Retrograde Fast Pathway Research Articles

Ablation for Atrioventricular Nodal Reentrant Tachycardia with a Prolonged PR Interval During Sinus Rhythm: The Risk of Delayed Higher‐Degree Atrioventricular Block

Delayed higher-degree atrioventricular (AV) block can develop after slow pathway ablation for AV nodal reentrant tachycardia with a preexisting first-degree AV block. Retrograde fast pathway ablation is considered as an alternative approach for patients with a markedly prolonged PR interval and no demonstrable anterograde fast pathway function at baseline. This study aimed to determine the long-term reliability of AV conduction after retrograde fast pathway ablation in comparison to slow pathway ablation in patients with AV nodal reentrant tachycardia and a first-degree AV block at baseline. Among 43 patients with AV nodal reentrant tachycardia and a prolonged PR interval (defined as >or=200 msec), 10 patients without demonstrable dual pathway physiology underwent ablation of the retrograde fast pathway, and 33 patients with dual pathway physiology underwent slow pathway ablation. Persisting intraprocedural second- or third-degree AV block requiring pacemaker implantation occurred in one patient (10%) after retrograde fast pathway ablation and in one patient (3%) after slow pathway ablation. During the long-term follow-up of 61 +/- 39 months after retrograde fast pathway ablation, no delayed second- or third-degree AV block occurred, and the PR interval remained unchanged (308 +/- 60 msec vs 304 +/- 52 msec). During the follow-up of 37 +/- 25 months after slow pathway ablation, a delayed complete heart block developed in two patients, and a second-degree AV block developed in two patients. Three patients aged 66, 75, and 76 years died suddenly of unknown cause 4, 16, and 48 months following slow pathway ablation, respectively. Slow pathway ablation was associated with a significant risk of a delayed higher-degree AV block in patients with AV nodal reentrant tachycardia and a prolonged PR interval at baseline. Retrograde fast pathway ablation for patients with a first-degree AV block and no demonstrable dual pathway physiology was associated with a higher intraprocedural risk of complete AV block but did not result in the development of higher-degree AV block during the long-term follow-up of up to 9 years.

Atrial activation during atrioventricular nodal reentrant tachycardia: Studies on retrograde fast pathway conduction

Detailed right and left septal mapping of retrograde atrial activation during typical atrioventricular nodal reentrant tachycardia (AVNRT) has not been undertaken and may provide insight into the complex physiology of AVNRT, especially the anatomic localization of the fast and slow pathways. The purpose of this study was to investigate the pattern of retrograde atrial activation during typical AVNRT by means of right-sided and left-sided septal mapping and implementation of pacing maneuvers for separating atrial and ventricular electrograms recorded during tachycardia. Twenty-two patients with slow-fast AVNRT were studied by means of simultaneous His-bundle recordings from the right and left sides of the septum. Patterns of retrograde atrial activation were recorded during tachycardia following specific pacing maneuvers and during right ventricular apical (RVA) pacing at the tachycardia cycle length. The pattern of retrograde atrial activation could be mapped in 17 of 22 patients during AVNRT. In 9 (53%) patients, the earliest retrograde atrial activation was recorded on the left side of the septum, in 3 (17%) patients on the right side, and in 5 (29%) patients both right and left atrial septal electrograms occurred simultaneously. Stimulus to atrial electrogram times recorded during RVA pacing in 14 patients were 138.5 ms from the right His bundle, 134.5 ms from the left His bundle, and 148.0 ms from the ostium of the coronary sinus (P <.001). The predominant site of earliest retrograde atrial activation during RVA pacing was the left side of the septum (10 patients [71%]). Only 8 (57%) of 14 patients demonstrated concordance in the pattern of retrograde atrial activation during AVNRT and RVA pacing. Earliest retrograde atrial activation during AVNRT is most often recorded on the left side of the septum. Breakthrough of atrial activation may be discordant from that observed during RVA pacing.

The Different Ablation Effects on Atrioventricular Nodal Reentrant Tachycardia in Children with and without Dual Nodal Pathways

Previous studies in adults have shown a significant shortening of the fast pathway effective refractory period (ERP) after successful slow pathway ablation. However, information on atrioventricular nodal reentrant tachycardia (AVNRT) in children is limited. The purpose of this retrospective study was to investigate the different effects of radiofrequency (RF) catheter ablation in pediatric AVNRT patients between those with and without dual atrioventricular (AV) nodal pathways. From January 1992 to August 2004, a total 67 pediatric patients with AVNRT underwent an electrophysiologic study and RF catheter ablation at our institution. We compared the electrophysiologic characteristics between those obtained before and after ablation in the children with AVNRT with and without dual AV nodal pathways. Dual AV nodal pathways were found in 37 (55%) of 67 children, including 36 (54%) with antegrade and 10 (15%) with retrograde dual AV nodal pathways. The antegrade and retrograde fast pathway ERPs in children with dual AV nodal pathways were both longer than the antegrade and retrograde ERPs in children without dual AV nodal pathways (300 +/- 68 vs 264 +/- 58 ms, P = 0.004; 415 +/- 70 vs 250 +/- 45 ms, P < 0.001) before ablation. In children with antegrade dual AV nodal pathways, the antegrade fast pathway ERP decreased from 300 +/- 68 ms to 258 +/- 62 ms (P = 0.008). The retrograde fast pathway ERP also decreased after successful ablation in the children with retrograde dual AV nodal pathways (415 +/- 70 vs. 358 +/- 72 ms, P = 0.026). The dual AV nodal physiology could not be commonly demonstrated in pediatric patients with inducible AVNRT. After a successful slow pathway ablation, the fast pathway ERP shortened significantly in the children with dual AV nodal pathways.

Inducible Atrioventricular Nodal Reentrant Echo Behind Organic 2:1 Infra‐Hisian Block During Sinus Rhythm

A 77-year-old male patient with an intermittent 2:1 infra-Hisian block during sinus rhythm was presented with dizziness and near-syncope. During electrophysiological (EP) study, dual atrioventricular (AV) nodal pathways and retrograde fast pathway were easily induced by atrial and ventricular programmed stimulation, respectively. A typical slow-fast AV nodal reentrant echo beat also could be demonstrated by single atrial extrastimulation. Atrioventricular nodal reentrant tachycardia (AVNRT) can occasionally exhibit 2:1 AV block. Conversely, AV nodal reentry property had been rarely reported behind 2:1 infra-Hisian block. The EP presentation from this case may support the notion that tissues below the His are not part of the reentrant circuit of AVNRT.

Results from electrophysiological and pharmacological assessments suggest concealed atrio-Hisian fibers constitute retrograde limbs in reentrant circuits of slow-fast type atrioventricular nodal reentrant tachycardias in one-third of patients

Backgrounds: Some of the retrograde fast pathways (rFPs) in slow-fast type AV nodal reentrant tachycardias (AVNRTs) have been reported to exhibit little decremental property with short VA conduction time and high 2:1 VA block (VAB) rate and to be resistant to agents that suppress AV nodal conduction. The mechamisms for these “Kent bundle-like behaviors” of rFPs, however, have not been clearly elucidated.

Electrophysiological Characteristics of Junctional Rhythm During Ablation of the Slow Pathway in Different Types of Atrioventricular Nodal Reentrant Tachycardia

