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Atrioventricular nodal reentrant tachycardia (AVNRT) is a common arrhythmia encountered in clinical practice. Catheter ablation reduces duration of hospitalization and improves quality of life in patients with this arrhythmia.1 AVNRT is occasionally seen in patients at an old age; however, ablation therapy has not been fully investigated in nonagenarians. In patients with a long PR interval at baseline, antegrade fast pathway conduction may be absent and slow pathway ablation for AVNRT can lead to atrioventricular (AV) block.2,3 Bifascicular block at baseline was also recognized as a risk factor for AV block during ablation therapy; however, there are few reports that discuss the combination of both conduction disorders. Here, we report a case of a nonagenarian with AVNRT and trifascicular block including prolonged PR interval treated with cryoablation. Key Teaching Points • Patients with trifascicular block have a high risk of atrioventricular block following slow pathway ablation. • The slow and fast pathways may be located close together in elderly patients. • Cryoablation is feasible in elderly patients with atrioventricular nodal reentrant tachycardia and trifascicular block.

The classical form of typical Atrio Ventricular Node Reentrant Tachycardia (AVNRT) is a "slow-fast" pathways tachycardia and the usual therapy is an ablation of the slow pathway since it carries a low risk of AV block. In patients with long PR interval and/or living on the anterograde slow pathway an alternative technique is required. We report a case of a 42-year-old lady with idiopathic restrictive cardiomyopathy, persistent atrial fibrillation status post pulmonary vein isolation (PVI) and PVC ablation with a systolic dysfunction, who presented with incessant slow narrow complex tachycardia of 110 bpm that appeared to be an AVNRT. Her baseline EKG revealed a first-degree AV block with a PR of 320 ms. EP study showed no evidence of anterograde fast pathway conduction. Given this fact, the decision was to attempt an ablation of the retrograde fast pathway. The fast pathway was mapped during tachycardia to its usual location into the anteroseptal region, then radiofrequency (RF) ablation in this location terminated tachycardia. After ablation, she continued to have her usual anterograde conduction through slow pathway and the tachycardia became uninducible. In special populations with prolonged PR interval or poor anterograde fast pathway conduction, fast pathway ablation is the required ablation for typical AVNRT. This article is protected by copyright. All rights reserved.

Background The management of patients with atrial fibrillation and an abnormally fast ventricular response has been through the use of pharmacologic agents. In those cases where rate control cannot be achieved pharmacologically, a standard approach has been atrioventricular (AV) junctional ablation and ventricular pacemaker implantation to achieve a stable ventricular rate. Long-term ventricular pacing has been shown to result in diminished ventricular function that can lead to heart failure. Objective To describe an experimental and clinical study demonstrating a modified form of AV junction ablation. Methods Ablation of the slow and fast AV nodal input does not produce AV block. Ablation of the connection between the two induces AV block, leaving the AV node and His bundle intact. Results Subsequently the escape heart rate is close to normal and responds well to exercise. Conclusion In a clinical study with a 42 month follow-up, the modified procedure resulted in significantly reduced pacemaker dependence and mortality compared to the standard AV ablation procedure.

Purpose Previous studies examined the right atrial (RA) input site of the antegrade fast pathway (AFp) (AFpI). However, the left atrial (LA) input to the atrioventricular (AV) node has not been extensively evaluated. In this study, we created three-dimensional (3-D) bi-atrial stimulus-ventricle (St-V) maps and analyzed the input site and characteristics of the AFp in both the RA and LA. Methods Forty-four patients diagnosed with atrial fibrillation or WPW syndrome were included in this study. Three-dimensional bi-atrial St-V mapping was performed using an electroanatomical mapping system. Sites exhibiting the minimal St-V interval (MinSt-V) were defined as AFpIs and were classified into seven segments, four in the RA (F, S, M, and I) and three in the LA (M1, M2, and M3). By combining the MinSt-V in the RA and LA, the AFpIs were classified into three types: RA, LA, and bi-atrial (BA) types. The clinical and electrophysiological characteristics were compared. Results AFpIs were most frequently observed at site S in the RA (34%) and M2 in the LA (50%), and the BA type was the most common (57%). AFpIs in the LA were recognized in 75% of the patients. There were no clinical or electrophysiological indicators for predicting AFpI sites. Conclusions Three-dimensional bi-atrial St-V maps could classify AFpIs in both the RA and LA. AFpIs in the LA were frequently recognized. There were no significant clinical or electrophysiological indicators for predicting AFpI sites, and 3-D bi-atrial St-V mapping was the only method to reveal the precise AFp input site.

We described a 15-year-old boy who underwent the catheter ablation for the nodoventricular (NV) tachycardia that had difficulty in differentiation from atrioventricular nodal reentrant tachycardia with upper common pathway. The modification of the fast pathway revealed an anterograde conduction of the NV fiber. We successfully performed the catheter ablation targeting for the right ventricular insertion site of the NV fiber.

