This study aims to evaluate the efficacy and safety of telmisartan as a cardioprotective agent in patients receiving doxorubicin-based chemotherapy, with the goal of reducing treatment-associated cardiotoxicity, optimizing therapeutic outcomes, and facilitating the safer administration of anthracycline regimens.
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.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
PREVENTION
Masking
NONE
Enrollment
36
Telmisartan administered orally once daily as cardioprotective therapy during doxorubicin-based chemotherapy.
Standard doxorubicin-based chemotherapy according to institutional protocol.
Tanta University
Tanta, El Gharbia, Egypt
Change in Left Ventricular Ejection Fraction (LVEF)
The primary outcome is the absolute change in left ventricular ejection fraction (LVEF) from baseline to the end of doxorubicin-based chemotherapy, assessed by echocardiography.
Time frame: Baseline to end of chemotherapy (approximately 12-18 weeks)
Change in High-Sensitivity Cardiac Troponin T (hs-cTnT) Levels
Measurement of serum hs-cTnT at baseline and at the end of doxorubicin-based chemotherapy to assess myocardial injury and cardiac stress in patients receiving telmisartan or standard care.
Time frame: Baseline (pre-chemotherapy) to end of chemotherapy (approximately 12-18 weeks)
Change in N-terminal pro-B-type Natriuretic Peptide (NT-proBNP) Levels
Measurement of serum NT-proBNP at baseline and at the end of doxorubicin-based chemotherapy. Any increase from baseline indicates early ventricular strain or subclinical heart failure in patients receiving telmisartan or standard care.
Time frame: Baseline to end of chemotherapy (approximately 12-18 weeks)
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