Telmisartan for Prevention of Doxorubicin-Induced Cardiotoxicity in Breast Cancer Patients

Doxorubicin remains one of the most effective chemotherapeutic agents for the treatment of a wide range of solid tumors and hematological malignancies. However, its clinical use is limited by dose-dependent cardiotoxicity, which may manifest as subclinical myocardial injury, left ventricular dysfunction, and progression to heart failure. The mechanisms underlying doxorubicin-induced cardiotoxicity are multifactorial, with oxidative stress recognized as a central pathway contributing to reactive oxygen species (ROS) generation, mitochondrial dysfunction, and cardiomyocyte injury. These effects highlight the need for strategies to reduce cardiovascular complications associated with doxorubicin therapy without compromising anticancer efficacy. Telmisartan, an angiotensin II type 1 receptor blocker (ARB), has demonstrated pharmacological effects beyond blood pressure control. Preclinical studies suggest that telmisartan may reduce oxidative stress, improve endothelial function, and preserve mitochondrial integrity, partly through modulation of peroxisome proliferator-activated receptor gamma (PPAR-γ) pathways. These effects may contribute to attenuation of cardiac remodeling and myocardial injury. Despite these observations, clinical evidence evaluating telmisartan for the prevention of doxorubicin-induced cardiotoxicity remains limited and inconclusive. Recent in vitro findings also indicate that telmisartan may enhance doxorubicin-induced apoptosis and cytotoxic efficacy in cancer cell lines. These findings raise the possibility that telmisartan could exert both cardioprotective and chemosensitizing effects. Considering this evidence gap, the present study is designed to investigate the cardioprotective role of telmisartan in patients undergoing doxorubicin-based chemotherapy.