Desynchronization: a novel model to induce heart failure

Thorac Cardiovasc Surg. 2009 Dec;57(8):441-8. doi: 10.1055/s-0029-1186070.

Abstract

Background: Previous large animal heart failure models led to inhomogeneous results. Therefore, we developed a novel model combining rapid pacing with forced ventricular desynchronization.

Methods: Heart failure was induced in 20 pigs during a pacing period of 21 days. Group A (n = 10) received one right ventricular lead (220 bpm). In group B (n = 10), two leads were implanted in different right ventricular regions with beat-to-beat alternation of activation sites (each lead 110 bpm). Sham-operated pigs (n = 6) served as controls. Hemodynamics were invasively evaluated and tissue was analyzed by immunohistochemistry and zymography.

Results: Hemodynamics were significantly more impaired in group B with an increase of pulmonary capillary wedge and central venous pressure and a reduction of cardiac index (control 4.3 +/- 0.1 l/min/m (2); A 3.6 +/- 0.2; B 2.9 +/- 0.2, P < 0.05). Heart-to-body weight ratio was significantly higher in group B. Histological analyses showed a significant increase of cell diameters and interstitial fibrosis with significantly higher collagen contents in group B.

Conclusion: The new model with a combination of rapid pacing and forced desynchronization of the ventricular contraction is superior to traditional heart failure models induced solely by rapid pacing.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Cardiac Pacing, Artificial / methods*
  • Collagen / metabolism
  • Cytoskeletal Proteins / metabolism
  • Disease Models, Animal*
  • Heart Failure / etiology*
  • Hemodynamics / physiology
  • Male
  • Matrix Metalloproteinase 2 / metabolism
  • Matrix Metalloproteinase 9 / metabolism
  • Myocardial Contraction / physiology
  • Myocytes, Cardiac / metabolism
  • Myocytes, Cardiac / pathology
  • Random Allocation
  • Single-Blind Method
  • Swine

Substances

  • Cytoskeletal Proteins
  • Collagen
  • Matrix Metalloproteinase 2
  • Matrix Metalloproteinase 9