Evidence against a role of physiological concentrations of estrogen in post-myocardial infarction remodeling

OBJECTIVES: The purpose of this study was to examine whether endogenous est rogen deficiency induced by ovariectomy affects chronic left ventricular dy sfunction post-myocardial infarction (MI). BACKGROUND: Epidemiologic findings suggest that mortality of postmenopausal women is increased after MI, but the underlying mechanisms are unknown. Ra ts were either not ovariectomized (non-OVX), ovariectomized (OVX) or ovarie ctomized and treated with subcutaneous 17-beta-estradiol (E-2) pellets (OVX + E-2). Two weeks later, animals were sham-operated (Sham) or left coronar y artery ligated (MI). Eight weeks later, in vivo echocardiographic and hem odynamic measurements were performed. Thereafter, hearts were isolated and perfused isovolumically. RESULTS: Mean infarct size was similar among the three MI groups. Ovariecto my decreased serum E-2 levels (11 +/- 4 vs. 49 +/- 11 pg/ml in non-OVX, p < 0.01) and increased body weight. These changes were reversed by E-2 replac ement. The degree of cardiac hypertrophy was similar for all groups post-MI . Left Ventricular diameters were increased post-MI (8.9 +/- 0.4 in non-OVX + MI vs. 6.7 +/- 0.2 mm in non-OVX + Sham hearts, p < 0.0001), but OVX or OVX + E-2 replacement did not alter left ventricular diameters in post-MI a nd Sham hearts. Left Ventricular fractional shortening was severely impaire d post-MI (19 +/- 2% vs. 50 +/- 3 in non-OVX + Sham hearts, p < 0.0001) wit h no influence of hormonal status. Left ventricular end-diastolic pressure, measured in vivo, was increased in all MI groups without significant diffe rences between groups. Pressure-volume curves, obtained in perfused hearts, demonstrated a right and downward shift with reduced maximum left ventricu lar developed pressure post-MI (75 +/- 6 vs. 108 +/- 3 mm Hg in non-OVX + S ham hearts, p < 0.001) and were also unaffected by either OVX or E-2 replac ement. CONCLUSIONS: Chronic endogenous estrogen deficiency does not have major eff ects on the development of cardiac hypertrophy, dysfunction and dilation po st-MI. (C) 1999 by the American College of Cardiology.