title: Ventricular arrhythmias following one-stage and two-stage coronary reperfusion: evidence for both reentry and enhanced automaticity.
abstract: We studied the effects of reperfusion in 60 dogs following a 30-45 minute period of left anterior descending coronary artery occlusion using electrocardiograms and composite electrogram recordings. One-stage reperfusion in 14 of 15 dogs produced ventricular arrhythmias which degenerated into ventricular fibrillation within 60 seconds. The onset of ventricular arrhythmias was associated with continuous electrical activity in epicardial and intramural electrograms recorded from the reperfused zone. Vagal slowing during reperfusion (64 +/- 8/min) did not prevent ventricular fibrillation (eight of eight dogs) and escape beats were often followed by one or more coupled ectopic beats associated with continuous electrical activity. Rapid atrial pacing (270/min) also did not prevent the appearance of ventricular arrhythmia with associated continuous electrical activity and ventricular fibrillation (six of six dogs) nor did 4 mg/kg lidocaine (15 of 16 dogs). In another group of 15 dogs reperfusion was performed in two stages resulting in no ventricular fibrillation but in 8 of 15 dogs ventricular arrhythmias were observed beginning within two minutes after reperfusion and lasting 20-30 minutes. These ventricular arrhythmias were not associated with continuous electrical activity in any of the recorded leads. Atrial pacing suppressed ventricular arrhythmias and idioventricular rate averaged 157 +/- 10/min versus 55 +/- 10/min pre-reperfusion control. The earliest site of activation indicated automatic foci arising in the subendocardium of the reperfused zone. Lidocaine (2-4 mg/kg) rapidly (less than 90 sec) restored normal sinus rhythm and suppressed automaticity (72 +/- 11/min) as did left anterior descending artery reocclusion (52 +/- 6/min). We conclude that both reentry and enhanced automaticity play a role in ventricular arrhythmias due to reperfusion. Lidocaine (2-4 mg/kg) suppresses automatic but not reentrant ventricular arrhythmias in this experimental setting.
authors.forename: G
authors.initials: G
authors.lastname: Kabell
authors.forename: B J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: J
authors.initials: J
authors.lastname: Brachmann
authors.forename: L
authors.initials: L
authors.lastname: Harrison
authors.forename: R
authors.initials: R
authors.lastname: Lazzara
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000503:physiopathology*; D005117:Cardiac Complexes, Premature / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial; D003326:Coronary Circulation / Q000187:drug effects; D003327:Coronary Disease / Q000503:physiopathology*; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography / Q000379:methods*; D006325:Heart Atria / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000503:physiopathology*; D008012:Lidocaine / Q000494:pharmacology; D013610:Tachycardia / Q000503:physiopathology; D014630:Vagus Nerve / Q000503:physiopathology; D014693:Ventricular Fibrillation / Q000503:physiopathology
chemical_list: D008012:Lidocaine