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Patients with left ventricle (LV) volume overload (VO) remain in a compensated state for many years although severe dilation is present. The myocardial capacity to fulfill its energetic demand may delay decompensation. We performed a gene expression profile, a model of chronic VO in rat LV with severe aortic valve regurgitation (AR) for 9 months, and focused on the study of genes associated with myocardial energetics.  Methods . LV gene expression profile was performed in rats after 9 months of AR and compared to sham-operated controls. LV glucose and fatty acid (FA) uptake was also evaluated  in vivo  by positron emission tomography in 8-week AR rats treated or not with fenofibrate, an activator of FA oxidation (FAO).  Results . Many LV genes associated with mitochondrial function and metabolism were downregulated in AR rats. FA  β -oxidation capacity was significantly impaired as early as two weeks after AR. Treatment with fenofibrate, a PPAR α  agonist, normalized both FA and glucose uptake while reducing LV dilation caused by AR.  Conclusion . Myocardial energy substrate preference is affected early in the evolution of LV-VO cardiomyopathy. Maintaining a relatively normal FA utilization in the myocardium could translate into less glucose uptake and possibly lesser LV remodeling.

Transcriptional Changes Associated with Long-Term Left Ventricle Volume Overload in Rats: Impact on Enzymes Related to Myocardial Energy Metabolism