Atherosclerosis is a slow, complex process involving many different cell types and their interactions producing excessive oxidant stress, increased inflammation, abnormal endotheliumdependent vasodilation, and localized increases in thrombogenic and decreases in fibrinolytic factors. Numerous factors incite these processes, but oxidized LDL particles seem the most essential component of this pathologic cascade. These oxidized particles set up a chain of biochemical events eventually leading to clinical atherosclerotic events. Statins have been shown to reduce such events by 40 to 50% when LDL cholesterol is lowered to less than 80 mg/dL. But in-vitro studies have shown that the provision of mevalonate, not cholesterol, can result in reversal of some of the beneficial effects of statins, suggesting that other mechanisms such as inhibiting the formation of the isoprenoids, farnesyl pyrophosphate and geranylgeranyl pyrophosphate, and thus prenylation of many cell-signaling proteins may be important in the preventive effects of statins. Clinically, these more rapid, non-lipid-altering effects may be more apparent in acute coronary syndromes. Now that we have more LDL-cholesterol lowering agents which lower LDL-cholesterol without blocking HMG CoA reductase, we may be better able to dissect and understand the importance of these non-lipid-altering effects of statins in human disease.
Keywords: Statin, atorvastatin, cerivastatin, fluvastatin, pravachol, HMG Co-A reductase inhibitor, hsCRP, LDL cholesterol, HDL cholesterol, myocardial infarction
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