Abstract

The chronic cardiotoxicity of the cytotoxic agents such as anthracyclines is one of the main factors, which limits their prolonged use. Clinically, this cardiotoxicity results in a cardiomyopathy with irreversible congestive heart failure, with high mortality. The molecular mechanisms, which could explain this cardiac toxicity, are complex but it seems distinct from the anticancer mechanism. Several hypotheses were advanced but it appears that the induction of an oxidative stress within myocardial tissue constitutes the common denominator. The prevention of this cardiotoxicity lies on: — a rigorous cardiac monitoring — the use of anthracyclines analogues with lower cardiotoxicity, — modifications of the protocols of administration. The myocardial protection, with cardioprotective agents targeting oxidative stress during chemotherapy would be of great interest for an optimal use of the anthracyclines.

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