Prediction and prevention of chemotherapy-induced cardiomyopathy: can it be done?

Although anthracyclines are highly effective at treating certain cancers, their use is limited by the potential for cardiotoxicity. Studies report a wide range of the incidence of cardiotoxicity, related to differences in definitions, chemotherapy regimens, and patient populations. The occurrence of clinical heart failure seems to be in the range of 1% to 5%, and asymptomatic decrease in left ventricular function is in the range of 5% to 20%.1,2 Toxicity can occur early (within 1 year) or late (particularly among children, where late cardiac abnormalities are detectable in two thirds of surviving patients).3 The occurrence of cardiomyopathy is related to cumulative dose of anthracycline (especially doxorubicin doses 550 mg/m), dosing schedule, age, gender, mediastinal irradiation, and combination with other agents, including trastuzumab.4 Other chemotherapy, including imatinib mesylate,5 can also cause cardiotoxicity, suggesting a broader potential for adverse cardiac effects from novel chemotherapy and, especially, from inhibitors of nonreceptor tyrosine kinases. Anthracycline-induced cardiomyopathy seems to have a similar impact on survival as other forms of heart failure.6 Thus, identification of individuals at risk, prevention, early diagnosis, and effective treatment are all important goals. Most of these needs have been addressed by uncontrolled or small studies, and guidelines have relatively sparse information on which to base recommendations for care, other than careful monitoring of left ventricular function and interrupting or discontinuing anthracyclines once significant decrease in ejection fraction is detected, which is often too late.7