Cardiotoxicity is heart damage that arises from certain drugs, such as those used for cancer treatment and develops in approximately 10% of patients with breast cancer who are treated with anthracyclines. It has been suggested that sodium-glucose transporter-2 (SGLT2) inhibitors may reduce the damage to the heart caused by anthracycline chemotherapy. The investigators wish to determine whether dapagliflozin (SGLT2 inhibitor) taken daily during chemotherapy will reduce the rate of cardiotoxicity.
Cardiac dysfunction is a major complication of cancer drug therapies, affecting approximately 10% of patients treated with anthracyclines. It has the worst prognosis of all cardiomyopathies and is currently thought to be a consequence of an energetic based mitochondrial dysfunction. This energy deficit could potentially be ameliorated by the putative cardiometabolic benefits of sodium-glucose transporter type 2 inhibition. In pilot data from patients with breast cancer, the investigators have demonstrated that cardiac magnetic resonance spectroscopy can identify and quantify the myocardial energetic deficit associated with anthracycline therapy. The purpose of this study is to determine whether sodium-glucose transporter type 2 inhibition has the potential to reverse the myocardial energetic deficit associated with anthracycline toxicity.
Study Type
INTERVENTIONAL
Allocation
RANDOMIZED
Purpose
BASIC_SCIENCE
Masking
NONE
Enrollment
70
Dapagliflozin 10mg in addition to standard clinical care
Standard clinical care
University of Aberdeen
Aberdeen, United Kingdom
Cardiac energetics
In vivo myocardial phosphocreatine/gamma-adenosine triphosphate (PCr/yATP) ratio by cardiac 31P cardiac magnetic resonance spectroscopy
Time frame: From enrolment to the end of treatment at the end of approximately 22 weeks
Myocardial Ca2+ influx
Myocardial Ca2+ influx assessed with manganese-enhanced magnetic resonance imaging (MEMRI)
Time frame: From enrolment to the end of treatment at the end of approximately 22 weeks
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