Abstract

During the last decade, the evidence that statins have potent effects in reducing death and myocardial infarction in patients following acute coronary syndromes has become overwhelming, both in patients with elevated cholesterol levels and in those with normal cholesterol levels.1,2 Beyond their intended impact on blood cholesterol levels, statins are also known to have multiple non-lipid effects that contribute to the reduction of cardiovascular morbidity and mortality.3,4 Statins may prevent acute thrombus formation at the site of plaque rupture by inhibiting platelet function and inhibiting platelet deposition on damaged vessels. They have also been shown to contribute to plaque stabilization, not only through a reduction in lipids but also as a result of reduced macrophage accumulation in atherosclerotic lesions and inhibition of expression of matrix metalloproteinases. Statins have anti-inflammatory properties; they reduce levels of high sensitivity C-reactive protein and, through attenuation of P-selectin expression, protect the ischaemic myocardium. Statins restore endothelial function before any significant reduction in cholesterol levels may have occurred. In the context of acute coronary syndromes, the statin-mediated improvement of vascular function by inhibiting the production of harmful intermediates of the cholesterol biosynthetic pathway appears to play a major role. Therefore, the effects of statins include an increase in nitric oxide bioavailability, reduced expression of endothelin-1, and increased expression of tissue plasminogen activator. Ongoing clinical trials with highly potent statins are now expected to provide valuable information about the most appropriate agents and doses to improve the treatment of patients with acute coronary syndromes.5 Despite these demonstrated beneficial effects of statins and the low incidence of undesired effects, the use of statins is still highly variable in daily clinical routine. Up to 30% of prescriptions are discontinued during the first year. … *Corresponding author. Tel: +49 89 7095 3438, Fax: +49 89 7095 6433, Email: christopher.heeschen{at}med.uni-muenchen.de

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