The use of statins in acute coronary syndromes: The mechanisms behind the outcomes

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Abstract
Lipid-lowering drugs, in particular statin treatments, have been shown to reduce the incidence of initial and recurrent coronary heart disease (CHD) events within several years of initiating therapy. This effect can be clinically detected within the first 1 to 2 years in randomized trials. Recent observational and clinical trial data suggest that lipid-lowering therapy initiated at the time of an acute coronary event can reduce recurrent events, and possibly all-cause mortality, in a much shorter period of time. The possible mechanisms by which this benefit occurs include the effect of reduced lipoprotein levels, as well as an independent effect of statins on endothelial function. Statins improve endothelial-dependent flow-mediated vasodilation by increasing the bioavailability of nitric oxide. They stabilize the plaque by modulating the inflammatory response within the vessel wall. They also decrease clot formation by decreasing the adherence of platelets to the ruptured plaque and by acting on the extrinsic coagulation cascade pathway. This review examines these effects of statins and lipoproteins on vascular function, as well as the clinical evidence supporting early treatment in acute coronary syndromes.

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