scholarly journals Association Between Renin-Angiotensin-Aldosterone System Inhibitors and COVID-19 Infection in South Korea

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 742-749 ◽  
Author(s):  
Minkook Son ◽  
Jeongkuk Seo ◽  
Sung Yang
Keyword(s):  
South Korea ◽  
Case Control ◽  
Host Cells ◽  
Severe Illness ◽  
National Health Insurance System ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Increased Risk ◽  
High Flow Oxygen ◽  
Raas Inhibitors

The severe acute respiratory syndrome coronavirus 2 is known to infect host cells by interacting with ACE2 (angiotensin-converting enzyme 2) expressed in the respiratory epithelium. There have been concerns on whether alterations of ACE2 expression by renin-angiotensin-aldosterone system (RAAS) inhibitors would contribute to the infectivity and severity of coronavirus disease 2019 (COVID-19). We performed a case-control study to investigate the association between RAAS inhibitors and risk and severity of COVID-19 infection in South Korea using the population-based data provided by the Korean National Health Insurance System. Of 16 281 subjects with hypertension, there were 950 (5.8%) confirmed COVID-19 cases. After case-control matching, multivariable-adjusted conditional logistic regression analysis was performed. The adjusted odds ratio and 95% CIs for COVID-19 infection and long-term hospitalization comparing exposure to RAAS inhibitors and nonexposure to RAAS inhibitors was 1.161 (0.958–1.407) and 0.863 (0.533–1.397), respectively. When comparing exposure to RAAS inhibitors and nonexposure to RAAS inhibitors for intensive care unit admission, high-flow oxygen therapy, and death, the adjusted odds ratios (95% CIs) were 1.515 (0.402–5.701), 0.663 (0.272–1.619), and 1.363 (0.513–3.662), respectively. In all analyses, P values were not significant ( P >0.05). The present study demonstrates the absence of an identifiable association between the exposure to RAAS inhibitors and risk and severity of COVID-19 infection, supporting the current medical guidelines and recommendations that patients should not discontinue RAAS inhibitors out of a concern that they are at increased risk for infection or severe illness of COVID-19.

RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM INHIBITORS AND COVID-19 COMPLICATIONS

2021 ◽  
Author(s):  
ARTHUR FIOROTTO DE MATTOS ◽  
NATHALIA SILVEIRA BARSOTTI ◽  
RAFAEL RIBEIRO ALMEIDA
Keyword(s):  
Rna Virus ◽  
Host Cells ◽  
Converting Enzyme ◽  
Respiratory Complications ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
The World ◽  
Raas Inhibitors ◽  
The Impact ◽  
Different Tissues

The world faces today a pandemic of unquestionable importance, caused by an infection with a new enveloped RNA virus that belongs to the Coronaviridae family. The new coronavirus (SARS-CoV 2) uses a glycoprotein present on its surface to bind to and infect host cells that express the angiotensin converting enzyme II (ACE-2). Although different tissues may be targeted by the virus, respiratory complications remain as the main cause of death. It has been demonstrated that Renin-Angiotensin-Aldosterone System (RAAS) inhibitors increase ACE-2 expression in animal models, raising the concern that patients under treatment with these drugs could become more susceptible to COVID-19 complications. Here, we discuss the impact of RAAS inhibitors on COVID-19 outcomes and show that no evidence so far supports that the use of these drugs could pose a risk to SARS-CoV 2-infected patients. In fact, clinical data suggest that RAAS inhibitors may even act in a protective way against COVID-19 complications and should not be discontinued.,

scholarly journals Comparison of renin–angiotensin–aldosterone system inhibitors with other antihypertensives in association with coronavirus disease-19 clinical outcomes: systematic review and meta-analysis

2020 ◽  
Author(s):  
Yihienew M. Bezabih ◽  
Alemayehu Bezabih ◽  
Endalkachew Aalamneh ◽  
Gregory M. Peterson ◽  
Woldesellassie M. Bezabhe
Keyword(s):  
Clinical Outcomes ◽  
Meta Analysis ◽  
Conclusive Evidence ◽  
Antihypertensive Drug Therapy ◽  
Severe Illness ◽  
Angiotensin Ii Receptor ◽  
Converting Enzyme Inhibitors ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Inhibitors

