Pathology of outofhospital death

What proportion of out-of-hospital deaths are caused by developing infarction, and what proportion are caused by a re-entrant arrhythmia? Sudden unexpected death in England must be reported to a coroner unless the victim was known to have coronary disease and had been seen by a doctor within the last two weeks. Depending on the practice of individual coroners, the proportion of unexpected deaths coming to necropsy is high. However, developing infarction cannot be recognised in most cases of sudden death because the earliest his-tological change (invasion by leucocytes) does not develop until 12-24 hours after the onset. Evidence must be sought by examination of the coronary arteries.

Occlusion of the infarct related coronary artery by thrombus is nearly always present in patients with ST elevation myocardial infarction admitted early to hospital2; this is almost certainly the event which causes the infarct, so that the presence of occlusive thrombus at necropsy is almost pathognomonic of developing infarction. In a consecutive series of 168 sudden coronary deaths (within six hours of onset of symptoms)3 in which the coronary arteries were examined by postmortem arteri-ography and histology of sections made at 3 mm intervals, occlusive thrombus was present in 30% of cases, and mural thrombus in 43%. In 8% of cases plaque fissuring only was present, and there was no acute lesion in

Figure 6.2. Necropsy findings in 168 cases of sudden coronary death in which the coronary arteries were examined by post mortem arteriography and histology of sections made at 3 mm intervals. Reproduced from Davies3 with permission of the American Heart Association.

Figure 6.1. Total case fatality in the UK heart attack study and case fatality outside hospital by age group. Reproduced from Norris1 with permission of BMJ Publishing Group.

Figure 6.2. Necropsy findings in 168 cases of sudden coronary death in which the coronary arteries were examined by post mortem arteriography and histology of sections made at 3 mm intervals. Reproduced from Davies3 with permission of the American Heart Association.

19% (fig 6.2). Thus from this series it appeared that perhaps 30% of sudden cardiac deaths were definitely caused by developing infarction, and in an additional 45% infarction was highly likely (because the finding of intralumi-nal thrombus is unusual in definite non-coronary death). In the remaining 25% infarction was unlikely because plaque fissuring is quite common in people who die from an unrelated cause.3

Postmortem arteriography and serial sectioning of the coronary arteries is not carried out routinely by hospital pathologists who frequently limit the procedure, as far as the heart is concerned, to cursory section of the coronary arteries. Histological examination is not routine, and in these circumstances neither non-occlusive thrombus nor plaque fissuring are often commented upon. In the UK heart attack study (UKHAS)4 1037 (83%) of the 1247 out-of-hospital coronary deaths which we recognised in people up to 75 years of age came to necropsy. Occlusive thrombus was recognised by hospital pathologists in 23% of cases, recent myocardial infarction in 20%, and an old myocardial scar in 56%. Stenoses of one or more coronary arteries were present in all cases.

Clinicopathological correlations In about half of the victims of out-of-hospital coronary death in the UKHAS study we were able to discover whether death had been truly sudden or if there had been prodromal symptoms (usually chest pain) before death. Of particular interest was that necropsy evidence of old infarction was more common and recent infarction less common in 124 victims who apparently had had no prodromal symptoms before death (70% and 11%) than in the 386 who had had prodromal chest pain (45% and 29%) (p < 0.001). However, occlusive thrombus was no more common in people with symptoms (26%) than in those without symptoms (29%). This latter finding is at variance with that of Davies3 who was able to show a much higher number of thrombi with serial sectioning of the arteries. Of the 168 cases of sudden cardiac death mentioned earlier, occlusive thrombus was more common when prodromal pain had been present than when it had been absent. To summarise the evidence from necropsies, it is impossible to give any reliable estimate of the proportion of sudden coronary deaths which were caused by developing infarction and what proportion were caused by "electrical" death. However, both the detailed anatomical studies of Davies3 and our own larger series of routine necropsies do support the existence of at least two separate mechanisms for out-of-hospital coronary death.

Resuscitation from out-of-hospital arrest Further evidence does, however, come from one of the earliest studies of patients resuscitated from out-of-hospital cardiac arrest.5 In Seattle, Washington, between 1970 and 1973, 146 patients were resuscitated from out-of-hospital ventricular fibrillation and were fol-

Figure 6.3. Two year survival after resuscitation from out-of-hospital arrest according to whether or not new pathological Q waves developed. Reproduced from Baum and colleagues5 with permission of the American Heart Association.

lowed for two years. The subsequent survival of the 17% of patients whose arrest was caused by Q wave infarction was significantly better (p < 0.005) than the survival of the 83% who did not develop new pathological Q waves (fig 6.3).5 It was this seminal observation that led to the recognition of "electrical" coronary death as a distinct pathological entity and its consequent electrophysiological investigation and treatment with implantable defibrillators. The Seattle findings also suggested that the majority of sudden deaths were "electrical". However, this conclusion, based on findings in a subset of survivors, may be incorrect in view of those from the detailed pathological examinations described above.3

Epidemiological studies The final arbiter of the classification of acute coronary events, both fatal and non-fatal, is the epidemiologist. Discussion of global differences in incidence of new coronary events and prevalence of the disease is not the purpose of this article. However, methods used by the World Health Organisation MONICA (monitoring trends and determinants in cardiovascular disease) investigators6 highlight the difficulties in exact definition. MONICA recognised both fatal and non-fatal events in the two categories of "definite" and "probable", and constructed their main analyses of incidence, mortality, and case fatality on "definite" only non-fatal events and "definite" plus "probable" fatal events. A third category of "unclassifiable" fatal events was also encountered; these were unexpected deaths in which no necropsy had been carried out and cause of death had been certified as coronary disease in the absence of definite evidence for or against the diagnosis. These deaths too were included in the analyses. MONICA definitions are not in dispute, but the problems in applying them to differing cultures with differing legal requirements for death certification are immense. From the epidemiologists' perspective the problem of "unclassifiable" deaths and the frequent unreliability of death certificates, particularly in the elderly, is very real. Different counting methods used by clinicians and epidemiologists yield differing results; this problem is discussed in a recent editorial.7 Of

Problems in defining the true natural history of myocardial infarction

• Two thirds to three quarters of fatal events occur outside hospital. Such deaths may be caused by infarction or may be electrical. Although it may be possible to differentiate these mechanisms in some individual cases, it is impossible to do this in the majority.

• Death certificates are unreliable; many deaths certified as being caused by coronary heart disease, particularly in the elderly, are in truth unclassifiable.

• About 25% of non-fatal infarctions are silent and medically unattended.

• These facts must be taken into account for interpretation of all community and epidemiological studies, and also for interpretation of demographic data which show geographical differences or secular changes in mortality from coronary heart disease.

of acute myocardial infarction? Of course only acute events rather than infarctions can be monitored. However, the most recent evidence from the MONICA study suggests that over a 10 year period in populations where mortality decreased, reduction in coronary event rates accounted for about two thirds of the decrease while reduced case fatality accounted for about one third.12

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