Slow/Fast Atrioventricular Nodal Reentrant Tachycardia Using the Inferolateral Left Atrial Slow Pathway: Role of the Resetting Response to Select the Ablation Target.

AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting ("slow") pathway and retrograde conduction over a rapidly conducting ("fast") pathway. A variety of drugs, such as beta blockers, digitalis, and calcium channel blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways respond in a quantitatively different manner to drugs such as beta-adrenergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refractoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. Thirteen patients with discontinuous AV nodal conduction properties and typical AVNRT were studied. Anterograde and retrograde AV nodal functional assessment was performed at baseline and following steady-state drug infusion of intravenous esmolol at a dose of 500 micrograms/kg for 1 minute, 150 micrograms/kg per minute for the next 4 minutes, followed by a continuous maintenance infusion of 50 to 100 micrograms/kg per minute. The anterograde effective refractory period of the fast pathway increased from 381 +/- 75 msec at baseline to 453 +/- 92 msec during the infusion of esmolol (P = 0.003). The anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 +/- 26 msec to 310 +/- 17 msec (P = 0.005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 +/- 59 msec) was significantly greater than the change in anterograde effective refractory period of the slow pathway (+21 +/- 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased from 276 +/- 46 msec to 376 +/- 61 msec during esmolol infusion (P = 0.03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion. In contrast to the effects of esmolol on refractoriness, the AH interval during anterograde slow pathway conduction prolonged to a far greater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). The beta-adrenergic antagonist, esmolol, has a quantitatively greater effect on anterograde refractoriness of the fast than the slow AV nodal pathway. However, the effects on conduction intervals during AVNRT are greater in the anterograde slow pathway than in the retrograde fast pathway. These observations suggest that the fast and slow pathways may have differential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinically useful method for demonstrating slow pathway conduction in some individuals with AVNRT.

Recurrent tachycardia after selective ablation of slow pathway in patients with atrioventricular nodal reentrant tachycardia

Pseudo–Atrial Fibrillation, Rare Manifestation of Multiple Anterograde Atrioventricular Nodal Pathways

We present a series of elderly patients older than 80 years who had recurrent palpitations for decades and who were subsequently diagnosed with atrioventricular (AV) nodal reentrant tachycardia (AVNRT). Through a retrospective chart analysis, we identified 12 patients (nine females and three males) aged 88 years ± 3.7 years (range: 80–92 years) seen at our center from 2015 to 2016 for recurrent palpitations and supraventricular tachycardia (SVT) who were ultimately diagnosed with AVNRT. These patients had palpitations and had been treated for anxiety and panic attacks for decades. They underwent electrophysiology (EP) study and successful ablation of the slow pathway. The demographic data, symptoms, and EP characteristics during the EP studies of the patients were evaluated. All 12 patients experienced palpitations and all but three had documented SVT on a loop recorder or an event monitor. During EP study, all patients displayed slow-pathway conduction. Nine patients demonstrated discontinuous AV nodal conduction curves, while three showed continuous AV nodal conduction curves. The observed tachycardia rates were 496.7 ms ± 25.7 ms. Three patients had atrial fibrillation (AF), which was noted during monitoring with the implanted loop recorders. Tachycardia was induced with both burst atrial pacing and atrial extrastimuli in five patients and with extrastimuli only in two patients. In five patients, no tachycardia induction was noted, but these individuals showed evidence of dual AV node physiology. Successful elimination of residual slow-pathway conduction postablation and/or noninducibility of tachycardia in the postablation period were achieved in all patients. All patients remained symptom-free over a period of one year. The patients who had AF in addition to AVNRT also did not present any recurrent AF following AVNRT ablation but are being monitored for recurrence. AVNRT in elderly people is often confused with panic attacks; hence, reports of panic attacks in elderly people should be properly evaluated for an arrhythmic etiology.

