Key result
causal verbs okay).
Why the study?
Antihypertensive therapy should induce regression of structural abnormalities, but the effects of adding transdermal 17 beta-estradiol on left ventricular anatomy and systolic performance in hypertensive postmenopausal women were unclear.
Does transdermal 17 beta-estradiol added to standard antihypertensive therapy improve left ventricular anatomy and performance in hypertensive postmenopausal women?
RCT (n=169)
Double-blind
Randomized
Does transdermal 17 beta-estradiol added to standard antihypertensive therapy improve left ventricular anatomy and performance in hypertensive postmenopausal women?
Transdermal 17 beta-estradiol combined with standard antihypertensive therapy may enhance the reduction of left ventricular mass in postmenopausal women with mild to moderate hypertension.
Answers are grounded in this paper and cite their sources.
May further reduce LV mass beyond BP control in hypertensive postmenopausal women; leaves open routine use pending CV outcome trials.[[1]](https://www.ahajournals.org/doi/pdf/10.1161/01.HYP.34.5.
To reduce cardiovascular complications, antihypertensive therapy should not only normalize blood pressure but also induce a regression of structural abnormalities, which are the expression of end-organ damage. We investigated the effects of transdermal 17 beta-estradiol, combined with standard antihypertensive therapy, on the modification of left ventricular anatomy and systolic performance in hypertensive postmenopausal women. In a randomized, double-blind, placebo-controlled study, we enrolled 169 postmenopausal women with mild or moderate hypertension. Eighty-six patients (group 1) received transdermal 17 beta-estradiol (50 mu g/d) and norethisterone acetate (2.5 mg/d, orally), and 83 patients (group 2) received placebo. At baseline, all women underwent M-mode and 2-D echocardiogram, which was repeated after 6, 12, and 18 months of follow-up. After 18 months of treatment, we observed a significant decrease in left ventricular diastolic septal and posterior wall thickness and mass in both groups. Furthermore, after 18 months, left ventricular mass was significantly less than in the estrogen-treated group. No significant modifications were observed in left ventricular systolic and diastolic dimensions or in systolic performance, as expressed by left ventricular fractional shortening. In conclusion, transdermal 17 beta-estradiol, which is associated with antihypertensive therapy, may contribute in the reduction of left ventricular mass in hypertensive postmenopausal women.
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MODENA et al. (1999) conducted an RCT in Mild or moderate hypertension (n=169). Transdermal 17 beta-estradiol and norethisterone acetate vs. Placebo was evaluated on Modification of left ventricular anatomy and systolic performance.
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