[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.