Fast Pathway Effective Refractory Period Research Articles

Circadian Variations of Electrical Properties of the Hearta

Cardiac refractoriness and electrical inducibility of supraventricular tachycardia (SVT) were assessed at intervals of 1 to 2 hours over a period of 22 hours in 38 patients (25 with paroxysmal SVT). Daily variability of effective refractory period (ERP) had a mean range of 35 +/- 14 mseconds for the atria, 79 +/- 65 mseconds for the AV node, 24 +/- 10 m seconds for the ventricles, 51 +/- 27 mseconds for the retrograde Kent bundle, and 35 +/- 17 mseconds for the antegrade Kent bundle. Between 11 PM and 8 AM there was a significant prolongation of the ERP of the atria (ANOVA, p less than 0.001), AV node (p = 0.002), right ventricle (p less than 0.001), and retrograde Kent bundle (p = 0.005), and a reduction in electrical induction of SVT from 75% to 42% (p less than 0.05) with respect to the first electrophysiologic study. This nocturnal prolongation was preceded by ERP shortening of all explored cardiac sites and by increased tachycardia inducibility between 8 and 10 PM. Six patients with dual AV nodal pathways showed a prolongation of the fast pathway ERP at midnight, whereas conduction through the slow pathway followed an unpredictable daily variability. These data indicate a circadian influence on refractoriness of normal cardiac tissues and accessory pathways that exerted a midnight protection against electrical inducibility of reciprocating tachycardia but a transient arrhythmia facilitation at the evening.

Effects of upright posture on atrioventricular nodal reentry and dual atrioventricular nodal pathways

The electrophysiologic effects of upright posture (45 ° upright tilt) were studied in 17 patients with dual atrioventricular (AV) nodal pathways, AV nodal reentry or both. Discontinuous AV nodal conduction curves were observed in 16 patients while supine, but in only 11 patients while upright. Fast pathway refractoriness was shortened: the anterograde fast pathway effective refractory period decreased from 360 ± 22 to 275 ± 14 ms (mean ± standard error of the mean), the anterograde fast pathway block cycle length shortened from 448 ± 28 to 348 ± 20 ms and the retrograde fast pathway block cycle length shortened from 425 ± 29 to 338 ± 24 ms (all p < 0.01). The anterograde slow pathway Mock cycle length shortened from 378 ± 29 to 316 ± 17 ms (p < 0.05). AV nodal reentrant tachycardia was induced in 5 patients while supine (2 sustained, 3 nonsustained) and in 6 patients while upright (4 sustained, 2 nonsustained). Tachycardia cycle length shortened during upright posture, from 413 ± 30 to 345 ± 22 ms (p < 0.01), primarily due to shortened anterograde slow pathway conduction time, from 322 ± 23 to 268 ± 20 ms (p < 0.05). Upright posture thus enhances conduction in patients with dual AV nodal pathways, facilitating AV nodal reentry. Electrophysiologic testing in the upright position may yield additional clinically important information in patients with dual AV nodal pathways.

