Effects of renin-angiotensin system blockers on outcomes from COVID-19: a systematic review and meta-analysis of randomized controlled trials.

IF 5.3 1区 医学 Q1 CARDIAC & CARDIOVASCULAR SYSTEMS
Matthew M Y Lee, Toru Kondo, Ross T Campbell, Mark C Petrie, Naveed Sattar, Scott D Solomon, Muthiah Vaduganathan, Pardeep S Jhund, John J V McMurray
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引用次数: 0

Abstract

Background and aims: Randomized controlled trials (RCTs) have assessed the effects of renin-angiotensin system (RAS) blockers in adults with coronavirus disease 2019 (COVID-19). This meta-analysis provides estimates of the safety and efficacy of treatment with (vs. without) RAS blockers from these trials.

Methods: PubMed, Web of Science, and ClinicalTrials.gov were searched (1 March-12 April 2023). Event/patient numbers were extracted, comparing angiotensin-converting enzyme (ACE) inhibitor/angiotensin-receptor blocker (ARB) treatment with no treatment, for the outcomes: intensive care unit (ICU) admission, mechanical ventilation, vasopressor use, acute kidney injury (AKI), renal replacement therapy (RRT), acute myocardial infarction, stroke/transient ischaemic attack, heart failure, thromboembolic events, and all-cause death. Fixed-effects meta-analysis estimates were pooled.

Results: Sixteen RCTs including 3492 patients were analysed. Compared with discontinuation of RAS blockers, continuation was not associated with increased risk of ICU [risk ratio (RR) 0.96, 0.66-1.41], ventilation (RR 0.77, 0.55-1.09), vasopressors (RR 0.92, 0.58-1.44), AKI (RR 1.01, 0.40-2.56), RRT (RR 1.01, 0.46-2.21), or thromboembolic events (RR 1.07, 0.36-3.19). RAS blocker initiation was not associated with increased risk of ICU (RR 0.71, 0.47-1.08), ventilation (RR 1.12, 0.91-1.38), AKI (RR 1.28, 0.89-1.86), RRT (RR 1.66, 0.89-3.12), or thromboembolic events (RR 1.20, 0.06-23.70), although vasopressor use increased (RR 1.27, 1.02-1.57). The RR for all-cause death in the continuation/discontinuation trials was 1.24 (0.80-1.92), and 1.22 (0.96-1.55) in the initiation trials. In patients with severe/critical COVID-19, RAS blocker initiation increased the risk of all-cause death (RR 1.31, 1.01-1.72).

Conclusion: ACE inhibitors and ARBs may be continued in non-severe COVID-19 infection, where indicated. Conversely, initiation of RAS blockers may be harmful in critically ill patients.PROSPERO registration number: CRD42023408926.

肾素-血管紧张素系统阻断剂对新冠肺炎结果的影响:随机对照试验的系统综述和荟萃分析。
背景和目的:随机对照试验(RCT)评估了肾素-血管紧张素系统(RAS)阻断剂对成年新冠肺炎患者的影响。这项荟萃分析提供了这些试验中使用(与不使用)RAS阻滞剂治疗的安全性和有效性的估计。方法:检索PubMed、Web of Science和ClinicalTrials.gov(2023年3月1日至4月12日)。提取事件/患者编号,比较ACE抑制剂/ARB治疗与未治疗的结果:重症监护室(ICU)入院、机械通气、血管升压药使用、急性肾损伤(AKI)、肾脏替代治疗(RRT)、急性心肌梗死、中风/短暂性脑缺血发作、心力衰竭、血栓栓塞事件和全因死亡。合并固定效应荟萃分析估计。结果:对16例随机对照试验(包括3492例患者)进行了分析。与停用RAS阻断剂相比,持续使用RAS阻断剂与ICU(RR 0.96,0.66-1.41)、通气(RR 0.77,0.55-1.09)、血管升压药(RR 0.92,0.58-1.44)、AKI(RR 1.01,0.40-2.56)、RRT(RR1.01,0.46-2.21)或血栓栓塞事件(RR 1.07,0.36-3.19)的风险增加无关。RAS阻断剂的使用与ICU风险增加无关(RR 0.71,0.47-1.08),通气(RR 1.12,0.91-1.38)、AKI(RR 1.28,0.89-1.86)、RRT(RR 1.66,0.89-3.12)或血栓栓塞事件(RR 1.20,0.06-23.70),尽管血管升压药的使用增加(RR 1.27,1.02-1.57)。继续/停止试验中全因死亡的RR为1.24(0.80-1.92),初始试验中为1.22(0.96-1.55)。在重症/危重型新冠肺炎患者中,RAS阻断剂的使用增加了全因死亡的风险(RR 1.31,1.01-1.72)。相反,RAS阻断剂的使用可能对危重患者有害。PROSPERO注册号:CRD42023408926。
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来源期刊
European Heart Journal - Cardiovascular Pharmacotherapy
European Heart Journal - Cardiovascular Pharmacotherapy Medicine-Cardiology and Cardiovascular Medicine
CiteScore
10.10
自引率
14.10%
发文量
65
期刊介绍: The European Heart Journal - Cardiovascular Pharmacotherapy (EHJ-CVP) is an international, peer-reviewed journal published in English, specifically dedicated to clinical cardiovascular pharmacology. EHJ-CVP publishes original articles focusing on clinical research involving both new and established drugs and methods, along with meta-analyses and topical reviews. The journal's primary aim is to enhance the pharmacological treatment of patients with cardiovascular disease by interpreting and integrating new scientific developments in this field. While the emphasis is on clinical topics, EHJ-CVP also considers basic research articles from fields such as physiology and molecular biology that contribute to the understanding of cardiovascular drug therapy. These may include articles related to new drug development and evaluation, the physiological and pharmacological basis of drug action, metabolism, drug interactions, and side effects.
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