Slow-fast form of atrioventricular nodal reentrant tachycardia with eccentric retrograde left-sided activation

A case of atypical AV nodal reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation, masquerading as tachycardia using a left-sided accessory pathway, is reported. Initially, it appeared that the tachycardia was a typical slow-fast form of AVNRT. The earliest retrograde activation, however, was registered at a site approximately 3 cm from the coronary sinus orifice (left atrial free wall), indicating atypical AVNRT. Atrial tachycardia and orthodromic AV reciprocating tachycardia using an accessory AV pathway were excluded. Slow pathway ablation at the posteroseptal right atrium eliminated the tachycardia. It was suggested that the anterograde limb of the tachycardia circuit was a slow AV nodal pathway with typical posteroseptal location, whereas the retrograde limb was a long atrionodal pathway connecting the compact AV node and the left atrial free wall near the mid-coronary sinus.     

Change in the retrograde atrial activation sequence following radiofrequency modification of the atrioventricular node: implications for the electrophysiologic circuit of a variant of atrioventricular nodal reentrant tachycardia

INTRODUCTION: Despite the great success in treating AV nodal reentrant tachycardia (AVNRT) with radiofrequency modification of the AV node, the dimensions of the electrophysiologic circuit of this arrhythmia remain unclear, and simple models fail to explain all tachycardia-related phenomena. METHODS AND RESULTS: We describe three unusual cases of supraventricular tachycardia (SVT). In all three cases, retrograde atrial activation during ventricular pacing or during SVT manifested local left atrial electrograms recorded from the coronary sinus preceding the septal atrial electrograms (eccentric activation), with earliest atrial activity at the lateral or posterolateral mitral annulus. Electrophysiologic maneuvers and observations were consistent with AVNRT as the mechanism in each case. In all cases, radiofrequency modification of the AV node eliminated inducible SVT and abolished dual pathway AV nodal physiology. The retrograde atrial activation sequence during ventricular pacing changed after ablation in each case, with septal atrial electrograms preceding left atrial electrograms recorded from the coronary sinus (concentric activation). CONCLUSION: The observations in these cases cannot be explained by the traditional model of slow, fast, and intermediate AV nodal pathways. A model incorporating a circuit close to the AV node with left atrial and coronary sinus connections is proposed.     

Electrophysiologic Spectrum of Atrioventricular Nodal Behavior in Patients with Atrioventricular Nodal Reentrant Tachycardia Undergoing Selective Fast or Slow Pathway Ablation

AV Nodal Behavior After Ablation. Introduction; The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT).
Methods and Results: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty-two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty-one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His-bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety-six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation.
Conclusion: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT: and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.     

Simultaneous antegrade dual AV node conduction initiates AV nodal re-entrant tachycardia (a rare initiation mechanism)

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.     

Electrophysiological mechanisms of conversion of typical to atypical atrioventricular nodal reentrant tachycardia occurring after radiofrequency catheter ablation of the slow pathway

This report presents an adult patient with conversion of typical to atypical atrioventricular nodal reentrant tachycardia (AVNRT) after slow pathway ablation. Application of radiofrequency energy (3 times) in the posteroseptal region changed the pattern of the atrioventricular (AV) node conduction curve from discontinuous to continuous, but did not change the continuous retrograde conduction curve. After ablation of the slow pathway, atrial extrastimulation induced atypical AVNRT. During tachycardia, the earliest atrial activation site changed from the His bundle region to the coronary sinus ostium. One additional radiofrequency current applied 5 mm upward from the initial ablation site made atypical AVNRT noninducible. These findings suggest that the mechanism of atypical AVNRT after slow pathway ablation is antegrade fast pathway conduction along with retrograde conduction through another slow pathway connected with the ablated antegrade slow pathway at a distal site. The loss of concealed conduction over the antegrade slow pathway may play an important role in the initiation of atypical AVNRT after slow pathway ablation.     

Atrial tachycardia with slow pathway conduction mimicking typical atrioventricular nodal reentrant tachycardia.

