Prevention of chemotherapy-induced left ventricular dysfunction

Abstract

Prevention of left ventricular dysfunction predominantly induced by anthracyclines and/or trastuzumab still represents a challenge for cardio-oncology today. Indeed, this complication threatens to limit the significant gain in cancer survival achieved to date. Oncology strategies with cumulative dose limitation, continuous infusion, dexrazoxane, and liposomal formulations have been shown to decrease the risk of anthracycline cardiotoxicity. The preventive use of ace inhibitors, sartans, and/or beta-blockers has not yet provided convincing evidence and the positive effect on left ventricular ejection fraction decline appears poor without a clear clinical relevance. Assessment of the cardiovascular risk profile is a key aspect of the baseline evaluation of any patient scheduled for cancer therapy. Control and/or correction of modifiable cardiovascular risk factors is the first form of primary prevention of cardiotoxicity. It will be necessary to select populations at higher risk of developing cardiac dysfunction, identify patients genetically predisposed to develop cardiotoxicity in order to build the most appropriate strategies to correctly and timely target cardioprotective therapies.

Therapeutic potential of extracellular vesicles derived from cardiac progenitor cells in rodent models of chemotherapy-induced cardiomyopathy

“…The incidence of this chemotherapy-induced cardiomyopathy (CCM) can be as high as 48% for those who have received the highest cumulative anthracycline doses and is exacerbated by the presence of other cardiovascular risk factors (3). These patients require careful monitoring, sometimes a reduction in dosing regimens or heart failure preventive therapies, whose benefit on improving patient outcomes still remains variable, especially after an anthracycline-based regimen (4,5). Hence, new therapeutic options are eagerly awaited.…”