title: Desynchronization: a novel model to induce heart failure.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Cardiology, Kerckhoff Heart and Thorax Center, Bad Nauheim, Germany. h.moellmann@kerckhoff-fgi.de
authors.forename: H
authors.initials: H
authors.lastname: Möllmann
authors.forename: S
authors.initials: S
authors.lastname: Voss
authors.forename: H M
authors.initials: HM
authors.lastname: Nef
authors.forename: M
authors.initials: M
authors.lastname: Lintz
authors.forename: C
authors.initials: C
authors.lastname: Oltenau
authors.forename: S
authors.initials: S
authors.lastname: Kostin
authors.forename: J
authors.initials: J
authors.lastname: Sperzel
authors.forename: C
authors.initials: C
authors.lastname: Troidl
authors.forename: W
authors.initials: W
authors.lastname: Skwara
authors.forename: A
authors.initials: A
authors.lastname: Rolf
authors.forename: C
authors.initials: C
authors.lastname: Hamm
authors.forename: A
authors.initials: A
authors.lastname: Elsässer
mesh_terms: D000818:Animals; D002304:Cardiac Pacing, Artificial / Q000379:methods*; D003094:Collagen / Q000378:metabolism; D003598:Cytoskeletal Proteins / Q000378:metabolism; D004195:Disease Models, Animal; D006333:Heart Failure / Q000209:etiology*; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D020778:Matrix Metalloproteinase 2 / Q000378:metabolism; D020780:Matrix Metalloproteinase 9 / Q000378:metabolism; D009200:Myocardial Contraction / Q000502:physiology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D011897:Random Allocation; D016037:Single-Blind Method; D013552:Swine
chemical_list: D003598:Cytoskeletal Proteins; D003094:Collagen; D020778:Matrix Metalloproteinase 2; D020780:Matrix Metalloproteinase 9