An asset allocation paradigm

Electrophysiological effects of 2 to 2.5 mg/kg iv disopyramide were studied in 10 patients with dual nodal pathways who used a slow pathway for anterograde and a fast pathway for retrograde conduction during paroxysmal supraventricular tachycardia (mean cycle length 308.5 +/- 37 ms; range 260-370 ms). Disopyramide terminated the tachycardia in six cases by production of ventriculoatrial block in five and by sinus overdrive in one. In the remaining four patients cycle length of the paroxysmal supraventricular tachycardia increased significantly from 270 +/- 8 ms to 377.5 +/- 28 ms. In all 10 patients disopyramide depressed retrograde fast pathway conduction manifest by an increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 296.5 +/- 25 ms to 358 +/- 60 ms, and increase in retrograde fast pathway effective refractory period from less than or equal to 246 +/- 34 ms to 325 +/- 36 ms; the drug abolished ventriculoatrial conduction in two cases. Anterograde slow pathway and fast pathway conduction properties were unchanged after disopyramide (atrial paced cycle length producing AH block 292 +/- 30 to 306.5 +/- 30 ms; effective refractory period of anterograde fast pathway less than or equal to 274 +/- 56 to 284 +/- 44 ms, before and after the drug, respectively) suggesting that anterograde conduction was not crucial either for sustainment or for failure to initiate paroxysmal supraventricular tachycardia after the drug. Paroxysmal supraventricular tachycardia could not be reinduced in six cases after disopyramide. In the other four the ventricular paced cycle lengths producing ventriculoatrial block (318 +/- 41 ms) and effective refractory period of retrograde fast pathway (320 +/- 28 ms) were shorter than the cycle length of reinduced paroxysmal supraventricular tachycardia (367.5 +/- 35 ms) allowing perpetuation of the tachycardia. We conclude that disopyramide breaks atrioventricular nodal re-entrant tachycardia by specific blockade of the retrograde fast pathway though the effect on anterograde atrioventricular nodal conduction is variable.

Selective blockade of retrograde fast pathway by intravenous disopyramide in paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways.

Electrophysiological effects of 2 to 2.5 mg/kg iv disopyramide were studied in 10 patients with dual nodal pathways who used a slow pathway for anterograde and a fast pathway for retrograde conduction during paroxysmal supraventricular tachycardia (mean cycle length 308.5 +/- 37 ms; range 260-370 ms). Disopyramide terminated the tachycardia in six cases by production of ventriculoatrial block in five and by sinus overdrive in one. In the remaining four patients cycle length of the paroxysmal supraventricular tachycardia increased significantly from 270 +/- 8 ms to 377.5 +/- 28 ms. In all 10 patients disopyramide depressed retrograde fast pathway conduction manifest by an increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 296.5 +/- 25 ms to 358 +/- 60 ms, and increase in retrograde fast pathway effective refractory period from less than or equal to 246 +/- 34 ms to 325 +/- 36 ms; the drug abolished ventriculoatrial conduction in two cases. Anterograde slow pathway and fast pathway conduction properties were unchanged after disopyramide (atrial paced cycle length producing AH block 292 +/- 30 to 306.5 +/- 30 ms; effective refractory period of anterograde fast pathway less than or equal to 274 +/- 56 to 284 +/- 44 ms, before and after the drug, respectively) suggesting that anterograde conduction was not crucial either for sustainment or for failure to initiate paroxysmal supraventricular tachycardia after the drug. Paroxysmal supraventricular tachycardia could not be reinduced in six cases after disopyramide. In the other four the ventricular paced cycle lengths producing ventriculoatrial block (318 +/- 41 ms) and effective refractory period of retrograde fast pathway (320 +/- 28 ms) were shorter than the cycle length of reinduced paroxysmal supraventricular tachycardia (367.5 +/- 35 ms) allowing perpetuation of the tachycardia. We conclude that disopyramide breaks atrioventricular nodal re-entrant tachycardia by specific blockade of the retrograde fast pathway though the effect on anterograde atrioventricular nodal conduction is variable.

Clinical, electrocardiographic, and electrophysiological observations of dual A-V nodal pathways.

