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Acute intoxication with verapamil (2400 mg) induced A-V dissociation and circulatory failure in a 38-year-old woman with no previous cardiac disease. Resumption of A-V conduction was observed after administration of orciprenalin, calcium gluconate, and dopamine, with no effect on blood pressure. Epinephrine infusion finally restored satisfactory blood pressure level and allowed a favorable outcome.

Dihydroquinidine (DQ) is contained in substantial amounts in quinidine salts, but its direct antiarrhythmic action has not been studied. The efficacy of oral DQ (300 mg t. i. d.) compared to disopyramide (D) (200 mg t.i.d.) was thus investigated using a double-blind crossover placebo-controlled protocol in 12 patients, aged 13 to 67 years, with chronic stable high frequency premature ventricular beats (PVB), defined as greater than 100 PVB/h during 48-72-h control Holter monitoring. The protocol included three 72-h treatment periods: DQ, D, and placebo at random. On days 2 and 3 of each period a 24-h Holter recording was carried out; drug blood levels were determined at peak (days 2 and 3) and trough time (day 3). No significant difference in the mean PVB/h was found between control (735 +/- 400) and placebo periods (564 +/- 388), or between the two Holter recordings of each period. Compared to placebo both DQ (106 +/- 113, p less than 0.005) and D (240 +/- 263, p less than 0.05) reduced the mean PVB/h, but the decrease was significantly higher with DQ (78 versus 53%, p less than 0.02). Nine patients (75%) on DQ and 5 (42%) on D had a greater than 70% decrease in mean PVB/h; complex PVBs were abolished in 3 of 6 patients on both treatments. On day 3, DQ plasma levels were 1.31 +/- 0.44 (peak) and 0.92 +/- 0.45 (trough) mg/l; D plasma levels were 2.88 +/- 0.64 (peak) and 2.02 +/- 0.31 (trough) mg/l; no significant difference was found between day 2 and day 3 samples.(ABSTRACT TRUNCATED AT 250 WORDS)

The electrophysiologic effects of oral encainide (75 to 150 mg daily) were evaluated in 14 patients (6 male and 8 female, aged 49 ± 9 years) with atrioventricular (AV) node reentrant tachycardia of the slow-fast type. The patients were studied in control conditions and after 2 to 12 days of treatment.Encainide increased the AH interval from 67 ± 10 to 82 ± 23 ms (p < 0.02). Anterograde Wenckebach cycle length was increased in three patients, reduced in four, unchanged in one; it was not measurable in the remaining patients because tachycardia was induced. Retrograde Wenckebach periodicity increased from 307 ± 71 to 401 ± 92 ms (p < 0.005) in all nine patients in whom it was measurable; complete retrograde block was observed in one patient. At the control study, tachycardia was induced in all patients, with a mean cycle length of 341 ± 50 ms; after encainide, tachycardia was inducible in only 1 patient, with an increase in cycle length from 270 to 320 ms; in the other patients, tachycardia was not inducible because of a lack of retrograde (11 patients) or anterograde (2 patients) conduction. The mean plasma concentrations of encainide and its metabolites O-demethyl-encainide and 3-methoxy-O-demethyl-encainide measured in 13 patients during the repeat study were 161 ± 304, 128 ± 100 and 95 ± 85 ng/ml, respectively; three poor metabolizers who presented a high concentration of the parent compound were observed in this series.All patients were discharged on encainide at a mean daily dose of 112 ± 39 mg. One patient dropped out of the study 1 month later because of neurologic side effects (blurred vision and vertigo). During a mean follow-up period of 24 ± 11 months, nine patients are completely free of attacks, three patients had only one recurrence and one patient had a marked reduction of attacks; no one complained of side effects.Encainide appears to be highly effective in preventing AV node reentrant tachycardia, mainly by depressing conduction in the retrograde limb of the reentrant circuit. The drug demonstrates long-term clinical efficacy and does not induce any significant side effect at the doses used in this trial.