AbstractIntroductionThe effects of renin–angiotensin–aldosterone system (RAAS) inhibitors on the clinical outcomes of coronavirus disease-19 (COVID-19) have been conflicting in different studies. This meta-analysis was undertaken to provide more conclusive evidence.MethodsA systematic search for published articles was performed in PubMed and EMBASE from January 5 2020 till May 5 2020. Studies that reported the clinical outcomes of patients with COVID-19, stratified by the class of concomitant antihypertensive drug therapy, were included. The Mantel-Haenszel random effects model was used to estimate pooled odds ratio (OR).ResultsA total of 6,997 patients with COVID-19 were included, and all of them had hypertension. The overall risk of poor patient outcomes (severe COVID-19 or death) was lower in patients taking RAAS inhibitors (OR=0.84, 95% CI: [0.73, 0.96]; P=0.017) compared with those receiving non-RAAS inhibitor antihypertensives. Patients taking angiotensin-I-converting enzyme inhibitors (ACEIs) were less likely to experience poor clinical outcomes (OR=0.73, 95% CI: [0.58-0.92]; P=0.01) compared with those receiving angiotensin-II receptor blockers (ARBs). In addition, comparison of ACEIs to the rest of non-ACEI antihypertensives gave a consistently decreased risk of poor COVID-19 outcome (OR=0.77, 95% CI: [0.63-0.93]; P=0.002). However, ARBs did not decrease the risk of poor COVID-19 outcomes compared to all other non-ARB antihypertensives (OR=1.13, 95% CI: [0.95-1.35]).ConclusionThe risk of developing severe illness or death from COVID-19 was lower in patients who received RAAS inhibitors compared with those who took non-RAAS inhibitors. ACEIs might be better in decreasing the severity and mortality of COVID-19 than ARBs.

scholarly journals Renin Angiotensin Aldosterone System Antagonism in 2019 Novel Coronavirus Acute Lung Injury

2021 ◽  
Author(s):  
Davide Ventura ◽  
Amy L Carr ◽  
R Duane Davis ◽  
Scott Silvestry ◽  
Linda Bogar ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Ii Receptor ◽  
Pulmonary Tissue ◽  
Renin Angiotensin Aldosterone System ◽  
Angiotensin Converting Enzyme 2 ◽  
Renin Angiotensin ◽  
Receptor Blockers ◽  
Membrane Bound ◽  
Raas Inhibitors ◽  
Novel Coronavirus

Abstract It has been established SARS-CoV-2 uses angiotensin-converting enzyme 2 (ACE2), a membrane-bound regulatory peptide, for host cell entry. Renin-angiotensin-aldosterone system (RAAS) inhibitors have been reported to increase ACE2 in type 2 pneumocytes pulmonary tissue. Controversy exists for the continuation of ACE inhibitors, angiotensin II receptor blockers (ARBs), and mineralocorticoid receptor antagonists (MRAs) in the current pandemic. ACE2 serves as regulatory enzyme in maintaining homeostasis between proinflammatory Angiotensin II and anti-inflammatory Angiotensin 1,7 peptides. Derangements in these peptides are associated with cardiovascular disease and are implicated in the progression of acute respiratory distress syndrome (ARDS). Augmentation of the ACE2/Ang1,7 axis represent a critical target in the supportive management of COVID-19 associated lung disease. Observational data describing the use of RAAS inhibitors in the setting of SARS-CoV-2 have not borne signals of harm to date. However, equipoise persists requiring an analysis of novel agents including recombinant human-ACE2 and existing RAAS inhibitors while balancing ongoing controversies associated with increased coronavirus infectivity and virulence.

scholarly journals Renin-angiotensin-aldosterone system inhibitors – a realm of confusion in COVID-19

2021 ◽  
Vol 4 (Special2) ◽  
pp. 389-394
Author(s):  
Angela Madalina Lazar
Keyword(s):  
Angiotensin Ii ◽  
Angiotensin Converting Enzyme ◽  
Current Knowledge ◽  
Angiotensin Receptor Blockers ◽  
Protective Effects ◽  
Converting Enzyme ◽  
Angiotensin I ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Raas Inhibitors