Background Coexistence of idiopathic left fascicular ventricular tachycardia (ILFVT) and atrioventricular nodal reentrant tachycardia (AVNRT) has been rarely reported. Objectives The study aimed at elucidating the prevalence of coexisted AVNRT in patients with ILFVT during longitudinal follow-up. The electrophysiological properties and clinical predictors of coexisted ILFVT and AVNRT were investigated. Methods From 1999 to 2017, a total of 108 patients (age: 33.7 ± 14.3, 84 male) with ILFVT from one tertiary center were consecutively enrolled. The prevalence of coexisted arrhythmias was explored during a longitudinal follow-up and the electrophysiological parameters from the index procedure were compared. Results During a mean follow-up period of 106.8 ± 69.5 months, 21 of 108 patients (19.4%) had coexisted AVNRT. The electrophysiological study demonstrated patients with coexisted ILFVT and AVNRT were characterized by more antegrade dual AV node conduction (52.4% vs. 19.5%, P = 0.002; 9.5%), shorter antegrade slow pathway effective refractory period (285.1 ± 34.1 ms vs. 329.2 ± 69.2 ms, P = 0.034), longer retrograde fast pathway effective refractory period (368.9 ± 56.7 ms vs. 312.5 ± 95.2, P = 0.036), and less VA dissociation (19.0% vs. 60.9%, P = 0.001) than those without a coexisted AVNRT. Multivariate logistic analysis showed that presence of antegrade dual AV nodal physiology and retrograde VA conduction could predict a coexisted AVNRT in patients with ILFVT (P = 0.005, OR: 4.80, 95% CI: 1.65-14.37 and P = 0.002, OR: 0.14, 95% CI: 0.04-0.49, respectively). Conclusion There was a high prevalence of coexisted AVNRT in patients with ILFVT during longitudinal follow-up. The presence of antegrade dual AV nodal physiology and retrograde VA conduction can predict the coexisted AVNRT in patients with ILFVT.

There have been remarkable strides and leaps in both the diagnostic elements, mechanisms, and treatment of cardiac arrhythmias in these last few decades. Paroxysmal Supraventricular Tachycardia (PSVT) with or without the Wolff-Parkinson-White syndrome ranks high among these maladies that witnessed a therapeutic revolution, perhaps like no other. In this chapter the author reviews the history of PSVT, and details the commonest variety of PSVT: AV nodal reentrant tachycardia (AVNRT), describing its incidence, manifestations and mechanisms, the case for, and against dual-pathway physiology, and an unifying concept linking the slow and fast pathways.

The Atrio Ventricular Junction (AVJ) is a well-defined anatomical region of the heart the physiology of which, despite extensive and numerous observations, it is not fully understood. The aim of this review is to present an up to date summary of old and more recent findings on histology, cellular electrophysiology and intracellular connectivity of this region. We have also attempted to relate our increasing understanding of nodal pathophysiology to the interpretation of the electrocardiographic (ECG) manifestations of AVN behavior. Bridging cellular observations with ECG analysis in a process we call "Precision Electrocardiology" renders this tool far more sensitive and clinically useful than the pattern analysis too often employed in the ECG interpretation.

Objectives: To determine the possible changes in the conducting properties of the fast pathway after modification of the atrioventricular slow pathway for AVNRT which leads to the failure of the induction of tachycardia. Methods: This study was conducted in the Cardiac electrophysiology Laboratory of Hayatabad Medical Complex, Peshawar, Pakistan from March 2017 to March 2018. All the patients underwent radiofrequency modification of the slow pathway for AVNRT. Patients in whom typical AVNRT was inducible with demonstration of dual AV nodal physiology were included in the study. Results: A total of 171 cases were included in the study, 42 (25%) were males, mean age recorded was 47±15 years. There were no significant changes pre and post ablation in the base line parameters like VV interval, atrioventricular nodal (AV nodal) Wenckebach cycle length, slow pathway effective refractory period (SPERP) or fast and slow pathways maximal Atrio His interval. However significant change was observed in the effective refractory period of the fast pathway 350±49 Vs 290±32 (p value 0.0001). The difference between slow and Fast pathway ERP was also decreased significantly 82±36 Vs 56±24 (p value 0.004). Conclusion: Our study showed that ablation of AV nodal slow pathway for atrioventricular nodal reentrant tachycardia leads to changes in the effective refractory period of the fast pathway. doi: https://doi.org/10.12669/pjms.35.5.473 How to cite this:Khan I, Shah B. Electrophysiological changes in the conducting properties of fast pathway following modification of the slow pathway of the atrio ventricular node for atrio ventricular nodal re-entrant tachycardia. Pak J Med Sci. 2019;35(5):1301-1305. doi: https://doi.org/10.12669/pjms.35.5.473 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

