Circulation, Vol 81, 1680-1687, Copyright © 1990 by American Heart Association
JK Williams, MR Adams and HS Klopfenstein
Although evidence indicates that estrogen replacement therapy reduces risk
of coronary heart disease, the mechanism remains unknown. Among the
possibilities are that estrogen replacement therapy may 1) inhibit growth
of atherosclerotic plaque and 2) decrease the prevalence of transient
myocardial ischemia and myocardial infarction by modulating vasomotion in
atherosclerotic coronary arteries. Using quantitative coronary angiography,
we determined vasomotor responses of atherosclerotic coronary arteries in
ovariectomized cynomolgus monkeys; six were given physiological estrogen
"replacement" by subcutaneous implants, and six were not. Intracoronary
infusion of the endothelium- dependent dilator acetylcholine (1 X 10(-6) M)
caused paradoxical constriction of coronary arteries (from 1.2 +/- 0.2 to
0.6 +/- 0.1 mm, p less than 0.05) in the estrogen-deficient monkeys.
However, acetylcholine tended to minimally dilate the left circumflex
coronary artery in estrogen-treated monkeys (from 1.2 +/- 0.2 to 1.5 +/-
0.2 mm, p greater than 0.2). Although estrogen replacement therapy reduced
plaque extent in coronary arteries, altered vasomotion was not related to
plaque extent. We conclude that estrogen modulates vasomotion of
atherosclerotic coronary arteries of monkeys and speculate that
estrogen-modulated constrictor responses of atherosclerotic coronary
arteries may reduce the incidence of coronary heart disease in
postmenopausal women.
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Estrogen modulates responses of atherosclerotic coronary arteries
Arteriosclerosis Research Center, Bowman Gray School of Medicine, Wake Forest University, Winston-Salem, North Carolina 27103.
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