Funding Acknowledgements None Introduction Cryoablation is considered a safe but somewhat less effective alternative to radiofrequency ablation (RF) for treatment of atrioventricular nodal reentry tachycardia (AVNRT). Additionally, it is traditionally performed with the aid of X-ray fluoroscopy as the principal imaging method causing radiation exposure, which is especially undesired in the pediatric population. Purpose The aim of our study was to assess feasibility, safety and success rate of nonfluoroscopic cryoablation for treatment of AVNRT. Methods Forty-eight consecutive patients with a diagnosed AVNRT (aged 40 ± 22 years, 29 (60%) female, 19 (40%) male) were included in the study. Among the study population, 14 (29%) were pediatric patients aged 11.5 ± 4.1 years. Cryoablation was used at the discretion of the operator. Only three dimensional electroanatomic mapping system and intracardiac electrograms were used to guide catheter movement and positioning. X-ray fluoroscopy was not used. The initial approach in all procedures was cryomapping in the region of the slow pathway during ongoing AVNRT, with a switch to cryoablation when termination of tachycardia within 20 seconds of reaching -30°C was achieved. When cryomapping was not possible due to catheter instability, cryoablation was used during ongoing AVNRT for up to 10 seconds at -70°C or lower. When AVNRT was not readily inducible, termination of slow pathway conduction was targeted with cryomapping during programmed stimulation with atrial extrastimuli. Procedural endpoint was noninducibility of AVNRT. Recorded residual slow pathway conduction was not considered a failure. Results Mean procedural duration was 79 ± 34 minutes. On average, 4 ± 2 cryoablations, with a 240 seconds of cryoablation time per each application. Cryoablation was used as a first choice in 45 (45/48, 93.7%) patients. In the remaining 3 patients (3/48, 6.3%) RF ablation failed as the first choice due to transient AV conduction disturbance and cryoablation had to be used to reach the endpoint. Cryoablation was unsuccessful only in 3 cases (6.6%) where RF ablation was needed to achieve procedural endpoint. Targeting termination of AVNRT during cryomapping or cryoablation was possible in 25 patients (25/48, 52%). In 14 patients AVNRT was not inducible and termination of the slow pathway conduction was targeted instead. In 9 patients inadvertent catheter tip contact mechanically terminated AVNRT or slow pathway conduction; site of mechanical termination was then targeted with cryoablation. After mean follow-up of 349 ± 201 days 47 patients were free of recurrence (47/48, 98%). There were no procedural complications. Conclusions In our study population with adult and pediatric patients, zero-fluoroscopy cryoablation of AVNRT proved feasible, safe and resulted in high success rates. Cryomapping or cryoablation for AVNRT termination was possible in approximately half of the procedures.

The Specialized Atrioventricular Ring Tissues Participate in the Circuit of Atrioventricular Nodal Reentrant Tachycardia

Multiple anterograde atrioventricular node pathways in patients with atrioventricular node reentrant tachycardia

Radiofrequency ablation of the "slow pathway" in atrioventricular nodal reentrant tachycardia (AVNRT) relies on tachycardia non-inducibility after ablation as success criterion. However, AVNRT is frequently non-inducible at baseline. Thus, autonomic enhancement using either atropine or isoproterenol is frequently used for arrhythmia induction before ablation. 80 patients (57 women, 23 men, age 50+/-14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01 mg/kg atropine or 0.5-1.0 microg/kg/min isoproterenol before ablation after baseline assessment of AV conduction. The effects of either drug on ante- and retrograde conduction was assessed by measuring sinus cycle length, PR and AH interval, antegrade and retrograde Wenckebach cycle length (WBCL), antegrade effective refractory period (ERP) of slow and fast pathway and maximal stimulus-to-H interval during slow and fast pathway conduction. Inducibility of AVNRT at baseline was not different between patients randomized to atropine (73%) and isoproterenol (58%) but was reduced after atropine (45%) compared to isoproterenol (93%, P<0.001). Of the 28 patients non-inducible at baseline isoproterenol rendered AVNRT inducible in 21, atropine in 4 patients. Dual AV nodal pathway physiology was present in 88% before and 50% after atropine compared to 83% before and 73% after isoproterenol. Whereas both drugs exerted similar effects on ante- and retrograde fast pathway conduction maximal SH interval during slow pathway conduction was significantly shorter after isoproterenol (300+/-48 ms vs. 374+/-113 ms, P=0.012). Isoproterenol yields higher AVNRT inducibility than atropine in patients non-inducible at baseline. This may be caused by a more pronounced effect on antegrade slow pathway conduction.

