Michael Schwarzl1, Francisco Ojeda2, Tanja Zeller3, Moritz Seiffert2, Peter M Becher2, Thomas Munzel4, Philipp S Wild4, Maria Blettner5, Karl J Lackner6, Norbert Pfeiffer7, Manfred E Beutel8, Stefan Blankenberg3, Dirk Westermann3. 1. Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany DZHK (German Centre for Cardiovascular Research), Partner site Hamburg/Kiel/Lübeck, Hamburg, Germany m.schwarzl@uke.de. 2. Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany. 3. Department of General and Interventional Cardiology, University Heart Center Hamburg-Eppendorf, Martinistr. 52, 20246 Hamburg, Germany DZHK (German Centre for Cardiovascular Research), Partner site Hamburg/Kiel/Lübeck, Hamburg, Germany. 4. Department of Medicine II, University Medical Center Mainz, Mainz, Germany. 5. Institute for Medical Biometrics, Epidemiology and Informatics (IMBEI), University Medical Center Mainz, Mainz, Germany. 6. Institute of Clinical Chemistry and Laboratory Medicine, University Medical Center Mainz, Mainz, Germany. 7. Department of Ophthalmology, University Medical Center Mainz, Mainz, Germany. 8. Department of Psychosomatic Medicine and Psychotherapy, University Medical Center Mainz, Mainz, Germany.
Abstract
AIMS: Left-ventricular (LV) remodelling impacts on the LV end-diastolic pressure-volume relationship (EDPVR), which is different in heart failure (HF) with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In a large-scale, population-based cohort (Gutenberg Health Study), we aimed to investigate alterations of the EDPVR in HF patients and their association to risk factors and all-cause mortality in non-HF individuals. METHODS AND RESULTS: Based on clinical and echocardiographic data, participants were divided into 'No HF' (n = 14487), HFrEF (n = 215), and HFpEF (n = 79). We estimated the position of the EDPVR and its stiffness-coefficient β from echocardiographic data using a single-beat method. The EDPVR was shifted rightward in HFrEF and leftward in HFpEF compared with 'No HF', while the stiffness-coefficient β was increased in both HFrEF and HFpEF. In 'No HF', a higher stiffness-coefficient β was associated with age, female gender, hypertension, diabetes, and obesity, while age and female gender were associated with a leftward shift of the EDPVR, whereas dyslipidaemia, obesity, smoking, and impaired renal function were associated with a rightward shift of the EDPVR. Both changes of the EDPVR were associated with increased all-cause mortality. CONCLUSION: In a large-scale, population-based cohort, we show distinct alterations of the EDPVR in HFrEF and HFpEF. Already in non-HF individuals, the presence of risk factors for HF is linked alterations of the EDPVR, which are associated with increased mortality. Published on behalf of the European Society of Cardiology. All rights reserved.
AIMS: Left-ventricular (LV) remodelling impacts on the LV end-diastolic pressure-volume relationship (EDPVR), which is different in heart failure (HF) with reduced ejection fraction (HFrEF) and HF with preserved ejection fraction (HFpEF). In a large-scale, population-based cohort (Gutenberg Health Study), we aimed to investigate alterations of the EDPVR in HF patients and their association to risk factors and all-cause mortality in non-HF individuals. METHODS AND RESULTS: Based on clinical and echocardiographic data, participants were divided into 'No HF' (n = 14487), HFrEF (n = 215), and HFpEF (n = 79). We estimated the position of the EDPVR and its stiffness-coefficient β from echocardiographic data using a single-beat method. The EDPVR was shifted rightward in HFrEF and leftward in HFpEF compared with 'No HF', while the stiffness-coefficient β was increased in both HFrEF and HFpEF. In 'No HF', a higher stiffness-coefficient β was associated with age, female gender, hypertension, diabetes, and obesity, while age and female gender were associated with a leftward shift of the EDPVR, whereas dyslipidaemia, obesity, smoking, and impaired renal function were associated with a rightward shift of the EDPVR. Both changes of the EDPVR were associated with increased all-cause mortality. CONCLUSION: In a large-scale, population-based cohort, we show distinct alterations of the EDPVR in HFrEF and HFpEF. Already in non-HF individuals, the presence of risk factors for HF is linked alterations of the EDPVR, which are associated with increased mortality. Published on behalf of the European Society of Cardiology. All rights reserved.
Authors: Christoph Sinning; Francisco Ojeda; Philipp S Wild; Renate B Schnabel; Michael Schwarzl; Sevenai Ohdah; Karl J Lackner; Norbert Pfeiffer; Matthias Michal; Maria Blettner; Thomas Munzel; Tibor Kempf; Kai C Wollert; Kari Kuulasmaa; Stefan Blankenberg; Veikko Salomaa; Dirk Westermann; Tanja Zeller Journal: Clin Res Cardiol Date: 2016-12-21 Impact factor: 5.460
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