Breast Cancer, Doxorubicin Induced Cardiomyopathy
Conditions
Keywords
Telmisartan, Anthracycline Cardiotoxicity, Troponin, NT-proBNP, Cardioprotection
Brief summary
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.
Detailed description
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.
Interventions
DRUGTelmisartan
Telmisartan administered orally once daily as cardioprotective therapy during doxorubicin-based chemotherapy.
Standard doxorubicin-based chemotherapy according to institutional protocol.
Sponsors
Tanta University
Study design
Allocation
RANDOMIZED
Intervention model
PARALLEL
Primary purpose
PREVENTION
Masking
NONE
Eligibility
Sex/Gender
FEMALE
Age
18 Years to 65 Years
Healthy volunteers
No
Inclusion criteria
* Female patients with breast cancer. * Age ≥18 \& ≤ 65 years. * Newly diagnosed, chemotherapy-naïve patients. * Baseline echocardiogram showing left ventricular ejection fraction (LVEF) ≥55%.
Exclusion criteria
* Presence of hypersensitivity to telmisartan. * History of cardiovascular disease (e.g., congestive heart failure, ischemic heart disease, arrhythmia). * Patients with any chronic liver or renal dysfunction; inflammatory diseases; autoimmune disease; acute cardiovascular events, eating disorders (anorexia, bulimia) or gastrointestinal disorders. * Baseline blood pressure ≥ 160/100 mmHg * Current or prior use of ARBs/ACE inhibitors * Current participation in another clinical trial within the past 30 days. * Pregnant or breastfeeding women.
Design outcomes
Primary
| Measure | Time frame | Description |
|---|---|---|
| Change in Left Ventricular Ejection Fraction (LVEF) | Baseline to end of chemotherapy (approximately 12-18 weeks) | 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. |
Secondary
| Measure | Time frame | Description |
|---|---|---|
| Change in High-Sensitivity Cardiac Troponin T (hs-cTnT) Levels | Baseline (pre-chemotherapy) to end of chemotherapy (approximately 12-18 weeks) | 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. |
| Change in N-terminal pro-B-type Natriuretic Peptide (NT-proBNP) Levels | Baseline to end of chemotherapy (approximately 12-18 weeks) | 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. |
Countries
Egypt
Contacts
CONTACTMenna Ahmed
Outcome results
None listed