hg 

or higher, and peak of 15 mm Hg or higher), pressure halftime 

of 230 msec or higher, transvalvular gradients of 50% 

or higher than that observed before, wide intravalvular jet of 

tricuspid regurgitation, lower orifice area, visible thrombus 

on the prosthetic valve, and inability to demonstrate two 

different mobile echoes representing the valve leaflets 

in a high quality image. Indirect, nonspecific signs are an 

3, 6, 27 

enlarged right atrium and engorged inferior vena cava. 

After performance of TTE, the diagnosis should be 

confirmed by more specific modalities, namely fluoroscopy 

or TEE. 28 Fluoroscopy is a non-invasive method for 

detecting PVT, especially in patients with bileaflet prosthetic 

valves, and have high clinical suspicious for PVT and 

normal Doppler study. 29 Sensitivity, specificity, and positive 

and negative predictive values for the diagnosis of PVT in 

the mitral or aortic position by fluoroscopy are 87%, 78%, 

80%, and 91%. 28 Also, fluoroscopy has an important role for 

detecting the response to thrombolytic therapy. Thrombolysis 

significantly reduces the mean pressure gradient and 

improves valve leaflet opening angle. But some patients 

whose pressure gradient normalizes after thrombolytic 

infusion tend to continue to have concomitant abnormal 

leaflet motion at fluoroscopy, suggesting incomplete 

resolution of valve obstruction (pseudo responders). If lytic 

infusion is stopped at this time, the remaining thrombus 

could be the trigger for a late rethrombotic process. Thus, 

fluoroscopy should be carried out at regular intervals during 

therapy to confirm Doppler changes. 29 

TEE can correctly identify opening and closing angles in 

all patients, regardless of the prosthetic type. 30 TEE should 

be performed in selected patients even if fluoroscopy is 

negative because TEE is an invasive modality. On the other 

hand, fluoroscopy and TTE can correctly identify PVT in 

85% of all cases. Thus, fluoroscopy and TTE are quick, 

effective, and complementary diagnostic tools for the 

diagnosis of PVT in most patients. 28 Despite the scarcity of 

data on the role of TEE in diagnosing tricuspid PVT, it seems 

that if there is high clinical suspicion and other diagnostic 

modalities are not helpful, TEE will be help. 27 Furthermore, 

TEE is a superior modality for detecting the etiology of the 

obstruction (thrombus versus pannus), size, and location of 

the thrombus compared with TTE and fluoroscopy. 31 

Magnetic Resonance Imaging (MRI) and cardiac 

catheterization have limited diagnostic roles, because TEE and 

fluoroscopy can provide adequate data for decision-making. 

Since MRI is more expensive and time-consuming than 

echocardiography, it should be used only when prostheticvalve 

regurgitation or paravalvular leakage is suspected but 

not adequately visualized by echocardiography. 1 In contrast, 

Cardiac Multi-Detector Computer Tomography can provide 

sharp images to characterize quantitatively the reduced 

mobility of prosthetic leaflets or even directly visualize and 

distinguish between thrombus and pannus. 32-34 

Treatment 

There are different therapeutic modalities available for 

PVT such as heparin treatment, thrombolysis, surgery, or 

even in some cases only watchful waiting. Selecting one 

of these modalities is largely influenced by the presence of 

valvular obstruction, valve location (left- or right-sided), and 

clinical status. 6, 35 Surgery is more frequently performed for 

the treatment of left-sided PVT, not least in patients with 

either NYHA functional class III–IV symptoms or a large 

clot burden 36 and thrombolytic therapy is more favorable for 

right-sided PVT, because the risk of systemic embolization 

and recurrence rate is high by thrombolytic therapy in left- 

37, 38 

sided PVT. 

The conservative continued anticoagulation approach 

in patients with tricuspid PVT would only be appropriate 

if there is no significant hemodynamic compromise or 

a contraindication to either surgery or pharmacologic 

intervention is present. Shapira et al. reported that 

asymptomatic patients with tricuspid PVT who did not 

respond to thrombolytic therapy might be discharged from 

the hospital with long-term intensified anticoagulant therapy 

and close follow-up. The leaflet motion can be fully restored 

later. 6 However, Montorsi et al. proposed that leaflet mobility 

and duration of prosthetic valve symptoms were important 

factors in determining successful thrombolytic therapy. It 

may be because the amount of the thrombus that led to the 

stuck valve was minimal, thereby improving the chance of 

successful thrombolytic therapy. 29 

According the guidelines of the American Heart Association 

/American College of Cardiology (AHA/ACC) and the 

American College of Chest physicians (ACCP), in contrast to 

left-sided PVT, thrombolytic therapy is reasonable for rightsided 

PVT with NYHA functional class III-IV symptoms or 

a large clot burden. 36, 39 It is due to the high success rate and 




low incidence of embolism compared to left-sided PVT. The 

European Society of Cardiology guideline also recommends 

thrombolytic therapy for tricuspid PVT, but this guideline 

does not mention the NYHA functional class or clot burden. 40 

Long-standing symptoms even more than a month should 

not make one reluctant to use thrombolytic therapy. 6 If 

thrombolytic therapy fails, the presence of a large thrombus 

or pannus should be considered, which may require surgical 

intervention (thrombectomy or valve replacement). 

In contrast to left-sided PVT, there is limited information 

about thrombolytic therapy for tricuspid PVT. Various 

thrombolytic agents have been used for PVT, including 

streptokinase, urokinases, and tissue-type plasminogen 

activator (tPA). The choice of the thrombolytic agent depends 

on several factors, including cost, time to attain maximal 

pharmacologic effect, half-life of the thrombolytic agent, 

and hemorrhagic complications. Amongst the above agents, 

streptokinase is cheaper and has lower cerebral hemorrhage 

rates. In contrast, tPA has a faster effect reversion and 

faster reach to maximal pharmacologic effect. 3 Roudaut 

et al. indicated that patients treated by streptokinase had a 

significantly full success rate compared to patients treated 

by tPA or urokinases (86%, 68%, and 59%, respectively). 

Nonetheless, combined therapy improved the results of 

thrombolytic therapy in all the groups. 41 Also, they concluded 

that full success by thrombolytic therapy was higher in 

patients in NYHA functional classes I or II; nevertheless, 

they did not find a significant difference between patients 

with tilting-discs and bileaflet valves, or between patients 

with first episode of thrombosis and recurrent thrombotic 

episodes groups. 41 The dosage and route of the administration 

of thrombolytic therapy are different in various studies. 

Hering et al. recommended using streptokinase by starting 

a bolus dose of 250,000 IU over thirty minutes, followed 

by an intravenous infusion of 100,000 IU per hour (same 

as the therapy of our patient in the first episode of PVT), 

urokinase by the same protocol used in patients with acute 

pulmonary embolism, and t-PA at a dosage of 100 mg given 

over a period of two to five hours. 14 Caceres-Loriga et al. 

recommended using streptokinase by starting a bolus dose of 

250,000 IU over three minutes, followed by an intravenous 

infusion of 100,000 IU per hour (maximum duration of 

seventy-two hours), urokinase by starting a bolus dose of 

4500 U/kg, followed by an intravenous infusion of 4500 

U/kg/h (maximum duration of twenty-four to forty-eight 

hours), and tPA by starting a bolus dose of 15 mg over five 

minutes, followed by an intravenous infusion of 95 mg over 

ninety minutes. 3 Manteiga et al. used the short-course of 

thrombolytic therapy as a first line for PVT: streptokinase 

by starting a bolus dose of 250,000 IU over twenty minutes, 

followed by an intravenous infusion of 1,500,000 IU over 

ninety minutes, or tPA by starting a bolus dose of 10 mg, 

followed by an intravenous infusion of 90 mg over ninety 

minutes. They concluded that a successful rate by these 

regimes was 82%. 42 However, Alpert recommended another 

dose for streptokinase in right-sided PVT (starting a dose of 

500,000 IU over twenty minutes, followed by an intravenous 

infusion of 1,500,000 IU over ninety minutes). 43 Some 

other investigators have used direct intra-atrial infusion of 

thrombolytic for PVT. 44, 45 For the first time, Zhang et al. 

reported a case of tricuspid PVT, which was successfully 

treated by an intra-right atrium infusion of tPA. 

Recently, Tenecteplase (a genetically engineered variant 

of tPA which has a longer half-life than tPA and is resistant 

to inactivation by plasminogen activator inhibitor-1 46 ) has 

been utilized for PVT. Our literature search shows that 

Tenecteplase has been used in limited case repots for mitral 

or aortic PVT. 47-52 Although Tenecteplase has been prescribed 

in different doses and via different methods, we used this 

thrombolytic according to the dosing regimen employed 

for acute myocardial infarction. Data on Tenecteplase for 

the treatment of PVT are limited. Still, Melandri et al. in a 

review study about patients with acute myocardial infarction 

showed that this drug had some advantages compared with 

tPA. These advantages included being more fibrin-specific, 

usability in a single bolus dose, and having less non-cerebral 

bleeding. Be that as it may, mortality rates and intracranial 

hemorrhage rates were similar to those of tPA. 46 For the first 

time, we reported a successful use of Tenecteplase in our 

case 1 for the treatment of two episodes of recurrent tricuspid 

PVT. It seems that this drug might be a suitable alternative 

for the other types of tPA in the future. 

If thrombolytic therapy is successful, a continuous 

infusion of unfractionated heparin is indicated and should 

be initiated. Moreover, activated partial thromboplastin 

time should be maintained at twofold the baseline values, 

followed by conversion to oral anticoagulation combined 

with Aspirin (50 to 100 mg per day). 39 In contrast to leftsided 

PVT, guidelines do not provide a recommended INR 

for prostheses in the tricuspid position. 36, 39, 40 For bileaflet 

prosthetic valves in the mitral position, a range of 2.5 - 3.5 

is recommended, 2.0 - 3.0 in the aortic position for patients 

without additional risk factors for thromboembolism. 39 

However, Shapira et al. recommended target INR levels of 

3.5 - 4.0 for patients with tricuspid prostheses 6 and Zhang 

et al., in order to prevent future thrombotic complications 

of tricuspid PVT, considered target INR levels of 3.0 - 3.5. 

Recurrent tricuspid PVT 

A major disadvantage of thrombolytic therapy is the 

relatively high incidence of recurrent thrombosis during 

follow-up; however, data are limited about rethrombosis 

after thrombolytic therapy of tricuspid PVT. Recurrent 

rates after thrombolytic therapy vary from 11% to 31%. 3, 

53-58 

Overall, risk of recurrent thrombosis after thrombolytic 

therapy in left-sided prosthetic valves is higher than that in 

152



the tricuspid position. A meta-analysis showed that while 

the incidence of recurrent thrombosis in left-sided prosthetic 

valves was 20%, it was 14% in the tricuspid position. 14 As 

was mentioned earlier, the etiology of recurrent thrombosis 

is the same as that of the first episode. Also, the coexistence 

of thrombus and pannus tissue on a prosthetic valve is 

another factor that can explain the recurrence of PVT after 

successful thrombolytic therapy in a subset of patients. 53, 

56 

However, some recurrences may be the result of an 

uncompleted resolution of the initial thrombotic process 

rather than the result of a new thrombosis. Thus, after 

successful thrombolytic therapy, it is very important to 

follow up patients with serial clinical and echocardiographic 

examinations. 27 The results of rethrombolysis after PVT 

recurrence are comparable to those obtained after the first 

thrombolytic therapy, which is concordant with our case 1. 38, 

41, 58-62 

Therefore, rethrombolysis is safe with a high successful 

rate and is recommended in patients with recurrent tricuspid 

PVT. 

Choose a prosthetic valve: mechanical or biological 

Tricuspid valve replacement is one of the most challenging 

operations of cardiac surgery. Most cardiac surgeons 

undertake tricuspid valve surgery infrequently and usually 

perform tricuspid valve repair. Incidence of tricuspid 

valve replacement is approximately 0.7% of all valve 

replacements. 63 Although many studies have been performed 

to determine the preference between mechanical or biological 

valves in the tricuspid position, they have not reached the 

same conclusion yet. 63-69 As was mentioned before, because 

the risk of thrombosis is high in the tricuspid position and 

thrombus formation is lower in biological valves, 65, 66, 70 we 

recommend the use of biological valves in the tricuspid 

position, which is similar to that in re-replacement valve 

surgery (the same as our case 3). 

Conclusion 

Thrombosis in tricuspid prosthetic valves is high and 

in some cases, patients are symptom-free or have a mild 

complaint. Thus, regular visits after vale replacement are 

reasonable and if there is suspicion of PVT, other modalities 

(first TTE) are recommended. Herein, we reported three cases 

of tricuspid PVT with different conditions. The main cause 

of PVT in our cases was subtherapeutic anticoagulation. The 

first case was a woman who suffered from recurrent PVT. In 

this case we successfully used for the first time Tenecteplase 

for second and third episodes. Given that this drug can be 

used in a single dose and has acceptable efficacy compared 

to the other conventional thrombolytic agents, we would 

recommend Tenecteplase as a good alternative for PVT 

treatment. Also, this case shows us that thrombolytic therapy 

is a good option for recurrent tricuspid PVT, in contrast to 

left-sided PVT. The second case had fixed leaflets in open 

position, while the patient was symptomless. Thrombolytic 

therapy failed in this case; however, due to the patient’s 

chronic infection, we could not replace her valve. At six 

months’ follow-up, the motion of the leaflets was restricted 

and she was symptom-free. Thus, if thrombolytic therapy 

fails, surgery is not possible, the patient is symptom-free, 

and hemodynamic is stable, close observation with oral 

anticoagulant would be a reasonable course of action. The 

last case was a woman who had a large thrombus in the 

right atrium immediately after mitral and tricuspid valve 

replacement. We think that the cause of thrombus formation 

in this case was inadequate anticoagulation therapy. The 

patient underwent re-replacement surgery and a new 

biological valve was implanted in the tricuspid position. 

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Original Article 

Increased Carotid Artery Intima-Media Thickness in 

Pregnant Women with Gestational Diabetes Mellitus 

Gholamreza Yousefzadeh, MD 1 , Hashem Hojat, MD 1 , Ahmad Enhesari, MD 1 , 

Mostafa Shokoohi, MSc 2* , Nahid Eftekhari, MD 1 , Mehrdad Sheikhvatan, MD 3 

1 

Physiology Research Center, Kerman University of Medical Sciences, Kerman, Iran. 

2 

Research Center for Modeling in Health, Kerman University of Medical Sciences, Kerman, Iran. 

3 


Received 04 February 2012; Accepted 13 May 2012 

Abstract 

Background: Pregnant women with previous gestational diabetes mellitus are at increased risk of progressive carotid 

artery disorders. The current study evaluated carotid intima-media thickness (IMT) in pregnant women with gestational 

diabetes at two time points of mid-term and full-term pregnancy to determine whether gestational diabetes mellitus causes 

increased IMT. 

Methods: This cross-sectional study carried out at Afzalipour Hospital (Kerman, Iran) between 2009 and 2010, recruited 

50 women who were at high risk of gestational diabetes during pregnancy and had an oral glucose challenge test (OGCT) 

as screening for gestational diabetes. B-mode ultrasound scans were performed at baseline and at two time points of midterm 

pregnancy (20 to 24 weeks) and full-term pregnancy (36 to 38 weeks) on all the participants. The mean IMT of common 

carotids and internal carotid arteries from two walls (near and far walls) at four different angles was assessed. 

Results: An overall comparison between the impaired OGCT test group and the control group revealed significant 

differences in carotid IMT in the mid-term (0.65 ± 0.07 vs. 0.59 ± 0.06 mm; p value = 0.002) and full-term (0.65 ± 0.05 

vs. 0.59 ± 0.04 mm; p value < 0.001) pregnancy; however, the trend of the changes in carotid IMT during mid to full-term 

pregnancy was insignificant in each group (p value > 0.05). 

Conclusion: Carotid IMT was significantly higher in the women with gestational diabetes than that in the normoglycemic 

group in different trimesters. This finding denotes that atherosclerosis might start years before the diagnosis of gestational 

diabetes in vulnerable women. 


This paper should be cited as: Yousefzadeh G, Hojat H, Enhesari A, Shokoohi M, Eftekhari N, Sheikhvatan M. Increased Carotid 

Artery Intima-Media Thickness in Pregnant Women with Gestational Diabetes Mellitus. J TehUniv Heart Ctr 2012;7(4):156-159. 

Keywords: Pregnancy • Diabetes mellitus • Carotid arteries 

Introduction 

Screening for gestational diabetes mellitus is routinely 

programmed to prevent complications caused by elevated 

blood glucose levels in pregnancy, including macrosomia, 

Cesarean delivery, shoulder dystocia, neonatal metabolic 

problems, perinatal mortality, and pre-eclampsia. 1 Diabetes 

mellitus during pregnancy also appears to be associated 

* 

Corresponding Author: Mostafa Shokoohi, Research Center for Modeling in Health, Kerman University of Medical Sciences, Jihad Blvd, Shariati 

Street, Azadi Square, Kerman, Iran. 7619813159. Tel: +98 341 2263983. Fax: +98 341 2264079. E-mail: shokouhi.mostafa@gmail.com. 

156

Increased Carotid Artery Intima-Media Thickness in Pregnant Women with ... 

with an increased risk of cardiovascular diseases even in 

later life. 2 Moreover, this underlying co-morbidity is an 

independent risk factor for subsequent coronary artery 

disease. In this context, diabetes mellitus during pregnancy 

has been identified as a major etiology for atherosclerosis in 

large elastic arteries. 3 

One of the main indicators for assessing atherosclerotic 

lesions during this period is the increased intima-media 

thickness (IMT) of carotid arteries. 4 It has been well known 

that, as opposed to the blood flow through the other arteries of 

the maternal organs, the blood flow through the carotid artery 

is decreased during pregnancy, which has been attributed to 

pregnancy-mediated increased responsiveness of the carotid 

artery to vasoconstrictors and decreased responsiveness 

to vasodilators. 5 Also, the endothelial hypertrophy of the 

carotid artery can be a common finding, leading to changes 

in the carotid blood flow and its complications. 6, 7 Thus, 

increased carotid IMT can be deemed a validated endothelial 

dysfunction surrogate endpoint during pregnancy. 

Some studies have recently shown that pregnant women 

with previous gestational diabetes mellitus are at increased 

risk of carotid artery disorders. 8, 9 Be that as it may, the scarcity 

of research into this hypothesis means that it is still unknown 

whether or not gestational diabetes mellitus causes increased 

IMT. The current study was performed to evaluate carotid 

IMT in diabetic pregnant women with gestational diabetes 

and to ascertain if an impaired oral glucose challenge test 

(OGCT) correlates with the development of increased IMT. 

Methods 

This cohort study included 50 women ranging from 

18 to 35 years of age at high risk of diabetes during 

pregnancy. Gestational diabetes mellitus was screened 

with a one-hour 50 g oral glucose challenge test (OGCT). 

Abnormal results were, thereafter, confirmed with a threehour 

100 g oral glucose tolerance test (OGTT). Eligible 

women were nulliparous with a singleton pregnancy, had 

a normal blood pressure at the time of recruitment, and 

gave informed consent. Women with any of the following 

were excluded: family history of cardiovascular disorders; 

history of hypertension; anti-hypertensive and cholesterol 

medication use; hyperlipidemia; overt diabetes or fasting 

plasma glucose (FPG) > 125 mg/dl according to the 

American Diabetes Association (ADA) definition; 10 chronic 

renal or hepatic diseases; malignancies; recent hormonal 

medications; cigarette smoking; severe obesity (body 

mass index [BMI] > 35 kg/m 2 ); and history of infertility 

or polycystic ovarian disease. Those with the status of 

plaques/shadowing ( > 1.0 mm) at any carotid site were also 

excluded. The study protocol was approved by the Research 

and Ethics Committees at Kerman University of Medical 

Sciences. 


Baseline demographic variables were collected either 

from the women’s medical records or self-completed 

questionnaires at trial entry and comprised maternal age, 

height, weight, BMI, smoking status, and blood pressure 

at trial entry. Complete baseline data were available for 

all the women. All lipid and lipoprotein measurements 

were made at a central laboratory. Total cholesterol was 

measured enzymatically with standard methods and total 

triglyceride was measured via standard spectrophotometric 

techniques. After the precipitation of low-density lipoprotein 

(LDL) particle with phosphotungstic acid, high-density 

lipoprotein (HDL) cholesterol was measured enzymatically 

in the supernatant by a modification of the method for total 

cholesterol. 

B-mode ultrasound scans were performed at baseline 

and at two time points of mid-term pregnancy (20 to 24 

weeks) and full-term pregnancy (36 to 38 weeks) on all the 

participants. Carotid ultrasound scans were carried out by a 

single trained sonographer unaware of the study protocols 

and methodology. B-mode ultrasound images were equipped 

with a 7.5-MHz linear array transducer and captured with 

a GE log 200 ultrasound machine. The ultrasonic variable 

used in the statistical analysis was the mean of the IMT of 

common carotids and internal carotid arteries from two walls 

(near and far walls) at four different angles. 

The mean of carotid IMT was compared between the 

women with impaired OGCT and those who screened 

normal on OGCT at the two study time points. For the 

statistical analyses, the statistical software SPSS version 

19.0 for Windows (SPSS Inc., Chicago, IL) was used. The 

continuous variables, if normally distributed, were analyzed 

using the Student-test and presented as mean differences, 

while the Mann-Whitney test was employed for skewed 

data. A p value of 0.05 or less was considered to indicate 

statistical significance. 

Results 

The baseline characteristics of the pregnant women with 

impaired and normal OGCT tests are presented in Table 1. 

The two groups were similar in terms of pregnancy age, 

height, weight, BMI, and baseline laboratory parameters. 

There were no significant associations between carotid 

IMT and maternal indices, including the demographic 

variables and laboratory parameters. 

An overall comparison between the impaired OGCT test 

group and the control group via the Mann-Whitney U test 

revealed significant differences in carotid IMT in the midterm 

and full-term pregnancy (Table 2). The trend of the 

changes in carotid IMT during the mid-term to full-term 

pregnancy was, however, insignificant in each group. 