Junctional rhythm (JR) is commonly observed during radiofrequency (RF) ablation of the slow pathway for atrioventricular (AV) nodal reentrant tachycardia. However, the atrial activation pattern and conduction time from the His-bundle region to the atria recorded during JR in different types of AV nodal reentrant tachycardia have not been fully defined. Forty-five patients who underwent RF ablation of the slow pathway for AV nodal reentrant tachycardia were included; 27 patients with slow-fast, 11 patients with slow-intermediate, and 7 patients with fast-slow AV nodal reentrant tachycardia. The atrial activation pattern and HA interval (from the His-bundle potential to the atrial recording of the high right atrial catheter) during AV nodal reentrant tachycardia (HA(SVT)) and JR (HA(JR)) were analyzed. In all patients with slow-fast AV nodal reentrant tachycardia, the atrial activation sequence recorded during JR was similar to that of the retrograde fast pathway, and transient retrograde conduction block during JR was found in 1 (4%) patient. The HA(JR) was significantly shorter than the HA(SVT) (57 +/- 24 vs 68 +/- 21 ms, P < 0.01). In patients with slow-intermediate AV nodal reentrant tachycardia, the atrial activation sequence of the JR was similar to that of the retrograde fast pathway in 5 (45%), and to that of the retrograde intermediate pathway in 6 (55%) patients. Transient retrograde conduction block during JR was noted in 1 (9%) patient. The HA(JR) was also significantly shorter than the HA(SVT) (145 +/- 27 vs 168 +/- 29 ms, P = 0.014). In patients with fast-slow AV nodal reentrant tachycardia, retrograde conduction with block during JR was noted in 7 (100%) patients. The incidence of retrograde conduction block during JR was higher in fast-slow AV nodal reentrant tachycardia than slow-fast (7/7 vs 1/11, P < 0.01) and slow-intermediate AV nodal reentrant tachycardia (7/7 vs 1/27, P < 0.01). In patients with slow-fast and slow-intermediate AV nodal reentrant tachycardia, the JR during ablation of the slow pathway conducted to the atria through the fast or intermediate pathway. In patients with fast-slow AV nodal reentrant tachycardia, there was no retrograde conduction during JR. These findings suggested there were different characteristics of the JR during slow-pathway ablation of different types of AV nodal reentrant tachycardia.

Pace Mapping of Koch's Triangle Reduces Risk of Atrioventricular Block During Ablation of Atrioventricular Nodal Reentrant Tachycardia

Slow pathway (SP) ablation of AV nodal reentrant tachycardia (AVNRT) can be complicated by second- to third-degree AV block. We assessed the usefulness of pace mapping of Koch's triangle in preventing this complication. Nine hundred nine consecutive patients undergoing radiofrequency ablation of AVNRT were analyzed. Group 1 (n=487) underwent conventional slow pathway ablation. Group 2 (n=422) underwent ablation guided by pace mapping of Koch's triangle, which located the anterogradely conducting fast pathway (AFP) based on the shortest St-H interval obtained by stimulating the anteroseptal, midseptal, and posteroseptal aspects of Koch's triangle. In group 2, AFP was anteroseptal in 384 (91%), midseptal in 33 (7.8%), and posteroseptal or absent in 5 (1.2%). In 32 of 33 patients with midseptal AFP, slow pathway ablation was performed strictly in the posteroseptal area. In 4 of 5 patients with posteroseptal or no AFP, retrograde fast pathway was ablated. Two patients refused ablation. Persistent second- to third-degree AV block was induced in 7 (1.4%) of 487 group 1 patients versus 0 (0%) of 422 group 2 patients (P=0.038). Ablation was successful in all patients in whom ablation was performed. Pace mapping of Koch's triangle identifies patients in whom the AFP is absent or is abnormally close to the slow pathway. In these cases, guiding ablation helps to avoid AV block.

Characterization of subforms of AV nodal reentrant tachycardia.

Different subforms of AV nodal reentrant tachycardia (AVNRT) have been described ("Slow/Fast", "Slow/Slow" and "Fast/Slow"). Our aim is to improve definition of these subforms, based on systematic evaluation, in a large cohort of patients, of the site of earliest atrial activation, timing intervals, and evidence for the presence or absence of a lower common pathway (LCP). In 344 patients, AVNRT using a slow pathway (SP) for antegrade conduction and earliest atrial activation at the superior septum (i.e. retrograde fast pathway) was present in 81.4% (Slow/Fast). AVNRT using an SP for antegrade conduction and earliest atrial activation at the inferior septum or proximal coronary sinus (i.e. retrograde slow pathway; Slow/Slow) was present in 13.7%. AVNRT with a short A-H interval and retrograde SP conduction (Fast/Slow) was present in 4.9%. All timing intervals during tachycardia are dependent on autonomic tone. H-A intervals during tachycardia (H-A(t)) overlap in Slow/Slow and Slow/Fast AVNRT: Slow/Slow therefore may mimic Slow/Fast AVNRT. The H-A interval during pacing at the tachycardia cycle length (H-A(p)) better discriminates both subforms. The difference between H-A(p) and H-A(t) (Delta H-A) was significantly longer in Slow/Slow compared with Slow/Fast AVNRT (isoprenaline 0.5 microg/min: 27+/-18 ms vs. 1+/-9 ms; p<0.001). Delta H-A>15 ms had a specificity and sensitivity for Slow/Slow of 94% and 64%, respectively. A Delta H-A>15 ms, combined with other data, pointed to the presence of a long LCP in 36 of 43 evaluable Slow/Slow (84%) and all Fast/Slow, but in only 10% of Slow/Fast (p<0.001). Retrograde conduction during ventricular pacing at the tachycardia cycle length was present in only 6% of Fast/Slow. AVNRT subforms can be distinguished based on a systematic evaluation of atrial activation sequence, timing intervals and evidence for the presence of an LCP.

