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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

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