Mechanisms of acute coronary syndromes and the potential role of statins

The conventional concepts of the pathogenesis of acute coronary syndromes a re changing. High-risk lesions are not necessarily the angiographicaly 'tig ht' stenoses. Rather, vulnerable lesions are those that are unstable, with a large lipid core and a thin fibrous cap. Plaque instability is closely re lated to the development of inflammation within the intima and acute corona ry syndromes result from rupture of a vulnerable atherosclerotic plaque. St abilization of lesions by modification of structure and content, rather tha n simple improvement in the luminal diameter, provides a new therapeutic ta rget. Stabilization may be accomplished through lifestyle changes and appro priate pharmacologic therapy. In the past few years, it has become evident that a major beneficial effect of statins is to induce plaque stability and regression. In fact, statins, in addition to lowering low-density lipoprot ein cholesterol, have a variety of pleiotropic, or cholesterol-independent, effects that make them a particularly suitable choice in patients with acu te coronary syndromes. Among these are improvements in endothelial function , smooth muscle cells, thrombus formation/platelet function, and inflammati on. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.