Effects of statins in reducing thrombotic risk and modulating plaque vulnerability.
A large body of evidence demonstrates that statin therapy reduces risk for coronary events. This benefit probably stems in large part from lipid lowering, but lipid-independent cellular effects may also contribute. Statin therapy may lower the risk of thrombosis by reducing tissue factor expression and increasing plasminogen activators while reducing plasminogen-activator inhibitor. The statins may also improve endothelial function and reduce inflammatory response by increasing nitric oxide activity; all statins tested can decrease levels of C-reactive protein, a systemic marker of inflammation. Indeed, limiting inflammation may prove an important mechanism of statins' clinical benefits due to both lipid lowering and direct cellular effects. For example, attenuation of inflammation probably promotes maintained integrity of the fibrous cap of the atherosclerotic lesion by inhibiting processes that degrade the collagenous structure of the cap. Rupture of the fibrous cap causes most fatal coronary thrombosis.
Libby
Peter
P
Harvard Medical School and Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA.
Aikawa
Masanori
M
D000818:Animals; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D001707:Biopsy, Needle; D003328:Coronary Thrombosis / Q000517:prevention & control*; D004195:Disease Models, Animal; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D006937:Hypercholesterolemia / Q000188:drug therapy*; D007150:Immunohistochemistry; D011322:Primary Prevention / Q000379:methods*; D011817:Rabbits; D018570:Risk Assessment; D012307:Risk Factors; D012680:Sensitivity and Specificity; D020521:Stroke / Q000517:prevention & control*; D013923:Thromboembolism / Q000517:prevention & control
D000924:Anticholesteremic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors