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Abstract #3788

Creatine Kinase-Overexpression Improves Adriamycin-Induced Dysfunction and in vivo ATP Kinetics in Murine Hearts

Ashish Gupta1, Cory Rohlfsen1, Missy Leppo1, Vadappuram P. Chacko2, Yibin Wang3, Robert G. Weiss1

1Department of Medicine, Division of Cardiology, The Johns Hopkins University, Baltimore, MD, United States; 2Department of Radiology, Division of Magnetic Resonance Research, The Johns Hopkins University, Baltimore, MD, United States; 3University of California, Los Angeles, CA, United States

Adriamycin (ADR) is a commonly used life-saving antineoplastic agent that also causes dose-dependent cardiotoxicity. Impaired energy metabolism may contribute to contractile dysfunction in human heart failure and may play a role in ADR-induced cardiotoxicity. We overexpressed the myofibrillar isoform of creatine kinase (CK-M), the major cardiac energy reserve reaction, to test the hypothesis that increasing CK-M expression would improve energy metabolism and, in turn, improve contractile function in dysfunctional ADR hearts. 1H MRI and 31P MRS results reveal that CK-M overexpression improves depressed CK energetics and cardiac dysfunction in ADR hearts.