The importance of mechanical performance for development of myocardial infarction in man.

Abstract

In studies using an experimental infarction as a model it has been shown that factors increasing myocardial oxygen consumption will increase the size of infarction, while factors reducing the oxygen consumption have the opposite effect. The presence of catecholamines might be most important. It is suggested that local release of noradrenaline from the sympathetic nerve endings in ischemic myocardium can induce vigorous contractions and deleterious ischemia and result in cellular necrosis. A retrospective study was performed in 81 patients hospitalized in Göteborg in 1964-1965 due to attacks of severe chest pain with no previous documented myocardial infarction. In 31 of these patients definite congestive heart failure was seen at hospitalization or developed later. During 10 years of follow up the mortality was 48 per cent and an acute myocardial infarction was found in 64 per cent of the patients without congestive heart failure. In patients with congestive heart failure the mortality was 42 per cent, and 6.4 per cent had an acute myocardial infarction. The poor mechanical performance and a lower myocardial content of noradrenaline of the failing heart might protect from the acute myocardial infarction and instead be predisposed to a slow degeneration, pump failure, and serious arrhythmias. Severe angina pectoris and congestive heart failure might represent opposite ends of the spectrum of ischemic heart disease with similar degrees of luminal narrowing of the coronary arteries.