Acute effects of 17 beta-estradiol on ventricular and vascular hemodynamics in postmenopausal women

Because premenopausal women have lower cardiovascular morbidity than postme nopausal women, it has been proposed that estrogen may have a protective ro le. Estrogen is involved in smooth muscle relaxation both through its speci fic receptor as well as through calcium channel blockade. This study examin ed the acute effect of estradiol on invasive cardiovascular hemodynamics in 18 postmenopausal women (age 62.6 +/- 7.6 years, means +/- SD). The effect of estradiol on left ventricular chamber performance was studied in 9 wome n using simultaneous left ventricular pressure-volume recordings. In a furt her group of 9 women, the acute effect of estradiol on arterial function wa s assessed using input impedance (derived from simultaneous aortic pressure and flow recordings), pressure waveform analysis, and pulse wave velocity. After 2 mg micronized 17 beta -estradiol was administered, serum estradiol levels increased from 50.9 +/- 21.9 to 3,190 +/- 2,216 pmol/l, P < 0.0001. There was no effect of estradiol on either left ventricular inotropic or l usitropic function. There was no acute effect of estradiol on arterial impe dance, reflection coefficient, augmentation index, or pulse wave velocity. There was a trend to decreased heart rate and cardiac output in both groups of 9 women. Because heart rate and cardiac output were common to both hemo dynamic data sets, results for these parameters were pooled. Across all 18 women, there was a small but significant decrease in heart rate (69.2 +/- 1 0.4 vs. 67.2 +/- 9.9 beats/min, P = 0.02), as well as a significant decreas e in cardiac output (4.82 +/- 1.77 vs. 4.17 +/- 1.56 1/min, P = 0.002). Des pite achieving supraphysiological serum levels, this study found no signifi cant effect of acute 17<beta>-estradiol on ventricular or large artery func tion.