Author + information
- Received September 12, 1994
- Revision received May 22, 1995
- Accepted July 10, 1995
- Published online November 15, 1995.
- Sarah A. Samaan, MD and
- Michael H. Crawford, MD, FACC*
- ↵*Address for correspondence:Dr. Michael H. Crawford, The University of New Mexico Health Sciences Center, Department of Medicine, Cardiology Division 5-ACC 2211 Lomas Boulevard, Northeast, Albuquerque, New Mexico 87131.
Nonrandomized trials of postmenopausal estrogen replacement have shown a benefit in the prevention of coronary artery disease. Less clear are the specific mechanisms by which this occurs. Estrogen has beneficial effects on the lipid profile, with significant elevations in high density lipoprotein cholesterol and reductions in low density lipoprotein cholesterol reported. Also, antioxidant properties have been ascribed to estrogen. In addition, estrogen has been shown to prevent paradoxic vasoconstriction in atherosclerotic coronary arteries after acetylcholine and may have calcium channel-blocking and alpha2-inhibiting properties. Other proposed mechanisms of cardiovascular protection include reductions in serum fibrinogen and increases in prostacyclin biosynthesis. There is some evidence that cardiovascular biomechanics may be mildly depressed after menopause and that estrogen may normalize these changes by increasing ventricular contractility and, possibly, relaxation. Far less is known about the cardiovascular effects of progesterone, but overall it does not appear that the less androgenic progestins substantially modify the effects of estrogen. Because more women >50 years old die of cardiovascular disease than any other cause, further clinical investigations of the risks and benefits of estrogen replacement and combined estrogen and progesterone therapy are clearly needed.
- Received September 12, 1994.
- Revision received May 22, 1995.
- Accepted July 10, 1995.
- American College of Cardiology