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| __NOTOC__
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| {{CMG}} {{AE}} {{mitra}}{{MC}}
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| ==Overview==
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| ==Complications==
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| ===Acute Coronary Syndromes===
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| ===Heart Failure===
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| ===Cardiogenic Shock===
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| ===Myocarditis===
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| ===Pericarditis===
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| ===Arrhythmias ===
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| ==== Pathophysiology: ====
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| Respiratory disease is the main target of Covid-19. One-third of patients with the severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]].<sup>[1]</sup> Severe acute respiratory syndrome coronavirus 2 (SARS-CoV2) utilizes S-spike to bind to angiotensin-converting enzyme 2 (ACE2) receptors to enter the cells. Type 1 and type 2 [[pneumocytes]] exhibit ACE 2 receptors in the lung. Studies report that coronary [[endothelial cells]] in the heart and intrarenal endothelial cells and renal tubular epithelial cells in the kidney exhibit ACE2. ACE2 is an inverse regulator of the [[renin-angiotensin system]].<sup>[1][2][3]</sup> The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and endothelial cells.<sup>[4]</sup>
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| ==References ==
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| # Wang D, Hu B, Hu C, et al. Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus–Infected Pneumonia in Wuhan, China. JAMA. 2020;323(11):1061–1069. [[doi:10.1001/jama.2020.1585]]
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| # Xu Z, Shi L, Wang Y, et al. Pathological findings of COVID-19 associated with acute respiratory distress syndrome [published correction appears in Lancet Respir Med. 2020 Feb 25;:]. Lancet Respir Med. 2020;8(4):420‐422. doi:10.1016/S2213-2600(20)30076-X
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| # Zheng YY, Ma YT, Zhang JY, Xie X. COVID-19 and the cardiovascular system. Nat Rev Cardiol. 2020;17(5):259‐260. doi:10.1038/s41569-020-0360-5
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| # Xiong TY, Redwood S, Prendergast B, Chen M. Coronaviruses and the cardiovascular system: acute and long-term implications. Eur Heart J. 2020;41(19):1798‐1800. doi:10.1093/eurheartj/ehaa231
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