Abstract
The association of estrogen therapy with reduced levels of coronary artery disease in postmenopausal women has resulted in a burst of investigations into the mechanism(s) by which protection is offered. Findings published in the past year suggest that estrogen replacement alters every stage of the disease, from atherogenesis and plaque formation, to vascular reponsiveness in already diseased arteries. The lipid metabolic alterations caused by estrogen replacement therapy have been confirmed and appear unaffected by the concurrent use of progestins. Consensus reports have recommended that high cardiovascular disease risk be added to the indications for the use of postmenopausal hormone replacement.