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Evaluates the effect of falipamil on persistent atrial fibrillation induced by atrial pacing. Administration of the drug by slow intravenous injection; Similarity of the atrial anti-arrhythmic properties of falipamil to those of Class IA anti-arrhythmic agents; Justification of pacing-induced atrial fibrillation either because of the presence of documented atrial fibrillation or flutter or because of the possible involvement of the arrhythmia in the symptoms.

His bundle recordings and programmed electrical stimulation were performed in a 70-year-old woman with bidirectional tachycardia; the recordings demonstrated the infra-Hissian origin of the tachycardia. Occurrence of the His deflection slightly after the onset of ventricular depolarization suggested that the origin of the tachycardia was located near the His bundle bifurcation. Recording of three atrial sites during tachycardia allowed the study of retrograde atrial activation. Two sets of fairly constant and alternating VA intervals were recorded. This fact is consistent with two ventricular circuits used alternatively. The tachycardia could also be interrupted with a single atrial or ventricular premature beat. It is postulated that the tachycardia is due to macroreentry involving the two fascicles of the left branch. Thu study suggests that reentry may be a possible mechanism in some cases of bidirectional tachycardia. (PACE, Vol. 5, September-October, 1982) [ABSTRACT FROM AUTHOR]

Although pacing-induced ventriculo-atrial (VA) Wenckebach conduction has been previously described, the occurrence of this phenomenon during ventricular tachycardia has received little attention. The latter is defined as 2:2 VA block in which the conducted beats show progressive lengthening of VA conduction until the sequence is terminated by two or three blocked ventricular beats. This phenomenon was observed in a 16-year-old boy who underwent electrophysiologic study for ventricular tachycardia as a late complication of surgical correction of tetralogy of Fallot. During pacing-induced ventricular tachycardia with a morphology similar to that of the spontaneous tachycardia, 8:4 alternating VA block was observed. This sequence suggested that the AV node was the site of block, the 2:2 block being located at the upper level, and the VA Wenckebach block at the lower level. Alternate VA Wenckeboch conduction appears as a possible cause of variation in atrial depolarization intervals during ventricular tachycardias with short cycle lengths. [ABSTRACT FROM AUTHOR]

Evaluates the effect of hydroquinidine in patients with inducible ventricular tachycardias using programmed electrical stimulation. Relation of arrhythmia with coronary artery disease in patients; Method used for selection of the appropriate antiarrhythmic agent; Information on spontaneous sustained ventricular tachycardias.

The electrophysiological properties of falipamil (AQA-39), a new antiarrhythmic agent with bradycardic effect, were evaluated in 12 patients. Intravenous falipamil (1.5 mg/kg within 20 minutes) significantly prolonged sinus cycle length (control, 862 ± 148 msec; Falipamil, 941 ± 170 msec). The PR interval was significantly shorter due to AH interval shortening (P < 0.004). The antegrade Wenckebach point occurred at a higher rate. These findings were ascribed to an anticholinergic effect. The major electrophysiological findings included significant prolongation of the refractory periods of atrium and ventricle, whereas those of the AV node were not affected. Retrograde ventriculoatrial conduction present in 8 patients was not altered. In conclusion falipamil prolongs sinus cycle length and depresses atrial and ventricular functions, which is suggestive of antiarrhythmic properties at the atrial and ventricular levels. [ABSTRACT FROM AUTHOR]