AV Nodal Remodeling Induced by AFBackground An animal experiment showed that long-term atrial pacing or persistent atrial fibrillation (AF) caused electrical remodeling of the atrioventricular (AV) node. We aimed to test the hypothesis that persistent AF decreases the AV conductivity in human hearts. Methods and Results We retrospectively compared the cardiac electrophysiological properties between patients with paroxysmal AF who underwent catheter ablation (PXAF, N = 254) and those with persistent or longstanding persistent AF (PSAF, N = 213). The PSAF patients were more likely than PXAF patients to have longer atrial-His (AH) (96.3 ± 25.7 vs. 91.3 ± 20.4 milliseconds; P = 0.02) and His-ventricle (HV) (43.1 ± 9.4 vs. 41.2 ± 8.6 milliseconds; P = 0.02) intervals. The AV nodal effective refractory period (ERP) (299.1 ± 74.6 vs. 276.2 ± 58.9 milliseconds; P < 0.001) and Wenckebach cycle length (420.9 ± 80.3 vs. 386 ± 58.6 milliseconds; P < 0.001) were also more prolonged in the PSAF patients. We found a dual AV nodal physiology with a similar frequency in both groups. The AH interval, fast pathway ERP, and Wenckebach cycle length in the PSAF patients were more likely than in the PXAF patients to be prolonged among the patients without dual pathways, while those intergroup differences were never seen among the patients with dual pathways. In subgroup analyses including only PSAF patients, there was no difference in the AV conductivity between the patients with persistent AF and those with longstanding persistent AF. Conclusions Persistent AF may cause a mild decrease in the AV nodal function in human hearts. Electrical remodeling may be uncommon if dual AV nodal pathways are present, and its extent may not depend on the duration of persistent AF.

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A 66-year-old woman with palpitations was referred to our center for catheter ablation due to drug-refractory, common type atrioventricular nodal tachycardia (AVNRT). A selective slow pathway ablation was attempted. A fast junctional rhythm with transient ventriculoatrial block followed by transient prolongation of the A–H interval occurred immediately after the radiofrequency (RF) application at the coronary sinus ostium (CSOS) level. To assess the location of the fast pathway and His bundle, we sought to visualize the anatomy of the triangle of Koch (TOK) by three-dimensional computed tomography (CT).

Differential diagnoses of regularly irregular narrow QRS tachycardias are AV re-entrant tachycardia (AVRT) with alternating antegrade AVN pathways, atypical AV nodal re-entrant tachycardia (AVNRT) with alternating antegrade AVN pathways, and atrial tachycardia (AT) with alternating antegrade AVN pathways or with Wenckebach periodicity.

"2 for 1 phenomenon" is simultaneous anterograde conduction over the fast and slow pathways of the atrioventricular (AV) nodal pathway, leading to a double ventricular response from each atrial beat. This phenomenon can initiate AV nodal reentrant tachycardia (AVNRT). The unique induction of AVNRT was observed in a patient with an implantable cardioverter defibrillator in our case. Minimal to no retrograde invasion of the slow pathway from the anterogradely conducted fast pathway depolarization is the most accepted explanation.

Nowadays, slow pathway ablation is the first-line therapy for atrioventricular nodal reentrant tachycardia (AVNRT). However, it may cause inadvertent AV block especially inpatients with a prolonged PR interval on the baseline ECG. Retrograde fast pathway ablation may be attempted in such AVNRT patients as an alternative approach to maintain the original AV conduction over the slow pathway.

This is a typical example of a tachycardia-induced cardiomyopathy due to incessant tachycardia with moderately increased ventricular rate. This was due to nonreentrant atrioventricular nodal tachycardia that gave rise to two ventricular complexes for every atrial complex. It describes a rare finding of the presence of retrograde concealed conduction in the fast pathway. Curative catheter ablation led to improvement of symptoms with reversal of tachycardia-induced cardiomyopathy.

A 15-year-old girl with a history of paroxysmal supraventricular tachycardia underwent an electrophysiology study (EPS) for diagnosis and ablation. Her baseline electrocardiogram and echocardiogram were normal. At EPS, she had dual atrioventricular nodal (AVN) conduction, but isoproterenol was needed to initiate the slow-fast form of AVN reentry. Before ablation without any isoproterenol, she began to have a spontaneous block in the fast pathway with continuous conduction over the slow pathway. After ablation of the slow pathway, all complexes conducted over the fast pathway during a 25-year follow-up. Possible electrotonic interaction between the slow and fast pathways is proposed as the mechanism for this phenomenon.

