title: Anterior septal coronary artery infarction in the canine: a model of ventricular tachycardia with a subendocardial origin. Ablation and activation sequence mapping.
abstract: BACKGROUND
  In humans, chronic ventricular tachycardia (VT) is usually associated with myocardial infarcts that involve the interventricular septum. In an effort to more closely mimic the anatomic substrate that gives rise to chronic VT in humans, we developed a canine model of VT in which the anterior septal coronary artery was ligated. The site of earliest activation, the subsequent activation sequence, and the mechanism of VT associated with the resultant ventricular septal infarct was then evaluated to determine if this model accurately reflected the characteristics of human VT.
  
  
  RESULTS
  Seventeen dogs underwent occlusion-reperfusion ventricular septal infarcts. Four to 7 days later, electrophysiological studies were performed. VT was initiated by programmed electrical stimulation and terminated by pacing at a cycle length of 50% to 75% of the VT cycle length. Electrophysiological studies were performed using a 256-channel mapping system. A total of 15 VT morphologies were mapped in 9 animals. Fourteen of 15 morphologies had septal subendocardial sites of earliest activation and 1 had a septal midwall site of earliest activation. VT ablation was performed using a nitrous oxide cryoprobe and confirmed the site of earliest activation by subsequently rendering VT noninducible. Electrophysiological studies demonstrated four distinct VT activation sequences: (1) circular reentrant (n = 7), (2) concentric spread (n = 5), (3) figure-of-eight (n = 2), and (4) septal midwall (n = 1).
  
  
  CONCLUSIONS
  This canine model of ventricular septal infarction produces VTs with sites of earliest activation and activation sequences similar to those in humans. A reentrant mechanism as the basis of these arrhythmias is supported by the following observations: (1) all VT was initiated and terminated with programmed electrical stimulation; (2) VT activation sequences were consistent with reentry; and (3) precise interruption of the sequence terminated the VT and rendered it noninducible.
authors.affiliation: Department of Surgery, Washington University School of Medicine, Barnes Hospital, St Louis, MO.
authors.forename: J S
authors.initials: JS
authors.lastname: Tweddell
authors.forename: C K
authors.initials: CK
authors.lastname: Rokkas
authors.forename: A
authors.initials: A
authors.lastname: Harada
authors.forename: J S
authors.initials: JS
authors.lastname: Pirolo
authors.forename: B H
authors.initials: BH
authors.lastname: Branham
authors.forename: R B
authors.initials: RB
authors.lastname: Schuessler
authors.forename: J P
authors.initials: JP
authors.lastname: Boineau
authors.forename: J L
authors.initials: JL
authors.lastname: Cox
mesh_terms: D000818:Animals; D003326:Coronary Circulation; D003452:Cryosurgery; D004195:Disease Models, Animal; D004285:Dogs; D004594:Electrophysiology; D006346:Heart Septum; D007238:Infarction / Q000150:complications*; D017180:Tachycardia, Ventricular / Q000209:etiology* / Q000503:physiopathology* / Q000601:surgery