Abstract

COVID 19, caused by the SARS-CoV-2 virus, a newly discovered coronavirus, has caused the global pandemic of early 2020. The first case was described in December 2019 in Wuhan, China, and by March 2020, most countries around the world have put in place some of the strictest restrictions seen in decades in order to slow down the spread of the disease. Patients with pre-existing hypertension and cardiovascular comorbidities were reported to be at an increased risk of serious infections caused by SARS-CoV-2. Considering that those are among the most common chronic medical conditions in the Western world, the potential impact of it is huge. The proposed mechanism behind those associations is the expression of angiotensin converting enzyme II (ACE II) in those patients. Furthermore, the association between ACE inhibitors/AR blockers, which are among the most frequently prescribed medications, and serious cases of COVID 19 has been studied with the same mechanism in mind. The reports on the association between hypertension and COVID 19 morbidity and mortality are less clear, and the International Society of Hypertension even claims that there is none. The reports on the association between heart failure or coronary disease and COVID 19 are more uniform, and all seem to point to a greater risk from serious infections faced by patients with those comorbidities. A significant effort will need to be invested by the scientific community into finding strategies for protecting those patients from contracting the virus in the first place and then, once infected, into developing management plans aimed at preserving cardiac function as much as possible.

Highlights

  • The SARS-CoV-2 virus, a newly discovered member of the coronavirus family, was first described at the end of 2019 in Wuhan, China, as the third severe respiratory syndrome caused by a coronavirus [1]

  • Patients with pre-existing heart failure are more likely to have elevated angiotensin converting enzyme II (ACE II) expression due to the pathophysiology of CHF, which could increase the risk of infection [32]. He et al found the mortality of critically ill patients infected by SARS-CoV-2 who develop cardiac injury to be as high as 60% [33]. They found an elevation in N-terminal pro-B-type natriuretic peptide levels associated with the myocardial injury caused by COVID 19

  • A concern remains that some patients may be inclined to stop taking the prescribed medicines out of fear

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Summary

Introduction

The SARS-CoV-2 virus, a newly discovered member of the coronavirus family, was first described at the end of 2019 in Wuhan, China, as the third severe respiratory syndrome caused by a coronavirus [1]. Li et al reported a significantly higher prevalence of hypertension and other cardiovascular comorbidities among COVID 19 patients treated in the ICU compared to those who did not require ICU treatment [27] They reported that over 8% of those infected by SARS-CoV-2 developed cardiac injury [27]. He et al found the mortality of critically ill patients infected by SARS-CoV-2 who develop cardiac injury to be as high as 60% [33] They found an elevation in N-terminal pro-B-type natriuretic peptide levels (usually a biomarker for congestive heart failure) associated with the myocardial injury caused by COVID 19. Considered together, these studies point to an association between pre-existing cardiovascular comorbidities and adverse outcomes following SARS-CoV-2 infections. More research is needed into the exact impact of SARS-CoV-2 on the cardiovascular system in order to develop both protective and, potentially, curative strategies

Conclusions
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20. Marin GH
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