Physiopathology of unstable angina.

The majority of cases of unstable angina and myocardial infarction have a common origin : rupture of an atheromatous plaque complicated by intracoronary thrombosis. The nature of these ''high risk'' plaques is now well known : they are excentric, moderately severe lesions, the voluminous lipid centres of which are covered only by a thin unstable fibrous layer. The triggering factor of the rupture of an unstable plaque may be an increase in wall stress (spastic vasoconstriction, rise in blood pressure), and/or an inflammatory or haemorrhagic phenomenon within the plaque itself. Once the plaque has ruptured, the outcome to unstable angina or myocardial infarction is determined by two factors : the size and rapidity of constitution of the thrombus and the quality of the collateral circulation.