ARTERIAL REACTIVITY IS ENHANCED IN GENETIC MALES TAKING HIGH-DOSE ESTROGENS

Objectives. We sought to assess whether high dose estrogen treatment i s associated with enhanced arterial reactivity in genetic males. Backg round. Although estrogens have been shown to enhance arterial reactivi ty in women, and are thereby thought to confer cardiovascular benefit, the vascular effects of long-term estrogen therapy in genetic males i s unknown. Methods. We studied the arterial physiology of 30 genetic m ales-15 male to female transsexuals receiving long-term high dose estr ogen therapy and 15 healthy male control subjects matched for age, smo king history and vessel size. Using external vascular ultrasound, brac hial artery diameter was measured at rest, after how increase (causing endothelium-dependent dilation [EDD]) and after nitroglycerin (GTN), an endothelium-independent dilator. Blood pressure, cholesterol and te stosterone levels were also measured in each subject. Results. Total t estosterone and free testosterone index levels were lower in the trans sexuals compared with the control subjects (p < 0.001). In contrast, E DD was significantly higher in the transsexuals than in the control ma les (mean [+/- SD] 7.1 +/- 3.1% vs. 3.2 +/- 2.8%, p = 0.001), as was t he GTN response (21.2 +/- 6.7% vs. 14.6 +/- 3.3%, p = 0.002). Total an d high density lipoprotein cholesterol, blood pressure levels and base line vessel size were similar in the two groups. On multivariate analy sis, enhanced EDD was associated independently with estrogen therapy ( p = 0.02) and with low total cholesterol (p = 0.04). An enhanced GTN r esponse was also significantly associated with estrogen therapy (p = 0 .03). Conclusions. Long-term treatment with high dose estrogens is ass ociated with enhanced arterial reactivity in genetic males, which may be due to the effects of estrogen excess or androgen deprivation, or b oth. (C) 1997 by the American College of Cardiology.