Gholamreza Yousefzadeh et al. 

Table 1. Demographic characteristics and clinical data of GDM versus non-GDM women * 

Characteristics 

GDM group 

(n=25) 

Non-GDM group 

(n=25) 

Age (y) 24.4±3.6 25.1±4.2 0.259 

Height (cm) 159.4±5.5 161.5±7.3 0.276 

Weight (kg) 72.8±11.5 68.7±10.9 0.225 

Body mass index (kg/m 2 ) 28.7±4.5 26.5±4.5 0.109 

Systolic BP (mm Hg) 110.0±9.4 107.6±8.0 0.369 

Diastolic BP (mm Hg) 69.0±10.4 65.2±8.5 0.192 

Serum HDL (mg/dL) 49.0±8.7 49.0±10.5 0.987 

Serum LDL (mg/dL) 140.7±37.4 137.7±36.0 0.780 

Fasting blood sugar (mg/dL) 85.3±13.7 83.2±19.8 0.680 

Serum triglyceride (mg/dL) 183.5±67.0 178.0±61.0 0.775 

Serum cholesterol (mg/dL) 219.0±54.7 223.8±43.8 0.746 

* 

Data are presented as mean±SD 

GDM, Gestational diabetes mellitus; BP, Blood pressure; HDL, High-density lipoprotein; LDL, Low-density lipoprotein 

P value 

Table 2. Differences in carotid IMT in GDM versus non-GDM women * 

CIMT 

Mid-term pregnancy 

(mm) 

Full-term 

pregnancy(mm) 

GDM group 

(n=25) 

Non-GDM group 

(n=25) 

P value ** 

0.65±0.07 0.59±0.06 0.002 

0.65±0.05 0.59±0.04 < 0.001 

P value *** 0.989 0.992 

* 


** 

Between groups comparison 

*** 

Within groups comparison 

IMI, Intima-media thickness; GDM, Gestational diabetes mellitus; CIMT, 

Carotid intima-media thickness 

Discussion 

An increased carotid IMT can be observed not only in 

long-standing type II diabetic but also in newly detected type 

II diabetic patients. Especially in pregnant women, carotid 

IMT gradually increases from the first to the third trimester 

of normal pregnancy and regresses in the postpartum period. 

Nevertheless, the trend of the increase in pregnant women 

with gestational diabetes is still unclear. In our study, with the 

aid of carotid ultrasound, arterial examination was performed 

at mid-term and full-term pregnancy and both controls and 

the women with an impaired OGCT test were assessed 

and compared with regard to the changes in carotid IMT. 

We showed that although carotid IMT was more increased 

in those with impaired OGCT, the trend of this change was 

similar between the impaired and normal OGCT groups. 

Furthermore, we observed that carotid IMT was significantly 

higher in the diabetic group than in the normoglycemic 

group in different trimesters, but the trend of these gradual 

changes from the first to the third trimester was similar in 

both groups. Totally, effective glycemic control seems to be 

helpful for the prevention of increased carotid IMT. 

During the pregnancy period, peripheral vascular 

resistance is physiologically paralleled by improved 

macrovascular compliance. 11, 12 Some researchers have 

shown that 2-4 years after previous gestational diabetes 

mellitus, a significantly higher arterial stiffness can be 

found compared with reference women without a history of 

diabetes. 13 Pregnancies complicated by diabetes not only are 

associated with increased carotid IMT but also can lead to 

increased maternal arterial stiffness. 9 

This study demonstrates increased IMT of the carotid artery 

in a group of women who had a pregnancy complicated by 

impaired OGCT. This finding is in line with the literature 

confirming that women with a history of gestational diabetes 

have a higher risk of developing increased carotid IMT. This 

change can potentially lead to cardiovascular diseases in 

later life. There are some explanations for this phenomenon. 

One of the first steps in the development of atherosclerosis is 

endothelial activation, followed by endothelial dysfunction. 

Thus, in diabetes mellitus, vascular endothelial activation 

or dysfunction is considered to play a key role in the 

development of many of the clinical manifestations related 

to carotid artery disease, several years after delivery. 

Association between parity and carotid artery disease 

can be affected by some underlying factors. Some 

epidemiological studies have found positive associations 

between parity and risk of carotid artery plaques in elderly 

women and, therefore, age of pregnancy can be a trigger 

for this phenomenon. 14 Also, multi-gravidity and previous 

history of coronary diseases have been also identified to be 

related to the appearance of carotid artery plaques. 15 Folate 

deficiency during pregnancy is another probable triggering 

factor for progressing carotid IMT. Folate deficiency is 

linked with hyperhomocystinemia, 16 which is associated with 

accelerated progression of atherosclerosis 17 and, thereby, 

158

Increased Carotid Artery Intima-Media Thickness in Pregnant Women with ... 

carotid artery IMT. Pregnancy is potentially a cause of folate 

deficiency. 18 Consequently, it is possible that multiparous 

women are at risk of prolonged folate deficiency; this may 

explain their susceptibility to the development of carotid 

artery IMT. 

In the present study, the main limitation was blood glucose 

controlled by insulin; we could not hold treatment because 

of ethical issues. Also, we did not assess the confounding 

effects of the triggering variables such as age of pregnancy, 

multi-parity, or medication during this period on increasing 

carotid IMT; that should be considered in further studies. 

Another weakness of this study would be the relatively small 

sample size. The study was designed to enroll 50women. 

Despite this, we feel that it provides valuable information. 

Prospective follow-up studies will also be needed and have 

meanwhile been started to determine whether diabetes during 

pregnancy itself is responsible for the increase in IMT. 

Conclusion 

In conclusion, an impaired OGCT test is proven to be 

an independent risk factor for increased carotid IMT and 

subsequent coronary artery disease. Even with this small 

study, we were able to find an increased IMT after diabetes 

appearance, which might be used as an indicator of a potential 

increased vascular risk. Furthermore, IMT measurements 

in diabetic pregnant women could offer an opportunity to 

identify a high-risk group of women who might benefit from 

early screening and preventive measures. These measures 

could include lifestyle interventions such as improving diet 

and physical activity as well as increased surveillance of 

blood pressure, serum lipids, and particularly blood glucose. 

Acknowledgment 

This study was a resident’s thesis and was financially 

supported by Kerman University of Medical Sciences. 


artery intima-media thickness in cardiovascular risk assessment by 

Framingham risk-score in type 2 diabetes: a retrospective cohort 

study. J Diabetes 2009;1:188-193. 

5. Akinci B, Demir T, Celtik A, Baris M, Yener S, Ozcan MA, Yuksel 

F, Secil M, Yesil S. Serum osteoprotegerin is associated with 

carotid intima media thickness in women with previous gestational 

diabetes. Diabetes Res Clin Pract 2008;82:172-178. 

6. Blaauw J, van Pampus MG, Van Doormaal JJ, Fokkema MR, Fidler 

V, Smit AJ, Aarnoudse JG. Increased intima-media thickness after 

early-onset preeclampsia. Obstet Gynecol 2006;107:1345-1351. 

7. Jovanović S, Jovanović A. Pregnancy is associated with hypotrophy 

of carotid artery endothelial and smooth muscle cells. Hum Reprod 

1998;13:1074-1078. 

8. Tarim E, Yigit F, Kilicdag E, Bagis T, Demircan S, Simsek 

E, Haydardedeoglu B, Yanik F. Early onset of subclinical 

atherosclerosis in women with gestational diabetes mellitus. 

Ultrasound Obstet Gynecol 2006;27:177-182. 

9. Savvidou MD, Anderson JM, Kaihura C, Nicolaides KH. Maternal 

arterial stiffness in pregnancies complicated by gestational and 

type 2 diabetes mellitus. Am J Obstet Gynecol 2010;203:274.e1-7. 

10. American Diabetes Association. Standards of medical care in 

diabetes-2011. Diabetes Care2011;34:11-61. 

11. Visontai Z, Lenard Z, Studinger P, Rigo J, Jr, Kollai M. Impaired 

baroreflex function during pregnancy is associated with stiffening 

of the carotid artery. Ultrasound Obstet Gynecol 2002;20:364-369. 

12. Mersich B, Rigó J, Jr, Besenyei C, Lénárd Z, Studinger P, Kollai M. 

Opposite changes in carotid versus aortic stiffness during healthy 

human pregnancy. Clin Sci 2005;109:103-107. 

13. Hu J, Norman M, Wallensteen M, Gennser G. Increased large 

arterial stiffness and impaired acetylcholine induced skin 

vasodilatation in women with previous gestational diabetes 

mellitus. Br J Obstet Gynaecol 1998;105:1279-1287. 

14. Humphries KH, Westendorp IC, Bots ML, Spinelli JJ, Carere 

RG, Hofman A. Parity and carotid artery atherosclerosis inelderly 

women: the Rotterdam Study. Stroke2001;32:2259-2264. 

15. Ness RB, Harris T, Cobb J, Flegal KM, Kelsey JL, Balanger A. 

Number of pregnancies and the subsequent risk of cardiovascular 

disease. N Engl J Med 1993;328:1528-1533. 

16. Boushey CJ, Beresford SA, Omenn GS, Motulsky AG. A 

quantitative assessment of plasma homocysteine as a risk factor for 

vascular disease. Probable benefits of increasing folic acid intakes. 

JAMA 1995;274:1049-1057. 

17. Selhub J, Jacques PF, Bostom AG, D’Agostino RB, Wilson PW, 

Belanger AJ, O’Leary DH, Wolf PA, Schaefer EJ, Rosenberg IH. 

Association between plasma homocysteine concentrations and 

extracranial carotid-artery stenosis. N Engl J Med1995;332:286- 

291. 

18. Mc Partlin J, Halligan A, Scott JM, Darling M, Weir DG. Accelerated 

folate breakdown in pregnancy. Lancet 1993;341:148-149. 

References 

1. Bo S, Valpreda S, Menato G, Bardelli C, Botto C, Gambino R, 

Rabbia C, Durazzo M, Cassader M, Massobrio M, Pagano G. 

Should we consider gestational diabetes a vascular risk factor 

Atherosclerosis 2007;194:72-79. 

2. Ben-Haroush A, Yogev Y, Hod M. Epidemiology of gestational 

diabetes mellitus and its association with type 2 diabetes. Diabet 

Med 2004;21:103-113. 

3. Vastagh I, Horváth T, Garamvölgyi Z, Rosta K, Folyovich A, Rigó 

J, Kollai M, Bereczki D, Somogyi A. Preserved structural and 

functional characteristics of common carotid artery in properly 

treated normoglycemic women with gestational diabetes mellitus. 

Acta Physiol Hung 2011;98:294-304. 

4. Ataoglu HE, Saler T, Uzunhasan I, Yenigun M, Yigit Z, Temiz LU, 

Saglam Z, Cetin F, Kumbasar B, Sar F. Additional value of carotid 




Right Ventricular Myocardial Tissue Velocities, 

Myocardial Performance Index, and Tricuspid Annular 

Plane Systolic Excursion in Totally Corrected Tetralogy 

of Fallot Patients 

Asadolah Tanasan, MD 1 , Keyhan Sayadpour Zanjani, MD 2* , Armen 

Kocharian, MD 2 , Abdolrazagh Kiani, MD 2 , Mohammad Ali Navabi, MD 2 

1 

Besat Hospital, Hamadan University of Medical Sciences, Hamadan, Iran. 

2 

Children’s Medical Center, Tehran University of Medical Sciences, Tehran, Iran. 

Received 03 November 2011; Accepted 16 May 2012 

Abstract 

Background: Longer survival after the total repair of the Tetralogy of Fallot increases the importance of late complications 

such as right ventricular dysfunction. This is a prospective study of the right ventricular function in totally corrected Tetralogy 

of Fallot patients versus healthy children. 

Methods: Thirty-two healthy children were prospectively compared with 30 totally corrected Tetralogy of Fallot patients. 

Right ventricular myocardial tissue velocities, right ventricular myocardial performance index, and tricuspid annular plane 

systolic excursion were investigated as well as the presence and severity of pulmonary regurgitation. 

Results: The two groups were age-and sex-matched. Mean systolic peak velocity (Sa) and tricuspid annular plane systolic 

excursion were significantly decreased, while myocardial performance index and early to late diastolic velocity (Ea/Aa) 

were significantly increased in the Tetralogy of Fallot patients. Early diastolic velocity (Ea) showed no significant difference 

between the two groups. Sa correlated significantly with tricuspid annular plane systolic excursion in both the normal children 

and totally corrected Tetralogy of Fallot patients. Myocardial performance index was significantly higher in the patients 

with moderate to severe pulmonary regurgitation than in those with mild regurgitation. However, there was no significant 

correlation between this index and right ventricular myocardial tissue velocities. 

Conclusion: In this study, systolic right ventricular function indices (Sa and tricuspid annular plane systolic excursion) 

were impaired in the totally corrected Tetralogy of Fallot patients. Myocardial performance index was affected by the severity 

of pulmonary regurgitation. 


This paper should be cited as: Tanasan A, Sayadpour Zanjani K, Kocharian A, Kiani A, Navabi MA. Right Ventricular Myocardial 

Tissue Velocities, Myocardial Performance Index, and Tricuspid Annular Plane Systolic Excursion in Totally Corrected Tetralogy of Fallot 

Patients. J Teh Univ Heart Ctr 2012;7(4):160-163. 

Keywords: Tetralogy of Fallot • Tricuspid valve • Elasticity imaging technique • Child • Heart ventricles 

* 

Corresponding Author: Keyhan Sayadpour Zanjani, Assistant Professor of Pediatric Cardiology, Tehran University of Medical Sciences, Children’s 

Medical Center, No.62, Dr Gharib Street, Tehran, Iran. 1419733151. Tel: +98 21 66911029. Fax: +98 21 66930024. E-mail: sayadpour@tums.ac.ir. 

160

Right Ventricular Myocardial Tissue Velocities, Myocardial Performance Index ... 


Introduction 

Although excellent outcomes have been achieved long 

after the total correction of the Tetralogy of Fallot (TOF) in 

the developed countries, right ventricular (RV) dysfunction 

may still cause mortality and morbidity. 1, 2 Pulmonary 

regurgitation (PR) has a detrimental effect on the RV 

diastolic function. 3 Late systolic RV dysfunction has been 

reported after the correction of the TOF in the developed 

countries. 4 The long-term survival after the TOF repair in the 

developing countries is unknown; 5, 6 we, therefore, sought to 

focus on the earlier RV function in these patients. We used 

the right ventricular myocardial performance index (RVMPI 

or Tei index), tricuspid annular plane systolic excursion 

(TAPSE), and myocardial tissue velocities for the evaluation 

of the RV systolic and diastolic functions in totally corrected 

TOF patients. 7 

Methods 

Thirty consecutive totally corrected TOF patients, who 

referred to our Outpatient Clinic between July 2008 and 

July 2009, were enrolled in the study and written informed 

consent was obtained from all of them. The study population 

underwent surgery using valved trans-annular patches, nonvalved 

trans-annular patches, or sub-annular patches at 

a mean age of 3.6 ± 3.2 years. Thirty-two normal healthy 

children with innocent murmur were selected as the control 

group. 

The inclusion criteria for this study included classic TOF 

with pulmonary stenosis. The exclusion criteria were other 

variants of the TOF (pulmonary atresia with ventricular septal 

defect [VSD], absent pulmonary valve, and double-outlet 

RV) and the presence of a significant residual abnormality 

(VSD, valvular or peripheral pulmonary stenosis, or tricuspid 

regurgitation) other than PR. 

Echocardiography was performed using a single 

echocardiographic scanner (MicroMaxx Ultrasound System, 

Sonosite Inc., USA). RVMPI was measured using continuous 

pulse wave Doppler of the pulmonary and tricuspid valves. 

The formula a-b/b was used, where a was the time interval 

between cessation and onset of tricuspid inflow and b was 

pulmonary ejection time. 7 

The systolic displacement of the lateral portion of the 

tricuspid annular plan (TAPSE) was measured on the 

M-mode tracing under a two-dimensional echocardiogram 

in the four-chamber view. 8 

The averages of the RV systolic (Sa), early diastolic (Ea), 

and late diastolic velocities (Aa) in three cardiac cycles were 

measured using tissue Doppler echocardiography. 4 Threemillimeter 

Doppler sample volume was applied parallel 

to the RV free wall at the tricuspid valvular level to avoid 

sampling the right-heart cavities due to normal cardiac 

movement. 

Severity of PR was assessed by color and continues 

Doppler studies in the parasternal short-axis view. Duration 

of the PR flow to total diastolic time (PR index and PRi) 

was measured. PRi ≥ 70% was defined as mild PR, while 

9, 10 

the lower values were defined as moderate to severe PR. 

The severity of PR was also assessed on the color Doppler 

imaging. The presence of persistent retrograde color flow 

from the distal main pulmonary artery or branches that 

extend into the RV was defined as moderate to severe PR. 3 

The study was approved by the local Ethics Committee and 

it was conducted in accordance with good clinical practice 

and the Declaration of Helsinki. 

For the statistical analyses, the statistical software 

SPSS version 13.0 for Windows (SPSS Inc., Chicago, IL) 

was used. An independent samples t-test was performed 

to compare the RV function indices between the normal 

children and TOF patients. A bivariate correlation was 

performed using the Pearson correlation coefficient 

between the RV function indices. Statistical significance 

was inferred at a p value < 0.05. 

Results 

The 32 normal healthy children (17 males and 15 females 

at a mean age of 5.6 ± 3.8 years) and the 30 totally corrected 

TOF patients (17 males and 13 females at a mean age of 

6.4 ± 4.1 years) were age- and sex-matched. PR severity 

was evaluated in all of the totally corrected TOF patients, 

of whom 15 had valved trans-annular, 8 non-valved transannular, 

and 7 sub-annular patches. 

There were statistically significant differences in RVMPI, 

TAPSE, and myocardial tissue velocities (Sa, Aa, and Ea/ 

Aa) between the healthy children and totally corrected TOF 

patients. There was no significant difference in Ea (Table 1). 

Table 1. Indices of the RV function in the totally corrected TOF patients and 

normal healthy children * 

Variable TOF group Normal group P value 

RVMPI 0.3±0.1 0.2±0.1 0.001 

TAPSE (mm) 13.6±2.9 16.3±3.3 0.001 

Sa (cm/s) 8.6±8.9 11.4±2.2 < 0.001 

Ea (cm/s) 10.9±3.3 11.9±2.1 > 0.05 

Aa (cm/s) 5.9±1.8 8.2±2.1 < 0.001 

Ea/Aa 2.0±0.8 1.5±0.4 0.015 

* 


RV, Right ventricle; TOF, Tetralogy of Fallot; RVMPI, Right ventricular 

myocardial performance index; TAPSE, Tricuspid annular plain systolic 

excursion; Sa, RV systolic velocity; Ea, Early diastolic velocity; Aa, Late 

diastolic velocity 

The Pearson analysis showed a strong correlation between 



TAPSE and Sa both in the control (r = 0.755, p value < 0.001) 

and patient (r = 0.662, p value = 0.002) groups. There was 

a significant inverse correlation between Sa and RVMPI (p 

value = 0.001) in the control group but not in the patient 

group (p value = 0.054). There was no significant correlation 

between RVMPI and Ea/Aa in either group. 

PRi was measured in all the totally corrected TOF patients, 

of whom 13 had a value ≥ 70% (mild PR) and 17 had a value 

< 70% (moderate to severe PR). PRi < 50% was found in 2 

patients. There was a significant correlation between RVMPI 

and PRi (p value < 0.001) in the patient group. The RVMPI 

in patients with PRi < 70% was 0.42 ± 0.13, which differed 

significantly from the RVMPI (0.24 ± 0.1) in the patients 

with PRi ≥ 70% (p value < 0.05). In the 2 patients with PRi < 

50%, RVMPI was 0.62 and 0.47, respectively. There was no 

significant difference in the Ea/Aa ratio between the patients 

who had PRi ≥ 70% and those who had PRi < 70% (p value 

= 0.38). The Ea/Aa ratio was insignificantly higher in PRi 

< 70% (2.1 ± 9.4 vs. 1.85 ± 7.4; p value = 0.405). In the 2 

patients who had PRi < 50%, the Ea/Aa ratio was 4.57/1 and 

2.92/1, respectively (restrictive pattern). 

In the color flow Doppler assessment of PR, 11 patients 

had mild PR and 19 had moderate to severe PR. There was a 

significant correlation between PR severity in the retrograde 

color flow mapping and RVMPI (p value = 0.023), but there 

was no correlation between PR severity and Ea/Aa ratio (p 

value = 0.38). 

Discussion 

Advances in cardiac surgery and postoperative 

management in the developed countries have contributed 

to the excellent long-term outcome of the totally corrected 

TOF patients; 1 nevertheless, the long-term outcome of 

the corrected TOF surgery in developing countries is 

unknown. 5, 6 In the developed countries, PR and RV 

diastolic dysfunction is the most important outcome factor 

following the TOF repair. 2, 3 There are reports of the usage 

of pulmonary valve sparing surgery to decrease the severity 

of PR in the TOF patients. 11, 12 Intra- and postoperative 

management problems, delay in corrective surgery, and 

palliative surgery (aorto-pulmonary shunts) are probably 

additional contributory factors to the poor long-term 

outcome in developing countries. 5, 6 At follow-ups of the 

repaired TOF patients, simple and fast evaluation of the 

systolic and diastolic RV functions is of great importance. 

In our study, the RV systolic and diastolic function indices 

were clearly impaired in the TOF patients in comparison with 

the normal children at mid-term follow-ups (Table 1). A few 

studies have focused on the RV function at mid-term followup 

after the TOF repair. Pilla et al. evaluated the presence 

of mid-term RV dysfunction and health-related quality of 

life after the TOF repair in Brazil. 13 In their investigation, 

Asadolah Tanasan et al. 

