Cardiovascular disease--linking pathology and epidemiology.

Abstract

Coronary heart disease (CHD) in the form of myocardial infarction first came to attention early in the 20th century. Mortality from CHD increased dramatically after the First World War and had assumed epidemic proportions, particularly in the USA, by 1945. The ensuing research stemmed almost exclusively from the lipid infiltration hypothesis for atheroma. Using epidemiological methods, pathological evidence for the thrombotic component of CHD was demonstrated by Morris as early as 1951. Morris's main work was based, first, on routine autopsy records at the London (now Royal London) Hospital and, second, on the National Necropsy Survey relating physical activity at work to pathological findings. The indications from Morris's work that thrombosis contributes as much to clinical CHD as atheroma were in due course strengthened by the findings of clinical trials of aspirin, prospective studies incorporating measures of haemostatic function and further studies of pathology. Recognition of the thrombotic contribution to CHD does not materially alter approaches to prevention through lifestyle modifications but does have major implications for pharmacological measures. Thus, aspirin and thrombolytic therapy are mandatory in the acute stage of suspected myocardial infarction while aspirin is also part of accepted practice in the longer term in secondary prevention. The value of warfarin is being rediscovered, often at a lower and therefore safer intensity of anticoagulation than previously considered necessary. The effect that warfarin may have on the vessel wall as well as on occlusion of the lumen is helping to reconcile the two major hypotheses for the pathology of CHD. Much of our current knowledge about the origins, management and prevention of CHD stems from Morris's early studies linking pathology and epidemiology.