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SUMMARY In order to examine whether functional disturbances in the heart without significant lesions is a frequent cause of sudden cardiac death, two prospective autopsy studies were performed. In a series of 78 cases of myocardial ischaemia dying within 48 hours acute lesions in the major coronary arteries were found in 89 per cent in patients who had been on anticoagulant therapy at the onset of the acute disease and in 76 per cent of the untreated patients. The relative frequency of cases without acute coronary lesions, haemorrhage in fibrous plaque, rupture of necrotic plaque, and of thrombosis which was not secondary to rupture of plaques, was about the same whether the patients had died within 15 minutes or later. Thrombi secondary to rupturedplaques were not observed among those dying within 15 minutes, whereas such lesions were found in 28 per cent of the treated patients and in 27 per cent of the untreated patients who died later. This may be explained by assuming that it takes more than a few minutes for a sizable thrombus to form, and that the rupture itself is lethal. In another series of 38 cases sudden, unexpected death the blood supply of the sinus and atrioventricular nodes was particularly studied. Acute lesions in major coronary arteries was found in 75 per cent of the cases. There was no preferential location of the acute lesions to arteries supplying the dominant parts of the conductive system. In both autopsy series, platelet aggregates were found in the peripheral bed of the coronary arteries in several cases. It is concluded that the basic pathogenetic mechanisms are the same whether the patients are dying immediately or later with evidence of myocardial infarction. In the cases with no acute coronary lesion there is probably also a localized circulatory disturbance leading to myocardial infarction if the patient survives the initial period. On the basis of recent experimental evidence, it is proposed that one precipitating factor for such a localized circulatory disturbance could be intravascular platelet aggregation.