Mathias Orban1,2, Stéphanie Bieber3,4, Angelina Kraechan1,5, Johannes C Hellmuth5,6, Maximilian Muenchhoff5,7,8, Clemens Scherer1,5,2, Ines Schroeder9, Michael Irlbeck9, Stefan Kaeaeb5,2, Steffen Massberg1,2, Joerg Hausleiter1,2, Ulrich Grabmaier1,5,2, Ludwig T Weckbach10,11,12,13. 1. Medizinische Klinik und Poliklinik I, Klinikum der Universitaet Muenchen, Ludwig-Maximilians-University, Marchioninistraße 15, 81377, Munich, Germany. 2. DZHK (German Centre for Cardiovascular Research), Partner Site, Munich, Germany. 3. Medizinische Klinik und Poliklinik I, Klinikum der Universitaet Muenchen, Ludwig-Maximilians-University, Marchioninistraße 15, 81377, Munich, Germany. Stephanie.Bieber@med.uni-muenchen.de. 4. COVID-19 Registry of the LMU Munich (CORKUM), University Hospital, LMU Munich, Munich, Germany. Stephanie.Bieber@med.uni-muenchen.de. 5. COVID-19 Registry of the LMU Munich (CORKUM), University Hospital, LMU Munich, Munich, Germany. 6. Medizinische Klinik und Poliklinik III, Klinikum der Universitaet Muenchen, Ludwig-Maximilians-University, Munich, Germany. 7. Max Von Pettenkofer Institute and Gene Center, Virology, National Reference Center for Retroviruses, Faculty of Medicine, LMU Muenchen, Munich, Germany. 8. DZIF (German Center for Infection Research), Partner Site, Munich, Germany. 9. Department of Anaesthesiology, Ludwig-Maximilians-University, Munich, Germany. 10. Medizinische Klinik und Poliklinik I, Klinikum der Universitaet Muenchen, Ludwig-Maximilians-University, Marchioninistraße 15, 81377, Munich, Germany. Ludwig.Weckbach@med.uni-muenchen.de. 11. COVID-19 Registry of the LMU Munich (CORKUM), University Hospital, LMU Munich, Munich, Germany. Ludwig.Weckbach@med.uni-muenchen.de. 12. DZHK (German Centre for Cardiovascular Research), Partner Site, Munich, Germany. Ludwig.Weckbach@med.uni-muenchen.de. 13. Institute of Cardiovascular Physiology and Pathophysiology, Biomedical Center, Ludwig-Maximilians-University, Planegg-Martinsried, Germany. Ludwig.Weckbach@med.uni-muenchen.de.
Abstract
PURPOSE: SARS-COV-2 infection can develop into a multi-organ disease. Although pathophysiological mechanisms of COVID-19-associated myocardial injury have been studied throughout the pandemic course in 2019, its morphological characterisation is still unclear. With this study, we aimed to characterise echocardiographic patterns of ventricular function in patients with COVID-19-associated myocardial injury. METHODS: We prospectively assessed 32 patients hospitalised with COVID-19 and presence or absence of elevated high sensitive troponin T (hsTNT+ vs. hsTNT-) by comprehensive three-dimensional (3D) and strain echocardiography. RESULTS: A minority (34.3%) of patients had normal ventricular function, whereas 65.7% had left and/or right ventricular dysfunction defined by impaired left and/or right ventricular ejection fraction and strain measurements. Concomitant biventricular dysfunction was common in hsTNT+ patients. We observed impaired left ventricular (LV) global longitudinal strain (GLS) in patients with myocardial injury (-13.9% vs. -17.7% for hsTNT+ vs. hsTNT-, p = 0.005) but preserved LV ejection fraction (52% vs. 59%, p = 0.074). Further, in these patients, right ventricular (RV) systolic function was impaired with lower RV ejection fraction (40% vs. 49%, p = 0.001) and reduced RV free wall strain (-18.5% vs. -28.3%, p = 0.003). Myocardial dysfunction partially recovered in hsTNT + patients after 52 days of follow-up. In particular, LV-GLS and RV-FWS significantly improved from baseline to follow-up (LV-GLS: -13.9% to -16.5%, p = 0.013; RV-FWS: -18.5% to -22.3%, p = 0.037). CONCLUSION: In patients with COVID-19-associated myocardial injury, comprehensive 3D and strain echocardiography revealed LV dysfunction by GLS and RV dysfunction, which partially resolved at 2-month follow-up. TRIAL REGISTRATION: COVID-19 Registry of the LMU University Hospital Munich (CORKUM), WHO trial ID DRKS00021225.
PURPOSE:SARS-COV-2 infection can develop into a multi-organ disease. Although pathophysiological mechanisms of COVID-19-associated myocardial injury have been studied throughout the pandemic course in 2019, its morphological characterisation is still unclear. With this study, we aimed to characterise echocardiographic patterns of ventricular function in patients with COVID-19-associated myocardial injury. METHODS: We prospectively assessed 32 patients hospitalised with COVID-19 and presence or absence of elevated high sensitive troponin T (hsTNT+ vs. hsTNT-) by comprehensive three-dimensional (3D) and strain echocardiography. RESULTS: A minority (34.3%) of patients had normal ventricular function, whereas 65.7% had left and/or right ventricular dysfunction defined by impaired left and/or right ventricular ejection fraction and strain measurements. Concomitant biventricular dysfunction was common in hsTNT+ patients. We observed impaired left ventricular (LV) global longitudinal strain (GLS) in patients with myocardial injury (-13.9% vs. -17.7% for hsTNT+ vs. hsTNT-, p = 0.005) but preserved LV ejection fraction (52% vs. 59%, p = 0.074). Further, in these patients, right ventricular (RV) systolic function was impaired with lower RV ejection fraction (40% vs. 49%, p = 0.001) and reduced RV free wall strain (-18.5% vs. -28.3%, p = 0.003). Myocardial dysfunction partially recovered in hsTNT + patients after 52 days of follow-up. In particular, LV-GLS and RV-FWS significantly improved from baseline to follow-up (LV-GLS: -13.9% to -16.5%, p = 0.013; RV-FWS: -18.5% to -22.3%, p = 0.037). CONCLUSION: In patients with COVID-19-associated myocardial injury, comprehensive 3D and strain echocardiography revealed LV dysfunction by GLS and RV dysfunction, which partially resolved at 2-month follow-up. TRIAL REGISTRATION: COVID-19 Registry of the LMU University Hospital Munich (CORKUM), WHO trial ID DRKS00021225.
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