Differential Effects of Adenosine on Antegrade Fast Pathway, Antegrade Slow Pathway, and Retrograde Fast Pathway in Atrioventricular Nodal Reentry

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 ± 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 ± 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 ± 0.5, 4.2 ± 1.6, and 8.5 ± 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.

Pacemapping of the triangle of Koch: a simple method to reduce the risk of atrioventricular block during radiofrequency ablation of atrioventricular node reentrant tachycardia.

Slow pathway ablation in common AVNRT can be complicated by total AV block. When radiofrequency energy is delivered to the posterior aspect of the triangle of Koch, total AV block may be the consequence of the absence of anterograde conduction along the fast pathway or of inadvertent damage to a fast pathway abnormally located close to the slow pathway. To localize the anterogradely conducting fast pathway, the triangle of Koch was pacemapped in 72 patients who underwent the ablation of common AVNRT. In all cases, before ablation the St-H interval was calculated by stimulating the anteroseptal (AS), mid-septal (MS), and posteroseptal (PS) aspect of the triangle of Koch at a rate slightly faster than the sinus rate. In all patients, common AVNRT was induced. In 64 (89%) of 72 patients (group A) the shortest St-H interval was recorded on stimulating the AS region. In six (8%) patients (group B) the shortest St-H interval was recorded on stimulating the MS region. Finally, in two (3%) patients (group C) the shortest St-H interval was recorded stimulating in the PS region. In group C, AH interval, calculated on stimulating in the AS region, was significantly longer than in patients of groups A and B (200 +/- 99 ms vs 64 +/- 18 and 62 +/- 3, respectively). In group A, on stimulating in the AS, MS, and PS regions, the AH interval remained constant in all patients. In contrast, in groups B and C on stimulation in the MS and PS regions, AH interval shortened (in group B from 56 +/- 8 to 27 +/- 37 and 37 +/- 14, respectively; in group C from 200 +/- 99 to 170 +/- 100 and to 137 +/- 109, respectively). In groups A and B, a posteroseptal slow pathway, and in group C, an anteroseptal retrograde fast pathway were successfully ablated without AV block. Pacemapping of the triangle of Koch can help to recognize patients in whom the anterograde conducting fast pathway is abnormally located far from the anteroseptal region or in whom anterograde conduction of the fast pathway is absent. In these cases the risk of AV block can be reduced by performing slow pathway ablation in a site sufficiently far from the site of the anterograde fast pathway or ablating the retrogradely conducting fast pathway.

Variable responsiveness of anterograde and retrograde fast pathway conduction to adenosine in patients with typical AV-nodal reentry tachycardia

Adenosine is known as a substance which depresses predominantly the slow pathway of the av-node. However, the effect of adenosine on the anterograde and retrograde fast pathway (FP) has not been studied in a large patient population. Ninety-one patients with inducible typical av-nodal reentrant tachycardias (AVNRT) were included. The clinically used dosage of 12 mg adenosine was administered subsequently as bolus injection during a constant atrial and ventricular pacing (500 ms) in all patients. Electrophysiological av-nodal parameters were determined. A higher responsiveness of the anterograde compared to the retrograde FP was observed: the majority of patients (76%) blocked anterogradely and 55% blocked retrogradely within the FP after the administration of 12 mg adenosine. Thirty-six percent of all patients revealed a differential behaviour to adenosine. Sixteen percent of all patients were completely resistant to adenosine ( P=0.012). Electrophysiological parameters did not predict the responsiveness of the FP to adenosine. In patients with typical AVNRT the anterograde FP shows a higher sensitivity than the retrograde FP to adenosine.This might reflect an anatomical and/or functional distinction between anterograde and retrograde FP. The variable response to adenosine could be due to individual anatomical and electrophysiological heterogenity of the perinodal tissue and the av-node.