Atrioventricular nodal reentrant tachycardia (AVNRT) should be classified as typical or atypical. The term ‘fast-slow AVNRT’ is rather misleading. Retrograde atrial activation during tachycardia should not be relied upon as a diagnostic criterion. Both typical and atypical atrioventricular nodal reentrant tachycardia are compatible with varying retrograde atrial activation patterns. Attempts at establishing the presence of a ‘lower common pathway’ are probably of no practical significance. When the diagnosis of AVNRT is established, ablation should be only directed towards the anatomic position of the slow pathway. If right septal attempts are unsuccessful, the left septal side should be tried. Ablation targeting earliest atrial activation sites during typical atrioventricular nodal reentrant tachycardia or the fast pathway in general for any kind of typical or atypical atrioventricular nodal reentrant tachycardia, are not justified. In this review we discuss current concepts about the tachycardia circuit, electrophysiologic diagnosis, and ablation of this arrhythmia.

The reported electrocardiogram shows several atrial extrasystoles (AEs) sometimes occurring in couplets. The former beat of each couplet is nonconducted, whereas the latter triggers a supraventricular tachycardia with negative P waves in inferior leads and RP > PR. This suggests an atypical atrioventricular nodal reentrant tachycardia involving the fast pathway anterogradely and the slow pathway retrogradely. The tachycardia is never precipitated by single AEs. The blocked AE of each pair is pivotal in tachycardia initiation, allowing the subsequent impulse to conduct down the fast pathway. A concealed slow pathway penetration during the blocked AE is invoked as the key mechanism.

Background: In typical atrioventricular nodal reentrant tachycardia, radiofrequency (RF) ablation of the slow pathway (SP) is known to change the effective refractory period of the fast pathway (ERPFP) after successful RF ablation of the SP. The purpose of this study was to ascertain the mechanism of the ERPFP changes after SP ablation by comparing the results of both cryo- and RF ablation. Methods and Results: A total of 112 patients were enrolled prospectively and their electrophysiological properties analyzed before and after successful SP ablation. Patients were grouped into cryoablation (n=54) and RF ablation (n=58) groups and each group was subdivided into complete ablation (CG) and modification (MG) based on the presence of the SP after successful ablation. CG was performed in 64 patients: 30 by cryoablation and 34 by RF ablation. In patients who underwent complete SP ablation, the ERPFP was shortened significantly after cryoablation (375±74 vs. 281±39ms, P

A 53-year-old man with previous aortic valve surgery presented with paroxysmal narrow complex tachycardia, induced by exercise. His PR interval was greater than 400 ms when in sinus rhythm and atrioventricular nodal reentry tachycardia (AVNRT) was diagnosed with invasive electrophysiological studies. Single echoes were repeatedly inducible with single-paced extrastimuli. Cryotherapy was then used to ablate the fast pathway using single echoes to monitor anterograde slow pathway and retrograde fast pathway function during ablation. PACE 2012; 35:e47–e51)

AVNRT is the most common paroxysmal supraventricular tachycardia seen in adults. It occurs as a result of dual AV nodal physiology in which an ectopic beat from the atrium or the ventricle conducts along either a slowly conducting or fast pathway and retrogradely along the other pathway which is no longer refractory. In the case of a typical AVNRT this occurs antegradely along the slow pathway and retrogradely along the fast pathway resulting in a short RP tachycardia. In an atypical AVNRT conduction occurs antegradely along the fast pathway and retrogradely along the slow pathway resulting a long RP tachycardia. It is important to carefully map during tachycardia and perform the relevant maneuvers in order to help establish the diagnosis. AVNRT is treatable with catheter ablation and this is highly successful with a low recurrence rate.

We read with interest the paper by Katritsis et al. 1 published in Europace recently. In this study, the authors sought to assess the prevalence, electrophysiological characteristics, and mechanism underlying atypical atrioventricular nodal re-entrant tachycardia (AVNRT), which is not clinically well-defined. It was shown that the atrial-His (AH) interval in atypical ‘fast-slow’ (F-S) AVNRT is longer than His-atrial (HA) interval in typical ‘slow-fast’ (S-F) AVNRT, implying that different fast conduction pathways are utilized in these two types of tachycardia. However, we are holding the following interpretations: …

Case presentation A 65-year-old woman was suffering from recurrent paroxysmal atrial fibrillation and was being treated with propafenone 150 mg tid. Continuous ECG recording strips of lead V1 are shown in Figure 1. The QRS complexes are associated into groups separated from each other by pauses. Although several P waves are not clearly discernible because they are superimposed on the T waves, analysis of the recordings reveals regular atrial activity with P-P intervals of 520 ms (Figure 2). Often the P waves are partially buried within a coincidental ventricular complex, causing subtle QRS alterations that result in relatively wide “pseudo-r” waves. This occurs with the fourth beat in the top strip of Figure 1, the 13th beat of the middle strip, and the third beat of the bottom strip. The P-R intervals undergo progressive prolongation until a ventricular pause occurs. Such a sequence indicates a Wenckebach atrioventricular (AV) nodal conduction mechanism. During the tachycardia, the morphology of the QRS complexes is typical for left bundle branch block (LBBB). However, the ventricular beats that follow a pause at times are relatively narrow but on other occasions show an LBBB configuration. These late QRS complexes are clearly dissociated from, and independent of, the near-synchronous P wave (Figures 1 and 2). What is the mechanism underlying the beats ending the pauses?

