Abstract
Background:
Gender differences with respect to clinical presentation and outcome of cardiovascular disease have prompted examination of sex-specific factors that may influence cardiovascular physiology and pathophysiology. The rationale for evaluating control of contractility by estrogen derives from preclinical data demonstrating that 17β-estradiol (17β-E2) can attenuate the myocardial response to adrenergic stimulation.
Methods:
The effects of two doses of intracoronary 17β-E2 (150 and 300 ng/min) were tested on the left ventricular (LV) inotropic response to intravenous dobutamine in postmenopausal women who had undergone diagnostic cardiac catheterization. Peak positive LV+dP/dt (LV+dP/dtmax) was obtained from analysis of LV pressure recorded by a micromanometer catheter.
Results:
The study was terminated prematurely after the manufacturer stopped production of 17β-E2, and data from 7 patients who had completed the study were analyzed. Intracoronary 17β-E2 had no effect on basal LV+dP/dtmax (1299 ± 60 mm Hg/sec [mean ± SE] at control vs, 1299 ± 46 mm Hg/sec with 17β-E2). Intracoronary 17β-E2 also had no significant effect on the LV+dP/dtmax response to dobutamine (1672 ± 95 mm Hg/sec with dobutamine alone vs. 1639 ± 73 with dobutamine and 17β-E2, p = 0.51).
Conclusions:
In humans, no evidence of an acute moderate or large effect of 17β-E2 on adrenergically stimulated contractility was documented; a small effect size could not be excluded.
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