High variability of retrograde fast pathway sensitivity to adenosine.

Adenosine is widely used as a tool to assess the effectiveness of radiofrequency ablation of concealed accessory pathways. The goal of this study was to determine the reliability of this test by studying the retrograde fast pathway sensibility in a large patient population with typical atrioventricular (AV) nodal reentry tachycardias. We sought also to determine whether AV nodal properties were predictive of a retrograde fast pathway sensitivity to adenosine. In all, 124 patients with inducible AV nodal reentrant tachycardia were included in this study. All patients received a clinically used standard dose of 12 mg adenosine during ventricular pacing, with 500 ms and a constant ventriculoatrial (VA) conduction via the fast pathway. Electrophysiologic parameters of the AV node were determined in all patients in order to correlate them with the adenosine sensitivity of the retrograde pathway. In 74 patients, the injection of 12 mg adenosine resulted in a transient VA block, whereas no VA block occurred in the remaining 50 patients. In two patients, concealed accessory pathways were unmasked after the injection of adenosine. The adenosine sensitivity of the retrograde fast pathway was associated with longer retrograde conduction times and cycle lengths during AV nodal reentrant tachycardias. This study shows a high variability of retrograde fast pathway sensitivity to adenosine. Thus, in 40% of patients the lack of VA block after adenosine injection is not specific for persistent accessory pathway function after radiofrequency ablation. Electrophysiologic properties of patients with AV nodal reentrant tachycardias were different in patients with and without adenosine-sensitive retrograde fast pathways, possibly indicating differential patterns of penetration of the retrograde fast pathway into the compact AV node.

Retrograde fast pathway ablation for atrioventricular nodal reentry associated with markedly prolonged PR intervals

Three patients with typical atrioventricular nodal reentrant tachycardia (AVNRT) and markedly prolonged PR intervals (>300 ms) without dual pathway physiology at baseline or during isoproterenol infusion underwent successful fast pathway ablation and remained asymptomatic without recurrent AVNRT, atrioventricular block, or symptomatic bradycardia for a mean of 19 months. In patients with recurrent AVNRT and markedly prolonged PR intervals, selective ablation of the retrograde fast pathway can eliminate AVNRT without further impairment of anterograde atrioventricular nodal function.

Differential effect of adenosine on anterograde and retrograde fast pathway conduction in patients with atrioventricular nodal reentrant tachycardia.

Several studies have shown that the fast pathway is more responsive to adenosine than the slow pathway in patients with AV nodal reentrant tachycardia. Little information is available regarding the effect of adenosine on anterograde and retrograde fast pathway conduction. The effects of adenosine on anterograde and retrograde fast pathway conduction were evaluated in 116 patients (mean age 47 +/- 16 years) with typical AV nodal reentrant tachycardia. Each patient received 12 mg of adenosine during ventricular pacing at a cycle length 20 msec longer than the fast pathway VA block cycle length and during sinus rhythm or atrial pacing at 20 msec longer than the fast pathway AV block cycle length. Anterograde block occurred in 98% of patients compared with retrograde fast pathway block in 62% of patients (P < 0.001). Unresponsiveness of the retrograde fast pathway to adenosine was associated with a shorter AV block cycle length (374 +/- 78 vs 333 +/- 74 msec, P < 0.01), a shorter VA block cycle length (383 +/- 121 vs 307 +/- 49 msec, P < 0.001), and a shorter VA interval during tachycardia (53 +/- 23 vs 41 +/- 17 msec, P < 0.01). Although anterograde fast pathway conduction is almost always blocked by 12 mg of adenosine, retrograde fast pathway conduction is not blocked by adenosine in 38% of patients with typical AV nodal reentrant tachycardia. This indicates that the anterograde and retrograde fast pathways may be anatomically and/or functionally distinct. Unresponsiveness of VA conduction to adenosine is not a reliable indicator of an accessory pathway.