Background: Atrioventricular nodal reentrant tachycardia (AVNRT) can usually be induced by atrial stimulation. However, it seldom may be induced with only ventricular stimulation, especially the fast-slow form of AVNRT. The purpose of this retrospective study was to investigate the specific electrophysiological characteristics in patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation. Methods: The total population consisted of 1,497 patients associated with AVNRT, and 106 (8.4%) of them had the fast-slow form of AVNRT and 1,373 (91.7%) the slow-fast form of AVNRT. In patients with the fast-slow form of AVNRT, the AVNRT could be induced with only ventricular stimulation in 16 patients, Group 1; with only atrial stimulation or both atrial and ventricular stimulation in 90 patients, Group 2; and with only atrial stimulation in 13 patients, Group 3. We also divided these patients with slow-fast form AVNRT (n = 1,373) into two groups: those that could be induced only by ventricular stimulation (Group 4; n = 45, 3%) and those that could be induced by atrial stimulation only or by both atrial and ventricular stimulation (n = 1.328, 97%). Results: Patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a lower incidence of an antegrade dual AVN physiology (0% vs 71.1% and 92%, P < 0.001), a lower incidence of multiple form AVNRT (31% vs 69% and 85%, P = 0.009), and a more significant retrograde functional refractory period (FRP) difference (99 ± 102 vs 30 ± 57 ms, P < 0.001) than those that could be induced with only atrial stimulation or both atrial and ventricular stimulation. The occurrence of tachycardia stimulated with only ventricular stimulation was more frequently demonstrated in patients with the fast-slow form of AVNRT than in those with the slow-fast form of AVNRT (15% vs 3%, P < 0.001). Patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a higher incidence of retrograde dual AVN physiology (75% vs 4%, P < 0.001), a longer pacing cycle length of retrograde 1:1 fast and slow pathway conduction (475 ± 63 ms vs 366 ± 64 ms, P < 0.001; 449 ± 138 ms vs 370 ± 85 ms, P = 0.009), a longer retrograde effective refractory period of the fast pathway (360 ± 124 ms vs 285 ± 62 ms, P = 0.003), and a longer retrograde FRP of the fast and slow pathway (428 ± 85 ms vs 362 ± 47 ms, P < 0.001 and 522 ± 106 vs 456 ± 97 ms, P = 0.026) than those with the slow-fast form of AVNRT that could be induced with only ventricular stimulation. Conclusion: This study demonstrated that patients with the fast-slow form of AVNRT that could be induced with only ventricular stimulation had a different incidence of the antegrade and retrograde dual AVN physiology and the specific electrophysiological characteristics. The mechanism of the AVNRT stimulated only with ventricular stimulation was supposed to be different in patients with the slow-fast and fast-slow forms of AVNRT.

The fast pathway effective refractory period (ERP) has been reported to decrease after slow pathway modification with radiofrequency (RF) energy. How the fast pathway ERP changes during the ablation application has not been reported with either RF or cryoenergy.Using the unique features of cryotherapy, this study assesses the short-term changes in fast pathway ERP during cryomodification of the slow pathway and examines whether these changes are a useful marker for successful slow pathway modification in children.Nineteen pediatric patients (median age 15.1 years, range 9.6-19.6 years; weight 60.7 kg, range 35.6-130.2 kg) with anterograde dual AV nodal physiology underwent slow pathway modification with catheter-based cryoablation. Programmed stimulation was performed during cryoapplications after reaching -25 degrees C to assess fast pathway and slow pathway conduction. Data were analyzed from 59 of 237 cryoapplications where the fast pathway ERP was measured more than once (n = 13 patients).For 23 of 59 applications where the slow pathway was modified, the fast pathway ERP significantly increased during cryotherapy (Delta = 33.5 ms, P.0001). The magnitude of fast pathway ERP prolongation during cryotherapy was larger when the slow pathway was modified than when there was no effect on slow pathway conduction (33.5 +/- 30.5 vs 5.8 +/- 18.9 ms, P =.0005). Prolongation of fast pathway ERP by/=20 ms had 70% sensitivity and 72% specificity for predicting slow pathway modification. Following termination of cryoapplications, which resulted in slow pathway modification, the fast pathway ERP had significantly decreased from baseline (difference 44.5 ms, P.0001). The effect on fast pathway ERP was not related to changes in cycle length during (R(2) = 0.04, P = .045) or after ablation (R(2) = 0.13, P = .012).The fast pathway ERP prolongs during cryoapplications that result in slow pathway modification and shortens after termination of cryoapplications. The magnitude of fast pathway ERP prolongation during cryoapplication may be useful as a marker for successful slow pathway modification.

