REVIEW ARTICLE
The evolving role of statins in the management of atherosclerosis
Carl J. Vaughan, MD, MRCPIa,
Antonio M. Gotto, Jr., MD, DPhil, FACCa and
Craig T. Basson, MD, PhD, FACCa
a Division of Cardiology, Department of Medicine, Weill Medical College of Cornell University, The New York Presbyterian Hospital, Starr 4, 525 East 68th Street, New York, New York 10021.USA
Manuscript received February 23, 1999;
revised manuscript received August 3, 1999,
accepted October 5, 1999.
Reprint requests and correspondence: Dr. Craig T. Basson, Director, Molecular Cardiology, Cardiology Division, Department of Medicine, Weill Medical College of Cornell University, Starr 4, 525 East 68th Street, New York, New York 10021.
ctbasson{at}mail.med.cornell.edu
Significant advances in the management of cardiovascular disease have been made possible by the development of 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors—"statins." Initial studies explored the impact of statin therapy on coronary artery disease (CAD) progression and regression. Although the angiographic changes were small, associated clinical responses appeared significant. Subsequent large prospective placebo-controlled clinical trials with statins demonstrated benefit in the secondary and primary prevention of CAD in subjects with elevated cholesterol levels. More recently, the efficacy of statins has been extended to the primary prevention of CAD in subjects with average cholesterol levels. Recent studies also suggest that statins have benefits beyond the coronary vascular bed and are capable of reducing ischemic stroke risk by approximately one-third in patients with evidence of vascular disease. In addition to lowering low-density lipoprotein (LDL) cholesterol, statin therapy appears to exhibit pleiotropic effects on many components of atherosclerosis including plaque thrombogenicity, cellular migration, endothelial function and thrombotic tendency. Growing clinical and experimental evidence indicates that the beneficial actions of statins occur rapidly and yield potentially clinically important anti- ischemic effects as early as one month after commencement of therapy. Future investigations are warranted to determine threshold LDL values in primary prevention studies, and to elucidate effects of statins other than LDL lowering. Finally, given the rapid and protean effects of statins on determinants of platelet reactivity, coagulation, and endothelial function, further research may establish a role for statin therapy in acute coronary syndromes.
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Abbreviations and Acronyms
| | AFCAPS/TexCAPS | = Air Force/Texas Coronary Atherosclerosis Prevention Study | | CAD | = coronary artery disease | | CARE | = Cholesterol and Recurrent Events trial | | HDL | = high-density lipoprotein cholesterol | | HMG CoA | = 3-hydroxy-3-methylglutaryl coenzyme A | | LDL | = low-density lipoprotein cholesterol | | LIPID | = Long-term Intervention with Pravastatin in Ischemic Disease study | | MI | = myocardial infarction | | NCEP | = National Cholesterol Education Program | | 4S | = Scandinavian Simvastatin Survival Study | | WOSCOPS | = West of Scotland Coronary Prevention Study |
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