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Cardiotropin-1 and myocardial strain change heterogeneously in cardiomyopathy

D Dean Potter1, Philip A Araoz, Leong L Ng

  • 1Division of Cardiovascular Surgery, University of Leicester, Leicester, United Kingdom.

The Journal of Surgical Research
|June 19, 2007
PubMed

Insights

Heart failure pacing causes uneven changes in cardiotrophin-1 (CT-1) and wall motion, particularly near the pacemaker. These regional differences in CT-1 may explain myocyte hypertrophy and maintained function in these areas.

Area of Science:

  • Cardiovascular Research
  • Biomedical Engineering
  • Cardiac Electrophysiology

Background:

  • Heart failure pacing induces heterogeneous changes in myocardial wall stress and myocyte diameter.
  • Cardiotrophin-1 (CT-1) is a cytokine implicated in left ventricular (LV) remodeling.
  • Understanding regional variations in CT-1 and LV strain is crucial for managing heart failure.

Purpose of the Study:

  • To measure regional changes in cardiotrophin-1 (CT-1) in a canine pacing-induced heart failure model.
  • To assess regional changes in left ventricular (LV) strain using magnetic resonance imaging (MRI).
  • To correlate regional CT-1 levels with regional LV strain and remodeling.

Main Methods:

  • Dilated cardiomyopathy was induced in dogs via rapid ventricular pacing.
  • Regional myocardial CT-1 levels were measured from biopsies of different LV walls.
  • Tissue-tagged MRI was used to quantify regional LV strain, specifically minimal principal strain (MPS).

Main Results:

  • Pacing significantly altered LV ejection fraction and end-diastolic volume.
  • Significant regional differences in CT-1 levels and MPS were observed.
  • CT-1 increased and MPS decreased significantly in the inferior and septal walls, closest to the pacing lead.

Conclusions:

  • The pacing model results in heterogeneous changes in regional CT-1 and wall motion (MPS).
  • The most pronounced changes in CT-1 and MPS occurred in the inferior and septal walls.
  • Regional CT-1 variations may underlie observed myocyte hypertrophy and preserved ventricular function in specific regions.
Abstract

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