Myocardial creatine kinase expression after left ventricular assist device support

Academic Article

Abstract

  • 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. © 2002 by the American College of Cardiology Foundation.
  • Authors

    Digital Object Identifier (doi)

    Author List

  • Park SJ; Zhang J; Ye Y; Ormaza S; Liang P; Bank AJ; Miller LW; Bache RJ
  • Start Page

  • 1773
  • End Page

  • 1779
  • Volume

  • 39
  • Issue

  • 11