Atrioventricular nodal reentrant tachycardia and persistent left superior vena cava: A tough nut to crack. Successful ablation with transseptal approach

Objective The electrophysiological parameters of atrioventricular conduction function in patients with atrioventricular nodal reentry tachycardia (AVNRT) were analyzed, and to explore the effect of different ablation endpoints on atrioventricular conduction function in patients with AVNRT. Methods 96 cases with AVNRT underwent radiofrequency catheter ablation (RFCA) of slow conduction pathway.According to whether the slow pathway eliminated, the patients were divided into the slow pathway disappeared group and slow tracks remaining group.Preoperative and postoperative intracavitary electrophysiological examination and atrioventricular function data were recorded, including before and after radiofrequency ablation of bundle of HIS, PA, AH, HV interval, atrioventricular prequel venturi point(AVN-WKB), ventriculoatrial retrograde venturi point(VAN-WKB), atrioventricular node prequel effective refractory period(AVB-WKB). Patients were followed up by telephone for a year.Then, a comparative analysis of preoperative and postoperative was done. Results RFCA of AVNRT patients with atrioventricular node prequel time effect: RFCA and preoperative ratio, after his bundle electrogram PA, ah, HV interval had no significant changes(P>0.05). Effect of RFCA surgery on patients with AVNRT refractory atrioventricular node prequel: compared with RFCA before surgery, postoperative slow pathway disappear fast pathway shortening of effective refractory period[preoperative(287.5±46.2)ms, postoperative(260.2±55.6)ms, t=2.901, P=0.005], slow pathway effective refractory period[disappear preoperative(243.3±43.2), postoperative(0.0±0.0)ms, t=43.290, P=0.000], AV node Wenckebach point in advance before operation[(261.3±44.3)ms, postoperative(293.2±46.2)ms, t=3.828, P=0.000]; group after slow pathway to improve fast pathway effective refractory period without obvious change(P>0.05), the slow pathway effective refractory period in high concentration[preoperative(242.2±42.8)ms, postoperative(281.2±41.3)ms, t=3.879, P=0.000], atrioventricular node Wenckebach point in advance before operation[(261.5±43.5)ms, postoperative(291.3±46.5)ms, t=2.769, P=0.007]. Comparison between groups, after slow pathway disappeared group fast pathway effective refractory period was significantly shorter in the slow diameter improvement group, but between the two groups in the atrioventricular node Wenckebach point differences was not statistically significant(P>0.05). There was no recurrence in the follow-up after a year of slow path loss and slow pathway. Conclusion RFCA caused by slow pathway to disappear or modified two slow pathway ablation right AVNRT patients atrioventricular time had no effect, but all the atrioventricular junction the prequel's point advance.The atrioventricular node slow pathway disappear fast and effective pathway refractory period shortened, slow pathway improved the slow pathway effective refractory period.RFCA surgery done by the slow pathway disappeared or slow pathway ablation is effective in patients with AVNRT, and there was no significant recurrence rate in both groups within 1 year. Key words: Ablation; Tachycardia; Atrioventricular conduction function

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Both the typical (slow-fast (S/F)) and atypical (slow-slow (S/S) and fast-slow (F/S)) forms of the AV nodal reentrant tachycardias (AVNRT) are usually amenable to the classical slow pathway (SP) ablation at the inferoseptal atrial region. However, rare cases of unusual forms AVNRT do not involve an SP in the tachycardia circuits (TC), and they are resistant to the classical SP ablation. The characteristics of the atypical AVNRTs not involving an SP in the TCs remain to be elucidated. A total of 1252 AVNRTs induced during the electrophysiological study in 950 cases were analyzed. Both the anterograde and retrograde limbs of the TC were classified into the fast pathway (FP) or SP according to the A-H (AHI) and H-A intervals (HAI) during the tachycardia; the anterograde FP: AHI of &lt;220 ms, anterograde SP: AHI of ≥220 ms, retrograde FP: HAI of &lt;120 ms, and retrograde SP: HAI of ≥120 ms. Accordingly, each tachycardia was classified into one of the S/F, S/S, F/S and fast-fast (F / F) forms . There were 998 S/F forms (79.7%), 119 S/S forms (9.5%), 129 F/S forms (10.3%) and 6 F / F forms (0.5%). The F / F forms were induced by atrial or ventricular extrastimulation without an associated jump-up in the AHI and HAI, and they were characterized by a shorter tachycardia cycle length (260±55 ms), short AHI (153±39 ms) and HAI (107±19 ms) during the tachycardia, earliest retrograde atrial activation (ERAA) at the right superoseptum (n=2) or midseptum (n=4), and 2nd degree AV block without a tachycardia interruption. The retrograde atrial activation sequence during the F / F forms was identical to that during ventricular pacing. The tachycardias could be entrained from the RV, and they resumed with a V-A-V sequence after the cessation of the entrainment pacing. The classical SP ablation at the right inferoseptal region was unsuccessful in all 6 cases with the F / F forms . The successful ablation was achieved at the right superoseptum (n=2) or midseptum (n=4) without creating AV block in all 6 cases. The F / F forms of atypical AVNRT not involving a classical SP in the TC were observed in 0.5% of all AVNRT cases. The results of this study suggested that the TC was smaller and confined to the superior part of the AV nodal area in this extremely rare form of AVNRT.

