Cardiac toxicity after anthracycline chemotherapy in childhood

The clinical use of anthracyclines, a family of chemotherapeutic agents wit h efficacy against many solid tumors and leukemias is limited by unique cum ulative dose-limiting cardiotoxicity. Overt heart failure occurs in 4.5% to 7% of patients treated with anthracyclines and the incidence of cardiac fu nction abnormalities increases with the time, Anthracycline-induced congest ive heart failure is usually due to permanent changes in the myocardium, ch anges most consistent with the contractile failure of cardiomyopathy. Altho ugh the causes of anthracycline-induced cardiotoxicity are probably many, a large body of evidence points to free-radical-mediated myocyte damage. The risk of developing cardiac heart failure is modified by the presence of ce rtain risk factors that reduce cardiac tolerance to anthracyclines. Age and female gender seem to have an important role in the anthracycline cardioto xicity. This cardiotoxicity can be divided, on the base of when it started, into acute, subacute and progressive late, chronic form. Various invasive and non-invasive methods have been used to measure the extent of cardiac da mage done. Depending on the sensitivity of the method employed, the proport ion of hearts found to be damaged has varied widely. Attempts to ameliorate anthracycline cardiotoxicity have been directed toward: 1. decreasing myoc ardial concentrations of anthracyclines and their metabolites, 2. developin g less cardiotoxic analogous, and 3. concurrently administering cardioprote ctants to attenuate the effects of anthracyclines on the heart. Much progre ss has been made in terms of monitoring of clinical and subclinical anthrac ycline cardiotoxicity, finding alternative schedules, introducing special c arriers of anthracyclines and using cardioprotecting agents. It is hoped th at with all these effects and with results of ongoing and future trials, we will be able to reduce further or even eliminate anthracycline cardiotoxic ity.