Pathological concepts in acute coronary thrombosis: relevance to treatment.

Coronary thrombosis and myocardial infarction It is a little over a decade since the acute management of myocardial infarction underwent a revolution with direct intervention on the coronary occlusive lesion. This approach had validity only if the coronary occlusion caused infarction. The evidence generated by coronary angiography soon after the onset of pain, the frequent restoration of coronary blood flow by therapeutic thrombolysis, and the apparent benefit to the threatened myocardium soon dispelled any reasonable clinical doubt that thrombotic occlusion was the prime cause of myocardial infarction. It had not always been so.' For more than half a century pathologists had been comfortable with the orthodox concept that coronary thrombosis was the cause of myocardial infarction. In the 1970's, however, some pathologists proposed the maverick concept that coronary thrombosis was inconstant and was a secondary consequence of infarction.2 The validity of the orthodox concept was re-examined by several workers. A prevalence of thrombotic occlusion in regional myocardial infarction of some 90-97% was revealed.~3 Post-mortem evidence being of necessity retrospective, uncertainties about the time relation between occlusion and infarction persisted. In 1974 I started a prospective clinico-pathological necropsy study that used radiofibrinogen given in life as a marker of the timing of thrombus formation. A 100% incidence of acute coronary occlusion was confirmed in acute fatal myocardial infarction, all but one lesion being thrombotic. Also certain aspects of the study, in particular retrospective anatomical reconstruction of the underlying plaque and the demonstration of the different ages of thrombus, have contributed to the understanding of the clinical features of acute ischaemic syndromes. A substantially lower incidence and even the absence of coronary thrombosis has usually been reported in diffuse subendocardial infarction.'568 It is important to distinguish this entity from regional infarction.9 Diffuse subendocardial damage occurs in the presence of widespread severe obstructive coronary disease. Critically severe ischaemia is equitably distributed by greatly enlarged anastomoses, which are particularly extensive in the subendocardial plexus.7-'0 The putative final insult is usually extracoronary-for example, tachycardia, hypoxia, or heart failure-but it can be a fresh thrombotic occlusion.