Cardiac arrest and COVID-19: inflammation, angiotensin-converting enzyme 2, and the destabilization of non-significant coronary artery disease-a case report.

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info:eu-repo/semantics/altIdentifier/doi/10.1093/ehjcr/ytaa475

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info:eu-repo/semantics/altIdentifier/pmid/33542974

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info:eu-repo/semantics/altIdentifier/eissn/2514-2119

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_85FF7468C3C99

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info:eu-repo/semantics/openAccess , CC BY-NC 4.0 , https://creativecommons.org/licenses/by-nc/4.0/



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S. Colombier et al., « Cardiac arrest and COVID-19: inflammation, angiotensin-converting enzyme 2, and the destabilization of non-significant coronary artery disease-a case report. », Serveur académique Lausannois, ID : 10.1093/ehjcr/ytaa475


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The new β-coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) appears to exhibit cardiovascular pathogenicity through use of angiotensin-converting enzyme 2 (ACE2) for cell entry and the development of a major systemic inflammation. Furthermore, cardiovascular comorbidities increase susceptibility to SARS-CoV-2 infection and the development of a severe form of COronaVIrus Disease 2019 (COVID-19). We describe the case of a COVID-19 patient whose inaugural presentation was a refractory cardiac arrest secondary to the destabilization of known, non-significant coronary artery disease. Patient was supported by venoarterial extracorporeal life support. After 12 h of support, cardiac function remained stable on low vasopressor support but the patient remained in a coma and brainstem death was diagnosed. Myocardial injury is frequently seen among critically unwell COVID-19 patients and increases the risk of mortality. This case illustrates several potential mechanisms that are thought to drive the cardiac complications seen in COVID-19. We present the potential role of inflammation and ACE2 in the pathophysiology of COVID-19.

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