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1 Department of Hypertension and Vascular Research, Henry Ford Health System, Detroit, MI, USA
2 Department of Biostatistics, Henry Ford Health System, Detroit, MI, USA
* To whom correspondence should be addressed. E-mail: xpyang1{at}hfhs.org.
Premenopausal women are much less prone to develop cardiovascular disease than men of similar age, but this advantage no longer applies after menopause. We previously found that male mice have a significantly higher rate of cardiac rupture than females during the acute phase of myocardial infarction (MI); however, the effects of sexual hormones on chronic remodeling are unknown. We hypothesized that estrogen (E) may protect the heart from chronic remodeling and deterioration of function post-MI, whereas testosterone (T) may have adverse effects. 4-week-old mice of both genders were divided into 4 groups: females, 1) sham-ovariectomy+placebo (s-ovx+P), 2) s-ovx+T, 3) ovx+P, and 4) ovx+T; and males, 1) sham-castration+P (s-cas+P), 2) s-cas+17
-estradiol (E), 3) cas+P, and 4) cas+E. MI was induced 6 weeks later. Echocardiography was performed to assess cardiac function and left ventricular dimensions (LVD). Myocyte cross-sectional area (MCSA) was measured at the end of the study. In females, both testosterone and ovariectomy decreased ejection fraction (EF) and increased LVD, and when combined they aggravated cardiac function and remodeling further. Testosterone significantly increased MCSA. In males, castration or estrogen increased EF and reduced LVD, while castration significantly reduced MCSA. Our data suggest that estrogen prevents deterioration of cardiac function and remodeling after MI, but testosterone worsens cardiac dysfunction and remodeling and has a pronounced effect when estrogen levels are reduced.
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