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. 2023 Feb;71(2):71–80. doi: 10.1177/10815589221141841

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© 2023 American Federation for Medical Research

This article is made available via the PMC Open Access Subset for unrestricted re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the COVID-19 pandemic or until permissions are revoked in writing. Upon expiration of these permissions, PMC is granted a perpetual license to make this article available via PMC and Europe PMC, consistent with existing copyright protections.

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Figure 1. — The SARS-Cov-2 enters via respiration and is localized in pneumocytes via ACE2- that is dominant in bronchiolar epithelium and can active immune response (innate and adaptive) against COVID-19. Pneumonia and ARDS are main problems in COVID-19. Inflammation, pro-inflammatory cytokines release, and CS lead to the structural and functional (mechanical and electrical) CVD (cardiomyopathy, endomyocardial, pericarditis, arrhythmia, etc.) and coagulopathy (microthrombi, thromboembolism, ischemia, DIC, etc.).

ANG, angiotensin; ACE, angiotensin-converting enzyme; ARDS, acute respiratory distress syndrome; CS, cytokine storm; CVD, cardiovascular disease; DIC, disseminated intravascular coagulation.