Effects of pharmacological autonomic blockade on dual atrioventricular nodal pathways physiology in patients with slow-fast atrioventricular nodal reentrant tachycardia.

The purpose of this study was to investigate the atrioventricular AV nodal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 +/- 17 years) with clinical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71%) of 17 patients still demonstrated AV nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 +/- 105 ms vs 630 +/- 80 ms, P < 0.005) and AV blocking cycle length (365 +/- 64 ms vs 338 +/- 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and functional refractory period of the fast pathway (369 +/- 67 ms vs 305 +/- 73 ms, P < 0.005; 408 +/- 56 ms vs 350 +/- 62 ms, P < 0.005) and the slow pathway (271 +/- 30 ms vs 258 +/- 27 ms, P < 0.01; 344 +/- 60 ms vs 295 +/- 50 ms, P < 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 +/- 94 ms vs 326 +/- 89 ms, NS) and effective refractory period of retrograde fast pathway (228 +/- 38 ms vs 240 +/- 80 ms, NS) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the decreased inducibility of clinical AVNRT.

Differential effects of adenosine on antegrade and retrograde fast pathway conduction in atrioventricular nodal reentry

Although adenosine depresses antegrade atrioventricular (AV) nodal conduction, the effects of adenosine on antegrade and retrograde fast pathway conduction in AV nodal reentry have not been determined. In 17 patients (five men, 12 women, mean age 49 +/- 12 years) with common slow-fast AV nodal reentrant tachycardia, the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation while the antegrade and retrograde fast pathway conduction remained intact. During high right atrial pacing at a mean pacing cycle length of 474 +/- 36 msec, adenosine was rapidly injected intravenously at an initial dose of 0.5 mg followed by stepwise increases of 0.5 mg or 1.0 mg given at 5-minute intervals until second-degree AV block developed. During right ventricular apical pacing at the same pacing cycle lengths (mean 474 +/- 36 msec) as those in the study of antegrade conduction, intravenous injection of incremental doses of adenosine was repeated until ventriculoatrial (VA) block occurred. The adenosine-induced prolongation of VA conduction was also determined in the presence of verapamil (loading dose 0.15 mg/kg, maintenance dose 0.005 mg/kg/min) in seven of 17 patients. The dose of adenosine required to produce AV block, the increase in the atrio-His interval by 50% and the maximal response were 3.4 +/- 1.4 mg, 1.8 +/- 0.6 mg, and 58% +/- 5%, respectively. On the other hand, the dose of adenosine required to produce VA block, the increase in the VA interval by 50%, and the maximal response were 8.2 +/- 2.9 mg, 3.4 +/- 0.6 mg, and 20% +/- 5%, respectively, in the control and 3.7 +/- 0.5 mg, 3.5 +/- 0.7 mg, and 23% +/- 5%, respectively, in the presence of verapamil. In conclusion, adenosine has a differential potency to depress AV and VA conduction in patients with AV nodal reentry, with greater potency for slowing antegrade fast than retrograde fast pathway conduction. Verapamil had an additive effect to adenosine on slowing retrograde VA conduction, which further supports the evidence that the retrograde fast pathway in part involves an AV nodal-like structure.

Effects of Enhanced Parasympathetic Tone on Atrioventricular Nodal Conduction During Atrioventricular Nodal Reentrant Tachycardia

The effects of various physiologic and pharmacologic stimuli on the anterograde slow pathway in patients with atrioventricular nodal reentrant tachycardia are well characterized. We sought to further characterize the nature of anterograde and retrograde conduction during tachycardia and to define the differential input of the parasympathetic nervous system to these pathways. A custom-made neck suction collar was placed to stimulate the carotid body baroreceptors during supraventricular tachycardia. Neck suction at −60 mm Hg was applied and changes in tachycardia cycle length, AH, and ventriculoatrial intervals were measured in 20 patients. These measurements were repeated after intravenous administration of 10 mg of edrophonium to enhance vagal tone. We observed a 15 ± 6 ms increase in tachycardia cycle length from baseline (p <0.0001) and a 14 ± 6 ms increase in AH interval (p <0.0001), but no change in the VA interval with neck suction alone. The tachycardia cycle length prolonged 26 ± 55 ms (p <0.0001) with edrophonium and an additional 12 ± 43 ms (p <0.001) with neck suction after edrophonium. There was no change in the VA interval before or after edrophonium during neck suction. There were 10 tachycardia terminations in 8 patients during anterograde slow pathway block during neck suction, with tachycardia cycle length prolongation and mean AH prolongation before termination of 45 ± 37 ms (vs 15 ± 7 ms increase in AH interval without tachycardia termination, p = 0.10). There were 12 tachycardia terminations in 4 patients with retrograde block during neck suction, only after edrophonium, without any preceding change in tachycardia cycle length during 11 episodes. We conclude that anterograde slow pathway demonstrates gradual conduction slowing with parasympathetic enhancement, whereas retrograde fast pathway responds with abrupt block.