In 45 (25%) of 182 patients with various cardiac arrhythmias, dual A-V nodal pathways (DPWs) were diagnosed with atrial extrastimulus technique at least at one or more basic cycle lengths and/or after intravenous administration of atropine (1 mg). The jump of discontinuous A1A2, H1H2 curve of these 45 ranged from 25 to 235 (92±56) msec and the jump of A1A2, A2H2 curve ranged from 40 to 260 (107±55) msec. The fast pathway FRP (functional refractory period), slow pathway FRP, fast pathway ERP (effective refractory period) and slow pathway ERP was 464±87 msec, 532±91 msec, 404±96 msec and 328±70 msec, respectively. DPWs were demonstrated in 10 (59%) of 17 patients with paroxysmal supraventricular tachycardia (PSVT), 3 (5%) of 55 with WPW syndrome, 2 (20%) of 10 with paroxysmal atrial fibrillation, 11 (29%) of 38 with sick sinus syndrome, 10 (38%) of 26 with first degree and/or second degree A-V (AH) block, none of 3 with second degree HV block, 3 (27%) of 11 with bundle branch block and 6 (27%) of 22 with the other cardiac arrhythmias. In 17 patients with PSVT, seven demonstrated A-V nodal reentrant tachycardia. Six of these 7 had evidence of DPWs. In the other 7 of the 17, concealed accessory pathway was demonstrated. Three of these 7 had DPWs, which did not constitute the reentrant circuit. Twenty-eight of 45 patients (62%) with DPWs had one or more electrophysiological abnormalities suggesting A-V nodal dysfunction: 1) prolonged AH interval (>130 msec) during sinus rhythm (10 patients), 2) atrial pacing rates of 130 or less inducing A-V nodal Wenckebach periods (24 patients), 3) prolonged A-V nodal ERP or slow pathway ERP (>400 msec) (8 patients), and 4) prolonged A-V nodal FRP or fast pathway FRP (>500 msec) ( 16 patients). However, in most patients, atropine improved A-V nodal dysfunction. We consider that DPWs are a common electrophysiological finding and have a strong association not only with PSVT but also with A-V nodal dysfunction.

Determinants of fast- and slow-pathway conduction in patients with dual atrioventricular nodal pathways.

Electrophysiological studies were performed in two patients with documented paroxysmal supraventricular tachycardia and dual atrioventricular (AV) nodal pathways as defined by the atrial extra-stimulus technique. Both patients manifested two ranges of A-H intervals (AV nodal conduction times) at critical cycle lengths, reflecting fast- and slow-pathway conduction. The occurrence of fast- and slow-pathway conduction at the same cycle length depended on a long fast-pathway effective refractory period relative to the spontaneous or driven cycle length. At critical cycle lengths with fast-pathway conduction, a shift to slow-pathway conduction could be induced by a premature atrial impulse falling within the effective refractory period of the fast pathway. Repetitive retrograde concealed conduction to the fast pathway then maintained antegrade slow-pathway conduction. Resumption of fast-pathway conduction was induced with premature atrial impulses falling within the effective refractory periods of both the fast and the slow pathways, allowing recovery of the fast pathway for antegrade conduction. Atrial echoes and AV nodal reentrant paroxysmal supraventricular tachycardia occurred when sufficient slow-pathway delay was achieved to allow recovery of the fast pathway for retrograde conduction.

Demonstration of dual A-V nodal pathways in patients with paroxysmal supraventricular tachycardia.

Electrophysiological evidence suggestive of dual atrioventricular (A-V) nodal pathways is presented in two patients with normal P-R interval and reentrant paroxysmal supraventricular tachycardia (PSVT). His bundle recordings and atrial stimulation were used to obtain this electrophysiological evidence. Refractory periods were measured with the atrial extra-stimulus technique. Plotting of H 1 -H 2 responses against A 1 -A 2 coupling intervals revealed that as A 1 -A 2 decreased, H 1 -H 2 decreased appropriately. At a critical A 1 -A 2 , a sudden marked increase in H 1 -H 2 occurred, suggesting failure of fast pathway, (defining the fast pathway effective refractory period ERP). Further shortening of A 1 -A 2 defined a second H 1 -H 2 curve. The longest A 1 -A 2 with no H 2 response was defined as the slow pathway ERP. Echo zones coincided with A 1 -A 2 intervals equal to or less than the fast pathway ERP. These results provide the first electrophysiological demonstration of dual A-V nodal pathways in patients with normal P-R interval and PSVT, as manifest by dual A-V nodal conduction times and refractory periods. Antegrade failure of the fast pathway with subsequent availability for retrograde conduction could allow A-V nodal reentry. These findings provide a basis for reentrance in some patients with reentrant PSVT.