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In patients with dual atrioventricular (A-V) nodal pathways, atrial extrastimulus testing induces either no echoes, single atrial echoes (Ae), or repetitive re-entrance (repetitive atrial and ventricular beating). We examined the fast and slow pathways properties in 38 patients with dual pathways in order to delineate the determinants of re-entrance. Seventeen patients had no Ae. Of these, six had no V-A conduction and 11, intact V-A conduction. The mean paced ventricular cycle length producing retrograde V-A block (VABCL) in this group (a measure of retrograde fast pathway refractoriness) was 552 +/- 32 msec (mean +/- SEM; 10 pts). In contrast, all 21 patients with Ae had intact V-A conduction with mean VABCL of 382 +/- 21 msec (14 pts) (P less than 0.05). Repetitive re-entrance occurred only when Ae conducted to the ventricles. Seven patients had only single Ae. The mean paced atrial cycle length producing Wenckebach periodicity (CLAWP) in this group (a measure of antegrade slow pathway refractoriness) was 490 +/- 31 msec (5 pts). Fourteen patients had repetitive re-entrance. The mean CLAWP in this group was 399 +/- 18 msec (8 pts) (P less than 0.05). In conclusion, our results suggest that in patients with dual pathway, the occurrence of single or repetitive re-entry is dependent upon measurable slow and fast pathway properties.

In patients with atrioventricular (A-V) nodal re-entrant paroxysmal supraventricular tachycardia (PSVT), atrial extrastimulus technique frequently reveals discontinuous A1-A2, H1-H2 curves suggestive of dual A-V nodal pathways. To further test the hypothesis that these curves in fact reflect dual A-V nodal pathways, a ventricular extrastimulus (VS) was coupled either to A2 at a fixed A1-A2 interval which reliably produced an A-V nodal re-entrant atrial echo (E) with a constant A2-E interval in two patients, or to QRS complex (V) during sustained PSVT with a constant E-E interval in one patient. Three response zones were defined: at longer A2-VS or V-VS coupling interval, VS manifested no effect on the timing of E (Zone 1). At closer A2-VS or V-VS coupling interval, VS conducted to the atrium, shortening the apparent A2-E or E-E interval (Zone 2). At shortest A2-VS or V-VS coupling interval, VS was blocked retrogradely, and no E was induced (Zone 3). The ability of VS to preempt control of the atria (Zone 2 response) strongly suggests the presence of dual A-V nodal pathways in these PSVT patients. If only a single pathway were present, VS would of necessity collide with the antegrade impulse and could not reach the atria. The Zone 3 response occurs because of retrograde refractoriness of the fast pathway. Failure of the echo during Zone 3 probably reflects concealed conduction to the fast pathway, or possibly interference in the slow pathway.

Electrophysiological studies in one patient with type B pre-excitation and dual A-V nodal pathway revealed several types of paroxysmal narrow QRS tachycardia (PSVT). One type of PSVT reflected antegrade fast A-V nodal pathway and retrograde anomalous pathway conduction. This PSVT was characterized by early retorgrade activation of right atrial appendage, P following QRS and cycle length of 290 to 350 msec. A second PSVT reflected antegrade slow A-V nodal pathway and retrograde anomalous pathway conduction. This PSVT was characterized by early retrograde activation of right atrial appendage, P following QRS, and cycle length of 440 msec. A third PSVT reflected A-V nodal re-entrance with antegrade slow pathway and retrograde fast pathway conduction. This PSVT was characterized by normal retrograde atrial activation sequences, P simultaneous with QRS, and cycle length of 320 msec. All PSVT inductions could be explained in terms of antegrade and retrograde properties of fast and slow A-V nodal and anomalous pathways.

