Electrophysiological effects of L 9394 (benzoyl-indolizine) in man.

The electrophysiological effects of L 9394 (benzoyl-indolizine), a substance chemically related to amiodarone, but devoid of iodine atoms, were investigated by programmed electrical stimulation of the heart in 12 patients with various forms of tachycardia. Four subjects had electrocardiographic evidence of the WPW syndrome and episodes of circus movement tachycardia. Paroxysmal supraventricular tachycardia, confined to the atrioventricular (AV) node, was found in 3 patients. In 2 cases, where a short PR interval was present, the main complaint was the occurrence of paroxysmal atrial fibrillation. In the remaining 3 instances, the arrhythmia consisted of slow ventricular tachycardia (1 case), supraventricular tachycardia of the focal type (1 case), and episodes of primary ventricular fibrillation, not related to acute myocardial ischaemia (1 case). L 9394 injected intravenously was seen to lengthen the transnodal conduction time as well as the effective and functional refractory periods of the node. Similar effects were found on the retrograde VA pathway. The drug had no action on the infra-Hisian conduction system, on the refractory periods of ventricular muscle, or on the refractory periods of accessory bypasses. The drug was injected during an episode of tachycardia in 6 cases with reproducible supraventricular re-entrant tachycardia. Three had a tachycardia circuit confined to the node. In those instances, the drug had beneficial effects (slowing and interruption of tachycardia, decrease or abolition of echo zone; loss of ability to induce tachycardia). In the other 3 cases, an accessory pathway was incorporated in the circuit. L 9394 interrupted the tachycardia in 2 instances (by anterograde AV block), but failed to protect all 3 patients against reinitiation of tachycardia by premature stimuli. It is concluded that L9394 does not share all the pharmacological properties of amiodarone and will not replace it in all its indications.

Two unusual cases of intra-atrial gap.

Two cases are described in which, during investigation of rhythm disturbances, it was shown that, by delivering atrial stimuli of increasing prematurity, a point was reached where the artificial stimulus failed to induce an atrial response. However, with even more premature stimulations, atrial responses were again observed. These observations are best explained by a gap phenomenon in which very early stimuli delivered during the effective refractory period of the atria were delayed long enough in the exit area around the pacing electrode to allow atrial recovery.