Risk of Cardiomyopathy in Breast Cancer: How Can We Attenuate the Risk of Heart Failure from Anthracyclines and Anti-HER2 Therapies?

purpose of reviewTo review cardiotoxicity of and strategies to prevent cardiotoxicity from anthracyclines and anti-HER2 agents used to treat breast cancer. RECENT

findingsAlthough not common, cardiotoxicity from anthracyclines and anti-HER2 therapies is a major consideration in the use of these agents, especially in the adjuvant setting. Modifications in anthracycline agent, dosing, or schedule or use of Dexrazoxane have been shown to ameliorate the mostly irreversible cardiotoxicity from anthracyclines. Dose delays have been the primary means of addressing the possibly reversible cardiotoxicity from the anti-HER2 agent, trastuzumab, whereas the other anti-HER2 therapies, pertuzumab, lapatinib, and neratinib, are relatively nontoxic to the myocardium. Data from recent randomized clinical trials suggest that the use of angiotensin-converting enzyme inhibitors (ACEi), angiotensin receptor blockers (ARBs), and beta blockers may prevent subclinical cardiotoxicity, as measured by decline in the left ventricular ejection fraction, associated with these agents. Longer-term follow-up will be needed to confirm their role in prevention of symptomatic cardiomyopathy and subsequent cardiovascular disease in women with breast cancer. Preliminary evidence suggests that the use of ACEi, ARB, and beta blockers during treatment with anthracyclines and trastuzumab may prevent subsequent cardiomyopathy. Larger trials with meaningful clinical endpoints are needed.