Statins and biomarkers of inflammation.

Clinical and epidemiologic studies convincingly demonstrate that increased levels of low-density lipoprotein cholesterol promote premature atherosclerosis. Several large clinical trials have demonstrated that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) decrease cardiovascular events. The beneficial effects of statins may extend to mechanisms beyond cholesterol reduction. Evidence for the pleiotropic effects of statins is provided by recent clinical trials in which the benefit of statin drugs is manifest early in the course of lipid-lowering therapy, well before plaque regression could occur. Inflammation is pivotal in all stages of atherosclerosis, and C-reactive protein (CRP), the prototypic marker of inflammation, has emerged as a cardiovascular risk marker. Statins reduce CRP levels, and this reduction in most studies does not correlate to reduction in cholesterol. In addition, statins have beneficial effects on endothelial function, monocyte-macrophages, and platelets. In this review we discuss the role of inflammation in atherosclerosis, the role of CRP as a risk marker, the clinical evidence implicating the anti-inflammatory effects of statins, and the cellular and molecular basis underlying the anti-inflammatory effects of statins.