Conventional concepts of the pathogenesis of acute coronary syndromes are changing. High-risk lesions are not necessarily the angiographically "tight" stenoses. Rather, unstable vulnerable lesions have large lipid cores and thin fibrous caps. Plaque instability relates closely to the development of inflammation within the intima. Acute coronary syndromes usually result from rupture of a vulnerable atherosclerotic plaque mechanistically linked to the inflammatory process. Stabilization of lesions, rather than percutaneous or surgical procedures, provides a new therapeutic target. Lipid lowering may stabilize lesions by mitigating the inflammatory response.