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Paroxysmal tachycardia with widened QRS complexes was recorded in an eleven-year old boy who had suffered from brain damage, which had resulted from an episode of ventricular fibrillation. Atrial stimulation produced an increased AV conduction, sudden disappearance of the His bundle deflection and a complete left bundle branch block pattern. Tachycardias of this morphology were initiated by early atrial and ventricular premature beats. The findings suggested the presence of a macro re-entry circuit, utilizing a slow AV node- nodoventricular bypass tract as the anterograde limb and the His-Purkinje system--fast AV node as the retrograde limb. This supposition found further support by serial sectioning of the AV junctional area of the heart, which revealed a nodoventricular tract, which originated from the posterior extension of the compact part of the atrioventricular node and inserted into the crest of the ventricular septum.

The effect of Ro 11-1781, a drug that affects calcium transport, in 10 patients with paroxysmal supraventricular tachycardia (PSVT), was studied by intracardiac recording and stimulation. The re-entry circuit involved an accessory pathway that conducted only in the ventriculo-atrial direction in 5 patients, and was confined to the A-V node in 5 cases. Prior to administration of Ro 11-1781 tachycardia could be initiated in all patients. An intravenous bolus of 2 mg/kg during PSVT terminated the tachycardia in all cases by blockade in the A-V node. Ro 11-1781 lengthened the A-V nodal conduction time as well as the functional and effective refractory period of the A-V node. The effective refractory period of the "fast" pathway was variably changed. After Ro 11-1781 the tachycardia zone was abolished in 3 cases, reduced in 3, increased in 3 and was converted to an echo zone in 1. The ability to sustain the PSVT was lost in one subject. The heart rate during PSVT was slowed following Ro 11-1781. Ro 11-1781 appears to be useful for the termination of PSVT, but its ability to prevent PSVT varies. Beneficial effects include abolition or narrowing of the tachycardia zone, loss of the ability to sustain PSVT and a reduction in heart rate during PSVT. The widening of the tachycardia zone may be harmful.

The effect of 2 mg/kg intravenous tiapamil was studied by programmed stimulation of the heart in 6 patients. Before tiapamil, sustained tachycardias were initiated in 5, and only atrial echoes in 1. In all patients, the reentrant circuit involved an accessory pathway conducting only in the ventriculoatrial direction. When administered during tachycardia, tiapamil promptly terminated the arrhythmia in 5 cases. Tiapamil lengthened the atrio-His (A-H) interval and the effective refractory period of the A-V node. As a result of these changes, it was not possible to initiate the tachycardia in 1 patient. In 1 case, tiapamil permitted the induction of sustained tachycardia, while only echoes had been initiated before the drug. In 2 cases, the tachycardia zone narrowed, in 2 others it widened following tiapamil. The ability to sustain the arrhythmia was lost in 1 patient. Tiapamil may be useful for the termination of reentrant supraventricular tachycardia involving concealed accessory pathways. Whether tiapamil prevents or favors the initiation of tachycardia in these patients depends on the interplay between the prolongation of the effective A-V nodal refractory period and the prolongation of the transnodal conduction time in individual patients.

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