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Chemotherapy‐induced cardiotoxicity: current practice and prospects of prophylaxis
Author(s) -
Gharib M.I.,
Burnett A.K.
Publication year - 2002
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/s1388-9842(01)00201-x
Subject(s) - medicine , cardiotoxicity , ifosfamide , chemotherapy , anthracycline , intensive care medicine , cardiomyopathy , cyclophosphamide , heart failure , troponin , cardiology , oncology , cancer , breast cancer , etoposide , myocardial infarction
Cardiotoxicity is a potential side effect of few chemotherapeutic agents. The anthracycline class of cytotoxic antibiotics are the most famous, but other chemotherapeutic agents can also cause serious cardiotoxicity and are not so well recognised. Examples include cyclophosphamide, ifosfamide, mitomycin and fluorouracil. Prediction and hence prophylaxis has always been a difficult task. Ideal monitoring techniques, upon which efficient prophylaxis depends, are yet to be determined. Current prophylaxis relies upon early detection of systolic and/or diastolic dysfunction. While somewhat useful, in some cases by the time defects are detected progression of chemotherapy‐induced cardiomyopathy is beyond prevention. Prophylaxis would be much more efficient if a biochemical marker of myocardiocyte damage could be reliably used to stop further chemotherapy at the correct time before irreversible progressive ‘macroscopic’ damage becomes evident upon imaging. Work is currently progressing to identify the role of markers such as troponins and natriuretic peptides in this regard.