Atrioventricular nodal conduction and refractoriness after intranodal collision from antegrade and retrograde impulses.

Animal studies have suggested that spontaneous or programmed ventricular beats that occur simultaneously with atrial activation may facilitate atrioventricular (AV) nodal conduction during subsequent atrial impulses. However, this possibility has not been systematically studied in the human heart. In the present study the AV nodal conduction during a programmed atrial premature beat (S2) was analyzed. The S2 was delivered after a series of atrial drive beats (SjSj) of constant duration; this was termed stimulation method I. The results were compared with stimulation method II, which was similar to method I except that a single ventricular beat (Vs) was introduced simultaneously with the last Sl. The longest and shortest possible paced atrial cycle lengths (CLs) were scanned during both methods. Twenty-six patients were studied: 14 with a normal PR and normal intraventricular conduction (NIVC), four with first-degree AV nodal block and NIVC, three with a complete left bundle branch block (LBBB) pattern, three with a complete right bundle branch block (RBBB) pattern, and two with an incomplete RBBB pattern. At the same SlS2 intervals, the AV nodal conduction times (S2112 intervals) were consistently shorter with method II than with method I except in three patients, two with complete RBBB and one with complete LBBB. The magnitude of S2H2 shortening with method II was more pronounced at the shorter basic CLs and shorter SlS2 intervals. During method I, the effective refractory period (ERP) of the AV node was measured in 13 patients, eight with NIVC and five with preexisting bundle branch block. With method II, the ERP of the AV node shortened in all but three patients (one with complete RBBB, one with incomplete RBBB and one with complete LBBB pattern), in whom this variable did not change. The findings suggest that intranodal collison from antegrade and retrograde impulses facilitates AV nodal conduction and shortens the ERP. The magnitude of this change is greater at shorter atrial CLs and is probably related to deeper intranodal penetration of a Vs. The shortening in AV nodal conduction and refractoriness is not noted in patients with bundle branch block when retrograde conduction delay or block in the bundle branches coexists with the antegrade counterpart producing delayed or ineffective input of Vs into the AV node.