[Etiology of acute coronary syndrome--unstable plaque]

Our perception of the mechanisms underlying the acute complications of atherosclerosis has significantly changed in the last decade. Most coronary thromboses result from a rupture or a fissure in the protective fibrous cap of atherosclerotic plaque, but less common from a superficial erosion. The extent of thrombosis is a determinant of the clinical picture of acute coronary syndromes. Until now, we held a high grade stenosis responsible for the vast majority of acute coronary syndromes. However, current findings establish the relevance of qualitative aspects of plaques as important determinants of the vulnerability of plaques, i.e. the risk to cause acute complications. Among morphologic and functional features of plaques, inflammation has emerged as a leading pathophysiologic mechanism. In addition to local effect of inflammation at the level of the unstable plaque itself, systemic factors of the inflammatory response may alter the thrombogenicity of a vulnerable plaque. Knowledge of the role of inflammation helps us to understand the mechanisms by which therapeutic efforts can reduce clinical events. The clinical benefits of dietary modifications, pharmacotherapy with statins, and ACE inhibitors may be due in part to an anti-inflammatory action.