Though patients with AV nodal reentry are now routinely cured by catheter ablation, the basic mechanism of this disorder is still under debate. The putative mechanism of AV node reentry was first discovered by the elegant work of Gordon Moe. He demonstrated the existence of dual pathways and echo beats in rabbits. Building on these seminal observations, the mechanism of AVNRT has burgeoned to include the possibility of left atrial input into the node. The first curative nonpharmacologic procedures involved surgical dissection around the AV node and the procedure was rapidly supplanted by catheter ablation procedures. The initial ablative procedure targeted the fast pathway, but later observations showed that ablation of the slow pathway was more effective and safer. Cure of AV nodal reentry which is the most common cause of paroxysmal supraventricular tachycardia became possible through the cooperative efforts of anatomists, physiologists, surgeons, and clinical electrophysiologists.

Background 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). Methods and results 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-At) 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-Ap) better discriminates both subforms. The difference between H-Ap and H-At (ΔH-A) was significantly longer in Slow/Slow compared with Slow/Fast AVNRT (isoprenaline 0.5 μg/min: 27 ± 18 ms vs. 1 ± 9 ms; p 15 ms had a specificity and sensitivity for Slow/Slow of 94% and 64%, respectively. A ΔH-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

Typical atrioventricular nodal reentrant tachycardia (AVNRT) is the most common paroxysmal supraventricular tachycardia among adults. The concept of dual pathway physiology remains widely accepted, although this physiology likely results from the functional properties of anisotropic tissue within the triangle of Koch, rather than anatomically distinct tracts of conduction. AVNRT is typically induced with anterograde block over the fast pathway and conduction over the slow pathway, with subsequent retrograde conduction over the fast pathway. On rare occasions, anterograde AV node conduction occurs simultaneously through fast and slow pathways resulting in two ventricular beats in response to one atrial beat. We report a case of AVNRT where the tachycardia is always induced by the same mechanism described above. Successful ablation was achieved by slow pathway modification.

This article describes the additional use of incremental atrial burst pacing (A1A1) and double atrial extrastimulation with a predefined fast pathway conducted A2 (A1A2A3), rather than single atrial extrastimulation (A1A2) only, to characterize typical atrioventricular nodal reentrant tachycardia (AVNRT). The authors noted an additional 32% of patients had multiple anterograde AV nodal physiology demonstrated when A1A1 or A1A2A3 protocols were deployed compared to more conventional A1A2 protocols. The A2H2max (449 +/- 147 vs 339 +/- 94 ms) and A3H3max (481 +/- 120 vs 389 +/- 85 ms) were higher in 31 patients where multiple jumps in the AV nodal conduction curve were obtained (group 1) compared to 192 patients where only single jump was obtained (group 2) (both P0.01). Postablation, the degree of reduction of A2H2max (49%) and A3H3max (50%) in group 1 was greater than in group 2 (38% and 42%, respectively, P0.05). In seven of group 1 patients in whom A1A2A3 stimulation was required to reveal multiple jumps, the A2H2max remained unchanged after ablation (237 +/- 89 vs 214 +/- 59, P0.05). A3H3max was the only parameter that shortened significantly after ablation. Generally, successful ablation resulted in loss of multiple discontinuities in A1A1/A1H1 or A2A3/A3H3 curves. In conclusion, a combination of A1A2, A1A1, and A1A2A3 are required to fully elucidate AVNRT. Significant shortening of AHmax or loss of multiple jumps after ablation indicates successful elimination of AVNRT in these patients.

Background— There is evidence that atypical fast–slow and typical atrioventricular nodal re-entrant tachycardia (AVNRT) do not use the same limb for fast conduction, but no data exist on patients who have presented with both typical and atypical forms of this tachycardia. We compared conduction intervals during typical and atypical AVNRT that occurred in the same patient. Methods and Results— In 20 of 1299 patients with AVNRT, both typical and atypical AVNRT were induced at electrophysiology study by pacing maneuvers and autonomic stimulation or occurred spontaneously. The mean age of the patients was 47.6±10.9 years (range, 32–75 years), and 11 patients (55%) were women. Tachycardia cycle lengths were 368.0±43.1 and 365.8±41.1 ms, and earliest retrograde activation was recorded at the coronary sinus ostium in 60% and 65% of patients with typical and atypical AVNRT, respectively. Thirteen patients (65%) displayed atypical AVNRT with fast–slow characteristics. By comparing conduction intervals during slow–fast and fast–slow AVNRT in the same patient, fast pathway conduction times during the 2 types of AVNRT were calculated. The mean difference between retrograde fast pathway conduction during slow–fast AVNRT and anterograde fast pathway conduction during fast–slow AVNRT was 41.8±39.7 ms and was significantly different when compared with the estimated between-measurement error ( P =0.0055). Conclusions— Our data provide further evidence that typical slow–fast and atypical fast–slow AVNRT use different anatomic pathways for fast conduction.

