Chemotherapy-Induced Heart Disease

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  • I. CHEMOTHERAPEUTIC AGENTS
    It is common for chemotherapeutic agents to be associated with myocardial damage reduction in ejection fraction and heart failure.
  • II. CARDIAC DAMAGE FROM ANTHRACYCLINES
    Anthracyclines contain an aromatic ring structure that intercalates in between DNA base pairs. The mechanism of cardiotoxicity appears to be inhibition of the function of topoisomerase II. This enzyme is critical in allowing DNA to undergo efficient repair. Most important, these agents generate free radicals that can damage cell membranes partly by lipid peroxidation. Amsacrine and mitoxantrone produce lower quantities of free radicals and cause less cardiotoxicity and cardiomyopathy compared with the doxorubicin, daunorubicin, idarubicin, and epirubicin. Cardiac tissues possess a low ability to detoxify these free radicals because of the presence of only small amounts of catalase that converts hydrogen peroxide to water.
  • III. CYCLOPHOSPHAMIDE
    Cyclophosphamide and ifosfamide high-dose therapy may cause severe cardiomyopathy and heart failure in patients undergoing stem cell transplantation. Acute myocyte necrosis, with damage to the endothelial lining of the heart, and hemorrhagic myopericarditis may occur with a 30% mortality rate. The ECG shows abnormal patterns and the chest x-ray is a good test for detecting heart failure. An echocardiogram is not a test used for the detection of heart failure, but it is useful in revealing weakness of the heart muscle, pericarditis, or pericardial effusions. Serious complications are more common in patients with pre¬existing heart disease, particularly in those with left ventricular dysfunction and an ejection fraction of less than 45%.
  • IV. 5-FLUOROURACIL
    This is a frequently used agent and its associated cardio-toxicity may be more common than previously thought.
  • BIBLIOGRAPHY
    Stone, R. M., Bridges, K. R., and Libby, P. Hematological-oncological disorders and cardiovascular disease. In Heart Disease, seventh edition. E. Braunwald, D. P. Zipes, and P. Libby, eds. W. B. Saunders, Philadelphia, 2005.