Ashish Gupta1,2,
Vadappuram P. Chacko3, Yibin Wang4, Robert G. Weiss2,5
1Department of
Medicine, Division of Cardiology, the Johns Hopkins University, School of
Medicine, Baltimore, MD, USA; 2Department of Radiology, Division of
Magnetic Resonance Research, the Johns Hopkins University , Baltimore, MD,
USA; 3Department of Radiology,Division of Magnetic Resonance
Research, the Johns Hopkins University School of Medicine, Baltimore, MD,
USA; 4Department of Anesthesiology & Medicine, University of
California, Los Angeles, CA, USA; 5Department of Medicine,
Division of Cardiology, the Johns Hopkins University School of Medicine,
Baltimore, MD, USA
Because it was hypothesized that failing heart is energy starved, we used a transgenic approach to augment ATP synthesis in failing hearts. The in vivo rate of ATP synthesis through cardiac creatine kinase (CK Flux) was measured using localized 31P MR triple repetition saturation transfer (TRiST) in healthy mice (n=11), others with heart failure (HF) following thoracic aortic constriction (TAC, n=10), and non-operated (n=8) and TAC (n=7) mice overexpressing the muscle isoform of creatine kinase (CK-M). CK flux was significantly increased in CK-M TAC hearts, indicating that CK-M overexpression offers a means to augment ATP delivery in HF.
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