[Pathophysiology of acute coronary syndrome].

This article reviews the current understanding of the pathophysiology of acute coronary syndrome and how these concepts have altered our clinical approach to the acute phase of coronary heart disease. Thrombosis due to erosion or, in most cases, rupture of a vulnerable atherosclerotic plaque underlies most acute coronary syndromes. The protective fibrous cap undergoes degradative processes controlled by inflammatory mediators that break down the interstitial collagen within the fibrous cap. Thrombus formation depends on factors in the solid-phase of the ruptured plaque as well as on fluid-phase determinants in blood. Depending on the degree of thrombus formation the subsequent obstruction of the coronary artery is followed clinically by unstable angina, non-ST- and ST-segment elevation myocardial infarction.