Our central hypothesis is that circulating components like cytokines generated in the host response to infection by the SARS-CoV-2 virus contribute to alterations in cardiac function that manifest as arrhythmias and/or diminished output ;and that these components can be identified using engineered, matured iPSC-derived-cardiac tissues. Our goal is to combine clinical and laboratory resources to robustly characterize the myocardial involvement in COVID-19, by pursuing the following specific aims:1. Adapt human iPSC derived cardiac tissue autoimmune cardiomyopathy model for the use of studying cardiomyopathy in COVID-19 patients. 2.Delineate contribution of cellular immunity, cytokines, and other serum components on the development of cardiomyopathy using engineered human iPS-derived cardiac tissues. 3. Identify transcriptomic changes in cardiomyocytes, fibroblasts and CD14+ cells that contribute to COVID-19 cardiomyopathy using single cell RNA-seq
