Abstract
Heart failure is associated with a significant change in the energy metabolism of the heart. We aimed to elucidate the altered energetics during the progression of heart failure. We used radioactive metabolic tracers to assess the substrate uptake. In a rat model of heart failure, the glucose uptake increased significantly at the stage of left ventricular hypertrophy, whereas the uptake of fatty acids decreased at the stage of heart failure, with decreased energy reserve during the transition of cardiac hypertrophy to failure. Metabolic modulator which enhances glucose oxidation ameliorated the decrease in cardiac function. We also validated the close correlation with mitochondrial membrane potentials and 99mtechnetium sestamibi (99mTc-MIBI) in vivo and at the organ level. The retention of 99mTc-MIBI signals was correlated with the severity of heart failure. Nuclear medicine is a powerful tool to understand the mechanism of cardiac remodeling in heart failure.
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