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. 2020 Oct 22;11:570681. doi: 10.3389/fimmu.2020.570681

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Copyright © 2020 Gopal, Marinelli and Alcorn

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential immune mechanisms of COVID-19 associated cardiovascular diseases. (A) SARS-CoV-2 enters the respiratory epithelium through the angiotensin-converting enzyme II (ACE2) receptor. The innate immune response induces various cytokines and chemokines to recruit macrophages and neutrophils to control the virus. (B, C) The hyperinflammatory cytokine storm increases vascular permeability, decreases gas exchange, stimulates pro-coagulation pathways, and subsequently causes ARDS. (D, E) Direct viral entry and inflammatory mediators can activate endothelial adhesion and clotting factors in the vascular space. Inflammatory cytokine storm, oxygen supply/demand mismatch due to hypoxia, endothelial activation, and dysregulation of clotting factors are likely mechanisms involved in triggering myocardial infarction in COVID-19 patients. (F) Direct viral entry, along with viral-induced inflammatory mediators increase myocarditis. All these pathological effects lead to arrhythmia, heart failure, and myocardial inflammation in multisystemic inflammatory syndrome. This figure was made in ^©BioRender—biorender.com.