35 patients at a median age of 6.1 years and 4.9 years of 

follow-up after surgery were compared with 36 sex- and 

age-matched healthy controls and RVMPI (0.34 vs. 0.2) 

demonstrated RV dysfunction in the patients compared with 

the controls. In adult patients late after the repair of the TOF, 

D’Andrea et al. detected a correlation between myocardial 

performance assessed at rest via tissue Doppler (TD) and 

cardiac performance during physical effort in adult patients 

(21.4 ± 3.8 years). 4 In their study, TD analysis showed lower 

Sa, Ea, Ea/Aa ratios in the corrected TOF patients compared 

to the normal group. In contrast to our study, the corrected 

TOF patients of their study had no significant PR, the mean 

age of the TOF patients was higher than that in our study 

(21.4 ± 3.8 vs. 6.3 ± 3.3 years), and the mean age of the 

corrected TOF patients was lower than that in our study (1.4 

± 0.5 vs. 3.6 ± 3.2 years). 4 In the Puranik et al. study, Sa 

and Ea were significantly lower in asymptomatic corrected 

adult TOF patients compared with their normal group. 14 

Similar to our study, there was significant PR but the age at 

corrective surgery was higher (6.6 vs. 3.6 years). Although 

the increased Ea/Aa ratio in our study, in contrast to the 

D’Andrea’s, may suggest the role of combined prolonged 

cyanosis and post-correction PR, a comparison with the 

Puranik study emphasizes the importance of other factors in 

4, 14 

the restrictive diastolic RV dysfunction in our patients. 

On the other hand, while our study demonstrates combined 

systolic dysfunction (decrease in both Sa and TAPSE) and 

restrictive RV dysfunction (increase in Ea/Aa ratio), the two 

other studies 4, 14 showed mild systolic dysfunction (decrease 

in Sa) associated with a significant decrease in Ea/Aa in adult 

corrected TOF patients. Frigola et al. reported that PR was an 

important factor of RV contractile dysfunction after the TOF 

repair. 15 These observations may suggest that the systolic and 

restrictive diastolic RV dysfunctions in our study probably 

originated through others mechanisms and they were present 

since the early postoperative period. In a study by Cullen 

et al, 16 patients with early restrictive physiology after the 

TOF repair had a clinical picture of low cardiac output and 

slow postoperative recovery but a study by Gatzoulis et al. 

suggested that late restrictive physiology predicted a superior 

exercise performance. 17 Further studies are clearly warranted 

about how the RV systolic and diastolic functions correlate 

with intra- and early postoperative management and PR. 

In addition to significant PR and prolonged preoperative 

cyanosis, intra- or early postoperative management may 

have been affected by systolic and restrictive diastolic RV 

functions in our study. 6 Although RVMPI was significantly 

correlated with PR severity (retrograde color flow and PRi), 

there was no significant correlation between RVMPI and 

Ea/Aa ratio. In our 2 patients with severe PR (PRi < 50%), 

the Ea/Aa ratio was significantly elevated. As RVMPI was 

not correlated with systolic and diastolic function indices 

(Sa, TAPSE, Ea, and Ea/Aa) but was allied to PR severity, 

RVMPI may have been affected more by PR severity than 

162

Right Ventricular Myocardial Tissue Velocities, Myocardial Performance Index ... 

by the RV function in the totally corrected TOF patients with 

restrictive physiology. In accordance with our study, Abd 

El Rahman et al. suggested that MPI was affected by the 

severity of PR in the presence of RV diastolic dysfunction. 18 

Yasuoka et al. showed that MPI obtained by pulsed wave 

Doppler was not different in patients with the TOF repair 

compared with normal children but RVMPI measured by 

tissue Doppler was significantly higher in patients with the 

TOF than in normal children. 19 

The current study had some limitations. The sample 

size was inadequate to compare the totally corrected TOF 

subgroups. Furthermore, half of the corrected TOF patients 

underwent valved trans-annular patch repair, which is a new 

technique for right ventricular outflow tract reconstruction. 

Conclusion 

RVMPI was significantly correlated with PR severity 

without the presence of a significant correlation between 

RVMPI (obtained by pulsed wave Doppler) and the RV 

function indices obtained by tissue Doppler imaging 

(EA, Aa, Ea/Aa, and Sa). We suggest that these indices, 

RVMPI by tissue Doppler and PRi, be measured basically 

at postoperative and follow-up evaluations. In addition, as 

TAPSE was significantly decreased in the totally corrected 

TOF patients and there was a significant correlation between 

TAPSE and Sa, we suggest that TAPSE be also measured as 

the global RV systolic function index. 


This study was approved and supported by Tehran 

University of Medical Sciences. 

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P, Mayer JE, Jr, del Nido PJ, Jonas RA. Long-term results after 

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Surg 2001;122:154-161. 

2. Knauth AL, Gauvreau K, Powell AJ, Landzberg MJ, Walsh 

EP, Lock JE, del Nido PJ, Geva T. Ventricular size and function 

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3. Bouzas B, Kilner PJ, Gatzoulis MA. Pulmonary regurgitation: not 

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5. Ho KW, Tan RS, Wong KY, Tan TH, Shankar S, Tan JL. Late 

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9. Festa P, Ait-Ali L, Minichilli F, Kristo I, Deiana M, Picano E. 

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Echocardiogr 2010;23:496-503. 

10. Li W, Davlouros PA, Kilner PJ, Pennell DJ, Gibson D, Henein 

MY, Gatzoulis MA. Doppler-echocardiographic assessment of 

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comparison with cardiovascular magnetic resonance imaging. Am 

Heart J 2004;147:165-172. 

11. Boni L, García E, Galletti L, Pérez A, Herrera D, Ramos V, 

Marianeschi SM, Comas JV. Current strategies in tetralogy of 

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ventricle/left ventricle pressures ratio. Eur J Cardiothorac Surg 

2009;35:885-889. 

12. Singh S, Pratap H, Agarwal S, Singh A, Satsangi DK. Pulmonary 

valve preservation in tetralogy of Fallot with a mildly hypoplastic 

annulus-should we do it Indian J Thorac Cardiovasc Surg 

2011;27:76-82. 

13. Pilla CB, Pereira CA, Fin AV, Aquino FV, Botta A, DalleMulle L, 

Ricachinevsky CP, Nogueira AJ, Lucchese FA, Rohde LE. Healthrelated 

quality of life and right ventricular function in the midterm 

follow-up assessment after tetralogy of Fallot repair. Pediatr 

Cardiol 2008;29:409-415. 

14. Puranik R, Greaves K, Hawker RE, Pressley LA, Robinson PJ, 

Celermajer DS. Abnormal right ventricular tissue velocities after 

repair of congenital heart disease-implications for late outcomes. 

Heart Lung Circ 2007;16:295-299. 

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Anatomy of Atrioventricular Node Artery and Pattern of 

Dominancy in Normal Coronary Subjects: A Comparison 

between Individuals with and without Isolated Right 

Bundle Branch Block 

Ali Kazemisaeid, MD, Marziyeh Pakbaz, MD * , Ahmad Yaminisharif, MD, 

Gholamreza Davoodi, MD, Masoumeh Lotfi Tokaldany, MD, Elham Hakki 

Kazazi, MD 


Received 24 December 2011; Accepted 20 May 2012 

Abstract 

Background: Isolated right bundle branch block (RBBB) is a common finding in the general population. The atrioventricular 

node (AVN) artery contributes to the blood supply of the right bundle branch. Our hypothesis was that the anatomy of the 

AVN artery and the pattern of dominancy differ between subjects with and without RBBB. 

Methods: We retrospectively studied the coronary angiography of 92 patients with RBBB and 184 age- and gendermatched 

controls without RBBB. All the subjects had angiographically proven normal coronary arteries. The dominant 

circulation and precise origin of the AVN artery were determined in each subject. Obtained data were compared between the 

two study groups. 

Results: There was no significant difference between the two groups in terms of dominancy (p value = 0.200). Origination 

of the AVN artery from the right circulatory system was more common in both groups, but this pattern was more prevalent 

in the cases than in the controls (p value = 0.021). There was a great variation of the AVN artery origin. In the total study 

population, the AVN artery was more commonly separated from a non crux origin than from the crux area. The prevalence of 

the non-crux origination of the AVN artery was significantly higher in the cases than in the controls (p value < 0.001). While 

the origination of the AVN artery from the right circulatory system was more common in both groups, the prevalence of the 

right origin of the AVN artery was significantly higher in the cases than in the controls. We observed that the AVN artery most 

commonly originated from the dominant artery but not necessarily from the crux. 

Conclusion: The anatomy of the AVN artery but not the pattern of dominancy is somewhat different in subjects with RBBB 

compared with normal individuals. 


This paper should be cited as: Kazemisaeid A, Pakbaz M, Yaminisharif A, Davoodi G, Lotfi Tokaldany M, Hakki Kazazi E. Anatomy 

of Atrioventricular Node Artery and Pattern of Dominancy in Normal Coronary Subjects; A Comparison Between Individuals With and 

Without Isolated Right Bundle Branch Block. J TehUniv Heart Ctr 2012;7(4):164-169. 

Keywords: Anatomy • Coronary vessels • Bundle-branch block 

* 

Corresponding Author: Marziyeh Pakbaz, Department of Cardiology, Tehran University of Medical Sciences, Tehran Heart Center, North Kargar 

Street, Tehran, Iran.1411713138. Tel: +98 21 88029256. Fax: +98 21 88029256. E-Mail: marzi.pakbaz@gmail.com. 

164

Anatomy of Atrioventricular Node Artery and Pattern of Dominancy in Normal ... 


Introduction 

The atrioventricular node (AVN) is an area of specialized 

tissue between the atria and the ventricles of the heart and 

specifically acts as an electrical relay station for electrical 

impulses, passing from the atria to the ventricles. The arterial 

blood supply of the AVN, which is quite variable, was the 

topic of anatomic, histologic, and radiologic research for 

many years. The origin of the blood supply to the conduction 

system is highly relevant to the clinical symptoms and 

surgical procedures. 1 Recognition of the anatomical variants 

of the arterial blood supply to the AVN may help overcome 

potential complications following ablation procedures or in 

mitral valve surgery. 

Isolated right bundle branch block (RBBB) is a common 

finding in the general population. RBBB may be associated 

with structural heart disease but many subjects with this 

conduction abnormality have no evidence of underlying 

heart disease. 2, 3 The blood supply to the proximal part of 

the right bundle branch is provided by the left anterior 

descending artery (LAD) or the AVN artery, and the distal 

part is mainly supplied by branches from the LAD. 4 

With regard to the contribution of the AVN artery to the 

blood supply of the right bundle branch, we postulated that 

RBBB may be associated with anatomical variations in the 

AVN artery. The aim of this study was to investigate the 

origin of the AVN artery in patients with isolated RBBB and 

to compare it with normal electrocardiogram individuals. 

Methods 

This case control study was conducted enrolling patients 

with normal coronary arteries or mild coronary artery 

disease who underwent coronary angiography between 2001 

and 2010 in Tehran Heart Center. Demographic features, 

coronary risk factors, drug history, history of cardiac events, 

electrocardiographic interpretation, echocardiographic 

findings, past history of coronary or any other type of 

intervention and open heart surgery, and the result of 

coronary angiography were drawn out of the computerized 

angiography database of Tehran Heart Center. Patients eligible 

for inclusion were men and women at least 20 years of age 

with documented RBBB on the surface electrocardiogram, 

mild or normal coronary arteries proven by angiography, and 

a normal ejection fraction (more than 50%). Major exclusion 

criteria included the presence of conduction abnormalities 

other than RBBB, history of using drugs affecting the heart 

conduction system such as beta adrenergic receptor blockers 

and antiarrhythmic agents, significant valvular heart disease 

(more than mild regurgitation or stenosis of any valve) on 

echocardiography study, and congenital or acquired structural 

heart disease that could be an etiology for developing RBBB 

such as atrial septal defect, ventricular septal defect, and 

pulmonary thromboembolism. Case selection was done 

with convenience non-probability sampling. Initially, 141 

patients were selected from the angiography database. 

Subsequently, the hospital records of these patients, 

including the history of symptoms, further evaluation of 

the electrocardiogram, echocardiographic findings, and 

coronary angiography report sheets, were reviewed in detail. 

First, the electrocardiogram and records were selected for 

further study if the electrocardiogram satisfied the criteria 

previously defined for typical RBBB by the World Health 

Organization and the International Society and Federation 

for Cardiology in 1985, as follows: 1) prolongation of QRS 

to 0.12 second or more; 2) an rsr’, rsR’, or rSR’ pattern and 

occasionally a wide and notched R pattern in lead V 1 

or V 2 

; 

3) an S wave duration longer than the R wave duration or 

greater than 40 ms in leads V 6 

and I; and 4) an R peak time 

greater than 0.05 second in lead V 1 

but normal in leads V 5 

and V 6 

. 5 

Of these criteria, the first three should be present for the 

diagnosis to be made. When a notched dominant R pattern is 

present in V 1 

, criterion 4 should be satisfied as well. 

Of the initial 141 patients selected, 49 subjects who did 

not meet the inclusion criteria were excluded. Finally, a 

total of 92 subjects were entered for final analysis. Control 

subjects, who underwent coronary angiography during the 

same period, were randomly extracted from the angiography 

database. The controls were matched by age and sex to 

the cases with a 2:1 ratio. Inclusion criteria other than 

electrocardiography findings were the same as those of the 

cases. For each group, the coronary angiography recorded on 

CDs was studied to determine the pattern and characteristics 

of the coronary anatomy and the origination of the AVN 

artery. The dominant circulation was also determined. 

The classification described by Popma JJ was used in the 

present study to define the dominant coronary circulation 6 : 

a) in a right dominant circulation, the posterior descending 

artery (PDA) and at least one posterolateral branch (PLB) 

originate from the right coronary artery (RCA); b) in a left 

dominant circulation, the PDA and all of the PLBs originate 

from the left coronary artery; and c) In a co-dominant 

circulation, the PDA originates from the RCA and all of the 

PLBs originate from the left coronary artery. 

In order to determine the origin of the AVN artery, the 

dominant artery was ascertained. Based on the knowledge 

that the AVN artery most commonly originates from the 

crux, 7 if a branch to the AVN region originated from the 

dominant artery at the area of the crux, it was considered 

the AVN artery. If such a branch was not detected, other 

segments of the dominant artery and thereafter the nondominant 

artery were evaluated in multiple views. At the 

end, the origin of the AVN artery was classified to be from 

the right, left, or dual circulation (if both circulatory systems 

gave rise to the AVN blood supply). If the AVN artery was 

not originated from the crux, we determined the specific 



Ali Kazemisaeid et al. 

artery giving rise to it. 

Statistical analysis was performed using SPSS version 

15.0 software. Results for the quantitative variables were 

reported as mean ± standard deviation and as frequencies for 

the qualitative variables. The mean values of the quantitative 

variables of the two study groups were compared using the 

Student t-test. The frequency distributions of the qualitative 

variables, obtained from the two study groups, were 

compared using the chi-square test. A p value ≤ 0.05 was 

considered a statistically significant difference. 

Results 

A total of 276 patients were involved, and 92 (33.3%) and 

184 (66.7%) subjects were grouped as cases and controls, 

respectively. The mean age for the case group (59.8% male) 

was 59.19 ± 10.93 years and for the controls (62.5% male) 

59.29 ± 10.94 years. In terms of dominancy, there was no 

significant difference between the study groups (p value = 0. 

200). Also, 75.0% of the cases versus 76.6% of the controls 

had right dominant, 12.0% of the cases versus 16.3% of the 

controls had left dominant, and 13.0% of the cases versus 

7.1% of the controls had co-dominant circulations (Figure 

1). By comparison, in terms of dominancy, there was no 

significant difference between the study groups. 

Figure 1. Comparison between the cases (individuals with right bundle 

branch block) and controls (individuals without right bundle branch block), 

showing the frequency of the distribution of the types of dominancy 

In the evaluation of the AVN artery origin, we determined 

whether it was originated from the right or left or whether 

it had a dual origin, whether or not it was from the crux. 

Furthermore, we determined the specific artery, from which 

the AVN artery branched (Tables 1 and 2). The crux was 

defined as the U-turn segment of the dominant artery. 

Of the total study population, the AVN origin was from 

the crux in 106 (38.4%) and from a non-crux origin in 169 

(61.2%) subjects (Table 1). 

Table 1. Variations of the AVN origin artery in the total study population 

Origin of AVN artery 

Number of subjects 

Undetermined 1 

Crux 106 

Non-crux origins 169 

Dual origin 

PLB and distal of LCX 2 

OM and distal of RCA 1 

Origin from LCX 

Distal of LCX 3 

Mid-part of LCX 1 

Origin from OM 40 

Origin from RCA 

Conus 3 

Proximal of RCA 7 

Distal of RCA 24 

Posterior descending artery 2 

Posterolateral branch 85 

Origin from Ramus 1 

Total 276 

AVN, Atrioventricular node; LCX, Left circumflex artery; RCA, Right 

coronary artery; OM, Obtuse marginal artery 

In one patient, the AVN origin was undetermined, probably 

because it was too small to be visualized. Only a minority of 

the patients had an AVN artery with a dual origin (2 of the 

cases and one of the controls), as is shown in Table 1. 

These special cases were omitted from the subsequent 

analysis of the AVN origin because of the very small number 

of such cases. The results after such an adjustment are 

depicted in Table 2. 

Table 2 illustrates that origination of the AVN artery from 

a non-crux origin was more common than origination from 

the crux in both groups. The prevalence of the non-crux 

origination of the AVN artery was significantly higher in the 

cases than in the controls (79.8% vs. 51.4%, respectively; p 

value < 0.001). 

Although origination from the right circulatory system 

was more common in both groups (82.0% of the cases and 

68.9% of the controls), the prevalence of the right origin of 

the AVN artery was significantly higher in the cases than in 

the controls (p value = 0.021) (Table 2). 

A more detailed comparison of the AVN artery origin 

between the cases and controls is illustrated in Figure 2. 

The most common origin of the AVN artery was the crux 

in the controls and the PLB in the cases when considering 

the frequency of the different non-crux origin variations of 

the AVN artery separately. Nevertheless, by integrating these 

166



subtypes and considering the single variant of the “non-crux 

origin of the AVN artery”, it became more common than the 

crux origin even slightly in the controls. 

We analyzed the association between the origin of the 

AVN artery and the type of dominancy in the whole study 

population and observed that the AVN artery most commonly 

originated from the dominant artery. In the case of the codominant 

circulation, it most commonly originated from the 

right circulation (Table 3). 

Table 2. Comparison of the AVN artery origin in individuals with right 

bundle branch block (cases) and individuals without right bundle branch 

block )controls) * 

AVN artery 

origin 

Total 

n=272 

Case 

n=89 

Control 

n=183 

Left 73 (26.8) 16 (18.0) 57 (31.1) 

Right 199 (73.2) 73 (82.0) 126 (68.9) 

Crux 107 (39.3) 18 (20.2) 89 (48.6) 

Non-crux 165 (60.7) 71 (79.8) 94 (51.4) 

* 

Data are presented as n )%( 

** 

Case vs. Control 

AVN, Atrioventricular node 

P value ** 

0.021 

< 0.001 

Figure 2. Frequency of the AVN artery origin in cases (individuals with 

right bundle branch block) and controls (individuals without right bundle 

branch block) 

AVN, Atrioventricular node; CX, Left circumflex artery; OM, Obtuse 

marginal artery; PDA, Posterior descending artery; PLB, Posterolateral 

branch artery; RCA, Right coronary artery 

Table 3. Association of the AVN artery origin with dominancy 

Dominancy 

Origin of the AVN artery 

from right circulation from left circulation 

Right dominant 87.9% 12.1% 

Left dominant 7.5% 92.5% 

Co-dominant 60.0% 40.0% 

AVN, Atrioventricular node 

Discussion 

The findings of the present study suggest that there is no 

relationship between the dominancy of the epicardial arteries 

and the presence of RBBB in subjects with normal coronary 

arteries. There was a great variation of the AVN artery origin 

among all the study subjects. In the total study population 

and also in each group, the AVN artery was more commonly 

separated from a non-crux origin than from the crux (61.2% 

versus 38.4%); this is in contrast to the conventional 

wisdom. 7 The prevalence of the non-crux origination of 

the AVN artery was significantly higher in the cases than 

in the controls. A dual artery supply of the AVN was a rare 

variation, only observed in 0.01% of the subjects. While 

the origination of the AVN artery from the right circulatory 

system was more common in both groups, the prevalence of 

the right origin of the AVN artery was significantly higher in 

the cases than in the controls. Finally, we observed that the 

AVN artery most commonly originated from the dominant 

artery but not necessarily from the crux. 

To this date, there has been no previous study aiming to 

specifically compare anatomic variations in the AVN artery 

in subjects with RBBB versus subjects with normal surface 

electrocardiograms. 

Table 4 represents the results of the previous studies that 

investigated the AVN artery origin. 8-14 All the studies showed 

that the AVN artery originated most commonly from the 

RCA, which was the most common dominant system. This 

led to the conclusion that the AVN artery usually branched 

from the dominant artery. However, this was not always the 

case as we observed some cases of the origination of the 

AVN artery from the non-dominant artery. These out-ofthe-rule 

variants were more commonly seen in the control 

group (15% of the controls versus 1% of the cases and 10% 

of the total study population). The results of the current 

study with regard to this variable were very close to the 

results of Ramanathan and his colleagues’ angiographybased 

study on an Indian population and somewhat different 

from other studies, suggesting that race might be a potential 

factor influencing the anatomic variables of the coronary 

artery. 14 Three per cent of the total population investigated 

by Ramanathan et al., showed origination of the AVN artery 

from the non-dominant artery. 

Pejković B et al., in an anatomic study of 150 human hearts, 

found that the artery supplying the AVN arose most frequently 

from the U- or V-shaped segment of the right (90%) or left 

(10%) coronary artery termed the ‘U-turn’ at the level of the 

crux. 15 Differently in our study, the AVN artery was more 

commonly separated from a non-crux origin than from the 

crux (61.2% versus 38.4%). In 72.1% of the subjects, it was 

a branch from the right circulation and in 26.4% from the left 

circulation. In line with our observation, Pejkovic B et al., also 

showed that the AVN artery origin depended on topographic 



Ali Kazemisaeid et al. 

arterial dominance: in cases with right or balanced arterial 

coronary vascularization, the AVN artery was a branch of the 

RCA, and in cases of left dominance the left coronary artery 

gave a branch to the AVN. 15 

Dual supply of the AVN was a rare variation in the present 

sample of individuals. Such a dual supply has been described 

in the literature previously. 8, 10, 12-14, 16, 17 The co-dominant 

circulation seems not to be related to the dual arterial blood 

supply of the AVN insofar as in our study none of the 3 

patients with dual supply were co-dominant (one was leftdominant 

and the other 2 were right-dominant). 

