Chemotherapy-induced cardiotoxicity: molecular mechanisms and prevention strategies

Abstract

Objective: Understand the molecular mechanisms involved in chemotherapy-induced cardiotoxicity and identify prevention strategies. Literature review: With advances in oncological therapies, patient  survival has significantly improved; however, this progress has been accompanied by an increase in cardiovascular complications, including cardiotoxicity. This phenomenon involves direct damage to cardiomyocytes, inflammatory infiltration, and alterations in myocardial perfusion. Drugs such as anthracyclines, trastuzumab, sunitinib, and 5-fluorouracil are frequently implicated in ventricular dysfunction and heart failure. Furthermore, factors such as advanced age, hypertension, diabetes, and exposure to mediastinal radiotherapy significantly increase the risk. The main pathophysiological mechanisms include oxidative stress, apoptosis, cellular necrosis, and impaired DNA and protein synthesis essential for cardiac function. Final considerations: Early detection of cardiotoxicity signs, combined with preventive interventions such as rigorous clinical monitoring and cardioprotective therapies, is essential to minimize the adverse impacts of cancer treatment and preserve patients' quality of life.