A 68-year-old woman with palpitations underwent electrophysiologic testing. During burst atrial pacing the PR interval exceeded the RR interval and induced a supraventricular tachycardia consistent with a typical AV nodal reentrant tachycardia (AVNRT). Radiofrequency ablation of the slow pathway during the tachycardia immediately produced 2 : 1 AV conduction. After slow AV nodal pathway ablation an atrial tachycardia (AT) remained inducible with the earliest atrial activation around the HB region. Radiofrequency ablation at the site of earliest atrial activation interrupted the AT without AV block. AT originating from the HB region with slow pathway conduction may mimic typical AVNRT.     

Selected Slow Pathway Ablation in a Patient with Corrected Transposition of the Great Arteries and Atrioventricular Nodal Reentrant Tachycardia

AVNRT in Corrected TGA. We report the first known case of AV nodal reentrant tachycardia (AVNRT) associated with a corrected transposition of the great arteries to be treated successfully by ablation of the slow pathway. Triple AV nodal pathways were observed in the anterograde direction and two types of AVNRT were induced. Input of the fast pathway to the AV node was located at the anterior portion of the left-sided A V annulus, while the input of the intermediate and slow pathways was located at the anteroseptal portion of the right-sided AV annulus. Radiofrequency energy ablation at the right anteroseptal site eliminated the intermediate and slow pathways.     

Atypical atrioventricular nodal reentrant tachycardia with eccentric coronary sinus activation: electrophysiological characteristics and essential effects of left-sided ablation inside the coronary sinus.

BACKGROUND: The precise electrophysiological characteristics and essential effects of left-sided ablation in atrioventricular nodal reentrant tachycardia (AVNRT) with eccentric coronary sinus (CS) activation (ECSA) have not been described. OBJECTIVE: The purpose of this study was to elucidate the tachycardia characteristics and essential effects of left-sided ablation in AVNRT with ECSA. METHODS: Electrophysiological and ablation data were reviewed in 340 patients with all forms of AVNRT. RESULTS: Among 360 AVNRTs in the 340 patients, there were 23 atypical AVNRTs (6%; 12 slow-slow and 11 fast-slow) in 18 (5%) patients who exhibited ECSA with the earliest retrograde atrial activation 11 +/- 5 mm inside the CS. The patients with ECSA during the tachycardia were significantly younger than those without (38 +/- 18 vs. 51 +/- 18 years; P<.01). The presence of upper (UCP) and lower common pathways (LCP) was suggested in three (17%) and 18 (100%) patients, respectively. An ablation exclusively targeting the earliest retrograde atrial activation inside the CS eliminated the tachycardias with the elimination (n = 12) or modification of the left-sided slow pathway (SP) conduction (n = 6) without any complications. The entire reentrant circuit was considered to reside on the left side in two patients (11%) because the bidirectional SP conduction was simultaneously eliminated after the ablation inside the CS. CONCLUSIONS: Atypical AVNRT with ECSA involved the left-sided SP as a retrograde limb, and the reentrant circuit was more frequently associated with evidence that suggested a UCP and LCP. Ablation exclusively targeting the earliest retrograde atrial activation inside the CS was highly effective in this entity.     

Radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia in children aided by the LocaLisa mapping system.

AIMS: In young patients, slow pathway ablation for treatment of atrioventricular nodal reentrant tachycardia (AVNRT) carries a small but definite risk of permanent AV block. The aim was to assess the efficacy of slow pathway ablation aided by the LocaLisa mapping system. PATIENTS AND METHODS: Radiofrequency (RF) modification of the slow AV nodal pathway was performed in 26 children < 19 years of age (median age 9.8 years, range 3-18.9). Three measures to limit the risk of AV block were applied: (1) use of LocaLisa, a non-fluoroscopic mapping system, to determine and mark the location of the AV node/His bundle axis, and monitor ablation catheter position, (2) continuous atrial stimulation during RF delivery to monitor AV conduction, and (3) gradual increase of RF power during RF ablation. RESULTS: AVNRT was rendered non-inducible in all patients. Dual AV physiology was abolished in 24/26 patients; 2 patients had single atrial echoes at the end of the procedure. At follow-up, AVNRT recurred in 3 patients (including the above 2), necessitating a second procedure. The median number of RF applications was 4 (3-8); median fluoroscopy time was 16 (7-33)min. One patient developed transient second-degree AV block, with full recovery within 6 weeks of the procedure. CONCLUSIONS: RF modification of the slow AV nodal pathway in children can be safely accomplished, achieving the ideal end-point of abolishing dual AV physiology, aided by use of the LocaLisa mapping system.     