Rusu MC et al., in an anatomic study of 50 human hearts, 

described five morphological types (each with distinctive 

subtypes) of the AVN artery: 1) type I (22%, the AVN artery 

from the U-turn of the RCA); 2) type II (18%, the AVN artery 

from the PDA); 3) type III (34%, the AVN artery from the 

PLB); 4) type IV (8%, the AVN artery from the bifurcation of 

the RCA into the PDA and the PLB-trifurcated RCA); and 5) 

type V (18%, the AVN artery from the circumflex artery). 18 

According to this type of classification, in our total study 

population the prevalence of each subtype was as follows: 

38.4% type I; 0.7% type II; 30.8% type III; 8.6% type IV; 

and 1.4% type V. We also observed additional subtypes such 

as origination from the OM, conus, proximal part of the RCA 

and ramus in 14.5%, 1.1%, 2.5%, and 0.3% of the subjects, 

respectively. Similar to the Russu study, the separation of the 

AVN artery from a non-crux origin was more common than 

that from the crux. Also in both studies, the most common 

non-crux origin of the AVN artery was from the PLB. The 

least common subtype in our study was origination from 

the PDA (and also ramus), in contrast to the Russu study, in 

which origination from the PDA was a common variation. 

By comparing the two study groups in our investigation, as 

is shown in Figure 2, this conclusion could be readily made 

that the origin of the AVN artery differed in the subjects with 

RBBB and those without RBBB. 

Conclusion 

According to our observations, there was no relationship 

between the dominancy of the epicardial arteries and the 

presence of RBBB in subjects with normal coronary arteries. 

There was a great variation of the AVN artery origin. Noncrux 

origination of the AVN artery was more common than 

the crux origination in both groups, and the prevalence of 

non-crux origination of the AVN artery was significantly 

higher in the cases than in the controls. Origination of the 

AVN artery from the right circulatory system was more 

common in both groups and the prevalence of the right origin 

of the AVN artery was significantly higher in the cases than 

in the controls. The AVN artery most commonly originated 

from the dominant artery but not necessarily from the crux. 




References 

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blood supply to the atrioventricular node. Clinical and surgical 

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2. Knilans TK. Right bundle branch block. In: Surawicz B, ed. Chou’s 

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6. Pompa JJ. Coronary arteriography. In: Bonow RO, Mann DL, 

Table 4. Origin of the AVN artery reported by various authors 

Author Study date Sample size 

Origin of AVN artery (%) 

RCA LCX Dual 

Vieweg et al. 1975 118 84 8 8 

Hutchison 1978 40 80 20 - 

Hadziselimović 1978 200 85 13 2 

Krupa 1993 120 90 10 - 

Futami et al. 2003 30 80 10 10 

Saremietal 2008 102 87 11 2 

Ramanathan et al. 2009 300 72 28 0 

The present study 2011 276 72.1 26.4 1.1 

AVN, Atrioventricular node; RCA, Right coronary artery; LCX, Left circumflex artery 

168



Zipes DP, Libby P, Braunwald E, eds. Braunwald’s Heart Disease, 

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electrophysiologic considerations. In: Bonow RO, Mann DL, 

Zipes DP, Libby P, Braunwald E, eds. Braunwald’s Heart Disease, 

A Textbook of Cardiovascular Medicine. 9th ed. Philadelphia: 

Saunders; 2011. p. 653-686. 

8. Vieweg WV, Alpert JS, Hagan AD. Origin of the sinoatrial node 

and atrioventricular node arteries in right, mixed, and left inferior 

emphasis systems. Cathet Cardiovasc Diagn 1975;1:361-373. 

9. Hutchinson MC. A study of the artrial arteries in man. J Anat 

1978;125:39-54. 

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human heart. Acta Anat (Basel) 1978;102:105-110. 

11. Krupa U. The atrioventricular nodal artery in the human heart. 

Folia Morphol (Warsz) 1993;52:G1-9. 

12. Futami C, Tanuma K, Tanuma Y, Saito T. The arterial blood supply 

of the conducting system in normal human hearts. Surg Radiol 

Anat 2003;25:42-49. 

13. Saremi F, Abolhoda A, Ashikyan O, Milliken JC, Narula J, 

Gurudevan SV, Kaushal K, Raney A. Arterial supply to sinuatrial 

and atrioventricular nodes: imaging with multidetector CT. 

Radiology 2008;246:99-107. 

14. Ramanathan L, Shetty P, Nayak SR, Krishnamurthy A, Chettiar 

GK, Chockalingam A. Origin of the sinoatrial and atrioventricular 

nodal arteries in South Indians: an angiographic study. Arq Bras 

Cardiol 2009;92:314-319. 

15. Pejković B, Krajnc I, Anderhuber F, Kosutić D. Anatomical aspects 

of the arterial blood supply to the sinoatrial and atrioventricular 

nodes of the human heart. J Int Med Res 2008;36:691-698. 

16. Krauss D, Carter JE, Jr, Feldman T. Anomalous connection between 

the sinus node artery and the A-V node artery. Cathet Cardiovasc 

Diagn 1993;29:236-239. 

17. James TN, Burch GE. The atrial coronary arteries in man. 

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18. Rusu MC, Ferechide D, Curca GC, Dermengiu D. Morph functional 

considerations on the atrioventricular node arterial vascularization. 

Rom J Leg Med 2009;17:101-110. 




Determinants of Length of Stay in Surgical Ward after 

Coronary Bypass Surgery: Glycosylated Hemoglobin as a 

Predictor in All Patients, Diabetic or Non-Diabetic 

Mahdi Najafi, MD * , Hamidreza Goodarzynejad, MD 


Received 03 March 2012; Accepted 23 July 2012 

Abstract 

Background: Reports on the determinants of morbidity in coronary artery bypass graft surgery (CABG) have focused on 

outcome measures such as length of postoperative stay in the Intensive Care Unit (ICU). We proposed that major comorbidities 

in the ICU hampered the prognostic effect of other weaker but important preventable risk factors with effect on patients’ 

length of hospitalization. So we aimed at evaluating postoperative length of stay in the ICU and surgical ward separately. 

Methods: We studied isolated CABG candidates who were not dialysis dependent. Preoperative, operative, and 

postoperative variables as well as all classic risk factors of coronary artery disease were recorded. Using multivariate 

analysis, we determined the independent predictors of length of stay in the ICU and in the surgical ward. 

Results: Independent predictors of extended length of stay in the surgical ward ( > 3 days) were a history of peripheral 

vascular disease, total administered insulin during a 24-hour period after surgery, glycosylated hemoglobin (HbA1c), last 

fasting blood sugar of the patients before surgery, and inotropic usage after cardiopulmonary bypass. The area under the 

Receiver Operating Characteristic Curve (AUC) was found to be 0.71 and Hosmer-Lemeshow (HL) goodness of fit statistic p 

value was 0.88. Independent predictors of extended length of stay in the ICU ( > 48 hours) were surgeon category, New York 

Heart Association functional class, intra-aortic balloon pump, postoperative arrhythmias, total administered insulin during 

a 24-hour period after surgery, and mean base excess of the first 6 postoperative hours (AUC = 0.70, HL p value = 0.94 ). 

Conclusion: This study revealed that the indices of glycemic control were the most important predictors of length of stay in 

the ward after cardiac surgery in all patients, diabetic or non-diabetic. However, because HbA1c level did not change under 

the influence of perioperative events, it could be deemed a valuable measure in predicting outcome in CABG candidates. 


This paper should be cited as: Najafi M, Goodarzynejad H. Determinants of Length of Stay in Surgical Ward after Coronary Bypass 

Surgery: Glycosylated Hemoglobin as a Predictor in All Patients, Diabetic or Non-Diabetic. J Teh Univ Heart Ctr 2012;7(4):170-176. 

Keywords: Coronary artery bypass • Treatment outcome • Hemoglobin A, glycosylated • Length of stay 

Introduction 

In a world of limited medical care resources, despite 

increasing demand for medical services, clinicians often 

need to identify patients that are likely to require a longer 

period of high dependency care after cardiac surgery. 

Coronary artery bypass graft surgery (CABG) has received 

particular attention as it is an expensive and commonly 

* 

Corresponding Author: Mahdi Najafi, Assistant Professor of Anesthesiology, Tehran Heart Center, Tehran University of Medical Sciences, Tehran 

Heart Center, North Karegar Street, Tehran, Iran. 1411713138. Tel: +98 21 88029600. Fax: +98 21 88029731. E-mail: najafik@sina.tums.ac.ir. 

170

Determinants of Length of Stay in Surgical Ward after Coronary Bypass Surgery ... 


performed procedure. 1, 2 Indeed, detection of patients who 

are likely to need a longer postoperative length of stay (LOS) 

for CABG would allow operations on these patients to be 

spread over the operating week. This would maximize the 

chance of the availability of the Intensive Care Unit (ICU) 

beds for other sick patients and also prevent the cancellations 

of operations. Moreover, prolonged ICU and ward stay in 

patients undergoing CABG increases overall hospital costs. 3 

LOS in hospital after cardiac surgery is among the most 

important determinants of outcome to have been studied 

so far. Many studies have reported the factors affecting the 

length of postoperative ICU stay. 4-12 A few investigators have 

evaluated total hospital LOS, 13-16 but to our knowledge, no 

study has assessed such predictors at cardiac surgical wards. 

Although the total time of hospital stay contains the time 

of stay in the ward, prolonged stay in the surgical ward is 

important itself inasmuch as it limits the number of available 

ICU beds because of a reduced throughput in the surgical 

ward, and as a consequence in the ICU unit. We proposed 

that the predictors of a prolonged ICU stay might be different 

from the predictors of a long postoperative stay in the 

hospital ward. 

Methods 

We prospectively studied a total of 570 consecutive patients 

undergoing elective CABG at Tehran Heart Center during 

a period of five months. Patients who underwent CABG 

combined with a heart valve repair or replacement, resection 

of a ventricular aneurysm, or other surgical procedures 

were excluded. The study was approved by the division of 

cardiothoracic surgery and by the research department of the 

hospital. 

Data were collected prospectively during the patients’ 

admission by interviews and physical examinations on the 

following variables: age; gender; body mass index (BMI); 

educational level; New York Heart Association (NYHA) 

functional class; number of diseased vessels; and left 

ventricular ejection fraction (LVEF). A history of myocardial 

infarction, smoking, alcohol abuse, opiate dependency, 

diabetes, hypercholesterolemia, hypertension, peripheral 

vascular disease, cerebrovascular disease, respiratory failure, 

and renal failure were also noted. 

Laboratory data included measured blood sugar in 

perioperative and glycated or glycosylated hemoglobin 

(HbA1c) at operation day. 

The patients’ data, risk factors, operation, and outcome 

data were recorded in a structured form. Perioperative 

medical characteristics were collected by research general 

practitioners. The data were transcribed onto the SPSS 

software by a data entry operator at a later date. 

Regarding educational level, three levels of education 

were categorized: 1 = primary school or lower; 2 = 

secondary school; and 3 = university/college or equivalents. 

Current smoker was defined as anybody who had smoked 

within one month of surgery. Alcohol abuse was defined 

as the consumption of alcohol despite recurrent adverse 

consequences. Daily regular use of opium products was 

defined as opium dependency according to the DSM-IV 

criteria. (American Psychiatric Association. Diagnostic 

and statistical manual of mental disorders: DSM-IV-TR. 

American Psychiatric Publishing, Inc.; 2000) Any cerebral 

neurological deficit induced by both cerebrovascular 

accident and transient ischemic attacks or previous cerebral 

surgery was defined as cerebrovascular disease. Peripheral 

vascular disease was defined as a history or any evidence 

of aneurysm or occlusive peripheral vascular disease on 

physical examination. After surgery, the patients who stayed 

in the ward for more than 2 consecutive days on the initial 

admission were classified as having a prolonged ward stay. 

A long cardiac surgical ICU stay was defined as > 2 days. 

The patients within the first 24 hours after bypass surgery 

were categorized into three groups according to the average 

amount of insulin intake: group 0 = zero U; group 1 = 1 to 

9 U; and group 2 = 10 or more U of insulin. The operations 

were performed by seven surgeons. The surgeons, in terms 

of mean total in-hospital duration of stay for the patients of 

each individual surgeon, were classified into 3 groups, as 

follows: 1 = total LOS < 8 days; 2 = 8 ≤ total LOS < 10 

days; and 3 = total LOS ≥ 10 days. 17 Central and peripheral 

circulations were measured by the amount of inotropic 

support and arterial blood gas parameters (base excess and pH 

in plasma), respectively. A wound infection was any wound 

infection in the sternum or leg incision following surgery. 

Postoperative arrhythmias were all observed rhythms that 

needed treatment rather than normal sinus rhythm. 

The numerical variables are presented as mean ± SD, 

while the categorized variables are summarized by absolute 

frequencies and percentages. The continuous variables 

were compared using the Student t-test, and the categorical 

variables were compared using the chi-square (or the 

Fisher exact test, as required) and the Mantel-Haenszel 

chi-square test for trend. A multivariate forward stepwise 

logistic regression model for risk factors predicting LOS 

in the ICU and the surgical ward was constructed. Through 

the multivariate forward stepwise analysis, the variables 

were entered into the logistic regression model according 

to their statistical significance (entering criterion p value ≤ 

0.15). The associations between the independent predictors 

and LOS in the ICU or the surgical ward in the final model 

were expressed as odds ratios (OR) with 95% CIs. Model 

discrimination was measured using the c statistic, which 

is equal to the area under the ROC (Receiver Operating 

Characteristic) curve. Model calibration was estimated 

using the Hosmer-Lemeshow (HL) goodness-of-fit statistic 

(higher p values imply that the model fits the observed data 

better). For the statistical analyses, the statistical software 



Mahdi Najafi et al. 

SPSS version 13.0 for Windows (SPSS Inc., Chicago, IL) 

and the statistical package SAS version 9.1 for Windows 

(SAS Institute Inc., Cary, NC, USA) were used. All the p 

values were two-tailed, with statistical significance defined 

by p value ≤ 0.05. 

Results 

The baseline characteristics, preoperative data, and 

outcome variables of the CABG patients according to LOS in 

the ICU are presented in Table 1. Overall, 380/570 (66.7%) 

patients were discharged from the ICU in ≤ 48 hours, and 190 

(33.3%) patients spent > 48 hours in the ICU. Table 2 shows 

the predictors of LOS in the ICU in the patients, undergoing 

bypass surgery. Three most important variables were intraaortic 

balloon pump support, mean 24 hours’ insulin intake 

of ≥ 10 units, and NYHA functional class, with odds ratios 

of 25.5, 2.3, and 2.2, respectively. 

The relationship between the LOS in the ICU and the 

Table 1. Baseline characteristics of the coronary artery bypass graft patients according to length of stay in the Intensive Care Unit 

ICU stay ≤ 48 hours (n=380) ICU stay > 48 hours (n=190) P value 

Age (y) 58.44±8.80 60.21±9.20 0.026 

Male sex 290 (76.3) 139 (73.2) 0.410 


Surgeon category 0.017 

1 218 (57.4) 102 (53.7) 

2 104 (27.4) 41 (21.6) 

3 58 (15.3) 47 (24.7) 

Cardiac risk factors 

Diabetes mellitus 159 (41.8) 74 (38.9) 0.508 

Hypertension 178 (46.8) 104 (54.7) 0.076 

Hyperlipidemia 264 (69.5) 136 (71.6) 0.605 

Cigarette smoking 138 (36.3) 68 (35.8) 0.902 

Family history of CAD 186 (48.9) 84 (44.2) 0.286 

Prior MI 187 (49.5) 100 (52.9) 0.440 

Prior CVA 10 (2.6) 12 (6.3) 0.031 

History of PVD 100 (26.3) 58 (30.5) 0.290 

NYHA functional class 0.032 

1 141 (37.1) 60 (31.6) 

2 193 (50.8) 93 (48.9) 

3 46 (12.1) 37 (19.5) 

LVEF (%) 48.88±9.80 47.78±11.38 0.253 

Number of diseased vessels 0.607 

1 12 (3.2) 9 (4.7) 

2 73 (19.2) 35 (18.4) 

3 295 (77.6) 146 (76.8) 

Operative details and complications 

Pump time (min) 68.45±20.36 73.19±25.24 0.025 

Number of grafts 3.70±0.94 3.79±0.99 0.265 

Intraoperative IABP-support 1 (0.3) 11 (5.8) < 0.001 

Endarterectomy 27 (7.1) 12 (6.3) 0.725 

Pacemaker dependents 33 (8.7) 20 (10.5) 0.475 

Inotropic drug use 148 (38.9) 90 (47.4) 0.055 

Arrhythmia 123 (32.4) 101 (53.2) < 0.001 

Perioperative MI 1 (0.3) 3 (1.6) 0.110 

Respiratory failure 56 (14.7) 48 (25.3) 0.002 

Wound infection 0 3 (1.6) 0.037 

Arterial blood gas parameters 

Mean BE within 6 hours after surgery (mmol/l) -5.42±2.55 -6.19±2.57 0.001 

pH < 7.34 within 6 hours after surgery 74 (19.5) 59 (31.1) 0.002 

Mean insulin intake within 24 hours after surgery < 0.001 

Zero U 193 (50.8) 69 (36.3) 

1 - 9 U 99 (26.1) 48 (25.3) 

≥ 10 U 88 (23.2) 73 (38.4) 

* 

Data are presented as mean±SD or n (%) 

ICU, Intensive Care Unit; CAD, Coronary artery disease; MI, Myocardial infarction; CVA, Cerebrovascular accident; PVD, Peripheral vascular disease; 

NYHA, New York Heart Association; LVEF, Left ventricular ejection fraction; IABP, Intra-aortic balloon pump; BE, Base excess 

172



Table 2. Predictors of length of stay in the Intensive Care Unit in patients undergoing bypass surgery 

Predictors 

Univariate analysis 

Multivariate analysis 

OR 

95% CI 

P value 

OR 

95% CI 

P value 

NYHA classification 

0.05 

0.02 

2 vs. 1 

1.13 

0.76-1.67 

1.17 0.77-1.79 

3 vs. 1 

1.89 

1.11-3.20 

2.15 1.22-3.79 

Surgeon category 

0.02 

0.04 

Group 2 vs. 1 

0.84 

0.54-1.29 

0.69 0.43-1.12 

Group 3 vs. 1 

1.73 

1.10-2.71 

1.47 0.91-2.38 

Intra-aortic balloon pump 

support 

23.29 

2.98-181.79 < 0.01 25.22 3.14-202.43 < 0.01 

Postoperative arrhythmia 

2.37 

1.65-3.38 

< 0.01 

1.95 1.33-2.86 

< 0.01 

Mean BE within 6 hours 

after surgery 

0.88 

0.82-0.95 

< 0.01 

0.90 0.83-0.97 

< 0.01 

Mean insulin intake within 

24 hours after surgery * 

1 vs. 0 

1.35 

0.87-2.10 

< 0.01 

1.31 0.82-2.09 

< 0.01 

2 vs. 0 

* 

Group 0 = Zero U 

Group 1 = 1 to 9 U 

Group 2 = ≥ 10 U 

2.32 

1.53-3.51 

2.27 1.45-3.55 

OR, Odds ratio; CI, Confidence interval; NYHA, New York Heart Association; BE, Base excess; AUC, Area under the Receiver Operating Characteristic 

Curve (c = 0.70) 

Table 3. Durations of Intensive Care Unit, surgical ward and total hospital stay as well as in-hospital mortality rate for both study groups * 

Group A 

Group B 

Patients with ICU stay ≤ 48h (n=380) 

Patients with ICU stay > 48h (n=190) 

P value 

ICU stay (hr) 27.38±9.30 85.79±34.87 

Surgical ward stay (d) 2.78±1.79 2.63±2.35 0.43 

Total hospital stay (d) 7.21±2.84 9.85±7.36 < 0.01 

In-hospital mortality 0 3 (1.6) 0.04 

* 


Table 4. Comparison of patients with regard to LOS in ward after CABG * 

Ward stay ≤ 3 days (n=426) Ward stay > 3 days (n=144) P value 

Male sex 

336 (78.9) 93 (64.6) < 0.01 


Education class ** < 0.01 

1 218 (51.2) 94 (65.3) 

2 133 (31.2) 36 (25.0) 

3 75 (17.6) 14 (9.7) 

Diabetes mellitus 153 (35.9) 80 (55.6) < 0.01 

Family history of CAD 191 (44.8) 79 (54.9) 0.04 

History of PVD 104 (24.4) 54 (37.5) < 0.01 

Inotropic drug use 166 (39.0) 72 (50.0) 0.02 

Postoperative arrhythmia 179 (42.0) 45 (31.3) 0.02 

HbA1C at operation day 5.83±1.58 6.55±1.90 < 0.01 

Last fasting blood sugar 103.58±30.41 119.45±46.88 < 0.01 

Mean insulin intake within 24 hours after surgery *** < 0.01 

0 220 (51.6) 42 (29.2) 

1 100 (23.5) 47 (32.6) 

2 106 (24.9) 55 (38.2) 

Mean BG within the first 24 hours after surgery (mg/dl) 167.41±26.28 176.49±28.10 < 0.01 

Blood urea nitrogen (mg/dl) 38.86±11.56 42.19±12.92 < 0.01 

Total cholesterol (mg/dl) 157.97±43.89 169.19±47.32 < 0.01 

* 


** 

1 = primary school or lower; 2 = secondary school; 3 = university/college or equivalents 

*** 

Group 0 = Zero U; Group 1 = 1 to 9 U; Group 2 ≥ 10 U 

LOS, Length of stay; CABG, Coronary artery bypass surgery; CAD, Coronary artery disease; PVD, Peripheral vascular disease; HbA1C, Glycosylated 

hemoglobin; BG, Blood glucose 




Table 5. Predictors of length of stay at surgical ward in patients undergoing bypass surgery 

Univariate analysis 

Multivariate analysis 

OR 95% CI P value OR 95% CI P value 

Peripheral vascular disease 1.858 1.241-2.781 < 0.01 1.568 1.013-2.426 0.04 

HbA1c 1.268 1.133-1.419 < 0.01 1.210 1.074-1.362 < 0.01 

Last fasting blood sugar 1.011 1.006-1.016 < 0.01 1.009 1.003-1.014 < 0.01 

Inotropic drug use 1.566 1.071-2.291 0.02 1.638 1.088-2.465 0.02 

Postoperative arrhythmia 0.627 0.420-0.937 0.02 0.531 0.343-0.822 0.01 

Mean insulin intake within 24 hours after surgery * < 0.01 < 0.01 

1 vs. 0 2.462 1.525-3.973 2.455 1.487-4.054 

2 vs. 0 2.718 1.709-4.321 2.708 1.648-4.450 

* 

Group 0 = Zero U 

Group 1 = 1 to 9 U 

Group 2 ≥ 10 U 

OR, Odds ratio; CI, Confidence interval; NYHA, New York Heart Association; HbA1c, Glycosylated hemoglobin 

surgical ward was investigated through a comparison of the 

average ICU, surgical ward, and total hospital stay as well 

as in-hospital mortality rate between two groups of ICU stay 

( ≤ 48 and > 48 hours) as listed in Table 3. The overall inhospital 

mortality rate was 0.5%. 

