Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has infected more than 6 million individuals worldwide, leading to the ongoing coronavirus disease 2019 (COVID-19) pandemic and significant morbidity and mortality. Patients with active myocardial injury (ie, elevated troponin levels) are at a very high risk, with mortality rates reaching as high as 40%.1,2 In particular, the subset of patients with evidence of myocardial injury and underlying cardiovascular disease are at exceedingly high risk, with mortality rates of nearly 70%.1,2 While several mechanisms have been postulated for how SARS-CoV-2 may damage the lungs, heart, and other organs, indirect damage from innate, cellular, and/or humoral immune responses, including a severe cytokine storm, is a leading hypothesis supported by numerous studies reporting significantly elevated inflammatory biomarkers in patients with COVID-19.
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Published: June 24, 2020. doi:10.1001/jamanetworkopen.2020.13556
Open Access: This is an open access article distributed under the terms of the CC-BY License. © 2020 Rabbani AB et al. JAMA Network Open.
Corresponding Author: Amir B. Rabbani, MD, Division of Cardiology, University of California, Los Angeles, 3500 Lomita Blvd, Ste M100, Torrance, CA 90505 (email@example.com).
Conflict of Interest Disclosures: None reported.
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