Dexrazoxane reduced clinical heart failure risk by 68% (RR 0.32; 95% CI 0.20-0.50) and statins reduced LVEF decline and cardiotoxicity rates (OR 0.41; 95% CI 0.27-0.63) in patients receiving anthracyclines; β-blockers reduced symptomatic heart failure risk (RR 0.29; 95% CI 0.10-0.85) and preserved LVEF with a mean difference of 3.44%; enalapril and ramipril had modest LVEF preservation effects; empagliflozin reduced cardiac dysfunction risk by 82% (RR 0.18; p=0.01) in high-risk breast cancer patients
Do pharmacologic cardioprotective therapies limit anthracycline-induced cardiotoxicity and preserve cardiac function?
Tailored, risk-based cardioprotective strategies guided by biomarkers and imaging show promise in limiting anthracycline-induced cardiotoxicity.
Several pharmacologic strategies offer potential benefit in limiting anthracycline-induced cardiotoxicity and preserving cardiac function. Tailored, risk-based approaches that incorporate cardioprotective therapies early in anthracycline treatment-guided by biomarkers and imaging-are most promising. Further large-scale randomised studies are required to establish optimal combinations and confirm long-term benefit.
Alotaibi et al. (Thu,) conducted a review in Patients treated with anthracycline-based chemotherapy including various cancers (breast, lymphoma, hematological malignancies), some with previous anthracycline exposure. Dexrazoxane reduced clinical heart failure risk by 68% (RR 0.32; 95% CI 0.20-0.50) and statins reduced LVEF decline and cardiotoxicity rates (OR 0.41; 95% CI 0.27-0.63) in patients receiving anthracyclines; β-blockers reduced symptomatic heart failure risk (RR 0.29; 95% CI 0.10-0.85) and preserved LVEF with a mean difference of 3.44%; enalapril and ramipril had modest LVEF preservation effects; empagliflozin reduced cardiac dysfunction risk by 82% (RR 0.18; p=0.01) in high-risk breast cancer patients.
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