title: Myocardial infarction does not preclude electrical and hemodynamic benefits of cardiac resynchronization therapy in dyssynchronous canine hearts.
abstract: BACKGROUND
  Several studies suggest that patients with ischemic cardiomyopathy benefit less from cardiac resynchronization therapy. In a novel animal model of dyssynchronous ischemic cardiomyopathy, we investigated the extent to which the presence of infarction influences the short-term efficacy of cardiac resynchronization therapy.
  
  
  RESULTS
  Experiments were performed in canine hearts with left bundle branch block (LBBB, n=19) and chronic myocardial infarction, created by embolization of the left anterior descending or left circumflex arteries followed by LBBB (LBBB+left anterior descending infarction [LADi; n=11] and LBBB+left circumflex infarction [LCXi; n=7], respectively). Pacing leads were positioned in the right atrium and right ventricle and at 8 sites on the left ventricular (LV) free wall. LV pump function was measured using the conductance catheter technique, and synchrony of electrical activation was measured using epicardial mapping and ECG. Average and maximal improvement in electric resynchronization and LV pump function by right ventricular+LV pacing was similar in the 3 groups; however, the site of optimal electrical and mechanical benefit was LV apical in LBBB hearts, LV midlateral in LBBB+LCXi hearts and LV basal-lateral in LBBB+LADi hearts. The best site of pacing was not the site of latest electrical activation but that providing the largest shortening of the QRS complex. During single-site LV pacing the range of atrioventricular delays yielding > or =70% of maximal hemodynamic effect was approximately 50% smaller in infarcted than noninfarcted LBBB hearts (P<0.05).
  
  
  CONCLUSIONS
  Cardiac resynchronization therapy can improve resynchronization and LV pump function to a similar degree in infarcted and noninfarcted hearts. Optimal lead positioning and timing of LV stimulation, however, require more attention in the infarcted hearts.
authors.affiliation: Departments of Physiology and Cardiothoracic Surgery, Cardiovascular Research Institute Maastricht, Maastricht, The Netherlands.
authors.forename: Leonard M
authors.initials: LM
authors.lastname: Rademakers
authors.forename: Roeland
authors.initials: R
authors.lastname: van Kerckhoven
authors.forename: Caroline J M
authors.initials: CJ
authors.lastname: van Deursen
authors.forename: Marc
authors.initials: M
authors.lastname: Strik
authors.forename: Arne
authors.initials: A
authors.lastname: van Hunnik
authors.forename: Marion
authors.initials: M
authors.lastname: Kuiper
authors.forename: Anniek
authors.initials: A
authors.lastname: Lampert
authors.forename: Catherine
authors.initials: C
authors.lastname: Klersy
authors.forename: Francisco
authors.initials: F
authors.lastname: Leyva
authors.forename: Angelo
authors.initials: A
authors.lastname: Auricchio
authors.forename: Jos G
authors.initials: JG
authors.lastname: Maessen
authors.forename: Frits W
authors.initials: FW
authors.lastname: Prinzen
mesh_terms: D000818:Animals; D002037:Bundle-Branch Block / Q000150:complications / Q000503:physiopathology / Q000628:therapy*; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D022062:Electrophysiologic Techniques, Cardiac; D005260:Female; D006329:Heart Conduction System / Q000503:physiopathology*; D006439:Hemodynamics; D008297:Male; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000150:complications / Q000473:pathology / Q000503:physiopathology*; D009206:Myocardium / Q000473:pathology; D020127:Recovery of Function; D013318:Stroke Volume; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure