scholarly journals Association of Angiotensin‐Converting Enzyme Inhibitors and Angiotensin Receptor Blockers with the Risk of Hospitalization and Death in Hypertensive Patients with Coronavirus Disease‐19

Author(s):  
Rohan Khera ◽  
Callahan Clark ◽  
Yuan Lu ◽  
Yinglong Guo ◽  
Sheng Ren ◽  
...  

Abstract Background Despite its clinical significance, the risk of severe infection requiring hospitalization among outpatients with SARS‐CoV‐2 infection who receive angiotensin‐converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs) remains uncertain. Methods and Results In a propensity score‐matched outpatient cohort (January – May 2020) of 2,263 Medicare Advantage and commercially insured individuals with hypertension and a positive outpatient SARS‐CoV‐2 test, we determined the association of ACE inhibitors and ARBs with COVID‐19 hospitalization. In a concurrent inpatient cohort of 7,933 hospitalized with COVID‐19, we tested their association with in‐hospital mortality. The robustness of the observations was assessed in a contemporary cohort (May – August). In the outpatient study, neither ACE inhibitors (HR, 0.77, 0.53–1.13, P=0.18), nor ARBs (HR, 0.88, 0.61–1.26, P=0.48), were associated with hospitalization risk. ACE inhibitors were associated with lower hospitalization risk in the older Medicare group (HR, 0.61, 0.41–0.93, P=0.02), but not the younger commercially insured group (HR, 2.14, 0.82–5.60, P=0.12; P‐interaction 0.09). Neither ACE inhibitors nor ARBs were associated with lower hospitalization risk in either population in the validation cohort. In the primary inpatient study cohort, neither ACE inhibitors (0.97, 0.81–1.16; P=0.74) nor ARBs (1.15, 0.95–1.38, P=0.15) were associated with in‐hospital mortality. These observations were consistent in the validation cohort. Conclusions ACE inhibitors and ARBs were not associated with COVID‐19 hospitalization or mortality. Despite early evidence for a potential association between ACE inhibitors and severe COVID‐19 prevention in older individuals, the inconsistency of this observation in recent data argues against a role for prophylaxis.

Author(s):  
Rohan Khera ◽  
Callahan Clark ◽  
Yuan Lu ◽  
Yinglong Guo ◽  
Sheng Ren ◽  
...  

Background: Whether angiotensin-converting enzyme (ACE) Inhibitors and angiotensin receptor blockers (ARBs) mitigate or exacerbate SARS-CoV-2 infection remains uncertain. In a national study, we evaluated the association of ACE inhibitors and ARB with coronavirus disease-19 (COVID-19) hospitalization and mortality among individuals with hypertension. Methods: Among Medicare Advantage and commercially insured individuals, we identified 2,263 people with hypertension, receiving ≥1 antihypertensive agents, and who had a positive outpatient SARS-CoV-2 test (outpatient cohort). In a propensity score-matched analysis, we determined the association of ACE inhibitors and ARBs with the risk of hospitalization for COVID-19. In a second study of 7,933 individuals with hypertension who were hospitalized with COVID-19 (inpatient cohort), we tested the association of these medications with in-hospital mortality. We stratified all our assessments by insurance groups. Results: Among individuals in the outpatient and inpatient cohorts, 31.9% and 29.8%, respectively, used ACE inhibitors and 32.3% and 28.1% used ARBs. In the outpatient study, over a median 30.0 (19.0 - 40.0) days after testing positive, 12.7% were hospitalized for COVID-19. In propensity score-matched analyses, neither ACE inhibitors (HR, 0.77 [0.53, 1.13], P = 0.18), nor ARBs (HR, 0.88 [0.61, 1.26], P = 0.48), were significantly associated with risk of hospitalization. In analyses stratified by insurance group, ACE inhibitors, but not ARBs, were associated with a significant lower risk of hospitalization in the Medicare group (HR, 0.61 [0.41, 0.93], P = 0.02), but not the commercially insured group (HR: 2.14 [0.82, 5.60], P = 0.12; P-interaction 0.09). In the inpatient study, 14.2% died, 59.5% survived to discharge, and 26.3% had an ongoing hospitalization. In propensity score-matched analyses, neither use of ACE inhibitor (0.97 [0.81, 1.16]; P = 0.74) nor ARB (1.15 [0.95, 1.38]; P = 0.15) was associated with risk of in-hospital mortality, in total or in the stratified analyses. Conclusions: The use of ACE inhibitors and ARBs was not associated with the risk of hospitalization or mortality among those infected with SARS-CoV-2. However, there was a nearly 40% lower risk of hospitalization with the use of ACE inhibitors in the Medicare population. This finding merits a clinical trial to evaluate the potential role of ACE inhibitors in reducing the risk of hospitalization among older individuals, who are at an elevated risk of adverse outcomes with the infection.