In all the patients studied, the LOS at the cardiac surgical 

ward ranged from 1 to 14 days (mean ± SD, 2.73 ± 1.99 

days) with a median of 2 days. Patients with a prolonged 

surgical ward stay (144/570, 25.3%) were more likely to be 

women and have diabetes, family history of coronary artery 

disease, history of peripheral disease, and lower educational 

level. 

Table 4 compares the patients’ characteristics by taking 

into consideration the LOS in the ward after cardiac surgery. 

Among the important factors that were significantly different 

between the two groups, i.e. LOS > 3 days and LOS ≤ 3 days, 

five factors were independent predictors. Three predictors 

were indices of glycemic control (Table 5). The area under 

the Receiver Operating Characteristic Curve (AUC) was 

found to be 0.71, which showed a good predictive accuracy 

in the variables included in the model. The model was also 

found to fit the data well since the Hosmer-Lemeshow p 

value was 0.88 (p < 0.05 indicated a poor fit). 

Discussion 

In the current study, we included preoperative, 

intraoperative, and immediate postoperative variables to 

find LOS determinants in 570 CABG patients after bypass 

surgery. The six variables of intra-aortic balloon pump 

(IABP), NYHA functional class, postoperative arrhythmia, 

24-hour average insulin intake, mean 6-hour BE, and surgeon 

category were found to be the independent predictors of 

an ICU LOS greater than 48 hours. We also found five 

predictors to be the independent risk factors for an increased 

cardiac surgical ward LOS. Considerable reports have been 

published on the predictors of LOS in the ICU following 

CABG 4-12 and some studies have investigated factors 

increasing postoperative hospital stay. 13-16 To our knowledge, 

however, no study has focused on the determinants of the 

LOS of cardiac surgical wards. Thus, we think that our study 

may contribute to the literature in this regard. 

Over the past two decades, attempts have been made to find 

the determinants of postoperative LOS in CABG patients. 

Be that as it may, a great disparity in type and number of 

independent variables analyzed has been reported. Although 

most of outcome studies with the focus on LOS have 

investigated only preoperative and intraoperative variables, 

there are some outcome research reports with immediate 

6, 13 

postoperative variables included. 

Poor cardiac output states, as reflected by the need for 

an IABP and inotropic therapy, have been identified as a 

predictor of a prolonged ICU stay in several studies. 6, 8, 9 In 

the present study, use of IABP was an ICU stay predictor, 

whereas inotropic support was a surgical ward stay predictor. 

Additionally, both reflected cardiac output. 

Need for an IABP was identified as an independent 

risk factor for ICU stay longer than 48 hours in three 

studies. 18-20 In contrast, Doering et al. showed that only early 

hemodynamic instability was indicative of an ICU stay 

longer than 24 hours, whereas postoperative IABP and use 

of inotropic drugs were not. 9 Michalopoulos et al. also noted 

that the number of inotropes, rather than inotrope use itself, 

was the significant factor. 6 

These differences may result from different treatment 

protocols or the way in which variables such as the use of 

inotropes were defined. Michaloupolous et al. used a 6- hour 

window for starting inotropic support after surgery and did 

not consider vasodilators. 6 By contrast, in the Doering et al. 

study, a 3-hour period was adopted and after-load reducers 

such as nitroprusside were considered in the definition of 

inotropic support. 9 Christakis et al. did not consider inotropic 

support alone, adding to IABP support in defining low output 

state. 7 

Some disparities in study results may be due to various 

study populations and treatment protocols, different cut-offs 

used to define a prolonged stay in the ICU (from ≥ 2 to 10 

174



days), 5, 14, 21-23 differences in variables definitions, and the 

large number of variables that could be considered. 4 

The main difference between our study and those described 

above is that we took into account surgeon category and 

amount of insulin administered during a 24-hour period after 

CABG. We found that a patient’s surgeon could potentially 

influence the duration of ICU stay and that there were 

differences in the average length of ICU stay between the 

surgeons at our hospital. 17 It may indicate the necessity of 

using a unique protocol for discharging the patients from 

the ICU and hospital after surgery. We also found that the 

LOS in the ICU and ward depended predominantly on the 

amount of insulin received by the patients during the first 24- 

hour postoperative period. In addition, we could not show 

any association between the LOS in the ICU and that in the 

surgical ward (Table 3). As a result, a prolonged stay in the 

ICU probably is not an independent predictor of surgical 

ward stay. 

We found that the blood glucose control indices, including 

HbA1c and last fasting blood sugar (FBS) before surgery, 

were the risk factors for an extended LOS in surgical wards 

in patients undergoing CABG, diabetic or non-diabetic. 

Finding both HbA1c and FBS as the determinants of 

the LOS in the surgical ward suggests that HbA1c is an 

independent predictor of hospital stay regardless of the level 

of blood sugar. However, as HbA1c is an index of glycemic 

control during previous months, its level is independent of 

perioperative events. It may, therefore, be a more stable 

and reliable perioperative marker. HbA1c has been used 

as a marker of short-term glycemic control in diabetic 

patients for many years. Recently, the American Diabetes 

Association included HbA1c in diabetes mellitus diagnosis 

criteria. 24 The role of HbA1c in predicting morbidity and 

mortality in non-diabetic healthy people has been suggested 

by some population-based studies. 25, 26 However, there is 

limited knowledge about the prognostic role of HbA1c for 

perioperative outcome, and the relationship between HbA1c 

and postoperative outcome in cardiovascular surgery is 

controversial. 27-30 

Our study revealed that HbA1c could predict postoperative 

LOS in the surgical ward and not in the ICU. This may be 

explained by the hampering effect of more important strong 

cofactors such as IABP and NYHA functional class. 

Conclusion 

Among the five predictors of the LOS in the surgical 

ward, three were the indices of glycemic control. HbA1c is 

the most reliable marker of outcome because its level is not 

influenced by perioperative events. Taking these findings 

into consideration, the prognostic role of HbA1c for the 

LOS following CABG is promising. We would, therefore, 

recommend its use as a simple predictor of outcome after 

cardiac surgery in daily practice. 

Acknowledgments 



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176



Obvious or Subclinical Right Ventricular Dysfunction in 

Diabetes Mellitus (Type II): An Echocardiographic Tissue 

Deformation Study 

Mozhgan Parsaee, MD * , Parvaneh Bahmanziari, MD, Maryam Ardeshiri, MD, 

Maryam Esmaeilzadeh, MD 

Rajaei Cardiovascular, Medical and Research Center, Tehran University of Medical Sciences, Tehran, 

Iran. 

Received 20 May 2011; Accepted 07 March 2012 

Abstract 

Background: Diabetes mellitus is capable of impairing the myocardial function. Several studies have documented the 

influential impact of diabetes mellitus on the left ventricular function. The right ventricular function plays a significant role 

in the overall myocardial contractility; hence, this study was undertaken to evaluate the effect of diabetes mellitus type II on 

the right ventricular function. 

Methods: Twenty-two diabetic patients without any coronary artery disease, hypertension, or left ventricular dysfunction 

were studied. The right ventricular end diastolic diameter, tricuspid plane systolic excursion, right ventricular inflow Doppler 

parameters, longitudinal myocardial velocities, and deformation indices from the basal and apical segments of the right 

ventricular free wall of the case group were measured. The control group consisted of 22 healthy individuals. 

Results: The tricuspid annular plane systolic excursion (TAPSE) and tricuspid peak early to peak late diastolic flow 

velocities ratio (E/A) in the diabetic patients were significantly lower than those of the control group patients (18.9 vs. 23.2, 

p value < 0.001 and 0.96 vs. 1.21, p value = 0.012), but there were no significant differences in the right ventricular end 

diastolic diameter and the right ventricular Tei index between the two groups (p value = 0.72). The right ventricular basal 

peak myocardial systolic velocity (SM) (12 cm/sec vs. 13.4 cm/sec; p value = 0.03), basal and apical right ventricular free 

wall systolic strain (-13.3% and -18.7% vs. -20.2% and -25.7%; p value = 0.001), and apical strain rate (-1.2 1/s vs. -1.6 1/s; 

p value = 0.008 ) were significantly lower in the study group. There was a weak correlation between the right ventricular 

function and HbA1c as well as the duration of diabetes mellitus and C-reactive protein. 

Conclusion: Our results suggest that diabetes mellitus type II can influence the right ventricular function in the absence of 

coronary artery disease, diastolic dysfunction, and pulmonary hypertension. 


This paper should be cited as: Parsaee M, Bahmanziari P, Ardeshiri M, Esmaeilzadeh M. Obvious or Subclinical Right Ventricular 

Dysfunction in Diabetes Mellitus (Type II): An Echocardiographic Tissue Deformation Study. J Teh Univ Heart Ctr 2012;7(4):177-181. 

Keywords: Echocardiography • Diabetes mellitus • Ventricular function, right 

* 

Corresponding Author: Mozhgan Parsaee, Assistant Professor of Cardiology, Department of Echocardiography, Rajaei Cardiovascular, Medical 

and Research Center, Vali-Asr Ave. Adjacent to Mellat Park, Tehran, Iran. 1996911151. Tel: +98 21 23922930. Fax: +98 21 2055594. E-mail: 

parsaeemozhgan@yahoo.com. 



Introduction 

Diabetes mellitus (DM) increases the risk of heart failure 

development even in the absence of coronary artery disease, 

hypertension, or other comorbidities 1, 2 and could result in 

a two to fourfold greater mortality in heart failure patients. 

Indeed, DM is capable of impairing the myocardial function: 

this is initially a clinically silent condition; nevertheless, if 

left unrecognized and insufficiently managed, it could beget 

overt diabetic cardiomyopathy. 

The right ventricular (RV) function plays a significant 

role in the overall myocardial contractility. 3 Nevertheless, 

most of the previous studies regarding diabetes-induced 

changes in myocardial dysfunction were dedicated to the left 

ventricle (LV) at the cost of ignoring the role of the right 

heart chambers. The existing literature of course does contain 

a limited number of studies on the RV cardiomyopathies of 

patients with DM type I; however, to our knowledge, there 

is only one recent study probing into DM type II drawing up 

on three-dimensional strain and strain rate. 

The objectives of the present study were to evaluate the 

RV systolic and diastolic functions using conventional 

echocardiography, tissue Doppler imaging (TDI), and 

deformation indices (strain and strain rate) in patients with 

DM type II and without coronary artery disease or LV 

dysfunction. 

Methods 

The study group was comprised of 22 diabetic patients (9 

men and 13 women) aged 55.6 ± 6.0 years. These patients 

either referred to the DM Clinic of Rajaei Cardiovascular, 

Medical and Research Center or were amongst the hospital 

stuff. The control group consisted of 22 healthy individuals 

(9 men and 13 women). All the diabetic patients enrolled 

in this study were asymptomatic, without any clinical 

evidence of either systolic or diastolic heart failure. The 

control subjects were considered to have a low probability 

of coronary disease or heart failure based on clinical data. 

Coronary artery disease was excluded if there was a 

negative Dobutamine stress echocardiographic examination 

or a negative treadmill exercise electrocardiographic test. 

In a few cases, coronary artery disease was excluded on the 

evidence of equivocal non-invasive stress tests and normal 

coronary angiograms. The other exclusion criteria included 

valvular or congenital heart disease, left ventricular ejection 

fraction (LVEF) less than 50%, rhythms other than normal 

sinus rhythm, documented pulmonary diseases or pulmonary 

hypertension, and tricuspid regurgitation more than a mild 

degree. 

All the diabetic patients were on a diet and treatment with 

oral hypoglycemic drugs. Plasma glucose and HbA1c were 

observed periodically and controlled by the endocrinologist 

Mozhgan Parsaee et al. 

in the aforementioned clinic. None of the patients had such 

diabetic complications as progressive and complex diabetic 

retinopathy, neuropathy, and nephropathy. 

The study participants in the two groups underwent 

echocardiographic examinations (Vivid 7, GE Vingmed). 

The variables measured are presented as follows: 

1. The RV dimension and tricuspid annular plane systolic 

excursion (TAPSE) were measured from the apical fourchamber 

view. 

2. The RV Doppler parameters of the diastolic function 

(peak early [A] and peak late diastolic flow velocity [E], 

together with their ratio [E/A] and deceleration time [DT]) 

were recorded. The trans-tricuspid flow was measured in the 

apical four-chamber view using pulsed Doppler, with the 

sample volume positioned at the tips of the tricuspid leaflets. 

The measurements were averaged from three end-expiratory 

cycles. 

3. TDI was conducted to assess the RV longitudinal 

myocardial function in the apical four-chamber view. Color 

TDI was used in addition to two-dimensional images, 

with adjustment of the depth and sector angle to obtain an 

acceptable frame rate. The TDI variables of peak systolic 

velocity (Sm), peak early diastolic velocity (Em), peak late 

diastolic velocity (Am), myocardial performance index 

(MPI), and acceleration time of the isovolumetric contraction 

time (IVCT) were analyzed online. 

4. The deformation indices were measured by adjusting the 

imaging angle to achieve a parallel alignment of the beam 

with the myocardial segment of interest. The images were 

stored on a remote archive of the echocardiography machine 

so that they could be analyzed offline. The myocardial 

deformation curves were investigated from the basal segment 

of the RV free wall, which belongs to the inflow part of the 

RV, and also from the apical segment, which belongs to the 

trabecular portion of the RV. 

5. The strain rate and stain were measured based on the 

standard deformation measurement, and the peak of the R 

on the electrocardiography (ECG) was utilized to define 

end diastole. End systole was determined using the pulsed 

Doppler velocity profile of the left ventricular outflow tract 

(LVOT) as the aortic valve closure, and the RV end systole 

was determined using the pulsed wave profile of the right 

ventricular outflow tract (RVOT) at end expiration. The 

analysis of the myocardial strain and strain rate data included 

the assessment of the systolic strain (є), peak systolic strain 

rate (SRs), and peak early diastolic strain rate (SRe). 

The data are expressed as Mean ± SD and percentages. The 

Student unpaired t-test was used to evaluate the differences 

between the groups, and the chi-square test was employed to 

compare the categorical variables. The Pearson correlation 

coefficients were utilized to pair the continuous variables. 

A two-tailed p value < 0.05 was considered significant. For 

the statistical analyses, the statistical software SPSS version 

17.0 for Windows (SPSS Inc., Chicago, IL) was used. 

178

Table 1. Demographic characteristics of the studied groups * Diabetic group Control subjects P value 

Table 2. Echocardiographic and Doppler data of the studied groups * Diabetic group Control subjects P value 

Obvious or Subclinical Right Ventricular Dysfunction in Diabetes Mellitus (Type II): ... 


Results 

The demographic characteristics and clinical parameters 

of the participants are depicted in Tables 1. There were no 

significant differences between the two groups in terms 

of sex, age, body mass index, creatinine, total cholesterol 

level, low-density lipoprotein cholesterol (LDL), highdensity 

lipoprotein cholesterol (HDL), and being a smoker. 

The diabetic group, however, showed a higher level of 

triglyceride (p value = 0.049), but this was statistically, and 

not clinically, significant. 

The echocardiographic and Doppler data of the studied 

groups are illustrated in Table 2. There were no significant 

differences between the two groups as regards the right 

ventricular end diastolic diameter (RVEDD) (mm), and 

tricuspid E velocity, whereas the tricuspid annular plane 

systolic excursion (TAPSE), and tricuspid E/A ratio of the 

diabetic patients (18.9 ± 2.1 vs. 23.2 ± 2.9 and 0.96 ± 0.2 

vs. 1.21 ± 0.3, respectively) were significantly lower. The 

tricuspid A velocity and E wave deceleration time of the 

diabetic patients (0.5 ± 0.1 m/s vs. 0.4 ± 0.1 m/s and 289.2 

± 67 msec vs. 250.9 ± 57.1 msec) were significantly higher. 

Age (y) 54.5±7.0 49.8±8.4 0.05 

Male 9 (40.9) 9 (40.9) 0.69 

Hypertension 9 (40.9) 4 (18.2) 0.07 

Smoking 2 (9.1) 3 (13.6) 0.82 

Body mass index (Kg/m 2 ) 28.7±3.1 26.4±3.8 0.05 

Systolic blood pressure (mm Hg) 125.6±15.4 120.5±13.4 0.28 

Diastolic blood pressure (mm Hg) 79.5±11.6 76.1±10.5 0.32 

Creatinine (mg/dl) 1.0±0.2 1.1±0.1 0.47 

Total cholesterol (mg/dl) 178.4±40.0 166.0 ±37.0 0.39 

Duration of diabetes (y) 7.0±3.0 - - 

Triglyceride (mg/dl) 186.0±82.0 130.0±67.0 0.04 

Low-density lipoprotein cholesterol (mg/dl) 90.0±26.0 89.0±27.0 0.96 

* 


Right ventricular end diastolic diameter (mm) 28.0±2.9 28.0±3.7 0.56 

Tricuspid annular plane systolic excursion (mm) 18.9±2.1 23.2±2.9 < 0.01 

Tricuspid E velocity (m/s) 0.47±0.05 0.46±0.08 0.52 

Tricuspid A velocity (m/s) 0.5±0.1 0.4±0.1 0.04 

Tricuspid deceleration time (msec) 289.2±67.0 250.9±57.1 0.04 

E/A ratio 0.9±0.2 1.2±0.3 0.01 

* 


E/A, Tricuspid peak early to peak late diastolic flow velocities ratio 

Table 3. Tissue Doppler imaging data of the studied groups * Diabetic group Control subjects P value 

Right ventricular basal segment Sm (cm/s) 12.0±1.9 13.4±2.1 0.03 

Right ventricular basal segment Em (cm/s) 8.5±2.1 11.6±2.4 < 0.01 

Right ventricular basal segment Am (cm/s) 12.6±2.7 14.7±3.3 0.03 

Myocardial performance index 0.42±0.11 0.40±0.09 0.72 

Acceleration time of the isovolumetric contraction time (ms) 37.8±8.4 35.4±8.4 0.45 

E/Em ratio 0.05±0.01 0.04±0.01 < 0.01 

* 


Sm, Peak myocardial systolic velocity; Em, Peak early diastolic velocity; Am, Peak late diastolic velocity; E, Peak late diastolic flow velocity 



Mozhgan Parsaee et al. 

Table 4. Deformation indices data of the studied groups * Diabetic group Control subjects P value 

Right ventricular basal Є (%) 

Right ventricular basal SRs (1/s) 

Right ventricular basal SRe (1/s) 

Right ventricular apical Є (%) 

Right ventricular apical SRs (1/s) 

Right ventricular apical SRe (1/s) 

* 


Є, Systolic stain; SRs, Peak systolic strain rate; SRe, Early diastolic strain rate 

-13.3±4.3 -20.2±7.3 < 0.01 

-1.0±0.5 -1.37±0.9 0.18 

0.9±0.3 1.2±0.5 0.05 

-18.7±4.3 -25.7±8.2 < 0.01 

-1.2±0.3 -1.6±0.6 < 0.01 

1.2±0.4 1.9±0.7 < 0.01 

The TDI data of the study population are shown in Table 

3, according to which the RV basal segment Sm, Em, Am, 

and E/Em (12 ± 1.9 cm/sec vs. 13.4 ± 2.1 cm/sec, 8.5 ± 2.1 

cm/sec vs. 11.6 ± 2.4 cm/sec, 12.6 ± 2.7 cm/sec vs. 14.7 ± 

3.3 cm/sec, and 0.05 ± 0.01 vs. 0.04 ± 0.01, respectively) 

were significantly lower in the case group than in the control 

group. There were no significant differences between the two 

groups with respect to the MPI of the RV and the acceleration 

time of the IVCT. 

The data on the deformation indices of the two study 

groups are demonstrated in Table 4, according to which the 

RV basal segment systolic strain (Є) and RV apical segment 

(Є, SRs, and SRe) of the case group were significantly lower 

than those in the control group (p value < 0.01). There were, 

however, no significant differences in regard to the RV basal 

segment SRs and SRe between the two groups. 

There were no significant correlations between HBA1c, 

duration of diabetes, C-reactive protein (CRP), and measures 

of the RV systolic or diastolic dysfunction (based on 

conventional Doppler, TDI data, or deformation indices). 

Discussion 

The present study shows that both systolic and diastolic 

RV functions are impaired in patients with DM type II and 

without coronary artery disease or ejection fractions of less 

than 50%. This finding was demonstrated by significantly 

lower RV systolic parameters (TAPSE, RV basal Sm, basal 

and apical RV free wall systolic strains, and apical SRs) and 

lower RV diastolic parameters (E/A ratios, Em, Am, E/Em 

ratios, and apical early diastolic strain rate [SRe]) in our case 

group than those in a normal, sex- and age-matched control 

group. There were no statistically significant differences in 

the RV basal segment SRs and SRe between the diabetic and 

control subjects, which may be due to difficulties in drawing 

basal RV strain rate curves. 

