Postmenopausal Hormone Therapy and Hypertension
March 1, 1999
Postmenopausal Hormone Therapy and Hypertension
Abstract & Commentary
Synopsis: Postmenopausal hormone therapy is not contraindicated in women with hypertension.
Source: Lloyd G, Jackson G. J Hum Hypertens 1998; 12:319-321.
Lloyd and jackson from the cardiothoracic Centre at Guy’s and St. Thomas’ Hospital in London reviewed the relationship between postmenopausal estrogen treatment and hypertension. They point out that a large number of in vivo and in vitro studies demonstrate that estrogen has multiple effects on the vascular system that are consistent with vasodilatation, not vasoconstriction. Clinical studies, such as the three year PEPI trial, have documented no significant effects of oral hormone therapy on blood pressure (either estrogen alone or estrogen combined with sequential progestational agents). In a prospective, randomized trial, transdermal estrogen administered to hypertensive women was associated with a 3 mm decrease in blood pressure.1 Lloyd and Jackson conclude that postmenopausal hormone therapy (PHT) either has no effect on blood pressure or a mild antihypertensive effect.
Comment By Leon Speroff, MD
Hypertension is both a risk factor for cardiovascular mortality and a common problem in older people. Therefore, it is important to realize that no relationship has been established between hypertension and the doses of estrogen used for postmenopausal therapy. Studies have either shown no effect or a small, but statistically significant, decrease in blood pressure due to estrogen treatment. This has been the case in both normotensive and hypertensive women. The addition of a progestin does not affect this response. Discontinuing hormone therapy in women with hypertension does not result in a decrease in blood pressure (an expected response if the treatment were raising blood pressure), and in some patients, discontinuation is followed by an increase in blood pressure.2 The rare cases of increased blood pressure due to oral estrogen therapy truly represent idiosyncratic reactions. Because of the protective effect of appropriate estrogen treatment on the risk of cardiovascular disease, it can be argued that a woman with controlled hypertension is in need of that specific benefit of estrogen. Indeed, in the Nurses’ Health Study, hypertensive women who used postmenopausal hormone therapy did have a reduced risk of coronary heart disease.3 Although this position has been challenged by the results of the HERS trial, the problems with the HERS (reviewed in a previous issue of Clinical Alert), combined with the large amount of evidence supporting a beneficial effect of estrogen do not support the contention that hypertension is a contraindication to postmenopausal therapy.
In view of the results of the HERS trial, is it reasonable to choose a progestational agent other than medroxyprogesterone acetate for hypertensive women? There is reason to believe that the continuous presence of medroxyprogesterone acetate could attenuate and even block the favorable effects of estrogen on atherosclerosis and vasomotor function. There is evidence in the monkey that medroxyprogesterone antagonizes the favorable effects of conjugated estrogens on both the process of atherosclerosis and vasodilatation, but progesterone did not interfere with the ability of estrogen to inhibit atherosclerosis. In a study of mechanisms involved in the regression of atheroscleorsis, conjugated estrogens did exert favorable activity (aortic connective tissue remodeling in response to lipid lowering) in the monkey, but medroxyprogesterone acetate prevented this action.4 At this time, I believe it is prudent to choose progestational agents other than medroxyprogesterone acetate in hormonal regimens for hypertensive women.
References
1. Manhem K, et al. J Hum Hypertens 1988;12:323-327.
2. Zarifis J, et al. Am J Hypertens 1995;8:1241-1242.
3. Grodstein F, et al. N Engl J Med 1996;335:453-461.
4. Register TC, et al. Arterioscler Thromb Vasc Biol 1998;18:1164-1171.
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