This Article Figures Only Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Park, S. J. Articles by Bache, R. J. Search for Related Content PubMed PubMed Citation Articles by Park, S. J. Articles by Bache, R. J.

CLINICAL STUDY

Myocardial creatine kinase expression after left ventricular assist device support

Soon J. Park, MD^*, Jianyi Zhang, MD, PhD^,*, Yun Ye, MD, MS, Sofia Ormaza, RN, MS, Peihua Liang, MS, Alan J. Bank, MD, Leslie W. Miller, MD and Robert J. Bache, MD

^* Department of Surgery, University of Minnesota, Minneapolis, Minnesota, USA
Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota, USA

Manuscript received September 6, 2001; revised manuscript received March 5, 2002, accepted March 6, 2002.

^* Reprint requests and correspondence: Dr. Jianyi Zhang, Cardiovascular Division, Department of Medicine, University of Minnesota Medical School, Mayo Mail Code 508, 420 Delaware Street SE, Minneapolis, Minnesota, USA 55455.
zhang047{at}tc.umn.edu

OBJECTIVES: We examined whether unloading of the left ventricle with a ventricular assist device (LVAD) can result in normalization of the creatine kinase (CK) abnormalities in the failing human heart.

BACKGROUND: Left ventricular failure is associated with a decrease of myocardial total CK activity and a fetal shift in CK isoform expression that results in an increase in the cytosolic brain type homodimeric-creatine kinase (CK-B) subunit and decreases of the cytosolic muscle-creatine kinase (CK-M) and CK-mitochondrial (CK-Mt) isoforms. The mechanisms of this abnormality are not known.

METHODS: Total CK activity and CK protein isoform expression (Western blotting) were examined in 11 patients with end-stage cardiomyopathy. In 7 patients, myocardial tissue was also obtained after 4.1 ± 1.1 months of left ventricular assist device (LVAD) support.

RESULTS: Left ventricular unloading produced by LVAD implantation resulted in a 270% ± 114% increase in total CK activity (p < 0.01) that was associated with a 69% ± 18% increase in CK-M protein expression (p < 0.01) and a 121% ± 69% increase in CK-Mt protein expression (p < 0.01), but no significant change in CK-B expression.

CONCLUSIONS: Systolic and diastolic unloading provided by the LVAD resulted in increases of total CK activity as well as CK-Mt and CK-M protein expression. The failure of CK-B expression to decrease suggests that abnormalities other than increased loading are responsible for the increase in CK-B expression in the failing heart.

Abbreviations and Acronyms   ADP   adenosine 5"-diphosphate   ATP   adenosine triphosphate   CK   creatine kinase   CK-Mt   creatine kinase-mitochondrial   LV   left ventricle   LVAD   left ventricular assist device   Mg   magnesium   PCr   phosphocreatine   SDS-PAGE   sodium dodecyl sulfate-polyacrylamide gel electrophoresis

This article has been cited by other articles:

				J. S. Ingwall Energy metabolism in heart failure and remodelling Cardiovasc Res, February 15, 2009; 81(3): 412 - 419. [Abstract] [Full Text] [PDF]

				M. E. Cullen, A. H.Y. Yuen, L. E. Felkin, R. T. Smolenski, J. L. Hall, S. Grindle, L. W. Miller, E. J. Birks, M. H. Yacoub, and P. J.R. Barton Myocardial Expression of the Arginine:Glycine Amidinotransferase Gene Is Elevated in Heart Failure and Normalized After Recovery: Potential Implications for Local Creatine Synthesis Circulation, July 4, 2006; 114(1_suppl): I-16 - I-20. [Abstract] [Full Text] [PDF]

				K. M. Minhas, R. M. Saraiva, K. H. Schuleri, S. Lehrke, M. Zheng, A. P. Saliaris, C. E. Berry, K. M. Vandegaer, D. Li, and J. M. Hare Xanthine Oxidoreductase Inhibition Causes Reverse Remodeling in Rats With Dilated Cardiomyopathy Circ. Res., February 3, 2006; 98(2): 271 - 279. [Abstract] [Full Text] [PDF]

				T. Takaseya, M. Ishimatsu, E. Tayama, A. Nishi, T. Akasu, and S. Aoyagi Mechanical unloading improves intracellular Ca2+ regulation in rats with doxorubicin-induced cardiomyopathy J. Am. Coll. Cardiol., December 7, 2004; 44(11): 2239 - 2246. [Abstract] [Full Text] [PDF]

				J. S. Ingwall and R. G. Weiss Is the Failing Heart Energy Starved?: On Using Chemical Energy to Support Cardiac Function Circ. Res., July 23, 2004; 95(2): 135 - 145. [Abstract] [Full Text] [PDF]