Anthracycline-induced cardiotoxicity
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Bentham Science Publishers
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The anthracyclines constitute a group of drugs widely used for the treatment of a variety of human tumors. However, the development of irreversible cardiotoxicity has limited their use. Anthracycline-induced cardiotoxicity can persist for years with no clinical symptoms. However, its prognosis becomes poor after the development of overt heart failure, possibly even worse than ischemic or idiopathic dilated cardiomyopathies. Due to the successful action of anthracyclines as chemotherapic agents, several strategies have been tried to prevent/ attenuate their side effects. Although anthracycline-induced injury appears to be multifactorial, a common denominator among most of the proposed mechanisms is cellular damage mediated by reactive oxygen species. However, it remains controversial as to whether antioxidants can prevent such side effects given that different mechanisms may be involved in acute versus chronic toxicity. The present review applies a multisided approach to the critical evaluation of various hypotheses proposed over the last decade on the role of oxidative stress in cardiotoxicity induced by doxorubicin, the most used anthracycline agent. The clinical diagnosis and treatment is also discussed. © 2008 Bentham Science Publishers Ltd.
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Cardiomyopathy DNA damage Doxorubicin Free radicals Oxidative stress Reactive Oxygen Species alpha tocopherol amifostine anthracycline derivative antioxidant ascorbic acid beta adrenergic receptor blocking agent beta carotene cannabinoid 1 receptor cannabinoid 1 receptor antagonist cyclophosphamide cytarabine digoxin dipeptidyl carboxypeptidase inhibitor DNA topoisomerase (ATP hydrolysing) doxorubicin flavonoid glutathione idarubicin inducible nitric oxide synthase lycopene olive oil polyphenol derivative probucol razoxane reactive nitrogen species reactive oxygen metabolite retinol selenium ubiquinone unindexed drug antioxidant activity aspartate aminotransferase blood level cardiomyopathy cardiotoxicity cardiovascular risk clinical feature creatine kinase blood level diagnostic value dose response drug dose reduction drug efficacy drug induced disease drug safety drug withdrawal early diagnosis ECG abnormality echocardiography electrocardiography follow up health care cost heart arrhythmia heart failure heart muscle biopsy heart protection heart transplantation human hypotension incidence lactate dehydrogenase blood level neoplasm nonhuman oxidative stress pathogenesis primary prevention prognosis protein expression QRS complex QT prolongation review risk factor side effect single drug dose ST segment tachycardia Animals Antibiotics, Antineoplastic Calcium DNA Damage Electrocardiography Heart Humans Oxidative Stress
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Cardiovascular and Hematological Agents in Medicinal Chemistry, v. 6, n. 4, p. 278-281, 2008.
