title: Facilitation of reentry by lidocaine in canine myocardial infarction.
abstract: Despite continuing controversies regarding its antiarrhythmic and antifibrillatory efficacy lidocaine is frequently used for the treatment of ventricular arrhythmias occurring in the early phase of acute myocardial infarction (MI). The authors studied the effects of lidocaine in 18 consecutive MI dogs 1-4 days (2.8 +/- 0.3 day) after the two-stage left anterior descending coronary artery (LAD) ligation and in 11 dogs, in which the LAD and the distal branches of the left circumflex artery was ligated 12-75 (mean 35) days prior to study. Electrophysiologic testing was performed in anesthetized post-infarction dogs using single, double or triple programmed extrastimuli or rapid bursts (3 beats at 240-420/min) delivered to the right ventricular outflow tract. Inducibility of SMVT (uniform QRS morphology lasting > 30 sec at a rate of > 250 beat/min) after an i.v. bolus of lidocaine (3-6 mg/kg) was compared in the same animal to the pre-drug state. During the control state, SMVT was inducible in 6/18 dogs. After the administration of lidocaine, electrically induced SMVT was initiated in additionally 9 dogs (which were previously non-inducible; post-lidocaine vs control p < 0.02). Sustained reentry was induced by 3 mg/kg lidocaine in 5 dogs (310 +/- 62 beat/min) and by 6 mg/kg in 4 (261 +/- 52 beat/min). In the 8 survivors of the chronic MI group, SMVT was inducible before lidocaine administration in one, but in 7 after lidocaine. The antiarrhythmic agent induced further rate-dependent slowing of conduction in the peri-infarction subepicardium, which at a critical value of rate and amount of conduction delay resulted in sustained reentrant monomorphic tachycardia. These results show that lidocaine has arrhythmogenic/proarrhythmic actions in these canine models of MI probably due to its depressant effect on moderately sick cardiac tissue. The 'modification' of the functional properties of the arrhythmia substrate by lidocaine can promote the formation of new reentrant pathways leading to manifest sustained ventricular reentry under electrophysiologic study.
authors.affiliation: Department of Medicine, Oklahoma University Health Sciences Center, Oklahoma City.
authors.forename: T
authors.initials: T
authors.lastname: Fazekas
authors.forename: B J
authors.initials: BJ
authors.lastname: Scherlag
authors.forename: P
authors.initials: P
authors.lastname: Mabo
authors.forename: E
authors.initials: E
authors.lastname: Patterson
authors.forename: R
authors.initials: R
authors.lastname: Lazzara
mesh_terms: D000208:Acute Disease; D000818:Animals; D002908:Chronic Disease; D004285:Dogs; D004562:Electrocardiography; D004594:Electrophysiology; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D007275:Injections, Intravenous; D008012:Lidocaine / Q000627:therapeutic use / Q000633:toxicity*; D008297:Male; D009203:Myocardial Infarction / Q000503:physiopathology*; D017180:Tachycardia, Ventricular / Q000139:chemically induced / Q000188:drug therapy* / Q000503:physiopathology; D016171:Torsades de Pointes / Q000139:chemically induced / Q000503:physiopathology
chemical_list: D008012:Lidocaine