Cardiotoxicity in Pediatric AML

Pediatric acute myeloid leukemia (AML) therapy is associated with a significant risk of short- and long-term cardiotoxicity largely related to its inclusion of high doses of anthracycline chemotherapy. Cardiotoxicity most commonly manifests as asymptomatic left ventricular systolic dysfunction, which can progress to symptomatic heart failure. Cardiotoxicity may limit anthracycline delivery; its occurrence during pediatric AML therapy has been associated with inferior event-free and overall survival due to higher treatment-related mortality and higher relapse risk. Thus, cardioprotection is critical to preserving cardiac function and maximizing delivery of effective AML therapy. Dexrazoxane reduces short- and long-term cardiotoxicity without compromising cancer survival. Liposomal encapsulation of anthracyclines is cardioprotective in adults; however, its efficacy in reducing cardiotoxicity among children with AML remains under investigation. Current measures of primary cardioprotection may reduce but not eliminate cardiotoxicity; close monitoring of cardiac function during therapy and long-term follow-up remains essential. Anthracycline dose modifications in response to cardiotoxicity should be considered with caution to avoid compromising cancer survival. Additional cardioprotective measures may be considered in response to significant cardiotoxicity. Cardiac-directed medications, such as angiotensin-converting enzyme inhibitors and beta blockers, may support cardiac recovery when initiated early in the course of anthracycline-related cardiac dysfunction. Finally, careful management of cardiovascular risk factors such as hypertension and diabetes can reduce long-term cardiovascular risk in childhood AML survivors.