Why the study?
SARS-CoV-2 infects the heart, and hospitalized patients without prior heart disease frequently show significant heart tissue injury assessed by increased blood troponin levels.
SARS-CoV-2 infection directly injures human iPSC-derived cardiomyocytes, causing structural disorganization and functional impairment that may explain the clinical cardiac injury and decreased ejection fraction observed in COVID-19 patients.
Direct SARS-CoV-2 effects on iPSC-cardiomyocytes warrant caution in attributing clinical injury; leaves open mechanisms in patients.
SARS-CoV-2 infects multiple organs, including the heart. Analyses of hospitalized patients show that a substantial number without prior indication of heart disease or comorbidities show significant injury to heart tissue, assessed by increased levels of troponin in blood. We studied the cell biological and physiological effects of virus infection of healthy human iPSC-derived cardiomyocytes in culture. Virus infection with interleukins disorganizes myofibrils, increases cell size and the numbers of multinucleated cells, and suppresses the expression of proteins of the contractile apparatus. Viral infection of cardiomyocytes in culture triggers release of troponin similar to elevation in levels of COVID-19 patients with heart disease. Viral infection in the presence of interleukins slows down and desynchronizes the beating of cardiomyocytes in culture. The cell-level physiological changes are similar to decreases in left ventricular ejection seen in imaging of patients' hearts. These observations suggest that direct injury to heart tissue by virus can be one underlying cause of heart disease in COVID-19.
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A 2023 study studied this question.
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