Supraventricular tachycardia (SVT) is the most common and best known cardiac arrhythmia in both children and adults, with an estimated prevalence of 2.25 per 1,000 in the normal population worldwide.1 –3 These supraventricular arrhythmias are often repetitive, occasionally persistent, and rarely life threatening.4 Macroreentry through an anomalous atrioventricular (AV) pathway is by far the most frequent mechanism of SVT in children (80%) and accounts for ∼30% of SVT cases in adults.

A 52-year-old woman presented with left ventricular (LV) dysfunction and incessant narrow complex tachycardia. Electrocardiogram and clinical picture were suggestive of a permanent form of junctional reciprocating tachycardia, but electrophysiology study showed the tachycardia to be a fast-slow form of atrioventricular nodal reentrant tachycardia (AVNRT). Slow pathway ablation terminated the tachycardia and the LV dysfunction resolved completely at follow-up. Fast-slow AVNRT has not been reported to present in incessant form, and the mechanism in this patient was absent retrograde fast pathway conduction resulting in easy initiation and maintenance of tachycardia.

BACKGROUND: It is suggested that the adenosine resistance of retrograde fast pathway in slow-fast atrioventricular nodal reentrant tachycardia (AVNRT) confirms the participation of a concealed retrograde atrio-Hisian pathway rather than the conventional fast pathway in the arrhythmia circuit of slow-fast AVNRT.OBJECTIVE: To prospectively assess the retrograde fast pathway response to the intravenous administration of adenosine in patients with typical AVNRT and the control group.METHODS: Electrophysiological parameters and adenosine sensitivity of retrograde fast pathway were studied in 21 consecutive patients (18 women; mean age 57 ± 10 years) with slow-fast AVNRT and 24 patients (11 women; mean age 46 ± 16 years) as the control group.RESULTS: Fifteen (71%) patients with AVNRT and 18 (75%) patients in the control group developed transient ventriculoatrial (VA) block after the intravenous administration of adenosine (P = .79). In patients with slow-fast AVNRT, female sex (P = .003), longer VA interval during right ventricular pacing (P < .001), and longer tachycardia cycle length (P < .001) predicted transient VA block after the intravenous administration of adenosine. In patients in the control group, a shorter VA interval during fixed rate right ventricular apical pacing (P = .009) and the presence of dual atrioventricular nodal physiology (P = .002) were associated with the adenosine resistance of the retrograde fast pathway.CONCLUSIONS: The prevalence of the adenosine resistance of retrograde fast pathway's conduction is comparable between patients with and those without slow-fast AVNRT. This finding can be explained better by the existence of an insulated intranodal tract with Purkinje-like properties or a superior atrionodal connection to the nodo-Hisian region of the atrioventricular node rather than the presence of an atrio-Hisian pathway.

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.

A case of a 60-year-old male with irregular AV nodal reentrant tachycardia of the common type is reported. Electrophysiological study revealed multiple antegrade slowly conducting AV nodal pathways and one exclusively retrogradely conducting fast AV nodal pathway. Despite the recommendation for slow pathway ablation as the treatment of choice in patients with AVNRT, first pathway ablation was successfully performed in this case due to the risk of total A V block of ablating the slow pathways. The present report shows that there is the rare patient in whom fast pathway ablation is required for curative treatment of AV nodal reentrant tachycardia.

Para-Hisian pacing at high output simultaneously captures the His bundle or proximal right bundle, as well as the adjacent ventricular myocardium. At lower output, direct His-bundle, or right-bundle, capture is lost which causes an increase in the stimulus to atrium interval. We describe a case with an increment of 68 ms with capture of the His bundle. This seems to be a paradoxical response, which however can be explained by the presence of retrograde dual AV-node physiology. Continuation of this phenomenon could be related to concealed anterograde invasion of the fast pathway thereby maintaining the retrograde activation during para-Hisian pacing on the slow pathway despite paced cycle lengths (His to His intervals) where retrograde fast pathway conduction proved to be possible.

Incessant Nonreentrant AVNT by Multiple Pathways. In patients with dual AV nodal physiology, simultaneous anterograde fast and slow pathway conduction resulting in an unusual form of nonreentrant A V nodal tachycardia has been observed. We describe the case of a young patient with an incessant form of complex supraventricular tachycardia who underwent electrophysiologic evaluation, which showed simultaneous conduction via multiple AV nodal pathways that caused a unique form of incessant nonreentrant AV nodal tachycardia. Radiofreqeuncy ablation of the spatially closed intermediate and slow pathways effectively treated the tachycardia. The electrophysiologic determinants of simultaneous conduction through the multiple nodal pathways and the apparently different behavior of the fast pathway before and after ablation are discussed.

