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 postmyocardial 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.
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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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