Traditional concepts of the pathogenesis of acute coronary syndromes have changed over the last few years. In particular it has been demonstrated that high-risk lesions are not necessarily angiographically severe. Rather, unstable high risk lesions are the ones composed of large lipid cores and thin fibrous caps. It is now widely accepted that plaque instability is related to the development of inflammation within the intima. A consequence of this is that stabilization of lesions provides a new therapeutic target. Furthermore, there is growing evidence that statins may stabilize lesions by altering the inflammatory response. A brief overview of these developments and their impact on clinical practice is presented.
Farzaneh-Far, A; Rudd, J; Weissberg, PL
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