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Review
. 2021 Dec:11:200121.
doi: 10.1016/j.ijcrp.2021.200121. Epub 2021 Nov 13.

Hypertension and its management in COVID-19 patients: The assorted view

Gaber El-Saber Batiha  1 , Abdulrahim Gari  2   3 , Norhan Elshony  1 , Hazem M Shaheen  1 , Murtala Bello Abubakar  4   5 , Sherif Babatunde Adeyemi  6   7 , Hayder M Al-Kuraishy  8
Affiliations
Review

Hypertension and its management in COVID-19 patients: The assorted view

Gaber El-Saber Batiha et al. Int J Cardiol Cardiovasc Risk Prev. 2021 Dec.

Abstract

Background: Coronavirus disease 2019 (COVID-19) is suspected to mainly be more deleterious in patients with underlying cardiovascular diseases (CVD). There is a strong association between hypertension and COVID-19 severity. The binding of SARS-CoV-2 to the angiotensin-converting enzyme 2 (ACE2) leads to deregulation of the renin-angiotensin-aldosterone system (RAAS) through down-regulation of ACE2 with subsequent increment of the harmful Ang II serum levels and reduction of the protective Ang-(1-7). Both angiotensin receptor blockers (ARBs) and angiotensin-converting enzyme inhibitors (ACEIs) are commonly used to manage hypertension.

Objective: Objective was to illustrate the potential link between hypertension and COVID-19 regarding the role of angiotensin receptor blockers (ARBs) and angiotensin-converting enzyme inhibitors (ACEIs) in hypertensive patients with COVID-19.

Methods: We carried out comprehensive databases search from late December 2019 to early January 2021 by using online engines of Web of Science, Research gate, Scopus, Google Scholar, and PubMed for published and preprinted articles.

Results: The present study's findings showed that hypertension is regarded as an independent risk factor for COVID-19 severity. Both ACEIs and ARBs are beneficial in managing hypertensive patients.

Conclusion: This study concluded that hypertension increases COVID-19 severity due to underlying endothelial dysfunctions and coagulopathy. COVID-19 might augment the hypertensive complications due to down-regulation of ACE2. The use of ACEIs or ARBs might be beneficial in the management of hypertensive patients with COVID-19.

Keywords: ACE2; Coronavirus disease 2019; Hypertension; SARS-CoV-2.

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Conflict of interest statement

The authors declare no conflict of interests.

Figures

Fig. 1
Fig. 1
Flow-chart showing method and search strategy.
Fig. 2
Fig. 2
Structure of SARS-CoV-2. (M) Matrix, (S) spike glycoprotein, (N) N protein, (E) E protein, (HE) hemagglutination.
Fig. 3
Fig. 3
Coronavirus entry and replication inside the host cell. (1) Spike protein on the virion attaches to the cell-surface protein (ACE2), TMPRSS2, an enzyme that helps the virion to enter. (2) RNA is released by the virion. (3) Some RNAs are translated into proteins by the cell's machinery. (4) Formation of a replication complex by some of the proteins to make more RNAs. (5) Assembling of the proteins and RNAs into a new virion in the Golgi. (6) Release of new viruses.
Fig. 4
Fig. 4
Renin-angiotensin-aldosterone system (RAAS) in SARS-CoV-2 infection. AngI is converted to AngII by the action of the angiotensin-converting enzyme (ACE). AngII acts angiotensin receptor type 1(AT1R), leads to vasoconstriction, inflammation, fibrosis, lung damage, and oedema. However, the action of AngII on the AT2R produces a reverse effect. ACE2 converts AngII to Ang1-7, which acts on the Mas receptor leading to vasodilation and lung protection. SARS-CoV-2 causes down-regulation of ACE2 with subsequent activation of RAAS, which causes dual effects.
See this image and copyright information in PMC

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