Currently, there is a persisting dispute regarding the renin-angiotensin-aldosterone-system (RAAS) inhibitors' safety of use in COVID-19 pandemics. On one side, RAAS inhibitors appear to determine an overexpression of ACE2, the receptor of SARS-CoV-2. Therefore, they could increase the risk of SARS-CoV-2 infection and its degree of severity. On the other side, the discontinuation of RAAS leads to cardiovascular decompensation and has been discouraged by the major medical societies. Also, large-cohort studies report beneficial or at least neutral effects for the RAAS inhibitors in COVID-19 patients. Worldwide, millions of patients receive RAAS inhibitors for the treatment of hypertension and other important comorbidities. In this context, knowledge of the exact effect of these medications becomes of crucial significance. This paper aims to fill in a gap in the current knowledge and presents a putative mechanism by which RAAS inhibitor administration's beneficial results can be explained better. RAAS inhibitors can be beneficial, as they counteract the excessive detrimental activation of the classical angiotensin-converting enzyme (ACE) axis, decreasing the angiotensin II levels. The angiotensin receptor blockers (ARBs) increase the angiotensin II levels, while the angiotensin-converting enzyme inhibitors (ACEI) increase the angiotensin I levels; these substrates will compete with the SARS-CoV-2 for the ACE2 binding, decreasing the viral infectivity. In addition, following the RAAS inhibitors treatment, the up-regulated ACE2 will cleave these substrates (angiotensin I and II), particularly to angiotensin 1-7 that possesses vasodilator, protective effects.

scholarly journals Meta-analysis of effect of renin–angiotensin–aldosterone system blockers on contrast-induced nephropathy

2020 ◽  
Vol 21 (2) ◽  
pp. 147032032091958
Author(s):  
Weidong Wang ◽  
Wei Qu ◽  
Dan Sun ◽  
Xiaodan Liu
Keyword(s):  
Older People ◽  
Sample Size ◽  
Meta Analysis ◽  
Control Group ◽  
Inclusion Criteria ◽  
Contrast Induced Nephropathy ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Increased Risk ◽  
Larger Sample

Background: The purpose of this study was to systematically evaluate the effect of renin–angiotensin–aldosterone system blockers on the incidence of contrast-induced nephropathy in patients undergoing coronary angiography or percutaneous coronary intervention. Methods: A systematic literature search of several databases was conducted to identify studies that met the inclusion criteria. A total of 12 studies with 14 trials that performed studies on a total of 4864 patients (2484 treated with renin–angiotensin–aldosterone system blockers and 2380 in the control group) were included. The primary endpoint was the overall incidence of contrast-induced nephropathy. Analyses were performed with STATA version 12.0. Results: The overall contrast-induced nephropathy incidence in renin–angiotensin–aldosterone system blocker and control groups was 10.43% and 6.81%, respectively. The pooled relative risk of contrast-induced nephropathy incidence was 1.22 (95% confidence interval: 0.81–1.84) in the renin–angiotensin–aldosterone system blocker group. An increased risk of developing contrast-induced nephropathy in the renin–angiotensin–aldosterone system blocker group was observed among older people, non-Asians, chronic users, and studies with larger sample size, and the pooled RRs and 95% confidence intervals were 2.02 (1.21–3.36), 2.30 (1.41–3.76), 1.69 (1.10–2.59) and 1.83 (1.28–2.63), respectively. Conclusions: Intervention with renin–angiotensin–aldosterone system blockers was associated with an increased risk of contrast-induced nephropathy among non-Asians, chronic users, older people, and studies with larger sample size. Large clinical trials with strict inclusion criteria are needed to confirm our results and to evaluate the effect further.

scholarly journals Renin-Angiotensin-Aldosterone System peptide profiles in patients with COVID-19

2021 ◽  
Author(s):  
Alexander Kutz ◽  
Anna Conen ◽  
Claudia Gregoriano ◽  
Sebastian Haubitz ◽  
Daniel Koch ◽  
...  
Keyword(s):  
Respiratory Infections ◽  
Tertiary Care ◽  
Plasma Renin ◽  
Adverse Outcomes ◽  
Care Hospital ◽  
Renin Angiotensin Aldosterone System ◽  
Peptide Profile ◽  
Renin Angiotensin ◽  
Subgroup Analyses ◽  
Raas Inhibitors

