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Meta-Analysis
. 2019 Sep 1;124(5):789-794.
doi: 10.1016/j.amjcard.2019.05.046. Epub 2019 Jun 6.

Meta-Analysis Comparing Usefulness of Beta Blockers to Preserve Left Ventricular Function During Anthracycline Therapy

Affiliations
Meta-Analysis

Meta-Analysis Comparing Usefulness of Beta Blockers to Preserve Left Ventricular Function During Anthracycline Therapy

Priyank Shah et al. Am J Cardiol. .

Abstract

The purpose of this analysis was to evaluate the cardioprotective benefit of β blockers in preventing anthracycline-induced cardiotoxicity (AIC) in breast cancer patients. Anthracyclines are the cornerstone treatment for breast cancer. Yet, their use has declined in the last decade due to associated AIC. Although β blockers may protect left ventricular (LV) function, previous trials were underpowered with equivocal results. The authors systematically searched online databases through August 2018 for studies evaluating effectiveness of β blockers in preventing AIC in breast cancer patients. We analyzed 9 studies including 771 patients. Data on converting-enzyme inhibitors, trastuzumab, or other malignancies were excluded. The primary outcome was comparison of postchemotherapy LV ejection fraction (LVEF) between β blocker and placebo. Secondary outcomes were changes in global longitudinal strain, LV end-diastolic diameter (LVEDD), and diastolic function parameters, as assessed by 2D echocardiogram and MRI. The mean pre-chemotherapy LVEF was >60% in all studies. Our pooled analysis demonstrated significantly higher LVEF postchemotherapy in the β blocker group in comparison to placebo: mean difference -3.84 with 95% confidence interval [-(6.19 to 1.48) p = 0.001]. The absolute change in EF also favored β blockers: mean difference -3.66 with 95% confidence interval [-(6.20 to 1.12) p = 0.005]. Diastolic function, global longitudinal strain, and LVEDD were also preserved by β blockers, but only LVEDD reached statistical significance. In conclusion, this study suggests that β blockers during anthracycline chemotherapy may prevent cardiotoxicity by preserving LV function.

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