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06.12.2018 | Original Research | Ausgabe 3/2019 Open Access

Heart Failure Reviews 3/2019

Protective role of beta-blockers in chemotherapy-induced cardiotoxicity—a systematic review and meta-analysis of carvedilol

Zeitschrift:
Heart Failure Reviews > Ausgabe 3/2019
Autoren:
Shan Huang, Qin Zhao, Zhi-gang Yang, Kai-yue Diao, Yong He, Ke Shi, Meng-ting Shen, Hang Fu, Ying-kun Guo
Wichtige Hinweise

Electronic supplementary material

The online version of this article (https://​doi.​org/​10.​1007/​s10741-018-9755-3) contains supplementary material, which is available to authorized users.
Shan Huang and Qin Zhao are co-first authors.
Zhi-gang Yang and Ying-kun Guo jointly supervised this work and should be considered as co-corresponding authors.

Abstract

Some randomized controlled trials (RCTs) have tested the efficacy of beta-blockers as prophylactic agents on cancer therapy-induced cardiotoxicity; however, the quality of this evidence remains undetermined. This systematic review and meta-analysis study aims to evaluate the prophylactic effects of beta-blockers, especially carvedilol, on chemotherapy-induced cardiotoxicity. RCTs were identified by searching the MEDLINE (PubMed), Embase (OvidSP), Cochrane CENTRAL (OvidSP), etc., until December 2017. Inclusion criteria were randomized clinical trial and adult cancer patients started beta-blockers before chemotherapy. We evaluated the mean differences (MD) by fixed- or random-effects model and the odds ratio by Peto’s method. Primary outcome was the left ventricular ejection fraction (LVEF) of patients after chemotherapy, and secondary outcomes were all-cause mortality, clinically overt cardiotoxicity, and other echocardiographic measurements. In total, we included six RCTs that used carvedilol as a prophylactic agent in patients receiving chemotherapy. The LVEF was not significantly distinct between those using carvedilol and placebo after chemotherapy (MD, 1.74; 95% confidence interval (CI), − 0.18 to 3.66; P = 0.08). The incidence of clinically overt cardiotoxicity was lower in the carvedilol group compared with the control group (Peto OR, 0.42; 95% CI, 0.20–0.89; P = 0.02). Furthermore, after chemotherapy, the LV end-diastolic diameter did not increase in the carvedilol group compared with the placebo group (MD, − 1.41; 95% CI, − 2.32 to − 0.50; P = 0.002). The prophylactic use of carvedilol exerted no impact on the early asymptomatic LVEF decrease but seemed to attenuate the frequency of clinically overt cardiotoxicity and prevent ventricular remodeling.

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