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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 chief target of Coronavirus disease 2019 (COVID-19). One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]].<ref name="pmid320315702">{{cite journal| author=Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J | display-authors=etal| title=Clinical Characteristics of 138 Hospitalized Patients With 2019 Novel Coronavirus-Infected Pneumonia in Wuhan, China. | journal=JAMA | year= 2020 | volume= | issue= | pages= | pmid=32031570 | doi=10.1001/jama.2020.1585 | pmc=7042881 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32031570 }}</ref>Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) 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]].<ref name="pmid320858462">{{cite journal| author=Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C | display-authors=etal| title=Pathological findings of COVID-19 associated with acute respiratory distress syndrome. | journal=Lancet Respir Med | year= 2020 | volume= 8 | issue= 4 | pages= 420-422 | pmid=32085846 | doi=10.1016/S2213-2600(20)30076-X | pmc=7164771 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32085846 }}</ref>The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and [[Endothelium|endothelial cells]].Elevated levels of [[Cytokine|cytokines]] as a result of the [[Systemic inflammatory response syndrome|systemic inflammatory response]] of the severe [[COVID-19|Coronavirus disease 2019]] (COVID-19) can cause injury to multiple organs, including [[Cardiac muscle|cardiac myocytes]].<ref name="pmid32186331">Xiong TY, Redwood S, Prendergast B, Chen M (2020) [https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&retmode=ref&cmd=prlinks&id=32186331 Coronaviruses and the cardiovascular system: acute and long-term implications.] ''Eur Heart J'' 41 (19):1798-1800. [http://dx.doi.org/10.1093/eurheartj/ehaa231 DOI:10.1093/eurheartj/ehaa231] PMID: [https://pubmed.gov/32186331 32186331]</ref> According to the data based on studies on previous [[Severe acute respiratory syndrome]] ([[Severe acute respiratory syndrome|SARS]]) and the [[Middle East respiratory syndrome coronavirus infection|Middle East respiratory syndrome]] ([[Middle East respiratory syndrome coronavirus infection|MERS]]) epidemic and the ongoing [[COVID-19]] outbreak, multiple mechanisms have been suggested for cardiac damage. <ref name="pmid32200663">{{cite journal| author=Clerkin KJ, Fried JA, Raikhelkar J, Sayer G, Griffin JM, Masoumi A | display-authors=etal| title=COVID-19 and Cardiovascular Disease. | journal=Circulation | year= 2020 | volume= 141 | issue= 20 | pages= 1648-1655 | pmid=32200663 | doi=10.1161/CIRCULATIONAHA.120.046941 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=32200663 }}</ref>
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| ==== Signs and Symptoms: ====
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| ==References ==
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| <references />
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