Anthracycline-Induced Cardiac Toxicity in Pediatric Acute Myeloid Leukemia
Acute myeloid leukemia (AML) is the most life-threatening form of leukemia requiring the most intensive treatment. While advances in its treatment have improved survival, chemotherapy exposure results in significant side effects. One type of drug, anthracyclines, increases the risk for heart complications.
Anthracycline-induced cardiac toxicity starts with heart cell injury and worsens over time to overt heart disease and heart failure. Therefore, efforts to improve the long-term cardiovascular health and mortality among AML survivors should be directed at early detection and prevention of cardiotoxicity. However, there are little data evaluating the factors that increase the risk for early-onset anthracycline-associated cardiac toxicity and its potential resolution in pediatric AML. Additionally, assessments of drugs such as dexrazoxane that might protect the heart from the damage cause by anthracyclines generally have not included AML patients.
The typical measures used to monitor heart function in childhood cancer may not detect injury until a serious amount of irreversible damage to the heart has taken place. Therefore identifying measures of cardiac function that might be early indicators of damage is important in order to prevent permanent cardiac dysfunction and improve the therapeutic benefit of cardio-protective drugs.
Therefore the proposed project aims to identify demographic and clinical correlates of early cardiotoxicity and to evaluate myocardial strain and strain rate as early sensitive markers for later dysfunction in an effort to improve the detection of high-risk patients. We also aim to assess the potential utility of dexrazoxane as a cardioprotective intervention in pediatric AML.