Cardiovascular Disorders and COVID-19: Difference between revisions

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==== Pathophysiology:                                                                                                                                                                                                                                                ====
==== Pathophysiology:                                                                                                                                                                                                                                                ====
Respiratory disease is the chief target of Covid-19. One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]].<ref name="pmid32031570">{{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-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>
Respiratory disease is the chief target of Covid-19. One-third of patients with severe disease also reported other symptoms including [[Cardiac arrhythmia|arrhythmia]]. 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]].<ref name="pmid32031570" /><ref name="pmid32085846">{{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 endothelial cells.<sup>[4]</sup>


==References                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                ==
==References                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                                ==


#      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]]
#      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
#      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
#     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
#     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
#     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
#     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
<references />

Revision as of 14:28, 12 June 2020


Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mitra Chitsazan, M.D.[2]Mandana Chitsazan, M.D. [3]

Overview

Complications

Acute Coronary Syndromes

Heart Failure

Cardiogenic Shock

Myocarditis

Pericarditis

Arrhythmias

Pathophysiology:

Respiratory disease is the chief target of Covid-19. One-third of patients with severe disease also reported other symptoms including arrhythmia. 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.[1][2] The interaction between SARS-CoV2 and ACE2 can bring about changes in ACE2 pathways prompting intense injury to the lung, heart, and endothelial cells.[4]

References

  1.      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
  2.     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
  3.     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
  1. ↑
  2. ↑ Xu Z, Shi L, Wang Y, Zhang J, Huang L, Zhang C; et al. (2020). "Pathological findings of COVID-19 associated with acute respiratory distress syndrome". Lancet Respir Med. 8 (4): 420–422. doi:10.1016/S2213-2600(20)30076-X. PMC 7164771 Check |pmc= value (help). PMID 32085846 Check |pmid= value (help).
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