The Epidemiology of Arterial Thrombosis

The epidemiology of clinically manifest ischaemic heart disease (IHD) is not the same as that of atheroma. For example, the rise in IHD incidence that has taken place since early this century has probably not been paralleled by a similar rise in atheroma. The National Necropsy Survey in the United Kingdom found no relationship between physical activity at work and atheroma, but a clear association between activity, on the one hand, and lumen-occlusive changes and myocardial scarring on the other. Later studies have shown an association between occupational and leisure activity and clinical IHD. These and other observations strongly suggest that some process (or processes) other than, or in addition to, the formation of atheroma causes clinical IHD. However, the pathology of the different syndromes usually considered as IHD is not homogeneous. Evidence of recent thrombosis is often found in those dying of myocardial infarction; it is less often found in “sudden death”, though advanced atheroma is a usual finding. Sudden deaths may be due to small, unrecognized platelet aggregates. Clearly, atheroma and thrombogenesis are both involved in the pathogenesis of clinical IHD, and quite possibly to different degrees in different neoole. But thrombogenesis has not been adequately investigated in population-based studies. The epidemiological evidence suggests the need to study this process as contributing not only to infarction and sudden death, but also possibly to the formation of atheroma itself.