Atrioventricular nodal reentrant tachycardia (AVNRT) accounts for about 60% of the patients presenting with paroxysmal supraventricular tachycardia (PSVT). It is the result of functional dissociation of AV nodal conduction into a so-called ‘fast pathway’ (FP) and ‘slow pathway’ (SP). The fast pathway forms the normal physiological conduction axis. It connects to the atrium in the anterior (superior) septum, close to the recording of the most proximal His bundle potential (Fig. 1). The atrio-His (AH) interval during conduction over the fast pathway generally is not longer than 220 ms. Conduction over the slow pathway, connecting to the atrium in the posterior (inferior) septum, can be revealed when an atrial impulse is blocked in the fast pathway (which generally has a longer antegrade effective refractory period than the slow pathway) leading to a sudden prolongation of the AH interval. Often the wavefront migrates back to the atrium over the fast pathway resulting in an AV nodal echo beat. Slow pathway conduction can be demonstrated in the majority of people. However, one-to-one antegrade conduction over the slow pathway, i.e. a situation where every consecutive atrial impulse is conducted over the slow pathway to the His bundle, is unusual. Therefore, perpetuation of reentry leading to AVNRT is often not possible. Even in the presence of one-to-one antegrade slow pathway conduction, a necessary prerequisite for sustained AVNRT, tachycardia may be non-inducible because of absent or weak retrograde fast pathway conduction. If reentry evolves, causing AVNRT, it uses the slow pathway as an antegrade link and the fast pathway as a retrograde link in 90% of patients: therefore, this ‘slow/

189: Clinical and electrophysiological data of patients with first degree AV block and AV node reentrant tachycardia

The anatomic location of atrioventricular (AV) bypass tracts (or accessory pathways) is variable, but these generally traverse the tricuspid or mitral annulus and insert into the atrium and ventricle near the AV ring. There is only 1 case report of an accessory pathway ablated in the left coronary cusp (LCC),1 and this pathway had bidirectional conduction, was not decremental, and was associated with an orthodromic tachycardia. We report here the first case of an antegrade slowly conducting, decremental, accessory pathway that was also successfully ablated in the aortic LCC. This pathway generated antidromic tachycardia having a QRS morphology mimicking those seen in outflow tract ventricular tachycardia. A 42-year-old woman was evaluated for palpitations and presyncope for 2 years. These were commonly associated with shortness of breath and chest heaviness that would resolve spontaneously. Her baseline ECG was normal without ventricular preexcitation. Echocardiogram, coronary angiogram, and thyroid function were also unremarkable. On her third presentation to a hospital, a broad complex tachycardia was captured (representative 12-lead ECG shown in Figure 1). The cycle length was 480 ms, the QRS duration was 150 ms, and a left bundle branch morphology with a right inferior axis was noted. She was referred for ablation of suspected ventricular outflow tract tachycardia. Consent was obtained for mapping and ablation of this tachycardia. During placement of catheters, a spontaneous initiation of tachycardia occurred, which was noted to have 1:1 AV association. A quadripolar catheter was placed at the right ventricular apex and His bundle, with a decapolar catheter in the coronary sinus. During ventricular pacing, retrograde conduction occurred with a long ventriculoatrial interval. Tachycardia was readily initiated with ventricular premature beats showing retrograde decremental conduction (Figure 2). An antegradely conducting accessory pathway was noted during atrial pacing maneuvers. During delivery of premature atrial stimulations, shortening of …