Key result
Short-term oral N-acetylcysteine did not prevent anthracycline-induced cardiomyopathy compared to control in patients with breast cancer or lymphoma.
Why the study?
Does short-term use of N-acetylcysteine prevent anthracycline-induced cardiomyopathy (LVEF reduction) in patients receiving chemotherapy for breast cancer or lymphoma?
RCT (n=103)
Open-label
1:1 computer-generated permuted block of 6
No
Does short-term use of N-acetylcysteine prevent anthracycline-induced cardiomyopathy (LVEF reduction) in patients receiving chemotherapy for breast cancer or lymphoma?
Short-term use of N-acetylcysteine did not prevent anthracycline-induced left ventricular ejection fraction reduction in a low-risk cohort of patients with breast cancer or lymphoma.
Answers are grounded in this paper and cite their sources.
Does not support short-term N-acetylcysteine for anthracycline cardioprotection; confirms lack of benefit in this RCT population.
BACKGROUND AND OBJECTIVES: We investigate to determine whether N-acetylcysteine (NAC) can prevent anthracycline-induced cardiotoxicity. SUBJECTS AND METHODS: A total of 103 patients were enrolled in this prospective randomized open label controlled trial. They are patients first diagnosed with breast cancer or lymphoma, who require chemotherapy, including anthracycline like adriamycine or epirubicine. Patients were randomized to the NAC group {n=50; 1200 mg orally every 8 hours starting before and ending after the intravenous infusion of anthracycline in all chemotherapy cycles (3-6)} or the control group (n=53). Primary outcome was the decrease in left ventricular ejection fraction (LVEF) absolutely ≥10% from the baseline and concomitantly <50% at 6-month. Composite of all-cause death, heart failure and readmission were compared. RESULTS: The primary outcome was not significantly different in the NAC and control groups {3/47 (6.4%) vs. 1/52 (1.9%), p=0.343}. The mean LVEF significantly decreased in both the NAC (from 64.5 to 60.8%, p=0.001) and control groups (from 64.1 to 61.3%, p<0.001) after the completion of whole chemotherapy. The mean LVEF change did not differ between the two groups (-3.64% in NAC vs. -2.78% in control group, p=0.502). Left ventricular (LV) end systolic dimension increased with higher trend in NAC by 3.08±4.56 mm as compared with 1.47±1.83 mm in the control group (p=0.064). LV end diastolic dimension did not change in each group and change does not differ in both. Peak E, A and E/A ratio change and cardiac enzymes were comparable in two groups. Cumulative 12-month event rate was 6% and 3.8% in the NAC group and the control group, respectively, with no difference (p=0.672). CONCLUSION: We cannot prove that NAC prevents anthracycline-induced cardiomyopathy.
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Jo et al. (2013) conducted an RCT in Anthracycline-induced cardiomyopathy (n=103). N-acetylcysteine vs. Control was evaluated on Decrease in LVEF absolutely ≥10% from baseline and concomitantly <50% at 6 months (p=0.343). Short-term oral N-acetylcysteine did not prevent anthracycline-induced cardiomyopathy compared to control in patients with breast cancer or lymphoma.
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