Abstract

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V 2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H 2A 2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated In 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 ± 27 vs 352 ± 40 ms, p < 0.01), but prolonged H 2A 2 interval in only 5 of 11 patients (37 ± 6 vs 60 ± 31 ms, p <0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H 2A 2 interval was prolonged. Correlation between the paced cycle length which Induced VA block, the shortest V 1H 2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H 2A 2 or H-Ae interval, the shortest V 1H 2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block. Our findings suggest that in AV nodal reentry, the retrograde limb is formed by the atrioventricular nodal-like structure, and the dissimilar effects of verapamil on VA conduction, H 2A 2 interval and H-Ae interval appear to be a result of our inability to achieve V 1H 2 and H-H intervals comparable to the paced cycle length that induced VA block.

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