Author + information
- Received July 21, 1989
- Revision received April 18, 1990
- Accepted May 2, 1990
- Published online November 1, 1990.
- Teresa Kus, MD, PhD∗,
- Marc Dubuc, MD,
- Chantal Lambert, PhD and
- Mohammad Shenasa, MD, PhD, FACC
- ↵∗Address for reprints: Teresa Kus, MD, PhD, Sacré-Coeur Hospital Research Center, 5400 Gouin Boulevard West, Montreal, Quebec, Canada H4J 1C5.
The efficacy of propafenone in preventing induction of ventricular tachycardia was evaluated in 25 consecutive patients (mean age 62 ± 8 years) with remote myocardial infarction who underwent programmed electrical stimulation for ventricular arrhythmia using up to three extrastimuli after basic drive at the right ventricular apex. In nine patients (Group A), propafenone prevented induction of sustained ventricular tachycardia (noninducible in four, nonsustained [<30 s] in five). In the other 16 patients (Group B), sustained ventricular tachycardia was still inducible; in 11 of the 16, the tachycardia configuration was unchanged but the cycle length was significantly longer (431 ± 99 versus 284 ± 44 ms, p < 0.001).
Propafenone did not significantly affect either sinus cycle length or AH and HV intervals. However, it prolonged QRS duration during sinus rhythm equally in both groups of patients. With ventricular pacing, propafenone also prolonged right ventricular effective and functional refractory periods and surface QRS duration. There was greater lengthening of the paced surface QRS duration when drug therapy was ineffective (for example, +35 ± 12 ms in Group A versus +69 ± 23 ms in Group B at a basic drive of 400 ms, p < 0.01). Drag-induced prolongation of a paced QRS complex >40 ms had a 94% positive predictive value for drug failure to prevent induction of ventricular tachycardia. Drug-induced percent prolongation of ventricular tachycardia cycle length in Group B did not correlate well with percent QRS prolongation. Rather, the best correlation was with percent prolongation of right ventricular effective (r = 0.72, p < 0.02) and functional (r = 0.73, p < 0.02) refractory periods at a basic drive of 400 ms.
These observations suggest that excessive prolongation of conduction time in presumably normal tissue reduces the ability of propafenone to prevent ventricular tachycardia induction. It is speculated that effects of a drug on conduction time in partially refractory abnormal tissue forming the reentrant circuit may play a role in determining the tachycardia cycle length in the presence of that drug.
- Received July 21, 1989.
- Revision received April 18, 1990.
- Accepted May 2, 1990.