Our results chime in with those of the Kosmala et al., 4 

study, which reported the impairment of both basal and apical 

segments of the RV free wall performance. In that study, 

however, the apical segments exhibited more pronounced 

systolic impairment than did the basal segments and it 

was concluded that the RV might be divided into the three 

components of the inflow or sinus, the trabecular, and the 

outflow portions. Geva et al., 5 stated that the inflow region, 

compared with the other parts of the RV, had significant 

predominance in fiber shortening and contribution to the 

global RV systolic function. As the basal segment of the RV 

free wall is a part of the inflow component, and the apical 

segment refers to the trabecular portion of the RV, they 

suggested that the differences seen in their cohort might be 

related to the regional inhomogeneity of the RV in patients 

with DM. 

The Kosmala et al., study 4 reported RV diastolic 

dysfunction in a non-uniform type I and type II diabetic 

cohort using TDI and demonstrated significantly lower 

values of Em and Em-to-Am ratio in the basal and midsegments 

and longer isovolumic relaxation time (IRTm) in 

the mid-segment. Nonetheless, that study failed to show 

any difference in the E/A ratio, Em, and systolic parameters 

(Sm and TAPSE) between the diabetic patients and normal 

subjects. Furthermore, the said study found no significant 

correlations between the estimated echocardiographic 

parameters and indices of diabetic control (plasma glucose 

and HbA1c) as well as the duration of diabetes. 

In another study, Kosmala et al., 4 evaluated non-uniform 

type I and type II diabetic groups and showed impairment 

of the RV systolic function according to deformation studies 

(RV systolic stain and SRs in the basal and apical segments 

of the RV free wall) and impairment of the RV diastolic 

function (decreased SRe in both RV segments). In a study by 

Karamitsos et al., 6 type I diabetic patients were found to have 

an impaired RV diastolic function (trans-tricuspid E velocity, 

A velocity, E/A ratio, Em, and Am). Nevertheless, the RV 

systolic function was preserved in the authors’ diabetic 

population. 

Consistent with the findings of the present study, Gaber 

et al., 7 assessed patients with DM type II and demonstrated 

impairment of the RV systolic and diastolic functions 

according to deformation studies via three-dimensional 

echocardiography (systolic strain, SRs, and SRe in both RV 

basal and apical segments). 

The present study, in agreement with some other similar 

studies, 4, 8, 9 found no importance for the impact of the 

180

Obvious or Subclinical Right Ventricular Dysfunction in Diabetes Mellitus (Type II): ... 


duration of diabetes on the RV function. This finding could 

suggest that controlling diabetes mellitus is more important 

than its duration. 

Med J 2008;11:65-74. 

9. Rowland TW, Martha PM, Jr, Reiter EO, Cunningham LN. The 

influence diabetes mellitus on cardiovascular function in children 

and adolescents. Int J Sports Med 1992;13:431-435. 

Conclusion 

Whether the RV diastolic abnormalities have prognostic 

implications in the clinical course of patients with DM 

type II remains to be investigated. We believe that serial 

echocardiography measurements are warranted in this 

diabetic population if the progression from subclinical 

RV involvement to symptomatic RV dysfunction is to be 

followed. In addition, subclinical RV systolic and diastolic 

abnormalities should be considered when planning 

pharmacotherapy to prevent the development of symptomatic 

RV dysfunction. 

Acknowledgments 

This research project was supported by Rajaei 

Cardiovascular, Medical and Research Center. Special 

thanks are due to the above-mentioned hospital’s personnel 

and nurses who enrolled in our control group. 

References 

1. Kosmala W, Colonna P, Przewlocka-Kosmala M, Mazurek W. 

Right ventricular dysfunction in asymptomatic diabetic patients. J 

Diabetes Care 2004;27:2736-2738. 

2. Dounis V, Siegmund T, Hansen A, Jensen J, Schumm-Draeger PM, 

von Bibra H. Global myocardial perfusion and diastolic function 

are impaired to a similar extent in patients with type 2 diabetes 

mellitus and in patients with coronary artery disease-evaluation by 

contrast echocardiography and pulsed tissue Doppler. Diabetologia 

2006;49:2729-2740. 

3. Van den Brom CE, Bosmans JW, Vlasblom R, Handoko LM, 

Huisman MC, Lubberink M, Molthoff CF, Lammertsma AA, 

Ouwens MD, Diamant M, Boer C. Diabetic cardiomyopathy in 

Zucker diabetic fatty rats: the forgotten right ventricle. J Cardiovasc 

Diabetologia 2010;9:25-32. 

4. Kosmala W, Przewlocka-Kosmala M, Mazurek W. Subclinical 

right ventricular dysfunction in diabetes mellitus-an ultrasonic 

strain/strain rate study. Diabet Med 2007;24:656-663. 

5. Geva T, Powell AJ, Crawford EC, Chung T, Colan SD. Evaluation 

of regional differences in right ventricular systolic function by 

acoustic quantification by echocardiography and cine magnetic 

resonance imaging. Circulation 1998;98:339-345. 

6. Karamitsos TD, Karvounis HI, Dalamanga EG, Papadopoulos 

CE, Didangellos TP, Karamitsos DT, Parharidis GE, Louridas GE. 

Early diastolic impairment of diabetic heart: the significance of 

right ventricle. Int J Cardiol 2007;114:218-223. 

7. Gaber R, Kotb NA. Early diagnosis of right ventricular dysfunction 

in type II diabetes mellitus: value of 3 dimensional strain/strain 

rate. Heart mirror J 2010;4:80-85. 

8. Elshahed GS, Ahmed MI, El-Beblawy NS, Kamal HM, lsmaiel 

MF, Bin Zheidan OAS. Evaluation of right and left ventricular 

systolic and diastolic function in patients with type I diabetes using 

echocardiography and tissue Doppler imaging. Suez Canal Univ 



Case Report 

Surgical Treatment of Amplatzer Embolus in a Secundum 

Atrial Septal Defect Patient 

Ahmet Baris Durukan, MD 1* , Hasan Alper Gurbuz, MD 1 , Murat Tavlasoglu, 

MD 2 , Nevriye Salman, MD 1 , Halil Ibrahim Ucar, MD 1 , Cem Yorgancioglu, 

MD 1 

1 

Medicana International Ankara Hospital, Ankara, Turkey. 

2 

Diyarbakir Military Hospital, Diyarbakir, Turkey. 

Received 18 August 2011; Accepted 23 January 2012 

Abstract 

A secundum atrial septal defect is the most common congenital heart defect. Transcatheter treatment of secundum atrial 

septal defects is a popular and less invasive alternative to surgery. Procedural complications may occur in a wide spectrum, 

particularly device embolus as the most emergent one, but luckily they do not commonly occur in the clinical setting. Mortality 

from adverse events related to transcatheter treatment strategies is twentyfold higher than that of primary elective surgical 

closure. Here, we report an Amplatzer device embolus in a secundum atrial septal defect patient. The device was successfully 

removed with surgery, postoperative course was uneventful, and the patient was discharged from the hospital on the 5 th 

postoperative day. 


This paper should be cited as: Durukan AB, Gurbuz HA, Tavlasoglu M, Salman N, Ucar HI, Yorgancioglu C. Surgical Treatment of 

Amplatzer Embolus in a Secundum Atrial Septal Defect Patient. J Teh Univ Heart Ctr 2012;7(4):182-184. 

Keywords: Heart septal defects, atrial • Septal occluder device • Surgical procedures, operative 

Introduction 

A secundum atrial septal defect (ASD) is the most 

common congenital heart defect, making up 10% of all 

congenital heart defects. Five to ten percent of children and 

30% of adults with congenital heart disease have the ostium 

secundum ASD. 1 ASD closure is indicated to prevent right 

ventricular volume overload due to left-to-right shunting 

over four years of age and to prevent arrhythmias and right 

heart failure in later decades. 2 

Transcatheter treatment of the secundum ASD is a popular 

and less invasive alternative to surgery. By 2008, 30000 

devices had been implanted. 2 Procedural complications 

do exist, luckily very rarely in the clinical setting. These 

complications increase morbidity and mortality rates 

compared to conventional surgical closure. 3 

Here, we report a case with the secundum ASD in which 

the atrial septal occluder device was embolized during the 

transcatheter procedure and was successfully treated with 

surgery. 

Case Report 

A 38-year-old, 160 cm tall, 65 kg woman was referred to 

our hospital with the diagnosis of the secundum ASD. She 

* 

Corresponding Author: Ahmet Baris Durukan, Medicana International Ankara Hospital, Umit Mahallesi 2463.sokak 4/18, 06810, Yenimahalle, 

Ankara, Turkey. Tel: +90 532 2273814. Fax: +90 312 2203170. E-mail: barisdurukan@yahoo.com. 

182

Surgical Treatment of Amplatzer Embolus in a Secundum Atrial Septal Defect Patient 


had initially referred to another hospital with the complaints 

of palpitation and shortness of breath. During cardiologic 

evaluation, echocardiography was performed and a secundum 

type ASD (pulmonary to systemic blood flow ratio [Qp/Qs]: 

2.0), first to second degree mitral regurgitation, and first 

to second degree tricuspid regurgitation were noted. There 

was a mild increase in the right ventricular dimensions. 

Pulmonary artery pressure was measured as 45 mm Hg. In 

our hospital, echocardiography was performed again and 

the anatomy was found suitable for the implantation of an 

ASD occluder device. During catheter closure, the occluder 

device was embolized. The patient was heparinized for 

systemic anticoagulation. It was not possible to retrieve 

the embolized device via catheterization procedures, and 

the patient was referred for emergency surgical removal. 

Surgical intervention was performed within forty-five 

minutes of embolization. The electrocardiogram was normal 

sinus rhythm. On chest X-ray, the ‘Amplatzer occluder 

Device’ was seen in the right pulmonary artery localization 

(Figure 1). 

was closed with a Teflon patch. Right pulmonary arteriotomy 

was performed proximal to the superior vena cava and the 

device was removed (Figures 2 and 3). Arteriotomy was 

closed primarily. The postoperative course was uneventful, 

and the patient was discharged on the 5 th postoperative day. 

Figure 2. Intraoperative image. The right pulmonary artery is opened and 

the septal occluder device (arrow) is being removed through the arteriotomy 

Figure 3. Removed "Amplatzer Occluder Device" 

Figure 1. Preoperative chest X-ray of the patient, performed following device 

embolization. The arrow points very clearly to the septal occluder device 

in the right pulmonary artery 

The patient underwent surgery under general anesthesia 

and with standard median sternotomy incision. There were 

pericardial adhesions. Once the pericardium had been 

opened, the ‘Amplatzer Occluder Device’ was easily palpated 

in the right pulmonary artery proximal to the superior vena 

cava. Cardiopulmonary bypass (CPB) under moderate 

hypothermia was established with aorto-bicaval cannulation 

(selective superior vena cava cannulation was performed). 

Myocardial management was provided by antegrade cold 

and terminal warm blood cardioplegia. Right atriotomy was 

performed. A 2.5 × 1.5 cm secundum type ASD was seen. It 

Discussion 

The approach has shifted from surgical closure to 

transcatheter procedures in the treatment of the secundum 

ASD, which is definitely a less invasive approach. Hospital 

stay is shorter with transcatheter treatment and cosmetic 

results are better. Return to work for adults and return to 

school for children are earlier than those with cardiac surgery. 

Developmental outcome has been reported to be better in 

cases treated with transcatheter procedures. Adverse events 

related with CPB are avoided. 4 Right ventricular functions 

are preserved better. 5 And most importantly, the incidence 

of minor or major complications is lower with transcatheter 

closure. 6 

Procedural complications like device malposition or 

embolization, atrial wall erosion, mitral regurgitation, 



Ahmet Baris Durukan et al. 

cardiac arrhythmia requiring treatment, sciatic nerve 

compression due to retroperitoneal hematoma, prolonged 

time for femoral vein hemostasis, access site hematoma, 

arteriovenous fistula formation, pericardial/pleural 

effusions, and transient ischemic attacks have been 

previously reported. 1, 2 Butera et al. 1 reported 0.7% 

malposition/embolization. Wilson et al. 2 reported device 

embolization in 2 out of 227 patients and one was again 

treated via the transcatheter route. Sarris et al. 7 reviewed 

data from 19 well-known European institutes; and in a 10- 

year period, 56 cases undergoing emergency surgery after 

catheter intervention were reported. Among the 56 cases, 

there were 22 embolization cases and 7 cases were due 

to the pulmonary artery. Surgical removal of the device, 

closure of the defect, and repair/replacement of the damaged 

cardiac structure were performed. Operative mortality was 

5.4%. Based on the EACTS reports, operative mortality 

for primary surgical ASD closure was 0.36% in the same 

time period. 7 Based on the FDA reports, in a 7-year period, 

mortality rates for transcatheter closure were similar to 

those of primary surgical closure (0.13%), but the mortality 

for the surgical management of a device adverse event 

(2.6%) was twentyfold higher than that for primary elective 

ASD closure. 3 

We managed to remove the device in a very short time, and 

the patient was discharged without any further complications. 

of the US Food and Drug Administration Manufacturer and User 

Facility Device Experience database for adverse events involving 

Amplatzer septal occluder devices and comparison with the 

Society of Thoracic Surgery congenital cardiac surgery database. 

J Thorac Cardiovasc Surg 2009;137:1334-1341. 

4. Visconti KJ, Bichell DP, Jonas RA, Newburger JW, Bellinger 

DC. Developmental outcome after surgical versus interventional 

closure of secundum atrial septal defect in children. Circulation 

1999;100:II145-150. 

5. Dhillon R, Josen M, Henein M, Redington A. Transcatheter closure 

of atrial septal defect preserves right ventricular function. Heart 

2002;87:461-465. 

6. Berger F, Vogel M, Alexi-Meskishvili V, Lange PE. Comparison of 

results and complications of surgical and Amplatzer device closure 

of atrial septal defects. J Thorac Cardiovasc Surg 1999;118:674- 

678. 

7. Sarris G, Kirvassilis G, Zavaropoulos P, Belli E, Berggren H, Carrel 

T, Comas JV, Corno AF, Daenen W, Di Carlo D, Ebels T, Fragat J, 

Hamilton L, Hraska V, Jacobs J, Lazarov S, Mavroudis C, Metras 

D, Rubay J, Schreiber C, Stellin G. Surgery for complications of 

transcatheter closure of atrial septal defects: a multi-institutional 

study from the European Congenital Heart Surgeons Association. 

Eur J Cardiothorac Surg 2010;37:1285-1290. 

Conclusion 

Transcatheter device closure of the ASD can lead to serious 

complications despite its advantages over surgical closure. 

But it should be kept in mind that even if most cases are 

successful, not only early, but also late complications may 

occur regardless of the size or type of the current devices. 

Surgical treatment of the complications may be mandatory 

and should be performed immediately, especially in cases 

of embolization. Surgery is quite effective in treatment, 

but it is a fact that operative mortality rises when surgery 

is performed for the treatment of complications. Operative 

mortality is much lower for primary surgical repair. 

References 

1. Butera G, Romagnoli E, Carminati M, Chessa M, Piazza L, Negura 

D, Giamberti A, Abella R, Pome G, Condoluci C, Frigiola A. 

Treatment of isolated secundum atrial septal defects: impact of age 

and defect morphology in 1,013 consecutive patients. Am Heart J 

2008;156:706-712. 

2. Wilson N, Smith J, Prommete B, O’Donnell C, Gentles TL, 

Ruygrok PN. Transcatheter closure of secundum atrial septal 

defects with the Amplatzer septal occluder in adults and childrenfollow-up 

closure rates, degree of mitral regurgitation and 

evolution of arrhythmias. Heart Lung Circ 2008;17:318-324. 

3. DiBardino DJ, McElhinney DB, Kaza AK, Mayer JE, Jr. Analysis 

184


Case Report 


Kyomars Abbasi, MD, Hossein Ahmadi, MD, Arezoo Zoroufian, MD, 

Mohammad Sahebjam, MD, Naghmeh Moshtaghi, MD, Seyed Hessamedin 

Abbasi, MD * 


Received 26 October 2011; Accepted 07 January 2012 

Abstract 

Blunt injury to the chest can affect any one or all components of the chest wall and thoracic cavity. The clinical presentation 

of patients with blunt chest trauma varies widely and ranges from minor reports of pain to florid shock. Traumatic tricuspid 

valve regurgitation is a rare cardiovascular complication of blunt chest trauma. Tricuspid valve regurgitation is usually 

begotten by disorders that cause the right ventricle to enlarge. Diagnosis is made by physical examination findings and is 

confirmed by echocardiography. We report two cases of severe tricuspid regurgitation secondary to the rupture of the chordae 

tendineae of the anterior leaflet following non-penetrating chest trauma. Both patients had uneventful postoperative courses. 


This paper should be cited as: Abbasi K, Ahmadi H, Zoroufian A, Sahebjam M, Moshtaghi N, Abbasi SH. Post-Traumatic Chordae 

Rupture of Tricuspid Valve. J Teh Univ Heart Ctr 2012;7(4):185-187. 

Keywords: Heart rapture • Tricuspid valve • Wounds and injuries 

Introduction 

Blunt thoracic trauma has become a regular occurrence 

courtesy of high-speed motor vehicle accidents, 1 especially 

in the last decade. 2 Such accidents are the principal cause of 

isolated tricuspid valve regurgitation (TR). 3 Traumatic TR 

is a rare cardiovascular complication of blunt chest trauma. 

The most frequently involved valve in blunt chest trauma is 

the aortic valve, followed by the mitral and tricuspid valves. 4 

Traumatic TR is usually well tolerated; 5 however, as far as 

treatment is concerned, the tricuspid valve replacement has 

been the conventional procedure, especially in cases with 

delayed presentation. 6 We herein report two cases of severe 

TR secondary to the rupture of the chordae tendineae of the 

anterior leaflet following non-penetrating chest trauma. 

Case Reports 

Case # 1 

A 28-year-old man was admitted to our hospital suffering 

from exertional dyspnea and palpitation. One year previously, 

he had sustained blunt chest trauma in a car accident, but 

no cardiac abnormality had been noticed at the time. His 

symptoms started about two months before his referral to us. 

At presentation, the patient had a blood pressure of 120/90 

mmHg and pulse of 70 beats/min. The electrocardiogram 

revealed sinus rhythm and right bundle branch block with 

left-axis deviation. Transthoracic echocardiography (TTE) 

demonstrated a normal left ventricle (LV) size, mild LV 

systolic dysfunction, septal motion abnormality due to the 

right ventricle (RV) volume overload, severe RV and right 

* 

Corresponding Author: Seyed-Hesameddin Abbasi, Tehran University of Medical Sciences, Tehran Heart Center, North Kargar Street, Tehran, Iran. 

1411713138. Tel: +98 21 88029720. Fax: +98 21 88029702. E-mail: abbasi@tehranheartcenter.org. 



atrium (RA) enlargement, and finally, severe low pressure 

TR due to the flail anterior leaflet of the tricuspid valve. 

Transesophageal echocardiography (TEE) was conducted 

as a complementary study and confirmed the flail leaflet 

secondary to the ruptured chordae. The patient was, therefore, 

scheduled for tricuspid valve repair. 

The operation was performed through median sternotomy. 

Following the institution of cardiopulmonary bypass (CPB), 

the heart was arrested via cardioplegia and the RA was 

explored: there was chordae rupture of the anterior leaflet. 

The rupture was repaired by first constructing two near 

chordae with 5/0 Gortex suture and then placing edge-toedge 

stitches on the edge of the three leaflets. Additionally, 

ring annuloplasty using a Carpenter (31mm) was performed. 

Postoperative TEE demonstrated mild to moderate TR and 

no significant tricuspid valve stenosis (TS) (tricuspid valve 

mean gradient = 2.5 mm Hg). The patient’s postoperative 

course was uneventful. 

Case # 2 

A 53-year-old man was referred to our hospital because of 

exertional dyspnea. One year previously, he had sustained 

multiple traumas in a bus accident. The accident left him in 

a deep coma for 17 days, after which he suffered a stroke, 

right hemi-paresis, and aphasia due to infarction in the left 

temporal lobe. Also, he had fractures in the left femoral 

bone, left tibia bone, right hand, and two ribs on the superior 

right side. At the time, no cardiac symptoms were detected 

but the patient was subjected to splenectomy. 

On admission, the electrocardiogram showed sinus rhythm, 

right bundle branch block with left-axis deviation. TTE 

revealed a normal LV size with mildly reduced LV systolic 

function, abnormal septal motion due to the RV volume 

overload, severe RV and RA enlargement with mild RV 

systolic dysfunction, and flail anterior tricuspid valve leaflet 

with severe low pressure TR. In addition, a large, mobile 

filamentous mass was detected on the tip of the flail leaflet, in 

favor of ruptured chordae. These findings were all confirmed 

by preoperative TEE, which also demonstrated an aneurismal 

inter-atrial septum with a small secondary type of atrial septal 

defect (ASD). Cardiac catheterization showed a small left-toright 

shunt with no evidence of coronary artery disease. 

Intraoperatively, the chest was explored via median 

sternotomy. CPB was instituted, the heart was arrested by 

cardioplegia, and the RA was explored. The anterior papillary 

muscle was ruptured, resulting in the prolapse of the anterior 

tricuspid leaflet. The De Vega technique was applied to the 

tricuspid annulus. Pledgeted 4/0 Prolene suture was used for 

the reconstruction of the anterior tricuspid valve papillary 

muscle to scar tissue in the base of the papillary muscle. 

Linear repair was thereafter performed for the closure of 

the ASD. Saline test was carried out next and the result was 

Kyomars Abbasi et al. 

so optimal that it obviated the need for TEE. Postoperative 

TTE revealed mild RV enlargement with mild systolic 

dysfunction. Doppler and contras study showed mild TR and 

no residual shunt flow. 

The patient made an uneventful recovery. One year after 

surgery now, the patient is well and asymptomatic with 

trivial TR on echocardiography. 

