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. 2020 Jun 10;61(6):381–395. doi: 10.1016/j.hjc.2020.05.004

Figure 1.

Figure 1

Clinical manifestations of cardiovascular disease after infection with SARS-CoV-2. (1) High ACE2 expression is detected in cardiac and vascular tissue and may therefore facilitate cellular entry of SARS-CoV-2 resulting in myocardial and vascular damage. (2) An aberrant T-cell and monocyte activation has been observed in patients with COVID-19 leading to a systemic hyperinflammatory response. Increased circulating proinflammatory cytokines may result in inflammatory cardiomyopathy or atherothrombosis, causing an acute coronary syndrome. Systemic inflammatory response can also activate the microvascular endothelium, provoking the dysfunction of the coronary microvasculature, and consequently resulting in myocardial ischemia and myocardial injury. (3) Decreased myocardial oxygen supply, due to severe COVID-19 respiratory complications and hypoxia, along with increased myocardial oxygen demand, mainly due to high systemic metabolic needs, can provoke myocardial injury and type 2 myocardial infarction. (4) The binding of SARS-CoV-2 to ACE2 is expected to lead to the internalization of ACE2 and loss of the external ACE2 catalytic effect. Therefore, the possible downregulation of ACE2 and the subsequent decrease of angiotensin 1-7 in patients with COVID-19 may also compromise heart function. This figure was created using Servier Medical Art templates, which are licensed under a Creative Commons Attribution 3.0 Unported License; https://smart.servier.com. ACE2: angiotensin-converting enzyme 2, MI: myocardial infarction, and SARS-CoV-2: severe acute respiratory syndrome coronavirus 2.