The pathogenesis of cardiac infarction

Abstract

Questions concerning coronary heart disease have been raised for more than 200 years, but the concept of coronary insufficiency is only 50 years old. The pathological anatomy of coronary insufficiency is variable, unexpectedly rich and stratified, and full of pecularities. “Coronary insufficiency” is the superimposed concept; “cardiac infarcts” and “inner myocardial layer damage” are subordinate. The logical connection linking all the morphological consequences of so-called coronary insufficiency is the elective necrosis of the parenchyma. The anatomically demonstrable equivalents of coronary insufficiency are, from the point of view of coronary perfusion, the result of an inadequate “vis a tergo”. This principle is enshrined in a complex of conditions which has to be disentangled if an individual case is to be analysed. The complex comprises three sets of factors: the critical narrowing of the lumen of the coronary arteries and all their branches leading to a given territory; the weight of the functioning mass of the cardiac muscle; the cardiac effort required of the heart during the critical period of damage. The presence of anastomoses between the coronary arteries is no proof of their functional efficiency or readiness in an emergency. The conditions which determine their responsiveness, particularly as far as time is concerned, are at the moment still not adequately known. The behaviour of ions at the membranes of living cells, particularly of muscle fibres, is a fundamental phenomenon, fascinating in its primitive aspects. A disturbance of cellular respiration, produced in the cardiac muscle “regularly” by the “inadequate vis a tergo” of coronary perfusion, leads to an exhaustion of energy stores, and to an increased influx of calcium ions. This activates the ATP-ase of the myofibrils, and thereby reduces the level of adenin nucleotides. This loss of energy-rich substances not only militates against the function of the muscle fibres, it also initiates their necrosis. The cardiac infarct is a phenomenon of a disturbed circulation — a “dyscirculatory” change. It is found in certain sites of predilection, whose choice becomes intelligible only through an understanding of the developmental history of the coronary arteries. The cardiac infarct is “coronary-dependent”! There are, however, also other forms of, and possibilities leading to, the development of myocardial necrosis. The nosology of the cardiac infarct clearly distinguishes the latter from these other forms. In damage of the inner layers of the myocardium infarcts do not develop by the confluence of necroses of individual fibres or of groups of fibres. Infarcts are not a phenomenon of addition, they do not have the “character of a mosaic”. As in other tissues, in the human myocardium also there are lysosomes. They are found in hypertrophied muscle fibres. Topical relations to zones of necrosis have not been found. Current views of arteriosclerosis applied to the coronary arteries as the main factor responsible for the myocardial infarct must be amplified by an additional consideration: If no account is taken of the relation between the tone of the coronary arteries and their filling, of possible spasms and paralysis, and of an inadequate homeostasis between these factors, the marked variability of the pattern of myocardial damage cannot be adequately understood. This “pathology of relations” must always be kept in mind.