Objective While evidence on the interface between severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2) infection and the renin-angiotensin-aldosterone-system (RAAS) is accumulating, clinical data on RAAS peptide alteration among coronavirus disease-19 (COVID-19) patients is missing. Design and Methods In this exploratory study, we prospectively included adult patients (aged ≥18 years) admitted between February 26 and April 30, 2020 to a tertiary care hospital in Switzerland. We assessed the association of an underlying SARS-CoV-2 infection and equilibrium serum levels of RAAS peptides in hospitalized COVID-19 patients 1:1 propensity-score matched with patients suffering from SARS-CoV-2-negative respiratory infections. Subgroup analyses involved stratification for taking RAAS inhibitors. Results COVID-19 patients had about 50% lower equilibrium serum RAAS peptide levels as compared with matched controls (angiotensin I: 31.6 vs. 66.8pmol/l, -52.7% [95%CI -68.5% to -36.9%]; angiotensin II: 37.7 vs. 92.5pmol/l, -59.2% [95%CI -72.1% to -46.3%]; angiotensin (1-5): 3.3 vs. 6.6pmol/l, -49.7% [95%CI -59.2% to -40.2%]; angiotensin (1-7): 4.8 vs. 7.6pmol/l, -64.9% [95%CI -84.5% to -45.3%]). While the plasma renin activity (PRA-S) was lower in COVID-19 patients (88.6 vs. 207.9pmol/l, -58.5% [95%CI -71.4% to -45.6%]), there was no difference of angiotensin-converting enzyme (ACE) and ACE2 plasma activity between the groups. Subgroup analyses revealed a pronounced RAAS peptide profile depression in COVID-19 patients among those not on RAAS inhibitors. Conclusions As compared with SARS-CoV-2-negative patients, we found a downregulated RAAS in presence of a SARS-CoV-2 infection. Whether the lower levels of the protective angiotensin (1-5) and (1-7) are linked to adverse outcomes in COVID-19 warrants further investigation.

scholarly journals Effect of Renin-Angiotensin-Aldosterone System Inhibitors on Short-Term Mortality After Sepsis

Hypertension ◽  
2020 ◽  
Vol 75 (2) ◽  
pp. 483-491 ◽  
Author(s):  
Wan-Ting Hsu ◽  
Brandon Patrick Galm ◽  
Gregory Schrank ◽  
Tzu-Chun Hsu ◽  
Shih-Hao Lee ◽  
...  
Keyword(s):  
Propensity Score ◽  
Meta Analysis ◽  
Hazard Ratio ◽  
Short Term ◽  
Renin Angiotensin Aldosterone System ◽  
Renin Angiotensin ◽  
Mortality Hazard ◽  
Short Term Mortality ◽  
Raas Inhibitors ◽  
Mortality Hazard Ratio

Antagonists of the renin-angiotensin-aldosterone system (RAAS), including ACEIs (angiotensin-converting enzyme inhibitors) and ARBs (angiotensin II receptor blockers), may prevent organ failure. We, therefore, investigated whether specific RAAS inhibitors are associated with reduced mortality in patients with sepsis.We conducted a population-based retrospective cohort study using multivariable propensity score–based regression to control for differences among patients using different RAAS inhibitors. A multivariable-adjusted Cox proportional-hazards regression model was used to determine the association between RAAS inhibitors and sepsis outcomes. To directly compare ACEI users, ARB users, and nonusers, a 3-way propensity score matching approach was performed. Results were pooled with previous evidence via a random-effects meta-analysis. A total of 52 727 patients were hospitalized with sepsis, of whom 7642 were prescribed an ACEI and 4237 were prescribed an ARB. Using propensity score–matched analyses, prior ACEI use was associated with decreased 30-day mortality (hazard ratio, 0.84 [95% CI, 0.75–0.94]) and 90-day mortality (hazard ratio, 0.83 [95% CI, 0.75–0.92]) compared with nonuse. Prior ARB use was associated with an improved 90-day survival (hazard ratio, 0.88 [95% CI, 0.83–0.94]). These results persisted in sensitivity analyses focusing on patients without cancer and patients with hypertension. By contrast, no beneficial effect was found for antecedent β-blockers exposure (hazard ratio, 0.99 [95% CI, 0.94–1.05]). The pooled estimates obtained from the meta-analysis was 0.71 (95% CI, 0.58–0.87) for prior use of ACEI/ARB.The short-term mortality after sepsis was substantially lower among those who were already established on RAAS inhibitor treatment when sepsis occurred.

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