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CLINICAL STUDIES

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

Stephanie Hügel, MD^*, Martin Reincke, MD^*, Hinrik Strömer, MD^*, Johannes Winning, MD^*, Michael Horn, PhD^*, Charlotte Dienesch^*, Patricia Mora^*, Harald H. H. W. Schmidt, MD, Bruno Allolio, MD^* and Stefan Neubauer, MD^*

^* Medizinische Universitätsklinik, Würzburg, Germany
Institut für Pharmakologie und Toxikologie, Universität Würzburg, Würzburg, Germany

Manuscript received December 31, 1998; revised manuscript received May 20, 1999, accepted June 28, 1999.

Reprint requests and correspondence: Dr. Stephanie Hügel, Medizinische Universitätsklinik, Josef-Schneider-Str. 2, 97080 Würzburg, Germany
huegel{at}mail.uni-wuerzburg.de

OBJECTIVES

The purpose of this study was to examine whether endogenous estrogen deficiency induced by ovariectomy affects chronic left ventricular dysfunction post–myocardial infarction (MI).

BACKGROUND

Epidemiologic findings suggest that mortality of postmenopausal women is increased after MI, but the underlying mechanisms are unknown.

METHODS

Rats were either not ovariectomized (non-OVX), ovariectomized (OVX) or ovariectomized and treated with subcutaneous 17-beta-estradiol (E₂) pellets (OVX + E₂). Two weeks later, animals were sham-operated (Sham) or left coronary artery ligated (MI). Eight weeks later, in vivo echocardiographic and hemodynamic measurements were performed. Thereafter, hearts were isolated and perfused isovolumically.

RESULTS

Mean infarct size was similar among the three MI groups. Ovariectomy decreased serum E₂ levels (11 ± 4 vs. 49 ± 11 pg/ml in non-OVX, p < 0.01) and increased body weight. These changes were reversed by E₂ replacement. 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 + E₂ replacement did not alter left ventricular diameters in post-MI and Sham hearts. Left ventricular fractional shortening was severely impaired post-MI (19 ± 2% vs. 50 ± 3 in non-OVX + Sham hearts, p < 0.0001) with no influence of hormonal status. Left ventricular end-diastolic pressure, measured in vivo, was increased in all MI groups without significant differences between groups. Pressure-volume curves, obtained in perfused hearts, demonstrated a right and downward shift with reduced maximum left ventricular developed pressure post-MI (75 ± 6 vs. 108 ± 3 mm Hg in non-OVX + Sham hearts, p < 0.001) and were also unaffected by either OVX or E₂ replacement.

CONCLUSIONS

Chronic endogenous estrogen deficiency does not have major effects on the development of cardiac hypertrophy, dysfunction and dilation post-MI.

Abbreviations and Acronyms   CHD = coronary heart disease   E2 = 17-beta-estradiol   EDP = end-diastolic pressure   eNOS = endothelial nitric oxide synthase   HR = heart rate   LV = left ventricle   LVDP = left ventricular developed pressure   MI = myocardial infarction   OVX = ovariectomy

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