Discussion 

Traumatic TR is a rare sequela in the wake of blunt thoracic 

trauma. The most likely cause is compression, decompression, 

or deceleration of the thorax. These mechanisms give rise to 

intraventricular pressure peaks, which in combination with a 

closed valve and the systolic pressure in the RV most often 

affect the chordae tendineae and the papillary muscles. 1 

TR frequently goes undiagnosed at blunt chest trauma 

because of its asymptomatic nature; sometimes several 

or even more than ten years elapse before a diagnosis is 

made. 7-10 Nevertheless, severe TR eventually leads to right 

ventricular dilatation and progressive right heart failure, 

even if it is associated with no pulmonary hypertension. 6 The 

clinical course of TR following blunt chest trauma varies 

largely. Little is known about the clinical course of isolated 

ruptured chordae tendineae. Indeed, the only detailed case to 

have been reported thus far is that by Kleikamp et al., whose 

patient developed TR due to ruptured chordae tendineae of 

the anterior leaflet seven years after a blunt chest trauma, 

which was surgically corrected. 1 It is deserving of note 

that the rupture of the chordae tendineae is believed to be 

the consequence of an acute increase in the RV pressure 

associated with a closed tricuspid valve. 11 

Conclusions 

The two cases presented herein demonstrate that the 

rupture of the chordae tendineae of the tricuspid valve could 

be another cause of TR following blunt chest trauma. This 

is, however, a condition that can be repaired surgically 

without the need for valve replacement. Advances in 

echocardiography have enabled earlier diagnosis and ergo 

more effective treatment. 

We recommend that physicians working at emergency 

departments be on the alert for this potential complication 

of non-penetrating chest trauma and subject all patients 

admitted to the emergency department due to blunt chest 

trauma to TTE or TEE for accurate diagnosis. 

References 

1. Kleikamp G, Schnepper U, Körtke H, Breymann T, Körfer R. 

186



Tricuspid valve regurgitation following blunt thoracic trauma. 

Chest 1992;102:1294-1296. 

2. Lin SJ, Chen CW, Chou CJ, Liu KT, Su HM, Lin TH, Voon WC, 

Lai WT, Sheu SH. Traumatic tricuspid insufficiency with chordae 

tendinae rupture: a case report and literature review. Kaohsiung J 

Med Sci 2006;22:626-629. 

3. Nelson M, Wells G. A case of traumatic tricuspid valve 

regurgitation caused by blunt chest trauma. J Am Soc Echocardiogr 

2007;20:198.e4-5. 

4. Colombo T, Russo C, Ciliberto GR, Lanfranconi M, Bruschi G, 

Agati S, Vitali E. Tricuspid regurgitation secondary to mitral valve 

disease: tricuspid annulus function as guide to tricuspid valve 

repair. Cardiovasc Surg 2001;9:369-377. 

5. Noera G, Sanguinetti M, Pensa P, Biagi B, Cremonesi A, Lodi R, 

Lessana A, Carbone C. Tricuspid valve incompetence caused by 

nonpenetrating thoracic trauma. Ann Thorac Surg 1991;51:320- 

322. 

6. Fujiwara K, Hisaoka T, Komai H, Nishimura Y, Yamamoto 

Sh, Okamura Y. Successful repair of traumatic tricuspid valve 

regurgitation. Jpn J Thorac Cardiovasc Surg 2005;53:259-262. 

7. Gayet C, Pierre B, Delahaye JP, Champsaur G, Andre-Fouet X, 

Rueff P. Traumatic tricuspid insufficiency. An underdiagnosed 

disease. Chest 1987;92:429-432. 

8. van Son JA, Danielson GK, Schaff HV, Miller FA, Jr. Traumatic 

tricuspid valve insufficiency. Experience in thirteen patients. J 

Thorac Cardiovasc Surg 1994;108:893-898. 

9. Holper K, Hahnel C, Augustin N, Meisner H. Operative correction 

of traumatic tricuspid insufficiency. Herz 1996;21:172-178. 

10. Maisano F, Lorusso R, Sandrelli L, Torracca L, Coletti G, La Canna 

G, Alfieri O. Valve repair for traumatic tricuspid regurgitation. Eur 

J Cardiothorac Surg 1996;10:867-873. 

11. dos Santos J, Jr, de Marchi CH, Bestetti RB, Corbucci HA, 

Pavarino PR. Ruptured chordae tendineae of the posterior leaflet of 

the tricuspid valve as a cause of tricuspid regurgitation following 

blunt chest trauma. Cardiovasc Pathol 2001;10:97-98. 



Case Report 

Late Diagnosis of Large Left Ventricular Pseudoaneurysm 

after Mitral Valve Replacement and Coronary Artery 

Bypass Surgery by Real-Time Three-Dimensional 

Echocardiography 

Mohammad Sahebjam, MD * , Abbas Salehiomran, MD, Neda Ghaffari-Marandi, 

MD, Azam Safir, MD 


Abstract 

One of the most serious complications of mitral valve replacement is left ventricular rupture and pseudoaneurysm 

formation, which is rare but potentially lethal. We herein present a late type of post mitral valve replacement and coronary 

artery bypass surgery pseudoaneurysm in a 74-year-old female, who was admitted to our hospital with a recent history of 

exertional dyspnea. She had the above-mentioned operation 10 months before. The diagnosis was made via two-dimensional 

and real-time three-dimensional transthoracic echocardiography. The prosthetic mitral valve was removed, and the large 

orifice of the pseudoaneurysm was closed by surgery. At one year's follow-up, the patient was in good condition. 


Received 17 August 2011; Accepted 04 February 2012 

This paper should be cited as: Sahebjam M, Salehiomran A, Ghaffari-Marandi N, Safir A. Late diagnosis of Large Left Ventricular 

Pseudoaneurysm after Mitral valve Replacement and Coronary Artery Bypass Surgery by Real-Time Three-Dimensional Echocardiography. 

J Teh Univ Heart Ctr 2012;7(4):188-190. 

Keywords: Echocardiography, three-dimensional • Mitral valve • Aneurysm, false 

Introduction 

One of the most serious complications of mitral valve 

replacement (MVR) is the left ventricular (LV) rupture and 

pseudoaneurysm formation, which is rare but potentially 

lethal. 1-4 According to the time of the LV rupture, it is 

classified into three categories: early; delayed; and late 

ruptures. Early types are those that happen in the operating 

room after cardiopulmonary bypass discontinuation, 

delayed types are events which occur several hours or days 

after surgery, and late ruptures are cases that happen days 

to years after MVR. 1, 2 Because of the high propensity of 

the pseudoaneurysm to enlargement and rupture, immediate 

surgical management is inevitable. 3-5 We report a case 

with a late diagnosis of the LV pseudoaneurysm following 

previous MVR and coronary artery bypass graft surgery 

(CABG), which was diagnosed via two-dimensional and 

real-time three-dimensional transthoracic echocardiography 

(RT 3D TTE). 

Case Report 

A 74-year-old female with a history of coronary artery 

* 

Corresponding Author: Mohammad Sahebjam, Assistant Professor of Cardiology, Echocardiography Department, Tehran Heart Center, Jalal Al 

Ahmad and North Kargar Intersection, Tehran, Iran. 1411713138. Tel: +98 21 88029600. Fax: +98 21 88029731. E-mail: msahebjam@yahoo.com. 

188

Late Diagnosis of Large Left Ventricular Pseudoaneurysm after Mitral Valve ... 

disease was admitted to our hospital with a history of 

exertional dyspnea (function class II) during recent 

months. She had a past history of CABG and MVR surgery 

approximately 10 months prior to her admission. 

The postoperative echocardiography, performed one 

week after surgery, showed mild LV hypertrophy with an 

ejection fraction of 50%, a prosthetic MV with an acceptable 

gradient, and a normal right ventricle size with a good 

systolic function. 

On present admission, the patient’s pulse rate was 90 per 

minute and regular, and her blood pressure was 130/70 mm 

Hg. The patient had 1+ edema in her lower limbs. Auscultation 

revealed fine crackles in both lung bases and III/VI systolic 

murmur. An electrocardiogram (ECG) showed left bundle 

branch block and inverted T wave in V5-V6 leads. 

TTE showed a large echolucent space with a narrow neck 

(about 1.8 - 2 cm in diameter) on the basal posterolateral portion 

of the LV (near the prosthetic MV) and the diameter of the 

cavity was about 70 mm, suggestive of a large pseudoaneurysm 

in the basal posterolateral portion of the LV with a to-and-fro 

flow on color Doppler (Figures 1 and 2). RT 3D TTE (Vivid 7 

/ GE / RT 3D probe) was performed in order to better reveal 

the spatial relations between the pseudoaneurysm and the 

adjacent cardiovascular and thoracic structures and to better 

delineate the pseudoaneurysm borders before surgery. RT 3D 

TTE showed a large pseudoaneurysm (80 × 52 mm), parallel 

to the free wall of the LV (Figure 3). Its orifice was about 20 

mm and was very close to the MV annulus. 


prosthetic MV was removed. In the posterolateral aspect of 

the LV just below the annulus of the MV, the large orifice 

of the pseudoaneurysm (about 20 mm in diameter) was 

found, which was closed with a pericardial patch (Figure 

4). After the closure of the defect, MVR with a bileaflet 

mechanical valve (St. Jude # 27) was performed and the 

patient was weaned from CPB without problems. Post-pump 

intraoperative transesophageal echocardiography confirmed 

the complete closure of the orifice of the pseudoaneurysm 

without a flow. The postoperative course was acceptable and 

the patient was discharged on 10 th postoperative day. TTE 

was performed before discharge and showed the prosthetic 

MV with an acceptable gradient, without paravalvular leak 

and a large echomixed cavity (7 × 3.8 cm) due to a previous 

pseudoaneurysm posterolateral to the LV, which was filled 

by a clot. At one year's follow-up, the patient was in good 

condition and was taking oral medications. 

Figure 2. Two-dimensional color Doppler echocardiography, showing 

a turbulent flow on the orifice of the pseudoaneurysm (arrow) and the 

pseudoaneurysm (asterisk) 

Figure 1. Two-dimensional echocardiography, showing the orifice of 

the pseudoaneurysm near the mitral valve sewing ring (arrow) and the 

pseudoaneurysm (asterisk) 

The patient underwent urgent surgery through median 

sternotomy using cardiopulmonary bypass. After mid 

sternotomy and moderate hypothermia (28 °C), the left 

atrium was opened. The prosthetic MV (St Jude # 27) 

remained intact, but the orifice of the LV pseudoaneurysm 

was unclear when visualized through the St Jude valve. The 

Figure 3. Three-dimensional echocardiography, showing the orifice of the 

pseudoaneurysm (arrow) and the pseudoaneurysm (asterisk) 



Mohammad Sahebjam et al. 

important for the operative approach plan. 

Conclusion 

The LV pseudoaneurysm is an important complication that 

may occur late after MVR and thus necessitates due heed on 

the part of cardiologists and cardiac surgeons. 

References 

Figure 4. The operation site. The black arrow points to the pseudoaneurysm 

orifice (PS) and the white arrow to the prosthetic mitral valve (MV) 

Discussion 

Rupture of the LV wall after MVR, albeit infrequent, 

is a fatal complication, especially in the delayed class. 4, 

6, 7 

The most frequent cause of the LV pseudoaneurysm is 

myocardial infarction secondary to atherosclerotic coronary 

artery disease, but many other causes may be responsible 

for the LV pseudoaneurysm such as trauma, infective 

endocarditis, inflammation, and cardiac surgery. 8 Congestive 

heart failure is the most common clinical presentation of the 

LV pseudoaneurysm but the rate of asymptomatic patients is 

more than 10%. 9 For the first time, Spellberg and O’Reilly 

reported post-MVR pseudoaneurysm, which was diagnosed 

via left ventriculography. 10 Two third of the LV ruptures are 

the early type, and the mortality rate of this category reaches 

near 50% despite early management. 10 Classification of 

the post-MVR pseudoaneurysm may be based on the time 

and location of the rupture. 1 Miller and co-workers also 

classified the LV pseudoaneurysm based on the location of 

the LV rupture and its relative location to the MV annulus. 10 

In patients with congestive heart failure symptoms, the 

mortality rate is high, particularly without surgery. One 

of the previous case series study reported 11 deaths in 35 

patients in non-operated cases with pseudoaneurysms. 9 

The initial technique for the diagnosis of postoperative 

complications is TTE. 1 Proper anatomic delineation is 

essential in order to plan appropriate therapy. Contrary 

to the post-myocardial infarction cases, these aneurysms 

following MVR tend to be sub-annular in location. 11 

Previously, pseudoaneurysm diagnosis was made by left 

ventriculography, while echocardiography and Cardiac 

Computed Tomography (CT) can be the other diagnostic 

approaches for these cases. 11 

The usage of RT 3D TTE in this case conferred better 

delineation of the pseudoaneurysm territory, which is 

1. Biyikoglu SF, Guray Y, Turkvatan A, Boyaci A, Katircioglu F. 

A serious complication late after mitral valve replacement: left 

ventricular rupture with pseudoaneurysm. J Am Soc Echocardiogr 

2008;21:1178.e1-3. 

2. Ono M, Wolf RK. Left ventricular pseudoaneurysm late after 

mitral valve replacement. Ann Thorac Surg 2002;73:1303-1305. 

3. Suda H, Ikeda K, Doi K, Shiraishi R, Furukawa K, Ito T. Successful 

repair of left ventricular pseudoaneurysm after mitral reoperation 

under hypothermic circulatory arrest. Jpn J Thorac Cardiovasc 

Surg 2003;51:18-20. 

4. Choi JB, Choi SH, Oh SK, Kim NH. Left ventricular 

pseudoaneurysm after coronary artery bypass and valve 

replacement for post-infarction mitral regurgitation. Tex Heart Inst 

J 2006;33:505-507. 

5. Nekkanti R, Nanda NC, Ansingkar KG, McGiffin DC. 

Transesophageal three-dimensional echocardiographic 

assessment of left ventricular pseudoaneurysm. Echocardiography 

2002;19:169-172. 

6. Kupari M, Verkkala K, Maamies T, Härtel G. Value of combined 

cross sectional and Doppler echocardiography in the detection of 

left ventricular pseudoaneurysm after mitral valve replacement. Br 

Heart J 1987;58:52-56. 

7. Honda K, Okamura Y, Nishiharu Y, Hayashi H. Patch repair 

of a giant left ventricular pseudoaneurysm after mitral valve 

replacement. Ann Thorac Surg 2011;91:1596-1597. 

8. Mahilmaran A, Nayar PG, Sheshadri M, Sudarsana G, Abraham 

KA. Left ventricular pseudoaneurysm caused by coronary spasm, 

myocardial infarction, and myocardial rupture. Tex Heart Inst J 

2002;29:122-125. 

9. Leitman M, Shmueli R, Stamler A, Krakover R, Hendler A, 

Vered Z. An unusual presentation of a large left ventricular 

pseudoaneurysm. Echocardiography 2006;23:403-404. 

10. Lanjewar C, Thakkar B, Kerkar P, Khandeparkar J. Submitral left 

ventricular Pseudoaneurysm after mitral valve replacement: early 

diagnosis and successful repair. Interact Cardiovasc Thorac Surg 

2007;6:505-507. 

11. Yeo TC, Malouf JF, Oh JK, Seward JB. Clinical profile and 

outcomein 52 patients with cardiac pseudoaneurysm. Ann Intern 

Med 1998;128:299-305. 

190


Letter to the Editor 

A Memorandum of "World 

Heart Day 2012": Myocardial 

Infarction Mortality in Women 

in Birjand, 2008-2009 

September 29th, 2012 is entitled "World Heart Day" and 

the theme of the current year is "One World, One Heart, One 

Home, and Focus on Women and Children". 

Cardiovascular diseases are the most common causes of 

mortality in women and men. 1 Various studies have probed 

into the differences in the clinical symptoms, risk factors, 

and prognoses between male and female patients with acute 

myocardial infarction (AMI). 2 

One study on AMI patients in Birjand, Iran (2008-2009) 

reported the following results: 

Out of 471 patients, 136 (28.9%) cases were women 

and 335 (71.1%) were men. The mean age of the females 

and males was 64.6 ± 13.6 years and 61.4 ± 13.95 years, 

respectively; p value = 0.001.The most prevalent cardiac risk 

factors in the women and men were hypertension (54.4% 

in women, 32.2% in men; p value < 0.001), dyslipidemia 

(30.1% in women, 18.5% in men; p value = 0.006), diabetes 

mellitus (18.4% in women, 14.9% in men; p value = 0.35), 

and smoking (3.7% in women, 22.7% in men; p value = 

0.04). 

Table 1 shows that the consumption of Aspirin and beta 

blockers was lower in the women than in the men, but 

there was no other difference between the two genders with 

respect to other treatments. In-hospital mortality was 11.5%: 

8.4% in the men and 19.1% in the women (p value = 0.001). 

One-month mortality was 12.9%; it was significantly higher 

in the women than in the men (22.1% in women, 9.2% in 

men; p value ≤ 0.001). Finally, in-hospital mortality and 

one-month mortality after AMI were significantly higher in 

the women. 

Factors such as old age, higher prevalence of diabetes 

mellitus and hypertension, delayed referral of women to 

physicians, and difference in clinical symptoms can be play 

a decisive role in this regard. 3 Indeed, women do not tend to 

deem cardiovascular diseases as their most fatal disease and 

thus fail to take their risk factors into consideration; that is 

why cardiovascular diseases are diagnosed later in women 

and are more acute. It is, therefore, necessary that educational 

programs be devised to raise women's knowledge about 

these fatal diseases. 

Table 1. Comparison of drug therapy in patient with acute myocardial 

infarction (AMI) according to sex 

Drug 

Female 

n (%) 

Male 

n (%) 

P value 

Beta-blocker 77 (56.6) 222 (66.3) 0.04 

ASA 107 (78.7) 302 (90.1) 0.01 

Statins 74 (54.4) 213 (63.6) 0.06 

ACE-I 40 (29.4) 105 (31.3) 0.68 

Streptokinase 12 (8.8) 46 (13.7) 0.14 

Clopidogrel 27 (19.9) 90 (26.9) 0.11 

Nitrate 104 (76.5) 280 (83.6) 0.07 

ASA, Acetylsalicylic acid; ACE-I, Angiotensin-converting enzyme 

inhibitors 

References 

1. Kazemi T, Sharifzadeh GR, Zarban A, Fesharakinia A, Rezvani 

MR, Moezy SA. Risk factors for premature myocardial infarction: 

a matched case-control study. J Res Health Sci 201;11:77-82. 

2. Abbasi SH, Kassaian SE. Women and coronary artery disease. Part 

I: basic considerations. J Teh Univ Heart Ctr 2011;6:109-116. 

3. Hosseini SK, Soleimani A, Karimi AA, Sadeghian S, Darabian S, 

Abbasi SH, Ahmadi SH, Zoroufian A, Mahmoodian M, Abbasi 

A. Clinical features, management and in-hospital outcome of ST 

elevation myocardial infarction (STEMI) in young adults under 40 

years of age. Monaldi Arch Chest Dis 2009;72:71-76. 

Toba Kazemi, MD 

Associate Professor of Cardiology, 

Birjand Atherosclerosis and Coronary Artery Research Center, 

Department of Cardiology, 

Birjand University of Medical Sciences (BUMS), 

Valiassr Hospital, Ghafari Avenue, 

Birjand, Iran. 

9717964151. 

Tel: +98 56 14443001-9. 

Fax: +98 56 14433004. 

E-mail: drtooba.kazemi@gmail.com. 

Gholam Reza Sharifzadeh, MSc 

Epidemiologist, 

Birjand University of Medical Sciences (BUMS), 

Pasdaran Avenue, 

Birjand, Iran. 

9717964151. 

Tel: +98 56 14443001-9. 

Fax: +98 56 14433004. 

E-mail: rezamood@yahoo.com. 



Photo Clinic 

Ball in Chest 

Mohammad Bagher Rahim, MD, Mohammad Hossein Mandegar, MD, 

Farideh Roshanali, MD * 

Shariati General Hospital, Tehran University of Medical Sciences, Tehran, Iran. 

A 50-year-old male underwent a check-up for an insurance company. Chest X-ray revealed a large ball-like lesion in the 

posterior mediastinum. The finding was confirmed by computed tomography (CT) scan (Figure 1). The patient was referred 

to our center, where he had a successful mass removal surgery (Figure 2). Pathology identified the mass as neurinoma. 

A 

B 

Figure 1. Chest X-ray (A) and computed tomography (CT) 

scan (B), revealing a large ball-like lesion in the chest (arrows) 

Figure 2. The removed mass 

J Teh Univ Heart Ctr 2012;7(4):192 

This paper should be cited as: Rahim MB, Mandegar MH, Roshanali F. Ball in Chest. J Teh Univ Heart Ctr 2012;7(4):192. 

Keywords: Mass chest X-Ray • Thorax • Neoplasms 

* 

Corresponding Author: Farideh Roshanali, Shriati Hospital, North Kargar Street, Tehran, Iran. Tel: +98 912 3093151. Fax: +98 21 88797353. 

E-mail: farideh_roshanali@yahoo.com. 

