title: Role of the Purkinje system in spontaneous ventricular tachycardia during acute ischemia in a canine model.
abstract: BACKGROUND
  A role for the Purkinje system in the development of spontaneous ventricular tachycardia (VT) during acute ischemia has been suspected but not proved. We used a three-dimensional activation mapping system incorporating Purkinje signals to characterize the mechanism and site of origin of spontaneous VT occurring in the first 30 minutes after coronary artery occlusion in a dog model.
  
  
  RESULTS
  The left anterior descending coronary artery was occluded in 48 dogs after instrumentation of the risk zone with 21 multipolar plunge needles, each recording 6 bipolar electrograms through the myocardial wall. VT of Purkinje origin was defined as a focal endocardial VT with a Purkinje potential identified before muscle potential on the electrode recording the earliest activity. Purkinje potentials were identified on an average of 10 of the 21 plunge needles. During atrial pacing at cycle lengths of 300 to 700 ms, a total of 25 VTs were observed from 18 of the 48 dogs (37.5%). Of the VTs, 15 (60.0%) were of focal Purkinje origin, 1 (4.0%) of focal endocardial origin, 2 (8.0%) of focal midmyocardial origin, and 2 (8.0%) of focal epicardial origin; 3 (12.0%) had a reentrant mechanism, whereas in 2 (8.0%), the mechanism could not be defined. The mean cycle length of all VTs was 265+/-17 ms (mean+/-SEM, n=25). Of the 25 VTs, 19 originated from an ischemic area as defined by significant decreases in voltages of muscle electrograms at the time of occurrence of the VT, 4 originated from an ischemic border zone, and the origin of 2 could not be determined.
  
  
  CONCLUSIONS
  In this model, VT with a focal mechanism is commonly seen in the early ischemic period. Sixty percent of the VTs were of focal Purkinje origin as characterized by three-dimensional activation mapping. The results of this study indicate that Purkinje tissue may play an important role in the development of early ischemic VT.
authors.affiliation: Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242, USA.
authors.forename: D O
authors.initials: DO
authors.lastname: Arnar
authors.forename: J R
authors.initials: JR
authors.lastname: Bullinga
authors.forename: J B
authors.initials: JB
authors.lastname: Martins
mesh_terms: D000818:Animals; D003331:Coronary Vessels / Q000503:physiopathology*; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography; D005260:Female; D006321:Heart / Q000502:physiology / Q000503:physiopathology; D008297:Male; D017202:Myocardial Ischemia / Q000150:complications / Q000503:physiopathology*; D011690:Purkinje Fibers / Q000502:physiology / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000473:pathology / Q000503:physiopathology*; D013997:Time Factors; D014693:Ventricular Fibrillation / Q000503:physiopathology; D016276:Ventricular Function