Gaetano Pietro Bulfamante1,2, Gianluca Lorenzo Perrucci3, Monica Falleni1,2, Elena Sommariva3, Delfina Tosi1, Carla Martinelli1, Paola Songia4, Paolo Poggio4, Stefano Carugo5, Giulio Pompilio3,6. 1. Unità di Anatomia Patologica, Dipartimento di Scienze della Salute, Università degli Studi di Milano, 20142 Milan, Italy. 2. Struttura Complessa di Anatomia Patologica e Genetica Medica, ASST Santi Paolo e Carlo, 20142 Milan, Italy. 3. Unità di Biologia Vascolare e Medicina Rigenerativa, Centro Cardiologico Monzino IRCCS, 20138 Milan, Italy. 4. Unità per lo Studio delle Patologie Aortiche, Valvolari e Coronariche, Centro Cardiologico Monzino IRCCS, 20138 Milano, Italy. 5. Unità di Cardiologia, Dipartimento di Scienze della Salute, Università degli Studi di Milano, 20142 Milan, Italy. 6. Dipartimento di Scienze Cliniche e di Comunità, Università degli Studi di Milano, 20122 Milan, Italy.
Abstract
AIMS: A considerable proportion of patients affected by coronavirus respiratory disease (COVID-19) develop cardiac injury. The viral impact in cardiomyocytes deserves, however, further investigations, especially in asymptomatic patients. METHODS: We investigated for SARS-CoV-2 presence and activity in heart tissues of six consecutive COVID-19 patients deceased from respiratory failure showing no signs of cardiac involvement and with no history of heart disease. Cardiac autopsy samples were collected within 2 h after death, and then analysed by digital PCR, Western blot, immunohistochemistry, immunofluorescence, RNAScope, and transmission electron microscopy assays. RESULTS: The presence of SARS-CoV-2 into cardiomyocytes was invariably detected in all assays. A variable pattern of cardiomyocyte injury was observed, spanning from absence of cell death and subcellular alterations hallmarks, to intracellular oedema and sarcomere ruptures. In addition, we found active viral transcription in cardiomyocytes, by detecting both sense and antisense SARS-CoV-2 spike RNA. CONCLUSIONS: In this autopsy analysis of patients with no clinical signs of cardiac involvement, the presence of SARS-CoV-2 in cardiomyocytes has been detected, determining variable patterns of intracellular damage. These findings suggest the need for cardiologic surveillance in surviving COVID-19 patients not displaying a cardiac phenotype.
AIMS: A considerable proportion of patients affected by coronavirus respiratory disease (COVID-19) develop cardiac injury. The viral impact in cardiomyocytes deserves, however, further investigations, especially in asymptomatic patients. METHODS: We investigated for SARS-CoV-2 presence and activity in heart tissues of six consecutive COVID-19patients deceased from respiratory failure showing no signs of cardiac involvement and with no history of heart disease. Cardiac autopsy samples were collected within 2 h after death, and then analysed by digital PCR, Western blot, immunohistochemistry, immunofluorescence, RNAScope, and transmission electron microscopy assays. RESULTS: The presence of SARS-CoV-2 into cardiomyocytes was invariably detected in all assays. A variable pattern of cardiomyocyte injury was observed, spanning from absence of cell death and subcellular alterations hallmarks, to intracellular oedema and sarcomere ruptures. In addition, we found active viral transcription in cardiomyocytes, by detecting both sense and antisense SARS-CoV-2spike RNA. CONCLUSIONS: In this autopsy analysis of patients with no clinical signs of cardiac involvement, the presence of SARS-CoV-2 in cardiomyocytes has been detected, determining variable patterns of intracellular damage. These findings suggest the need for cardiologic surveillance in surviving COVID-19patients not displaying a cardiac phenotype.
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