2020 ◽  
Vol 2020 (1) ◽  
pp. 1
Author(s):  
Adrian Sturza ◽  
Cătălin V. Marian ◽  
Danina M. Muntean ◽  
Octavian M. Crețu

The renin–angiotensin–aldosterone system (RAAS) has been recognized as a key player in the complex scenario of cardiovascular regulation. Aside from its role in the cardiovascular diseases, RAAS dysregulation has emerged as a central pathomechanism in the severe acute respiratory syndrome coronavirus 1 (SARS-CoV1) epidemic, dating back to 2002–2004, and the current COVID-19 pandemic with SARS-CoV2, with the latter involving the interaction with angiotensin-converting enzyme 2 (ACE2). ACE2 is the enzyme responsible for Ang 1-7 production that partly counteracts the RAAS effects and promotes nitric oxide synthase activation; moreover, it has also been reported to act as a receptor for both SARS viruses. In the setting of the ongoing COVID-19 pandemic, the SARS–ACE2 interaction is highly debated with respect to both viral infectivity and usage/discontinuation of RAAS medication—ACE inhibitors (ACEi) and angiotensin-receptor blockers (ARBs)—in diagnosed or suspected SARS-CoV2 patients. Since ACE inhibitors and ARBs are largely prescribed in cardiovascular pathology, a better understanding of the interaction between SARS-CoV2 and RAAS is urgently needed. In this review, we will briefly discuss the SARS-CoV2 and ACE2 interaction and why the discontinuation of RAAS medication is unsafe for either diagnosed or suspected SARS-CoV2 patients.


2021 ◽  
pp. 82-84
Author(s):  
A. Yogalakshmee ◽  
Manimekalai Manimekalai ◽  
Saranya Devi

Coronavirus 2019 (COVID-19) causing severe acute respiratory syndrome. (SARS-CoV-2), has affected more than seven million people worldwide. The virus enter the cell through angiotensin-converting enzyme (ACE)-2 receptor . Hypertension as well as cardiovascular disease coexist with COVID-19 have generated discussion on the management of patients with hypertension. Here we discuss the pathophysiology of SARS-CoV-2 infection with ACE2 receptors, the cardiovascular system, and the kidney. Result showing evidence on the use of antihypertensive medication such as ACE inhibitors and angiotensin receptor blockers in SHTN patients with COVID-19.


Author(s):  
Maximilian Tscharre ◽  
Patricia P. Wadowski ◽  
Constantin Weikert ◽  
Joseph Pultar ◽  
Beate Eichelberger ◽  
...  

Abstract Background In patients with acute coronary syndrome (ACS), angiotensin-converting enzyme (ACE) inhibitors are preferred over angiotensin receptor blockers (ARBs). However, in a recent pilot study, treatment with ACE inhibitors was associated with increased platelet reactivity compared to ARBs. Therefore, we sought to investigate the impact of renin-angiotensin-aldosterone system (RAAS) blockade with ACE inhibitors and ARBs on platelet aggregation in patients with ACS undergoing percutaneous coronary intervention. Methods On-treatment residual platelet reactivity in response to arachidonic acid (AA), adenosine diphosphate (ADP), SFLLRN, AYPGKF, and collagen was assessed by multiple electrode aggregometry (MEA) in 197 ACS patients on dual antiplatelet therapy (DAPT) with aspirin and either prasugrel or ticagrelor. Results One hundred sixty-five (83.7%) patients were treated with ACE inhibitors, 32 (16.3%) with ARBs. On-treatment residual AA- and ADP-inducible platelet reactivity was significantly higher in patients with ACE inhibitors (both p < 0.05). Likewise, SFLLRN was significantly higher in patients with ACE inhibitors (p = 0.036) and there was a trend for higher AYPGKF- and collagen-inducible platelet reactivity (p = 0.053 and p = 0.082). The incidence of high on-treatment residual platelet reactivity AA was significantly higher in patients with ACE inhibitors (52 [31.5%] vs. 3 [9.4%] patients; p = 0.019). Conclusion ACE inhibitors are associated with increased on-treatment residual platelet reactivity in ACS patients with potent DAPT. Further clinical trials are needed to elucidate the role of RAAS blockade with ACE inhibitors and ARBs in ACS patients treated according to current standards.


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