192


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Turkey 

14-16 November 2012 

Barcelona 

Spain 

http://www.essr2012.com/ 

http://www.asci2012.org 

www.wscts.org 

www.ests.org 

http://pennstatehershey.org/web/pedscpb/ 

home 

http://www.asaio.com 

http://www.TheNewOrleansConference. 

com 

http://www.roboticsurg301.net 

http://www.scandinavian-ats.org/ 

http://www. 

georgiahealthcardiacconference.com/ 



http://www.tkdcd.org 

http://thoracicsurgery2012.org/


INTERNATIONAL CARDIOVASCULAR MEETING 

AND CONGRESSES CALENDER (2012) 

Title Location Start Date End Date 

3rd Asia PCR/ SingLive 2012 

Singapore 

Republic of Singapore 

12 January 2012 


ISET 2012: International Symposium on Endovascular 

Therapy 

Miami Beach, Florida 

United States 



44th Ten-Day International Teaching Seminar on 

Cardiovascular Disease Epidemiology and Prevention 

Cape Town 

South Africa 



Ninth Gulf Heart Association Conference 

Muscat 

Oman 



22nd Annual Echo Hawaii 2012 

Big Island, HI 

United States 



6th Middle East Cardiovascular Congress & IVth 

International Congress of Cardiovascular Imaging 

Dubai 

UAE 



33rd Annual Seminar of The American Academy of 

Cardiovascular Perfusion 

New Orleans, Louisiana 

United States 



19th Annual Arrhythmias & the Heart: A Cardiovascular 

Update 

Kauai 

Hawaii 


03 February 2012 

31st Annual Scientific Meeting of the Belgian Society of 

Cardiology 

Brussels 

Belgium 



International Congress on Personalized Medicine: Up 

Close and Personalized (UPCP 2012) 

Florence 

Italy 



APCHF 2012 

6th Asian Pacific Congress of Heart Failure 

Chiang Mai 

Thailand 



Cardiovascular Research Technologies (CRT) 2012 

Washington DC 

United States 






Vascular Care 2012: New Technologies and Emerging 

Therapies 

Truckee, CA 

United States 



37th Annual Cardiovascular Conference at Snowbird 

Snowbird, UT 

United States 



Gulf Heart Association & Saudi Heart Association Annual 

Conference 

Riyadh 

Saudi Arabia 



10th International Kawasaki Disease Symposium 

Kyoto 

Japan 



13th International Forum for the Evaluation of 

Cardiovascular Care 

Nice 

France 



Icon 2012- International Congress for Endovascular 

Specialists 

Scottsdale, Arizona 

United States 



12th Annual International Symposium on Congenital Heart 

Disease (CHD) 

Florida 

United States 



11th Genoa Meeting on Hypertension, Diabetes and Renal 

Disease 

Genoa 

Italy 



2nd Annual Case Based Approach to Controversies in 

Cardiovascular Disease 

Dubai 

UAE 



Cardiovascular Disease Prevention 2012: Tenth Annual 

Comprehensive Symposium 

Miami Beach, Florida 

United States 



17th Annual Cardiology at Cancun: Topics in Clinical 

Cardiology: Focus on Heart Failure 

Cancun 

Mexico 


02 March 2012 

NCVH Latin America 

An International Approach to Lower Limb Interventions 

San Jose 

Costa Rica 


01 March 2012 

The Future of Genomic Medicine V 

La Jolla, California 

United States 

01 March 2012 

02 March 2012 

International Conference on Heart & Brain 

Paris 

France 

01 March 2012 

03 March 2012 

8th International Congress of Update in Cardiology and 

Cardiovascular Surgery 

Antalya 

Turkey 

01 March 2012 

04 March 2012 

2012 Hypertension Congress 

Cape Town 

South Africa 

03 March 2012 

05 March 2012 

Interventional Cardiology 2012: 27th Annual International 

Symposium 

Snowmass Village, CO 

United States 

04 March 2012 

09 March 2012 

10th National Congress of the Italian Society for 

Cardiovascular Prevention SIPREC 

Napoli 

Italy 

08 March 2012 

10 March 2012 

9th Mediterranean Meeting on Hypertension and 

Atherosclerosis 

Antalya 

Turkey 

14 March 2012 

18 March 2012 

12th Annual Spring Meeting on Cardiovascular Nursing 

Copenhagen 

Denmark 

16 March 2012 

17 March 2012 

76th Annual Scientific Meeting of the Japanese Circulation 

Society 

Fukuoka 

Japan 

16 March 2012 

18 March 2012 

The Houston Aortic Symposium - Frontiers in Cardiovascular 

Diseases: The Fifth in the Series 

Houston, TX 

United States 

22 March 2012 

24 March 2012



61st Annual American College of Cardiology Scientific 

Sessions 

Chicago 

United States 

24 March 2012 

27 March 2012 

Frontiers in CardioVascular Biology 2012 

London 


30 March 2012 

01 April 2012 

Cardiology in the Young 2012 

London 


02 April 2012 

04 April 2012 

German Society of Cardiology 78th Annual Meeting 2012 

(DGK 2012) 

Manheim 

Germany 

11 April 2012 

14 April 2012 

34th Charing Cross International Symposium 

London 


14 April 2012 

17 April 2012 

Arteriosclerosis, Thrombosis and Vascular Biology 2012 

Scientific Sessions 

Chicago, IL 

United States 

18 April 2012 

20 April 2012 

World Congress of Cardiology Scientific Sessions 

Dubai 

UAE 

18 April 2012 

21 April 2012 

18th Annual Interventional Cardiology Fellows Course 

Miami, FL 

United States 

19 April 2012 

22 April 2012 

7th Clinical Update on Cardiac MRI & CT 

Cannes 

France 

20 April 2012 

22 April 2012 

Portuguese Society of Cardiology 33rd Congress 2012 (SPC 

2012) 

Vilamoura 

Portugal 

22 April 2012 

24 April 2012 

Angioplasty Summit Transcatheter Cardiovascular 

Therapeutics Asia Pacific 2012 

Seoul 

Korea 

25 April 2012 

27 April 2012 

22nd European Meeting On Hypertension and 

Cardiovascular Protection 

London 


26 April 2012 

29 April 2012 

Concepts in Contemporary Cardiovascular Medicine 2012 

Houston, TX 

United States 

01 May 2012 

04 May 2012 

EuroPRevent 2012 

Dublin 

Ireland 

03 May 2012 

05 May 2012 

APSC Intervention and Imaging 2012 Subspecialty Congress 

Taipei 

Taiwan 

04 May 2012 

06 May 2012 

Taiwan Society of Cardiology 

Annual Convention & Scientific Sessions 

Taipei 

Taiwan 

05 May 2012 

06 May 2012 

Quality of Care and Outcomes Research in Cardiovascular 

Disease and Stroke 2012 Scientific Sessions 

Atlanta, GA 

United States 

9 May 2012 

9 May 2012 

SCAI 2012 Scientific Sessions 

Las Vegas 

United States 

09 May 2012 

12 May 2012 

Heart Rythm 2012 

Boston 

United States 

09 May 2012 

12 May 2012 

EuroPCR 2012 

Paris 

France 

15 May 2012 

18 May 2012 

Metabolic Syndrome, Type II Diabetes and Atherosclerosis 

Marrakesh 

Morocco 

16 May 2012 

20 May 2012 

2nd International Congress on Cardiac Problems in 

Pregnancy (CPP 2012) 

Berlin 

Germany 

17 May 2012 

20 May 2012 




Heart Failure Congress 2012 

Belgrade 

Serbia 

19 May 2012 

22 May 2012 

EAS 2012, the 80th European Atherosclerosis Society 

Congress 

Milan 

Italy 

25 May 2012 

28 May 2012 

New Cardiovascular Horizons 13th Annual Conference 

New Orleans 

United States 

06 June 2012 

09 June 2012 

6th Congress of the Asian Society of Cardiovascular 

Imaging 

Bangkok 

Thailand 

07 June 2012 

09 June 2012 

15th Annual 2011 Live Symposium of Complex Coronary 

and Vascular Cases 

C3 Complex Cardiovascular Catheter Therapeutics- 

Advanced Endovascular and Coronary Intervention 

Global Summit 2012 

New York, NY 

United States 

Orlando, FL 

United States 

13 June 2012 

19 June 2012 

16 June 2012 

23 June 2012 

The iCi 2012 - imaging in cardiovascular interventions 

Frankfurt 

Germany 

27 June 2012 

27 June 2012 

CSI 2012- European congress on congenital and structural 

interventions 

Frankfurt 

Germany 

28 June 2012 

30 June 2012 

The 9th Tunisian European Days of cardiology practice 

Hammam Sousse 

Tunisia 

28 June 2012 

30 June 2012 

25th World Congress of the International Union of 

Angiology 

Prague 

Czech Republic 

01 July 2012 

05 July 2012 

15th Annual Cardiothoracic Update and TEE Board 

Review 

South Carolina 

United States 

05 July 2012 

08 July 2012 

International Society for the Study of Hypertension in 

Pregnancy 18th World Congress 2012 (ISSHP 2012) 

Geneva 

Switzerland 

09 July 2012 

12 July 2012 

19th ASEAN Federation of Cardiology Congress 2012 

Singapore 

Republic of Singapore 

13 July 2012 

15 July 2012 

Basic Cardiovascular Sciences 2012 Scientific Sessions 

New Orleans, LA 

United States 

23 July 2012 

26 July 2012 

Ten-Day Seminar on the Epidemiology and Prevention 

of Cardiovascular Disease 

Tahoe City, CA 

United States 

22 July 2012 

03 August 2012 

6th Annual Australian and New Zealand Endovascular 

Therapies Meeting 2012 (Anzet 2012) 

Brisbane 

Australia 



60th Annual Scientific Meeting of the Cardiac Society of 

Australia and New Zealand (CSANZ 2012) 

Brisbane 

Australia 



European Society of Cardiology Congress 2012 

Munich 

Germany 



CIRSE 2012 /Cardiovascular and Interventional 

Radiological Society of Europe 

Lisbon 

Portugal 

15 September 2012 


High Blood Pressure Research 2012 Scientific Sessions 

Washington DC 

United States 



Hypertension Sydney 2012 

Sydney 

Australia 


04 October 2012 

28th Annual Echocardiography in Pediatric and Adult 

Congenital Heart Disease 

Rochester, MN 

United States 

07 October 2012 

10 October 2012


Information for Authors 

The first three consecutive issues of "The Journal of Tehran University Heart Center" were published under the title of 

"The Journal of Tehran Heart Center" with ISSN: 1735-5370. From the fourth issue onward, however, the journal has been 

entitled ‘’The Journal of Tehran University Heart Center" with ISSN:1735-8620. 

Scope of the journal 

"The Journal of Tehran University Heart Center" aims to publish the highest quality material, both clinical and scientific, 

on all aspects of Cardiovascular Medicine. It includes articles related to research findings, technical evaluations, and reviews. 

In addition, it provides a forum for the exchange of information on all aspects of Cardiovascular Medicine, including 

educational issues. "The journal of Tehran University Heart Center" is an international, English language, peer reviewed 

journal concerned with Cardiovascular Medicine. It is an official journal of the Cardiovascular Research Center of the Tehran 

University of Medical Sciences (in collaboration with the Iranian Society of Cardiac Surgeons) and is published quarterly. 

Papers submitted to this journal which do not adhere to the Instructions for Authors will be returned for appropriate revision 

to be in line with the Instructions for Authors. They may then be resubmitted. Submission of an article implies that the work 

described has not been published previously (except in the form of an abstract or as part of a published lecture or academic 

thesis), that it is not under consideration for publication elsewhere, that its publication is approved by all Authors and tacitly 

or explicitly by the responsible authorities where the work was carried out, and that, if accepted, it will not be published 

elsewhere in the same form, in English or in any other language, without the written consent of the publisher. 

Article Categories 

The Journal of Tehran University Heart Center” accepts the following categories of articles:” 

Guest Editorial 


Clinical and pre-clinical papers based on either normal subjects or patients and the result of cardiovascular pre-clinical 

research will be Considered for publication provided they have an obvious clinical relevance. 

Brief communication 

Case report 


"The Journal of Tehran University Heart Center" publishes a limited number of scholarly, comprehensive reviews whose 

aims are to summarize and critically evaluate research in the field addressed and identify future implications. Reviews should 

not exceed 5000 words. 

Letter to editor 

Letters to the editor must not exceed 500 words and should focus on a specific article published in "The Journal of 

Tehran University Heart Center" within the preceding 12 weeks. No original data may be included. Authors will receive prepublication 

proofs, and the authors of the article cited invited to reply. 

Submission of manuscripts 

Four double spaced copies on 8 1/2 × 11 in. paper should be sent to: 

Dr. A. Karimi, 

Editor in Chief, 

"The Journal of Tehran University Heart Center", 

Tehran Heart Center, 

North Kargar Street, 



Tehran, Iran. 

1411713138. 

Photocopies or good reproductions of illustrations are acceptable only on the spare copies. Included also should be a set 

of the electronic files of the manuscript on floppy - disk or CD-ROM. For preparation of electronic files, see the instructions 

herein below. 

Also, manuscripts can be submitted electronically via the journal’s website: http://jthc.tums.ac.ir. On-line submission 

allows the manuscript to be handled in electronic forms throughout the review process. 

Review of manuscripts 

All manuscripts correctly submitted to will first be reviewed by the Editors. Some manuscripts will be returned to authors 

at this stage if the paper is deemed inappropriate for publication in “The Journal of Tehran University Heart Center”, if the 

paper does not meet submission requirements, or if the paper is not deemed to have a sufficiently high priority. All papers 

considered suitable by the Editors to progress further in the review process will undergo appropriate peer review and all 

papers provisionally accepted for publication will undergo a detailed statistical review. 

Preparation of manuscripts 

All submitted manuscripts must not exceed 5000 words, including References, Figure Legends and Tables. The number of 

Tables, Figures and References should be appropriate to the manuscript content and should not be excessive. Authors should 

comply with the manuscript formatting and the ethical conventions of the “Uniform Requirements for Manuscripts Submitted 

to Biomedical Journals” issued by the International Committee of Medical Journal Editors ( http://www.icmje.org ). 

Style and spelling 

Authors whose first language is not English are requested to have their manuscripts checked carefully before submission. 

This will help expedite the review process and avoid confusion. Abbreviations of standard SI units of measurement only 

should be used. 

Declaration of Helsinki 

The Authors should state that their study complies with the Declaration of Helsinki that the locally appointed ethics 

committee has approved the research protocol and that informed consent has been obtained from the subjects (or their 

guardians). 

Clinical trials 

Authors should comply with the clinical trial registration statement from the ICMJE. More information can be found at 

www.icmje.org. Clinical trial reports should also comply with the Consolidated Standards of Reporting Trials (CONSORT) 

and include a flow diagram presenting the enrollment, intervention allocation, follow-up, and data analysis with number of 

subjects for each (www.consort-statement.org). Please also refer specifically to the CONSORT Checklist of items to include 

when reporting a randomized clinical trial. 

Section of the manuscripts 

Original articles should be divided into the following sections: (1) Title page, (2) Abstract and Keywords, (3) Introduction, 

(4) Methods, (5) Results, (6) Discussion, (7) Conclusion, (8) Acknowledgements, (9) References, (10) Figure legends, 

(11) Tables, (12) Figures. 

General format 

Prepare your manuscript text using a word processing package. Submissions of text in the form of PDF files are not


permitted. Manuscripts should be double-spaced, including text, tables, legends and references. Number each page. Please 

avoid footnotes; use instead, and as sparingly as possible, parenthesis within brackets. Enter text in the style and order of 

the Journal. Type references in the correct order and style of the journal. Type unjustified, without hyphenation, except for 

compound words. Type headings in the style of the journal. Use the TAB key once for paragraph indents. Where possible use 

Times New Roman for the text font and Symbol for the Greek and special characters. Use the word processing formatting 

features to indicate Bold, Italic, Greek, Maths, Superscript and subscript characters. Clearly identify unusual symbols and 

Greek letters. Differentiate between the letter o and zero, and the letters I and i and the number 1. Mark the approximate 

position of each figure and table. Check the final copy of your paper carefully, as any spelling mistakes and errors may be 

translated into the typeset version. 

Title page 

The title page should include the following: (1) the title, (2) the name (s) of authors and their highest degree ( no more 

than 12 authors are acceptable), (3) the institution (s) where work was performed, (4) institution, and location of all authors, 

(5) the address, telephone number, fax number and e-mail address of the corresponding author. 

Abstract 

All abstracts may not contain more than 250 words and should also be submitted as a separate file. The abstract should be 

formatted with the following heading: (1) Background, (2) Methods, (3) Results, (4) Conclusion. 

A maximum of six Keywords may be submitted. 

Figures 

The review process will not begin until all figures are received. Figures should be limited to the number necessary for 

clarity and must not duplicate data given in tables or in the text. They must be suitable for high quality reproduction and 

should be submitted in the desired final printed size so that reduction can be avoided. Figures should be no larger than 125 

(height)×180 (width) mm (5×7 inches) and should be submitted in a separate file from that of the manuscript. 

Electronic submission of figures 

Figures should be saved in TIFF format at a resolution of at least 300 pixels per inch at the final printed size for colour 

figures and photographs, and 1200 pixels per inch for black and white line drawings. Although some other formats can be 

translated into TIFF format by the publisher, the conversion may alter the tones, resolution and contrast of the image. Digital 

colour art should be submitted in CMYK rather than RGB format, as the printing process requires colours to be separated 

into CMYK and this conversion can alter the intensity and brightness of colours. Therefore authors should be satisfied with 

the colours in CMYK (both on screen and when printed) before submission. Please also keep in mind that colours can appear 

differently on different screens and printers. Failure to follow these guides could result in complications and delays. 

Photographs: Photographs should be of sufficiently high quality with respect to detail, contrast and fineness of grain to 

withstand the inevitable loss of contrast and detail inherent in the printing process. Please indicate the magnification by a rule 

on the photograph. Colour figures: There is a special charge for the inclusion of colour figures. Figure legends: These should 

be on a separate, numbered manuscript sheet grouped under the heading “Legends” on a separate sheet of the manuscript 

after the References. Define all symbols and abbreviations used in the figure. All abbreviations and should be redefined in 

the legend. 

Tables 

Tables should be typed with double spacing, but minimizing redundant space and each should be placed on a separate 

sheet. Tables should be submitted, wherever possible, in portraits, as opposed to landscape, layout. Each Table should be 

numbered in sequence using Arabic numerals. Tables should also have a title above and an explanatory footnote below. All 

abbreviations and should be redefined in the Footnote. 



Acknowledgements 

All sources of funding and support, and substantive contributions of individuals, should be noted in the Acknowledgements, 

positioned before the list of references. 

Reference format 

Number references sequentially and use Arabic number in superscript to cite the reference in the text. All references 

should be compiled at the end of the article in the Vancouver style. Complete information should be given for each reference 

including the title of the article, abbreviated journal title and page numbers. All authors should be listed. Personal communications; 

manuscripts in preparation and other unpublished data should not be cited in the reference list but may be mentioned 

in parentheses in the text. Authors should get permission from the source to cite unpublished data. 

Titles of journals should be abbreviated in accordance with Index Medicus (see list printed annually in the January issue 

of Index Medicus). If a journal is not listed in Index Medicus then its name should be written out in full. 

Article citation example: 

Journal citation example: 1. Schroeder S, Baumbach A, Mahrholdt H. The impact of untreated coronary dissections on the 

acute and long-term outcome after intravascular ultrasound guided PTCA. Eur Heart J 2000;21:137-145. 

Chapter citation example: 2. Nichols WW, O’Rourke MF. Aging, high blood pressure and disease in humans. In: Arnold 

E, ed. McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 3rd ed. London/Melbourne/ 

Auckland: Lea and Febiger; 1990. p. 398-420. 

Webpage citation example: 3. Panteghini M. Recommendations on use of biochemical markers in acute coronary syndrome: 

IFCC proposals. eJIFCC 14. http://www.ifcc.org/ejifcc/vol14no2/1402062003014n.htm (28 May 2004). Where the 

date in parenthesis refers to the access date. 

Statistics 

All manuscripts selected for publication will be reviewed for the appropriateness and accuracy of the statistical methods 

used and the interpretation of statistical results. All papers submitted should provide in their Methods section a subsection 

detailing the statistical methods, including the specific method used to summarize the data, the methods used to test their 

hypothesis testing and (if any) the level of significance used for hypothesis testing. 

Conflict of interest 

At submission, the editors require authors to disclose any financial association that might pose a conflict of interest in 

connection with the submitted article. All sources of funding for the work should be acknowledged in a footnote on the title 

page and in the Acknowledgements within the manuscript, as should all the institutional affiliations of the authors (including 

corporate appointments). Other kinds of associations, such as consultancies, stock ownership or other equity interest 

or patent-licensing arrangements should be disclosed to the editors in the cover letter at the time of the of submission. If no 

conflict of interest exists, please state this in the cover letter. 

Proofs 

Page proofs will be sent to the corresponding author. Please provide an e-mail address to enable page proofs to be sent 

as PDF files via e-mail. These should be checked thoroughly for any possible changes or typographic errors. Significant 

alterations instigated at this stage by the author will be charged to the author. It is the intention of the Editor to review, 

correct and publish your article as quickly as possible. To achieve this it is important that all of your corrections are returned 

to us in one all- inclusive mail or fax. Subsequent additional corrections will not be possible, so please ensure that your first 

communication is complete.


New Subscription: 

Surname: 

First Name: 

Hospital or Organization: 

Date of subscription: 

Full mail address: 

Subscription Form 


P.O.BOX: Tell: Fax: 

E-mail: 

Continuation of Subscription: 

The annual Subscription and postage rate: 100/000 Rials for Iran and US $ 100 including postage for other countries. 

Please liquidate the total amount of Subscription and postal charges into: 

Bank: Refah Branch Code: 1232 Account: Tehran Heart Center Account Number: 200001.28 

and send the original Bank slip along with Duly completed form of Subscription to the following addre 

ss: 


North Karegar Street, 

Tehran, Iran: 1411713138 

Tel: +98 21 88029720 

Fax: +98 21 88029702 

E-mail: jthc@tums.ac.ir 


New Subscription: 

Surname: 

First Name: 

Hospital or Organization: 

Date of subscription: 

Full mail address: 

Subscription Form 


P.O.BOX: Tell: Fax: 

E-mail: 

Continuation of Subscription: 

The annual Subscription and postage rate: 100/000 Rials for Iran and US $ 100 including postage for other countries. 

Please liquidate the total amount of Subscription and postal charges into: 

Bank: Refah Branch Code: 1232 Account: Tehran Heart Center Account Number: 200001.28 

and send the original Bank slip along with Duly completed form of Subscription to the following addre 

ss: 


North Karegar Street, 

Tehran, Iran: 1411713138 

Tel: +98 21 88029720 

Fax: +98 21 88029702 

E-mail: jthc@tums.ac.ir

THE JOURNAL OF TEHRAN UNIVERSITY HEART CENTER

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