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The efficacy of oral sotalol in preventing sustained ventricular tachycardia induction by invasive electrophysiological testing was assessed in 22 patients (60 +/- 9 years) with prior myocardial infarction. Programmed stimulation consisted of two basic drives followed by up to three extrastimuli at two right ventricular sites. At baseline, sustained monomorphic ventricular tachycardia was inducible in all patients. With sotalol (360 +/- 172 mg/day), it was no longer inducible in 10 patients; in 12 others, it remained inducible and its cycle length was only minimally prolonged (322 +/- 42 to 345 +/- 44 msec, p less than 0.05). Sotalol markedly prolonged sinus cycle length, uncorrected QT interval, and right ventricular effective and functional refractory periods, but had little effect on ventricular conduction time either in sinus rhythm or with right ventricular pacing. There was no significant difference in drug dose or in electrophysiologic effect of drug that related to efficacy, nor was there any correlation between drug-induced prolongation of ventricular tachycardia cycle length and its effects. Six patients received oral sotalol over the long term without spontaneous recurrence of ventricular tachycardia (follow-up: 23 +/- 18 months). These results demonstrate that sotalol is effective (45%) against sustained ventricular tachycardia induction at moderate doses and is well tolerated over a long term in the setting of remote myocardial infarction. However, its electrophysiologic effects as measured at invasive testing are not predictive of efficacy against ventricular tachycardia induction.

Holter monitoring, electrocardiographic (ECG) signal-averaging, body surface potential mapping (BSPM) for PQRST isoarea maps, and electrophysiologic study (EPS) were performed in 100 patients with syncope. Coronary artery disease (CAD) was found in 46 patients and other heart disease was found in 19. EPS was diagnostic in 44 patients, while Holter monitoring suggested a diagnosis in only 21 patients. Abnormal BSPM was frequently seen (56%), especially in CAD (70%), or with inducible ventricular tachycardia (VT) (87%). Late potentials were recorded in 13 patients with CAD; five had inducible VT. In seven other patients with VT, they were either absent or bundle branch block (BBB) was found. Thirteen deaths (three sudden) occurred in our series. EPS-guided therapy resulted in a low rate of total cardiac death. In conclusion, EPS had a higher diagnostic yield than Holter monitoring regardless of cardiac pathology. ECG signal-averaging was useful in predicting VT only in patients with CAD without BBB. BSPM was abnormal in most patients with cardiac disease, but poorly predicted VT.

The effects of class la antiarrhythmic drugs (procainamide, quinidine) on the right ventricular effective refractory period (VERP) and intraventricular conduction time were assessed during serial invasive electrophysiologic studies for sustained monomorphic ventricular tachycardia (VT). In 47 patients with remote myocardial infarction, sustained VT was inducible by up to two extrastimuli after the basic drive at one of two basic cycle lengths at the right ventricular apex. With oral drug administration, sustained VT was no longer inducible (group I) in 27 patients but remained inducible (group II) in 20 with the same protocol. Class la drugs prolonged the VERP in both groups, but there was greater lengthening when drugs were effective (e.g., +32 +/- 14 msec in group I vs +12 +/- 19 msec in group II; p less than 0.005, basic cycle length 600 to 700 msec). Prolongation of the VERP by greater than 30 msec had an 88% positive predictive value for prevention of sustained VT induction. In all except one patient in group I, drugs prolonged the VERP such that the coupling intervals that had resulted in sustained VT induction under control conditions were no longer attainable. In contrast, conduction time through the ventricle (surface QRS duration) in sinus rhythm and during right ventricular pacing was prolonged similarly regardless of efficacy (e.g., +33 +/- 21 msec vs +27 +/- 27 msec at a cycle length of 400 msec). The presence of similar plasma levels of drug did not imply equivalent prolongation of the VERP in the two groups. These results suggest that greater prolongation of the VERP by oral procainamide or quinidine correlates with drug efficacy against VT induction and is a better predictor of drug effect than achievement of a "therapeutic plasma level."

The electrophysiologic effects of intravenous propafenone were studied in 15 consecutive patients with accessory pathways. Thirteen patients had sustained orthodromic supraventricular tachycardia induced during baseline study, and two patients needed isoproterenol to render it sustained. In all except one patient, propafenone, 2 mg/kg given intravenously over a 10-minute period, was successful in converting the arrhythmia to sinus rhythm. Atrial fibrillation was inducible in 10 patients before propafenone, but was no longer inducible in seven of these patients after the drug. The HV interval (23 +/- 20 to 41 +/- 25 msec) and the anterograde (310 +/- 96 to 509 +/- 145 msec) and retrograde (256 +/- 30 to 334 +/- 105 msec) effective refractory periods of the bypass tract were all significantly prolonged after the drug. The pacing cycle length that produced conduction block over the bypass tract anterogradely (319 +/- 126 to 446 +/- 150 msec) and retrogradely (272 +/- 25 to 360 +/- 97 msec) was also increased. During orthodromic tachycardia, propafenone increased conduction time in both the anterograde and retrograde limbs of the tachycardia. Tachycardia terminated in the retrograde limb in 64% of the patients. We conclude that propafenone is very effective in terminating orthodromic tachycardia when given intravenously and that it should be considered in patients initially seen with atrial fibrillation and short refractory periods.