Antiatherothrombotic Properties of Statins: Implications for Cardiovascular Event Reduction

• Published in: JAMA : the journal of the American Medical Association 1998-05, Vol.279 (20), p.1643-1650
• Main Authors: Rosenson, Robert S, Tangney, Christine C
• Format: Article
• Language: English
• Subjects: Animals; Antithrombins - pharmacology; Antithrombins - therapeutic use; Biological and medical sciences; Cardiology; Cardiovascular Diseases - blood; Cardiovascular Diseases - prevention & control; Cardiovascular system; Cholesterol; Cholesterol, LDL - blood; Cholesterol, LDL - physiology; Clinical Trials as Topic; Coronary Disease - blood; Coronary Disease - prevention & control; Endothelium, Vascular - physiology; Fibrinogen; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology; Hydroxymethylglutaryl-CoA Reductase Inhibitors - therapeutic use; Hypolipidemic Agents - pharmacology; Hypolipidemic Agents - therapeutic use; Inflammation; Lipids; Lovastatin - pharmacology; Lovastatin - therapeutic use; Medical research; Medical sciences; Miscellaneous; Muscle, Smooth, Vascular - physiology; Pharmacology. Drug treatments; Platelet Aggregation; Pravastatin - pharmacology; Pravastatin - therapeutic use; Simvastatin - pharmacology; Simvastatin - therapeutic use; Thromboplastin; Thrombosis - physiopathology
• ISSN: 0098-7484; 1538-3598
• DOI: 10.1001/jama.279.20.1643

Clinical trials of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors or statin therapy have demonstrated that baseline or treated low-density lipoprotein (LDL) cholesterol levels are only weakly associated with net coronary angiographic change or cardiovascular events. The beneficial effects of statins on clinical events may involve nonlipid mechanisms that modify endothelial function, inflammatory responses, plaque stability, and thrombus formation. Experimental animal models suggest that statins may foster stability through a reduction in macrophages and cholesterol ester content and an increase in volume of collagen and smooth muscle cells. The thrombotic sequelae caused by plaque disruption is mitigated by statins through inhibition of platelet aggregation and maintenance of a favorable balance between prothrombotic and fibrinolytic mechanisms. These nonlipid properties of statins may help to explain the early and significant cardiovascular event reduction reported in several clinical trials of statin therapy.