[Genesis of myocardial infarction].
The causes of myocardial infarction (MI) are complex and multiple and may eventually be associated. Two main types of mechanism are thought to be implicated: Functional mechanisms: these are operative in prolonged angina: the difference between MI and angina pectoris is related to the duration of these phenomena and to the resistance of the myocardial cells to anoxia: unsatisfied increase in myocardial oxygen demand, as for example in exercise-induced myocardial infarction; sudden reduction in oxygen supply due to an excessive fall in coronary flow, inadequate vasodilatation, platelet aggregation or coronary spasm. Priviledged cases are presented to demonstrate the reality of these phenomena. These mechanisms can sometimes cause MI by themselves, even when the coronary arteries are normal (5% of cases), and nearly always complicate and aggravate obstruction due to an atheromatous plaque. Organic obstructive lesions: coronary obstruction observed in about 2/3 of cases, sometimes caused by rupture of an atheromatous plaque, is usually the result of coronary thrombosis. The predominance of this mechanism is an argument in favour of it being the principal cause of MI. However, other workers believe that thrombosis is a secondary phenomenon induced by stasis, functional mechanisms or severe stenosis. The clot itself would then cause obstruction even if the primary cause were to regress. Irrespective of the roles of each of these factors it would appear logical to treat the functional mechanisms assumed to be responsible and the coronary thrombosis before the myocardial cells are destroyed by the anoxia.
D003326:Coronary Circulation; D003327:Coronary Disease / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology; D006801:Humans; D009203:Myocardial Infarction / Q000209:etiology / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism; D010101:Oxygen Consumption; D010974:Platelet Aggregation; D014661:Vasoconstriction
Genèse de l'infarctus du myocarde.