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 extra-stimuli after basic drive at the right ventricular apex. In nine patients (Group A),
propafenone prevented induction of sustained
ventricular tachycardia (noninducible in four, nonsustained [less than 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 less than 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 less than 0.01).
Drug-induced prolongation of a paced QRS complex greater than 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.(ABSTRACT TRUNCATED AT 250 WORDS)