Mechanisms of acute coronary syndromes and the potential role of statins.

The conventional concepts of the pathogenesis of acute coronary syndromes are changing. High-risk lesions are not necessarily the angiographicaly 'tight' stenoses. Rather, vulnerable lesions are those that are unstable, with a large lipid core and a thin fibrous cap. Plaque instability is closely related to the development of inflammation within the intima and acute coronary syndromes result from rupture of a vulnerable atherosclerotic plaque. Stabilization of lesions by modification of structure and content, rather than simple improvement in the luminal diameter, provides a new therapeutic target. Stabilization may be accomplished through lifestyle changes and appropriate 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 lipoprotein cholesterol, have a variety of pleiotropic, or cholesterol-independent, effects that make them a particularly suitable choice in patients with acute coronary syndromes. Among these are improvements in endothelial function, smooth muscle cells, thrombus formation/platelet function, and inflammation.