Evidence of dual atrioventricular nodal pathwats (a sudden jump in H1-H2 at critical A1-A2 coupling intervals) was shown in 41 out of 397 patients studied with atrial extrastimulus techniques. In 27 of these 41, dual pathways were demonstrable during sinus rhythm, or at a cycle length close to sinus rhythm (CL1). In the remaining 14, dual pathways were only demonstrated at a shorter cycle length (CL2). All patients with dual pathways at cycle length who were also tested at cycle length (11 patients) had dual pathways demonstrable at both cycle lengths. In these 11 patients both fast and slow pathway effective refractory periods increased with decrease in cycle length. Twenth-two of the patients (54%) had either an aetiological factor strongly associated with atrioventricular nodal dysfunction or one or more abnormalities suggesting depressed atrioventricular nodal function. Dvaluation of fast pathway properties suggested that this pathway was intranodal. Seventeen of the patients had previously documented paroxysmal supraventricular tachycardia (group 1). Eight patients had recurrent palpitation without documented paroxysmal supraventricular tachycardia (group 2), and 16 patients had neither palpitation nor paroxysmal supraventricular tachycardia (group 3). Echo zones were demonstrated in 15 patients (88%) in group 1, no patients in group 2, and 2 patients (13%) in group 3.

Alternating Wenckebach periods are defined as episodes of 2:1 atrioventricular (A-V) block in which conducted P-R intervals progressively prolong, terminating in two or three blocked P waves. In this study, His bundle recordings were obtained in 13 patients with pacing-induced alternating Wenckebach periods. Three patterns were noted: Pattern 1 (one patient with a narrow QRS complex) was characterized by 2:1 block distal to the H deflection (block in the His bundle) and Wenckebach periods proximal to the H deflection, terminating with two blocked P waves. Pattern 2 (four patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with three blocked P waves. Pattern 3 (eight patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with two blocked P waves. Alternating Wenckebach periods are best explained by postulating two levels of block. When alternating Wenckebach periods are terminated by three blocked P waves (pattern 2), the condition may be explained by postulating 2:1 block (proximal level) and type I block (distal level). When alternating Wenckebach periods are terminated by two blocked P waves (patterns 1 and 3), the condition may be explained by postulating type I block (proximal level) and 2:1 block (distal level). Pattern 1 reflects block at two levels, the A-V node and His bundle. Patterns 2 and 3 most likely reflect horizontal dissociation within the A-V node.

Electrophysiological studies utilizing His bundle recordings and atrial extra-stimulus technique were performed in 17 patients (pts) with documented paroxysmal supraventricular tachycardia (PSVT) before and after 0.01 mg/kg, i.v., ouabain. Before ouabaine, echozones(EZ) were demonstrated in 11 patients. After ouabain, EZ were abolished in two, decreased in five, unchanged in three, and increased in one. In one patient, EZ was demonstrated only after ouabain. Eleven patients could sustain PSVT before ouabain; after ouabain, only six patients could sustain PSVT. Analysis of A1-A2, H1-H2 curves revealed 11 patients with discontinous (dual pathway) and six patients with smooth conduction curves. In dual pathway patients, both the fast and slow pathway curves were shifted rightward and upward after ouabain. The changes in EZ were dependent upon the relative rightward shifts of the two pathways. In patients with smooth curves, EZ tended to shift rightward with a critical A-H being achieved at longer A1-A2 intervals after ouabain. In conclusion, the effects of ouabain on PSVT were variable. Beneficial effects included abolition or decrease of EZ and loss of the ability to sustain PSVT. Potentially deleterious effects included widening or new de-elopment of EZ.

Three patients with paroxysmal supraventricular tachycardia (PSVT) had discontinuous ventriculo-artrial conduction curves (V1-V2, A1-A2), suggesting dual A-V nodal pathways. Ventricular echoes occurred simultaneously with sudden increase of V-A interval. These echoes were characterized by retrograde P waves occurring in front of QRS, suggesting utilization of a slow pathway for retrograde conduction and a fast pathway for antegrade conduction. In case one, atropine improved retrograde slow pathway and antegrade fast pathway conduction and made A-V nodal re-entry sustained, resulting in PSVT (with retrograde P in front of the QRS). In cases 2 and 3, atropine markedly shortened retrograde fast pathway refractory period and slightly improved antegrade slow pathway conduction. The discontinuous V1-V2, A1-A2 curves and echoes were no longer demonstrable. However, with improvement of retrograde fast pathway and antegrade slow pathway conduction, A-V nodal re-entrant echoes and PSVT were observed, utilizing the slow pathway for antegrade conduction and the fast pathway for retrograde conduction (P simultaneous with QRS).