Christian Möller1, Thomas Stiermaier1, Georg Brabant2, Tobias Graf1, Holger Thiele3, Ingo Eitel4. 1. Department of Cardiology, Angiology and Intensive Care Medicine, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Lübeck, Germany. 2. Department of Experimental and Clinical Endocrinology, Medical Clinic I, University Medical Center Lübeck, Lübeck, Germany. 3. Department of Internal Medicine-Cardiology, University of Leipzig-Heart Center, Leipzig, Germany. 4. Department of Cardiology, Angiology and Intensive Care Medicine, Medical Clinic II, University Heart Center Lübeck, Lübeck, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Kiel/Lübeck, Lübeck, Germany. Electronic address: ingo.eitel@uskh.de.
Abstract
BACKGROUND: The detailed pathomechanism of Takotsubo syndrome (TS) is still elusive. Due to the predominance of postmenopausal females, a potential role of sex hormones has been suggested. However, the limited available data are contradictory. The aim of this study was to comprehensively assess the role of sex hormone levels in a large cohort of TS patients. METHODS: Serum samples of 57 female TS patients and 57 female patients with myocardial infarction (MI), matched for age (±2years) and repolarization disturbances were analyzed for estradiol (E2), estrone (E1), testosterone and androstenedione using liquid chromatography-tandem mass spectrometry. RESULTS: There was no difference concerning the concentrations of E1 [pmol/l (IQR): 89.1 (62.5, 132.0) vs. 98.8 (63.3, 156.0), p=0,441], testosterone [nmol/l (IQR): 0.67 (0.46, 1.00) vs. 0.80 (0.49, 1.08), p=0.382] and androstenedione [nmol/l (IQR): 2.03 (1.57, 3.11) vs. 2.98 (1.48, 5.27), p=0.244] between female TS and MI patients. Regarding E2, the majority of patients demonstrated concentrations below the detection limit of 30pmol/l (TS: n=41/54, 75.9%; MI: n=32/53, 60.4%; p=0.078). The remaining individuals with detectable E2 concentrations did not show a significant difference between TS and MI patients [pmol/l (IQR): 40.5 (33.0, 53.3) vs. 54.1 (37.9, 60.9); p=0.20]. CONCLUSIONS: Altered sex hormone levels, especially an estradiol deficiency, could not be identified as a risk factor for TS.
BACKGROUND: The detailed pathomechanism of Takotsubo syndrome (TS) is still elusive. Due to the predominance of postmenopausal females, a potential role of sex hormones has been suggested. However, the limited available data are contradictory. The aim of this study was to comprehensively assess the role of sex hormone levels in a large cohort of TS patients. METHODS: Serum samples of 57 female TS patients and 57 female patients with myocardial infarction (MI), matched for age (±2years) and repolarization disturbances were analyzed for estradiol (E2), estrone (E1), testosterone and androstenedione using liquid chromatography-tandem mass spectrometry. RESULTS: There was no difference concerning the concentrations of E1 [pmol/l (IQR): 89.1 (62.5, 132.0) vs. 98.8 (63.3, 156.0), p=0,441], testosterone [nmol/l (IQR): 0.67 (0.46, 1.00) vs. 0.80 (0.49, 1.08), p=0.382] and androstenedione [nmol/l (IQR): 2.03 (1.57, 3.11) vs. 2.98 (1.48, 5.27), p=0.244] between female TS and MI patients. Regarding E2, the majority of patients demonstrated concentrations below the detection limit of 30pmol/l (TS: n=41/54, 75.9%; MI: n=32/53, 60.4%; p=0.078). The remaining individuals with detectable E2 concentrations did not show a significant difference between TS and MI patients [pmol/l (IQR): 40.5 (33.0, 53.3) vs. 54.1 (37.9, 60.9); p=0.20]. CONCLUSIONS: Altered sex hormone levels, especially an estradiol deficiency, could not be identified as a risk factor for TS.
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