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.
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