The pathophysiology and epidemiology of myocardial infarction. A review

Abstract

Myocardial infarction continues to represent a major cause of death in the Western world, and although there have been significant reductions in its incidence in recent years, some countries such as Scotland and Finland still have high mortality rates. Thrombotic occlusion, in association with varying degrees of plaque disruption and coronary artery spasm, represents the major cause of acute myocardial infarction (AMI). At the cellular level, this results in a shift towards anaerobic metabolism, depletion of energy stores, disrupted membrane integrity, alterations in ionic gradients, myocyte oedema, inhibition of contraction and a proarrhythmic potential. Reperfusion can exacerbate the damage, producing calcium ion accumulation and free radical generation. Infarct expansion and ventricular remodelling can often follow AMI as can additional necrosis, in the form of infarct extension/reinfarction. Rational and optimal treatment of AMI should be based on an understanding of the epidemiological influences and the pathophysiological processes involved. This review considers some of the important features in the pre-, peri- and postinfarction periods.