Myocardial creatine kinase expression after left ventricular assist device support

Soon J. Park, Jianyi Zhang, Yun Ye, Sofia Ormaza, Peihua Liang, Alan J. Bank, Leslie W. Miller, Robert J. Bache

Research output: Contribution to journalArticle

19 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)1773-1779
Number of pages7
JournalJournal of the American College of Cardiology
Volume39
Issue number11
DOIs
StatePublished - Jun 5 2002
Externally publishedYes

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MB Form Creatine Kinase
Heart-Assist Devices
Creatine Kinase
MM Form Creatine Kinase
Protein Isoforms
Protein Kinase C
BB Form Creatine Kinase
Fetal Movement
Cardiomyopathies
Heart Ventricles

ASJC Scopus subject areas

  • Nursing(all)

Cite this

Park, S. J., Zhang, J., Ye, Y., Ormaza, S., Liang, P., Bank, A. J., ... Bache, R. J. (2002). Myocardial creatine kinase expression after left ventricular assist device support. Journal of the American College of Cardiology, 39(11), 1773-1779. https://doi.org/10.1016/S0735-1097(02)01860-0

Myocardial creatine kinase expression after left ventricular assist device support. / Park, Soon J.; Zhang, Jianyi; Ye, Yun; Ormaza, Sofia; Liang, Peihua; Bank, Alan J.; Miller, Leslie W.; Bache, Robert J.

In: Journal of the American College of Cardiology, Vol. 39, No. 11, 05.06.2002, p. 1773-1779.

Research output: Contribution to journalArticle

Park, SJ, Zhang, J, Ye, Y, Ormaza, S, Liang, P, Bank, AJ, Miller, LW & Bache, RJ 2002, 'Myocardial creatine kinase expression after left ventricular assist device support', Journal of the American College of Cardiology, vol. 39, no. 11, pp. 1773-1779. https://doi.org/10.1016/S0735-1097(02)01860-0
Park, Soon J. ; Zhang, Jianyi ; Ye, Yun ; Ormaza, Sofia ; Liang, Peihua ; Bank, Alan J. ; Miller, Leslie W. ; Bache, Robert J. / Myocardial creatine kinase expression after left ventricular assist device support. In: Journal of the American College of Cardiology. 2002 ; Vol. 39, No. 11. pp. 1773-1779.
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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.",
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AU - Bank, Alan J.

AU - Miller, Leslie W.

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N2 - 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.

AB - 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.

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