Key result
17β-Estradiol increases LVEF by ~15% and reverses LV dysfunction in castrated male rats.
Why the study?
No data are available on heart function in chronic testosterone deficiency and on the effect of estrogen treatment.
Answers are grounded in this paper and cite their sources.
Reverses LV dysfunction in a rat model of testosterone deficiency; leaves open translation to men with HF.
No data are available on heart function in chronic testosterone deficiency and on the effect of estrogen treatment. Eighteen 4-week-old male Lewis rats were randomly divided into 3 groups (n = 6): 1 group of sham-operated rats and 2 groups of castrated rats. Sixty-six weeks after surgery, 1 castrated group received a dose of 17β-estradiol (10 μg/kg per day) and the remaining 2 groups received a placebo subcutaneously for 14 days. Left ventricular (LV) systolic and diastolic functions were measured by transthoracic echocardiography. Castration decreased LV ejection fraction (9%) and fractional shortening (15%) and deteriorated LV diastolic function (94%). 17β-Estradiol treatment increased LV ejection fraction (15%) and fractional shortening (31%) and improved LV diastolic function (48%). Plasma testosterone concentrations were decreased in both castrated groups. In conclusion, chronic testosterone deficiency induced LV systolic and diastolic dysfunction; these disorders were reversed by short-term treatment with 17β-estradiol.
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Baka et al. (2018) studied Chronic testosterone deficiency (n=18). 17β-estradiol vs. Placebo was evaluated on Left ventricular ejection fraction. 17β-Estradiol treatment increased left ventricular ejection fraction by 15% and fractional shortening by 31%, reversing left ventricular systolic and diastolic dysfunction in castrated male rats.
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