| Abstract: |
The use of anthracyclines, a family of chemotherapeutic agents with efficacy against many solid tumors and leukemias has been limited by their cardiotoxicity. This cardiotoxicity manifests as a reversible acute myopericarditis, an irreversible subacute cardiomyopathy and a progressive late, chronic form. It is particularly important in children who can be expected to survive decades after cure of their malignancy. The incidence of the subacute and late forms have been shown to increase with increasing peak and total cumulative anthracycline dose. Prevention of cardiotoxicity has been attempted by: (1) arbitrary limitation of total cumulative dose; (2) dose limitation guided by monitoring; (3) variation of administrative methods to decrease peak dose by the use of weekly divided boluses or continuous infusion; (4) liposomal encapsulation; (5) use of anthracycline analogues; and (6) concomitant administration of cardioprotective agents. The most promising cardioprotective agent, to date is an intracellular iron chelator which interferes with the formation of free radicals by the anthracyclines, thus limiting cardiac damage from lipid peroxidation. None of these methods has provided full cardiac protection, hence further study of the pathophysiology of anthracycline cardiotoxicity and its prevention is warranted as is long term monitoring of the cancer survivors who have received anthracyclines. |
