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1 Hypertension and Vascular Research Division, and 2 Biostatistics Department, Henry Ford Health System, Detroit, Michigan 48202
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. Mice (4 wk old) of both genders were divided into four groups: female groups consisted of 1) sham
ovariectomy (S-Ovx) + placebo (P) (S-Ovx + P), 2)
S-Ovx + T, 3) Ovx + P, and 4) Ovx + T; and male groups consisted of 1) sham castration
(S-Cas)+ P (S-Cas + P), 2) S-Cas + 17
-estradiol
(E), 3) Cas + P, and 4) Cas + E. MI was
induced 6 wk 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, whereas
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.
sexual hormones; cardiac dysfunction
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