Effects of lidocaine and diltiazem on recovery of electrophysiologic activity during partial reperfusion following severe myocardial ischemia in canine hearts.
The effects of lidocaine and diltiazem on recovery of electrophysiologic activity during partial reperfusion following severe myocardial ischemia were investigated in 28 dogs. The left anterior descending artery was ligated, and the distal end was connected to the carotid artery. Myocardial ischemia was induced by retrograde blood flow for 10 minutes, after which flow-limited reperfusion (30-60% of the coronary flow before ischemia) was performed. The dogs were divided according to the agent administered before ischemia into the following three groups: saline (group S, n = 11); lidocaine (group L, n = 8, 0.07 mg/kg/min by intravenous drip infusion following 2 mg/kg intravenous injection); and diltiazem (group D, n = 9, 0.02 mg/kg/min by intravenous drip infusion. There were no significant differences among the three groups in the incidence of ventricular tachyarrhythmia, which occurred as ventricular tachycardia (VT) or ventricular fibrillation (VF). In each group, the occurrence of VT was frequently preceded by delayed potential which was initiated after reperfusion, with depressed conduction in the epicardium, suggesting reentry (82%, 96%, and 87%, not significant). The determining factors for VT with degeneration into VF were long duration of VT in groups S and L (VT with degeneration into VF vs VT without, 1.2 +/- 0.2 seconds vs 0.6 +/- 0.1 seconds, P < .05, in group S and 11.6 +/- 2.5 seconds vs 2.2 +/- 0.4 seconds, P < .05, in group L), and decrease in average R-R interval during VT in groups L and D (195 +/- 8 ms vs 313 +/- 17 ms, P< .01, in group L and 201 +/- 11 ms vs 327 +/- 28 ms, P< 0.01, in group D). In addition, occurrence of epicardial electrophysiologic activity with reduced time from onset of the QRS complex in the surface electrocardiogram to the onset of the activity during VT preceded VF in group L (VT with degeneration into VF vs VT without, 130.0 +/- 15.1 ms vs 185.8 +/- 21.4 ms, P < .05), while that with prolongation of the time had this effect in group D (116.0 +/- 15.7 ms vs 69.0 +/- 10.7 ms, P < .05). It is concluded that, even when partial reperfusion is applied, neither lidocaine nor diltiazem suppresses VT because neither drug decreases delayed potential acting as a triggering factor or suppresses VF, since the alteration of the epicardial conductivity during VT can change the VT circuit to a smaller one.
Murasato
Y
Y
Second Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Kitakyushu, Japan.
Nagamoto
Y
Y
Urabe
T
T
Kuraoka
F
F
Nakashima
Y
Y
Kuroiwa
A
A
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage / Q000494:pharmacology*; D001783:Blood Flow Velocity; D003331:Coronary Vessels; D004110:Diltiazem / Q000008:administration & dosage / Q000494:pharmacology*; D004195:Disease Models, Animal; D004285:Dogs; D004562:Electrocardiography / Q000187:drug effects*; D006329:Heart Conduction System / Q000187:drug effects / Q000503:physiopathology; D007262:Infusions, Intravenous; D008012:Lidocaine / Q000008:administration & dosage / Q000494:pharmacology*; D017202:Myocardial Ischemia / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D015428:Myocardial Reperfusion Injury / Q000150:complications / Q000188:drug therapy / Q000503:physiopathology*; D011897:Random Allocation; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology; D016896:Treatment Outcome; D014665:Vasodilator Agents / Q000008:administration & dosage / Q000494:pharmacology*
D000889:Anti-Arrhythmia Agents; D014665:Vasodilator Agents; D008012:Lidocaine; D004110:Diltiazem