title: Right or left ventricular pacing in young minipigs with chronic atrioventricular block: long-term in vivo cardiac performance, morphology, electrophysiology, and cellular biology.
abstract: BACKGROUND
  Left ventricular (LV) dyssynchrony may occur as a result of right ventricular (RV) pacing and is a known risk factor for the development of heart failure. In children with complete atrioventricular block, pacing-induced dyssynchrony lasting for decades might be especially deleterious for LV function. To determine the hemodynamic and ultrastructural remodeling after either RV free wall or LV apical pacing, we used a chronic minipig model.
  
  
  RESULTS
  Fourteen piglets 8 weeks of age underwent atrioventricular node ablation and were paced from either the RV free wall or the LV apex at 120 bpm for 1 year (7 age-matched minipigs served as controls with spontaneous heart rates of 104 ± 5 bpm). Echocardiographic examinations, pressure-volume loops, patch-clamp investigations, and examinations of connexin43, calcium-handling proteins, and histomorphology were carried out. RV free wall-paced minipigs exhibited significantly more LV dyssynchrony than LV apex-paced animals, which was accompanied by worsening of LV function (maximum LV mechanical delay/LV ejection fraction: RV free wall pacing, 154 ± 36 ms/28 ± 3%, LV apical pacing, 52 ± 19 ms/45 ± 2%, control 47 ± 14 ms/62 ± 1%; P=0.0001). At the cellular level, both pacemaker groups exhibited a significant reduction in L-type calcium and peak sodium current, shortening of action potential duration and amplitude, increased cell capacity, and alterations in the calcium-handling proteins that were similar for RV free wall- and LV apex-paced animals.
  
  
  CONCLUSIONS
  The observed molecular remodeling seemed to be more dependent on heart rate than on dyssynchrony. LV apical pacing is associated with less dyssynchrony, a more physiological LV contraction pattern, and preserved LV function as opposed to RV free wall pacing.
authors.affiliation: Department of Paediatric Cardiology, University of Leipzig, Heart Centre, Germany. aida.salameh@med.uni-leipzig.de
authors.forename: Aida
authors.initials: A
authors.lastname: Salameh
authors.forename: Stefan
authors.initials: S
authors.lastname: Dhein
authors.forename: Katja
authors.initials: K
authors.lastname: Blanke
authors.forename: Ardawan
authors.initials: A
authors.lastname: Rastan
authors.forename: Bahi
authors.initials: B
authors.lastname: Hiyasat
authors.forename: Anna
authors.initials: A
authors.lastname: Dietze
authors.forename: Axel
authors.initials: A
authors.lastname: Sobiraij
authors.forename: Ingo
authors.initials: I
authors.lastname: Dähnert
authors.forename: Jan
authors.initials: J
authors.lastname: Janousek
mesh_terms: D000818:Animals; D054537:Atrioventricular Block / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D002304:Cardiac Pacing, Artificial; D002908:Chronic Disease; D018031:Connexin 43 / Q000378:metabolism; D004195:Disease Models, Animal; D004452:Echocardiography; D055724:Electrophysiological Phenomena; D006321:Heart / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology; D008297:Male; D009206:Myocardium / Q000166:cytology / Q000378:metabolism; D018408:Patch-Clamp Techniques; D013552:Swine; D013556:Swine, Miniature; D018487:Ventricular Dysfunction, Left / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*; D018497:Ventricular Dysfunction, Right / Q000000981:diagnostic imaging / Q000503:physiopathology* / Q000628:therapy*
chemical_list: D018031:Connexin 43