Cardiotropin-1 and Myocardial Strain Change Heterogeneously in Cardiomyopathy

D. Dean Potter, Philip A Araoz, Leong L. Ng, David G. Kruger, Jess L. Thompson, Chad E. Hamner, Joseph A. Rysavy, Jayawant Mandrekar, Thoralf M. Sundt

Research output: Contribution to journalArticle

16 Citations (Scopus)

Abstract

Background: The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging. Materials and methods: Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure. Results: After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Conclusion: The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.

Original languageEnglish (US)
Pages (from-to)277-283
Number of pages7
JournalJournal of Surgical Research
Volume141
Issue number2
DOIs
StatePublished - Aug 2007

Fingerprint

Cardiomyopathies
Heart Failure
Muscle Cells
Dogs
Ventricular Function
Dilated Cardiomyopathy
cardiotrophin 1
Stroke Volume
Hypertrophy
Magnetic Resonance Imaging
Cytokines
Biopsy

Keywords

  • cardiomyopathy
  • cardiotrophin-1
  • heart failure
  • magnetic resonance imaging
  • natriuretic peptides
  • strain analysis

ASJC Scopus subject areas

  • Surgery

Cite this

Potter, D. D., Araoz, P. A., Ng, L. L., Kruger, D. G., Thompson, J. L., Hamner, C. E., ... Sundt, T. M. (2007). Cardiotropin-1 and Myocardial Strain Change Heterogeneously in Cardiomyopathy. Journal of Surgical Research, 141(2), 277-283. https://doi.org/10.1016/j.jss.2006.12.539

Cardiotropin-1 and Myocardial Strain Change Heterogeneously in Cardiomyopathy. / Potter, D. Dean; Araoz, Philip A; Ng, Leong L.; Kruger, David G.; Thompson, Jess L.; Hamner, Chad E.; Rysavy, Joseph A.; Mandrekar, Jayawant; Sundt, Thoralf M.

In: Journal of Surgical Research, Vol. 141, No. 2, 08.2007, p. 277-283.

Research output: Contribution to journalArticle

Potter, DD, Araoz, PA, Ng, LL, Kruger, DG, Thompson, JL, Hamner, CE, Rysavy, JA, Mandrekar, J & Sundt, TM 2007, 'Cardiotropin-1 and Myocardial Strain Change Heterogeneously in Cardiomyopathy', Journal of Surgical Research, vol. 141, no. 2, pp. 277-283. https://doi.org/10.1016/j.jss.2006.12.539
Potter, D. Dean ; Araoz, Philip A ; Ng, Leong L. ; Kruger, David G. ; Thompson, Jess L. ; Hamner, Chad E. ; Rysavy, Joseph A. ; Mandrekar, Jayawant ; Sundt, Thoralf M. / Cardiotropin-1 and Myocardial Strain Change Heterogeneously in Cardiomyopathy. In: Journal of Surgical Research. 2007 ; Vol. 141, No. 2. pp. 277-283.
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abstract = "Background: The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging. Materials and methods: Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure. Results: After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Conclusion: The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.",
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AU - Potter, D. Dean

AU - Araoz, Philip A

AU - Ng, Leong L.

AU - Kruger, David G.

AU - Thompson, Jess L.

AU - Hamner, Chad E.

AU - Rysavy, Joseph A.

AU - Mandrekar, Jayawant

AU - Sundt, Thoralf M.

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N2 - Background: The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging. Materials and methods: Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure. Results: After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Conclusion: The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.

AB - Background: The pacing model of heart failure produces heterogeneous changes in wall stress and myocyte diameter. The purpose of this study was to measure regional changes in cardiotrophin-1 (CT-1), a cytokine thought to play a role in LV remodeling, and regional changes in LV strain as measured with magnetic resonance imaging. Materials and methods: Dilated cardiomyopathy was induced in nine mongrel dogs over 4 wk by rapid pacing using a right ventricular epicardial lead. Baseline CT-1 was measured from an apical myocardial biopsy, and regional CT-1 was measured from anterior, lateral, inferior, and septal walls after the induction of heart failure and in six control dogs. Tissue tagged images were divided into similar regions and minimal principal strain (MPS), ejection fraction, and ventricular volumes were compared after induction of heart failure. Results: After induction of heart failure, LV ejection fraction and end-diastolic volume differed significantly from baseline (P < 0.01 and P = 0.02, respectively). Additionally, regional CT-1 and MPS were significantly different (P < 0.01 for both). Cardiotrophin-1 increased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Minimum principal strain decreased significantly in the inferior and septal walls (both P < 0.01) but not in the anterior or lateral walls (both P = NS). Conclusion: The pacing model of heart failure produces heterogeneous changes in regional CT-1 and wall motion as measured by MPS. The greatest regional changes are closest to the pacemaker site: the inferior and septal walls. These differences in regional CT-1 may account for previously noted myocyte hypertrophy and preserved ventricular function in these regions.

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