Enigmas regarding the true extent and impact of tyrosine kinase inhibitor-related cardiotoxicity.

Cardiac sequelae of anticancer treatment remains a major concern among both oncologists and cardiologists caring for patients treated with potentially cardiotoxic regimens. While the toxicity of anthracyclines is well understood to destroy myocytes, the scenario with regard to newer agents, both monoclonal antibodies and small-molecule tyrosine kinase inhibitors, is substantially different. This article differentiates the toxicity of agents that directly destroy myocytes (type I agents) from those that are associated with cardiac damage more indirectly (type II agents). Some mechanistic considerations regarding type II toxicity, albeit not categorically proven, are presented.