Cardiotoxicity Chemotherapeutic agents may cause direct injury to the heart, either acutely, in the form of myocardial tissue injury or dysrhythmias, or in a delayed or chronic fashion associated with congestive heart failure. Anthracyclines Principal among the cardiotoxic agents are the anthracyclines, for which cardiac toxicity is the major dose-limiting toxicity. Acute toxicity These agents can result in acute cardiac dysfunction, particularly supraventricular tachyarrhythmias, within hours of bolus administration. Chronic toxicity Of greatest concern, however, is the chronic toxicity of anthracyclines that occurs weeks or months after administration. The pathogenesis of anthracycline-related cardiotoxicity is mediated, in part, by free radical formation with derangement of mitochondrial function.
Mediastinal radiation increases the risk of cardiac toxicity.
The cardiac toxicity is only minimally reversible. A variety of techniques can be used to monitor cardiac function and detect evidence of chemotherapy-induced injury. Percutaneous endomyocardial biopsy can detect subclinical injury to the heart. Cardiac dysfunction is manifested as congestive heart failure or dysrhythmias and can occur in persons who were previously asymptomatic. Recent technologic advances have enabled the use of liposomes as carriers for antineoplastic drugs.