Effects of slow pathway ablation on fast pathway function in patients with atrioventricular nodal reentrant tachycardia.

This study investigated whether fast pathway conduction properties are altered by slow pathway ablation in patients with AV nodal reentrant tachycardia. Forty consecutive patients who underwent successful ablation of the slow pathway were prospective subjects for the study. Isoproterenol was used to enhance conduction and to differentiate interactive mechanisms. Potential electrotonic interactions were assessed by comparing patients with and those without residual dual AV node physiology after slow pathway ablation. Paired and unpaired t-tests were used when appropriate P < 0.05 was considered statistically significant. In the entire study population, heart rates were not significantly different before and after slow pathway ablation (RR = 770 +/- 114 msec before and 745 +/- 99 msec after, P = 0.07). Anterograde fast pathway conduction properties were unchanged after slow pathway ablation (effective refractory period, 348 +/- 84 msec before and 336 +/- 86 msec after, P = 0.13; shortest 1:1 conduction, 410 +/- 93 msec before and 400 +/- 82 msec after, P = 0.39). Retrograde fast pathway characteristics also were similar before and after ablation. Neither anterograde nor retrograde fast pathway conduction properties during isoproterenol infusion were changed by slow pathway ablation. When the study population was further divided into patients with (n = 13) or without (n = 27) residual dual AV node physiology, no significant change was detected in fast pathway function in either group after slow pathway ablation. Fast pathway conduction characteristics were not affected by slow pathway ablation. In patients with AV nodal reentrant tachycardia, observations suggest that fast and slow pathways are functionally distinct.

Effects of adenosine triphosphate on ventriculoatrial conduction--usefulness and problems in assessment of catheter ablation of accessory pathways.

The effects of adenosine triphosphate (ATP) on ventriculoatrial (VA) conduction were examined before and after accessory pathway (AP) ablation, with emphasis on assessment of the complication of dual atrioventricular (AV) node pathway. By evaluating the differences in the response to ATP of APs and other pathways, we assessed the usefulness and problems of this method. Of 59 patients who underwent AP ablation, 31 showed pre-excitation and 28 had concealed APs. A dual AV node pathway was found in 9 patients (15.3%) before ablation. After ablation, a dual AV node pathway was newly found in 9 patients. Thus, the total number of patients with a dual AV node pathway was 18 (30.5%). VA conduction over APs was not blocked in 26 of 29 patients, but the remaining 3 APs were blocked transiently by ATP. ATP caused VA block over the AV node in 15 of 16 patients and a dual AV node pathway in all 11 patients. In contrast, VA conduction over the retrograde fast pathway was blocked in 9 of 14 patients with AV node re-entrant tachycardia. ATP has little effect on APs, so observation of the response to ATP provides a more reliable and useful means of evaluating successful ablation. With this method, however, it is important to consider the possibility of the presence of ATP-sensitive APs and ATP-resistant retrograde fast pathways. The influence of ablation-induced injury has not been fully clarified. It is therefore essential to take into account various data, including the comparison between data obtained before and after ablation.

Effects of isoproterenol in facilitating induction of slow-fast atrioventricular nodal reentrant tachycardia

We conclude that patients with poorer conduction properties of the anterograde slow and retrograde fast pathways usually need isoproterenol to facilitate induction of tachycardia, and isoproterenol infusion usually facilitates induction of tachycardia by enhancing the retrograde VA conduction.