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. 2021 Nov 16:ehab696. doi: 10.1093/eurheartj/ehab696

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This article has been co-published with permission in the European Heart Journal and Cardiovascular Research. © The European Society of Cardiology 2021. All rights reserved. The articles are identical except for minor stylistic and spelling differences in keeping with each journal’s style. Either citation can be used when citing this article.

This article is published and distributed under the terms of the Oxford University Press, Standard Journals Publication Model (https://academic.oup.com/journals/pages/open_access/funder_policies/chorus/standard_publication_model)

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.

PMC Copyright notice

Cardiovascular involvement in COVID-19—key manifestations and hypothetical mechanisms. SARS-CoV-2 anchors on transmembrane angiotensin-converting enzyme 2 to enter the host cells including type 2 pneumocytes, macrophages, endothelial cells, pericytes, and cardiac myocytes, leading to inflammation and multiorgan failure. In particular, the infection of endothelial cells or pericytes could lead to severe microvascular and macrovascular dysfunction. Furthermore, in conjunction with the immune over-reactivity, it can potentially destabilize atherosclerotic plaques and explain the development of the acute coronary syndrome. Infection of the respiratory tract, particularly of type 2 pneumocytes, by severe acute respiratory syndrome coronavirus 2 is manifested by the progression of systemic inflammation and immune cell overactivation, leading to a ‘cytokine storm’, which results in an elevated level of cytokines such as IL-6, IL-7, IL-22, and CXCL10. Subsequently, it is possible that activated T cells and macrophages may infiltrate infected myocardium, resulting in the development of fulminant myocarditis and severe cardiac damage. This process could be further intensified by the cytokine storm. Similarly, the viral invasion could cause cardiac myocyte damage directly leading to myocardial dysfunction and contribute to the development of arrhythmia. CXCL10, C-X-C motif chemokine ligand 10; IL-6, interleukin 6; SARS-CoV-2, severe acute respiratory syndrome coronavirus 2.