prognosis is, surprisingly, unclear. The MINAP database allowsconsideration of this issue. We assessed the relevance tosurvival of cardiac arrest. We were particularly interested inthe impact of cardiac arrest on survival in patients who werelater discharged alive from hospital. Similarly, we consideredwhether cardiac arrest influenced outcome after 30 days if thepatient lived to that point, and whether it influenced outcomeafter 1 year if the patient was alive at that time.We analysed data from 41,467 patients admitted with STsegmentelevation AMI between 2008 and 2010. Cardiac arrestwas surprisingly common, recorded for 4,240 individuals,10.2% of the population. Approximately 30% of patientsexperiencing cardiac arrest died before discharge.Without adjustment for other clinical factors, cardiac arrestwas associated with increased risk of 30-day mortality, aswere greater age, higher heart rate and lower blood pressureon admission to hospital. However, after adjustment forcovariates, cardiac arrest had association with mortality upto, but not after, 30-days. In other words, the occurrence ofcardiac arrest during the early stages of AMI is associatedwith increased risk of death only up to 30 days after the event.Our results suggest that, for patients surviving to dischargefrom hospital after AMI, cardiac arrest is associated withincreased risk of death by 30-days, but not thereafter. Patientsexperiencing cardiac arrest after AMI may merit intensivemonitoring for one month, but can be reassured that thisdramatic event has no apparent association with mortality riskafter that point.5. The effects of hourly differences in airpollution on the risk of myocardial infarction:case crossover analysis of the MINAP 25Dr Krishnan Bhaskaran – Lecturer in Statistical Epidemiology,London School of Hygiene and Tropical MedicineProf Paul Wilkinson – Professor in EnvironmentalEpidemiology, London School of Hygiene and Tropical MedicineA unique strength of MINAP for research is the availability oftiming data on acute coronary syndromes. As part of a studyinvestigating the associations between environmental exposuresand myocardial infarction (MI) risk, we linked 79288 MI eventsin MINAP by time and location to data on ambient pollutionlevels obtained from pollution monitoring stations in 15 largeconurbations in England and Wales during the period 2003-2006. We assigned times to individual MIs using the recordedtime of symptom onset, where it was available (74% of cases);for the remainder we used time of call for help, or time ofarrival at hospital. For each individual experiencing an MI, wecompared their exposure to five key pollutants at the time oftheir MI, with their exposure at the same time of day on otherdays in the same calendar month (when they did not have anMI). We also looked for associations between pollution levelsand MI risk that might be delayed (lagged) by up to 72 hours,since exposure to pollution at a particular time might affect MIrisk some time later.Higher ambient levels of small particles (known as PM10),and nitrogen dioxide (NO 2 ), which are typically traffic-related,appeared to be associated with transiently increased risk ofmyocardial infarction 1-6 hours after exposure (Figure 30.For every 10µg/m 3 increase in PM10 and NO 2 levels, MI riskwas estimated to increase by 1.2% and 1.1% respectively.Interestingly, we observed that later reductions in risk appearedto offset the initial risk increase; over a 3-day period, higherpollution levels were not associated with a net increase in MIrisk. This suggests that exposure to traffic-related air pollutionmay be associated with triggering MIs early in highly vulnerablepatients who would in any case have experienced an MI a littlelater. For ozone, carbon monoxide (CO) and sulphur dioxide (SO 2 )there was no evidence of any detrimental effect.Our study was the largest to date to investigate associationsbetween the commonly measured pollutants and myocardialinfarction risk at an hourly temporal resolution. MINAP’scoverage means that hospital admissions recorded shouldhave been representative of those occurring within theconurbations under study, though one must be mindful of thefact that MIs leading to death before hospital admission wouldhave been excluded from our analysis. A further strengthwas that we were able to use information within MINAP tovalidate MI diagnoses: 89% of diagnoses were backed up byelectrocardiogram (ECG) or blood marker data (troponin/creatine kinase) consistent with MI.Our results suggest that there may be limited potential forreducing the net burden of MI through reductions in pollutionalone, but that should not undermine calls for action onair pollution, which has well established associations withbroader health outcomes including overall, respiratory, andcardiovascular mortality. One implication of our findings isthat other, perhaps non-thrombotic, mechanisms are moreimportant drivers of this net mortality increases associatedwith higher pollution levels.25. Bhaskaran K, Hajat S, Armstrong B, Haines A, Herrett E, Wilkinson P,Smeeth L. The effects of hourly differences in air pollution on the risk of myocardialinfarction: case crossover analysis of the MINAP database. BMJ 2011;343:d5531doi98 MINAP How the NHS cares for patients with heart attack
Figure 30. Estimated excess risk of myocardial infarction over time associated with exposure to different pollutantsMINAP Eleventh Public Report 201299
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Myocardial IschaemiaNational Audit
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Myocardial Ischaemia National Audit
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ForewordThe annual MINAP Report, no
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Patients who received thrombolytic
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considering such factors as the age
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3. Improving quality,improving outc
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Alan KeysMINAP Steering Group patie
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Conquest Hospital, St Leonards onSe
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Cheltenham General Hospital, Chelte
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