Lower Common Pathway Within the AV Node. Introduction: Despite the ability to cure atrioventricular nodal reentrant tachycardia (AVNRT) by radiofrequency catheter ablation with a high success rate, the exact localization of the tachycardia circuit is still not well established. The presence of AV nodal tissue between the typical AVNRT circuit and the His bundle, constituting a lower common pathway (LCP), remains controversial. Methods and Results: Entrainment of AVNRT during para-Hisian stimulation allows accurate measurement of the His- to- atrial (HA) interval which is part of the same circuit as that of the tachycardia. With an LCP, during tachycardia, there is simultaneous conduction from the low turnaround of the circuit to the atrium (via the fast pathway) and to the His bundle (via the LCP). However, during entrainment by para-Hisian pacing, the impulse bas to retrogradely depolarize sequentially the LCP and the fast pathway. Therefore, in the presence of an LCP, the HA interval duration during tachycardia (HAt) should be shorter than that of during entrainment by para-Hisian stimulation (HAe). We considered an LCP present when Hae - HAt was ≥ 10 msec. Entrainment of typical AVNRT with para-Hisian stimulation was performed in 23 consecutive patients (21 females) with a mean age of 45 ± 17 years. LCP was considered to be present in 18 of 23 patients (78%). In addition, transient His-bundle dissociation from the ongoing tachycardia occurred in seven patients (30%). Conclusion: These results support the presence of a LCP during typical AVNRT.

During atrial fibrillation (AF), conventional electrophysiological techniques for assessment of refractory period or conduction velocity of the atrioventricular (AV) node cannot be used. We aimed at evaluating changes in AV nodal properties during administration of metoprolol from electrocardiogram data, and to support our findings with simulated data based on results from an electrophysiological study.Sixty patients (age 71 ± 9 years, 42 men) with permanent AF were included in the RATe control in Atrial Fibrillation (RATAF) study. Two 15 min segments, during baseline and metoprolol administration, starting at 2 pm were analysed in this study. Atrial fibrillatory rate (AFR), heart rate (HR), and AV nodal parameters were assessed. The AV nodal parameters account for the probability of an impulse not taking the fast pathway, the absolute refractory periods of the slow and fast pathways (aRPs and aRPf), representing the functional refractory period, and their respective prolongation in refractory period. In addition, simulated RR series were generated that mimic metoprolol administration through prolonged AV conduction interval and AV node effective refractory period. During metoprolol administration, AFR and HR were significantly decreased and aRP was significantly prolonged in both pathways (aRPs: 337 ± 60 vs. 398 ± 79 ms, P0.01; aRPf: 430 ± 91 vs. 517 ± 100 ms, P0.01). Similar results were found for the simulated RR series, both aRPs and aRPf being prolonged with metoprolol (aRPs: 413 ± 33 vs. 437 ± 43 ms, P = 0.01; aRPf: 465 ± 40 vs. 502 ± 69 ms, P = 0.02).The AV nodal parameters reflect expected changes after metoprolol administration, i.e. a prolongation in functional refractory period. The simulations confirmed that aRPs and aRPf may serve as an estimate of the functional refractory period.

This study was conducted to systematically characterize the excitable gap and conduction properties of the reentrant circuit during atrioventricular nodal reentrant tachycardia (AVNRT). Previous studies have attempted to analyze these properties by introducing single ventricular extrastimuli during tachycardia. These studies have been limited, however, by the inability of single extrastimuli to engage the circuit in the majority of patients studied. Thus, in most cases, the nature of the excitable gap and the conduction properties of the anterograde and retrograde limbs of the circuit during tachycardia remain undefined. In this series, 11 patients with typical AVNRT were studied. During tachycardia, both single and double ventricular extrastimuli (the first extrastimulus acting as a conditioning stimulus) were used to scan diastole. The resetting response of the reentrant circuit, as well as the conduction properties f the retrograde fast and anterograde slow pathways, was recorded and analyzed. Whereas atrial preexcitation and resetting of the reentrant circuit could be demonstrated in only 1 patient with single ventricular extrastimuli, resetting was achieved in all 11 patients with closely coupled double ventricular extrastimuli. Over the full range of coupling intervals used, no retrograde delay in fast pathway conduction could be demonstrated before tachycardia termination or ventricular refractoriness. Penetration of the reentrant circuit resulted in a progressive increasing delay in the anterograde portion of the subsequent return cycle and an increasing resetting response pattern in all cases. Thus, the reentrant circuit during AVNRT demonstrates heterogeneous excitability. While the fast pathway remains fully excitable during tachycardia, the slow pathway uniformly demonstrates decrementai conduction, resulting in an increasing resetting response pattern. An increasing resetting response pattern does not preclude the presence of fully excitable tissue within a reentrant circuit.