PHYSIOPATHOLOGY OF UNSTABLE ANGINA

The majority of cases of unstable angina and myocardial infarction hav e a common origin : rupture of an atheromatous plaque complicated by i ntracoronary thrombosis. The nature of these ''high risk'' plaques is now well known : they are excentric, moderately severe lesions, the vo luminous lipid centres of which are covered only by a thin unstable fi brous layer. The triggering factor of the rupture of an unstable plaqu e may be an increase in wall stress (spastic vasoconstriction, rise in blood pressure), and/or an inflammatory or haemorrhagic phenomenon wi thin the plaque itself. Once the plaque has ruptured, the outcome to u nstable 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.