title: Effects of lidocaine and diltiazem on ventricular tachyarrhythmia and dispersion of conduction during severe myocardial ischemia in canine hearts.
abstract: The purpose of this study was to investigate the effects of lidocaine and diltiazem on ventricular tachyarrhythmia and dispersion of conduction during severe myocardial ischemia in dogs. Myocardial ischemia was produced by a 10-min occlusion of the left anterior descending artery by the retrograde blood flow technique. Saline, lidocaine, and diltiazem were infused intravenously before and during occlusion in groups A (n = 16), B (n = 22) and C (n = 13), respectively. The incidence of ventricular tachycardia (VT) consisting of ten or more VPC was 19% in group A, 73% in group B and 31% in group C (A vs. B, P < 0.01), and that of ventricular fibrillation (VF) was 31%, 64%, and 15%, respectively (A vs. B, P < 0.05). The time of the onset of VT preceding VF was shorter in group B than in group A (207.9 +/- 13.9 vs. 353.2 +/- 70.7 sec, P < 0.05). The time taken to reach maximal dispersion of conduction delay in the epicardium was shorter in group B than in group A (192.1 +/- 11.9 vs. 337.5 +/- 38.2 sec, P < 0.01), and the dispersion of conduction delay in the intramyocardial layers was smaller in group B than in group A (229.9 +/- 24.5 vs. 360.0 +/- 35.6 sec, P < 0.01). The time taken to reach maximal dispersion of conduction delay in the endocardium was greater in group C than in group A (400.8 +/- 38.8 vs. 274.4 +/- 23.9 sec, P < 0.01). However, there were no significant differences among the three groups with regard to the maximal dispersion of conduction delay in the epicardium, in the endocardium, or intramyocardial layer. These results suggest that lidocaine increased ventricular tachyarrhythmia due to an acute increase in dispersion of conduction in the epicardium and intramural layer, and that diltiazem was not effective in preventing ventricular tachyarrhythmia and did not affect the dispersion of conduction in the epicardium or intramural layer despite improvement in the endocardium.
authors.affiliation: 2nd Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Murasato
authors.forename: Y
authors.initials: Y
authors.lastname: Nagamoto
authors.forename: T
authors.initials: T
authors.lastname: Urabe
authors.forename: F
authors.initials: F
authors.lastname: Kuraoka
authors.forename: Y
authors.initials: Y
authors.lastname: Nakashima
authors.forename: A
authors.initials: A
authors.lastname: Kuroiwa
mesh_terms: D000818:Animals; D002121:Calcium Channel Blockers / Q000494:pharmacology*; D004110:Diltiazem / Q000494:pharmacology*; D004285:Dogs; D006329:Heart Conduction System / Q000187:drug effects; D008012:Lidocaine / Q000009:adverse effects*; D017202:Myocardial Ischemia / Q000150:complications*; D026941:Sodium Channel Blockers; D017180:Tachycardia, Ventricular / Q000209:etiology*
chemical_list: D002121:Calcium Channel Blockers; D026941:Sodium Channel Blockers; D008012:Lidocaine; D004110:Diltiazem