Chemotherapeutic agents such as doxorubicin can cause serious adverse effects on the heart, leading to decreased left ventricular function and heart failure. The biochemical mechanisms for this are not fully understood, however, increased oxidative stress in cardiomyocytes as well as bioenergetic changes to the heart have been suggested as primary triggers for the functional decline. Here we show that hyperpolarized 13C magnetic resonance spectroscopy and CINE magnetic resonance imaging of the heart can detect metabolic as well as functional changes in a clinically relevant rat model of doxorubicin-induced cardiotoxicity, and that metabolic changes may precede functional abnormalities.
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