Programmed electrical stimulation and drugs identify two subgroups of ventricular tachycardias occurring 16-24 hours after occlusion of the left anterior descending artery.
BACKGROUND
Spontaneous sustained ventricular tachycardia (VT) occurring 16-24 hours after left anterior descending (LAD) coronary artery occlusion in the canine heart is most likely based on abnormal automaticity. In vitro, it has been demonstrated that the rate of the arrhythmia and the effect of overdrive pacing depends on the maximal diastolic potential (MDP). The MDP is also of importance in understanding the effect of antiarrhythmic drugs. To study 1) the possible presence of different responses to overdrive pacing and 2) the relation between the response to overdrive pacing and the effect of different antiarrhythmic drugs in the intact heart, we investigated the effect of 1) (prolonged) pacing and 2) lidocaine (3 mg/kg), verapamil (0.4-1.0 mg/kg), or flunarizine (2 mg/kg) during VT.


RESULTS
In 21 conscious dogs with chronic atrioventricular block, 60 sustained VTs were observed 1 day after LAD occlusion. During VT, pacing with interstimulus intervals of 400, 300, and 200 msec for 15, 60, and 120 seconds was done on 40 VTs. Based on their response to pacing, VTs were divided into a pacing-suppressible (PS group) and a pacing-nonsuppressible group (PNS group). The mean cycle length in the PS group was significantly longer (410 +/- 50 msec) than in the PNS group (360 +/- 35 msec, p less than or equal to 0.01). Suppression was directly related to the rate and duration of pacing. Spontaneous recurrence of VTs was observed after 26 +/- 45 seconds. Lidocaine and verapamil increased cycle length of the suppressible VTs and terminated them, whereas flunarizine had no effect. Except for verapamil, which increased cycle length of the VTs, no effects were seen in the PNS group.


CONCLUSIONS
In conscious dogs showing sustained VTs 16-24 hours after LAD occlusion, 1) the slower VTs can be suppressed by pacing, verapamil, and lidocaine but not by flunarizine, and 2) the faster VTs are not affected by pacing, lidocaine, and flunarizine, and are only slowed by verapamil. These findings are compatible with in vitro findings of abnormal automaticity, with the slower VTs originating from a higher MDP than the faster VTs.
Vos
M A
MA
Department of Cardiology, University Hospital, Maastricht, The Netherlands.
Gorgels
A P
AP
Leunissen
J D
JD
Havenith
M G
MG
Kriek
E
E
Smeets
J L
JL
Wellens
H J
HJ
D000818:Animals; D001157:Arterial Occlusive Diseases / Q000150:complications*; D002304:Cardiac Pacing, Artificial; D003327:Coronary Disease / Q000150:complications*; D004285:Dogs; D004562:Electrocardiography; D004594:Electrophysiology; D005260:Female; D005444:Flunarizine / Q000627:therapeutic use*; D008012:Lidocaine / Q000627:therapeutic use*; D008297:Male; D013610:Tachycardia / Q000188:drug therapy* / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D013997:Time Factors; D014700:Verapamil / Q000627:therapeutic use*
D008012:Lidocaine; D014700:Verapamil; D005444:Flunarizine