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* From the The Johns Hopkins Ciccarone Center for Prevention of Heart Disease (Drs. Braunstein, Kershner, Gerstenblith, Schulman, Post, and Blumenthal), Division of Cardiology, Department of Medicine, Johns Hopkins Hospital, Baltimore, MD; and the Thrombosis Research Section (Dr. Bray), Department of Medicine, Baylor College of Medicine, Houston, TX.
Correspondence to: Roger S. Blumenthal, MD, FCCP, Division of Cardiology, Johns Hopkins Hospital, 600 North Wolfe St, Carnegie 538, Baltimore, MD 21287; e-mail: rblument{at}jhmi.edu
Genetic variants of key hemostatic mediators increasingly have been proposed as risk factors for atherothrombosis. The Hormone and Estrogen/Progestin Replacement Study group recently reported that the initiation of estrogen replacement in postmenopausal women with known coronary heart disease is associated with an early increase in cardiovascular events. A putative genetic susceptibility factor has been proposed a potential mediator of this increased event risk. This review outlines the recent literature to support the premise for this important proposal. Genetic profiling has great potential to improve the safety and efficacy of individualized pharmacotherapy in postmenopausal women and other at-risk populations for the prevention of cardiovascular disease.
Key Words: arterial thrombosis estrogen therapy genetic polymorphisms hemostatic factors
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