Coronary Thrombosis and Myocardial Infarction

Abstract

If the oxygen supply falls below the current myocardial oxygen requirements for any length of time, this results in a general impairment of function with or without a disseminated destruction of the cardiac musculature or a myocardial infarction with a localized loss of myocardial function. One of the most important preconditions for the occurrence of an acute cardiac infarction is a stenosis of a coronary artery of 75% or more of its cross-sectional area. The acute event in the myocardium can be induced by a great number of extracardiac and cardiac pathological mechanisms: anemia, hypotension, shock, altered rheological properties of the blood such as paraproteinemias and polycythemia, cardiac arrhythmias etc. Transient spasms of the coronary arteries similarly lead to myocardial ischemia (Prinzmetal-angina). Even in the absence of angiographically demonstrable stenoses or occlusions of the coronary arteries disorders in the microcirculation can be the cause of ischemic events in the myocardium. This can occur through pathological changes of the terminal circulation in hypertension, autoaggressive diseases and endotoxinemia, as also through rheological changes in the course of autoaggressive diseases, paraproteinemias, polycythemia etc. Arrhythmias and acute ischemia syndromes can be induced through thrombocyte aggregates which become detached from arteriosclerotic plaques of the coronary arteries and are carried into the peripheral vascular region, but also through platelet aggregates which have developed in the systemic vascular system and have been transported into the coronary vessel system in general hypercoagulability, diabetes and hyperlipidemias. Emboli from thrombocyte aggregates in the coronary peripheral vascular region are often said to be the cause of cases of sudden heart death.