Radiofrequency Catheter Ablation of AtypicalAtrioventricular Nodal Reentrant Tachycardia

Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia, Introduction: Published reports of radiofrequency ablation of atypical atrioventricular nodal reentranttacbycardia (AVNRT) have been limited. We present our experience in 10 consecutive patientswith atypical AVNRT wbo underwent radiofrequency ablation of the "slow" AV nodal pathway.
Methods and Resttlts: there were 9 females and 1 male; their mean age was 44 ± 19 years (± SD), the mean AVNRT cycle length and ventriculoatrial (VA) interval at the His positionduring AVNRT were 340 ± 50 msec and 200 ± 70 msec, respectively. the slow pathway wassuccessfully ablated in all patients with a mean of 10 ± 7 radiofrequency energy applications inthe posteroseptal right atritim near the coronary sinus os. The mean procedure duration was 100 ± 35 minutes. There were no complications. In 4 patients, target sites were identified during sinus rhythm by mapping for possible slow pathway potentials, In the other 6 patients, target sites were identified by mapping retrograde atrial activation during AVNRT or ventricularpacing, The VA times at successful target sites were a mean of 45 ± 30 msec less tban the VAtime at the His cathetcr during AVNRT, There were no differences in success rate, number ofradiofrequency energy applications, or procedure duration between patients in whom mappingwas guided by possible slow pathway potentials or by retrograde atrial activation, During 6 ± 3 months of followup, 1 patient bad a recurrence of atypical AVNRT and underwent a secondablation procedure, which was successful.
Conclusion: Radiofrequency ablation of atypical AVNRT can be safely and effectivelyaccomplisbed when target sites are identified based either on possible slow pathway potentialsduring sinus rbytbm or retrograde atrial activation times during tachycardia.     

Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: Effects of slow pathway ablation and insights into the location of the reentrant circuit

BACKGROUND: The electrophysiologic mechanisms of different ventriculoatrial (VA) block patterns during atrioventricular nodal reentrant tachycardia (AVNRT) are poorly understood. OBJECTIVES: The purpose of this study was to characterize AVNRTs with different VA block patterns and to assess the effects of slow pathway ablation. METHODS: Electrophysiologic data from six AVNRT patients with different VA block patterns were reviewed. RESULTS: All AVNRTs were induced after a sudden AH "jump-up" with the earliest retrograde atrial activation at the right superoparaseptum. Different VA block patterns comprised Wenckebach His-atrial (HA) block (n = 4), 2:1 HA block (n = 1), and variable HA conduction times during fixed AVNRT cycle length (CL) (n = 1). Wenckebach HA block during AVNRT was preceded by gradual HA interval prolongation with fixed His-His (HH) interval and unchanged atrial activation sequence. AVNRT with 2:1 HA block was induced after slow pathway ablation for slow-slow AVNRT with 1:1 HA conduction, and earliest atrial activation shifted from right inferoparaseptum to superoparaseptum without change in AVNRT CL. The presence of a lower common pathway was suggested by a longer HA interval during ventricular pacing at AVNRT CL than during AVNRT (n = 5) or Wenckebach HA block during ventricular pacing at AVNRT CL (n = 1). In four patients, HA interval during ventricular pacing at AVNRT CL was unusually long (188 +/- 30 ms). Ablations at the right inferoparaseptum rendered AVNRT noninducible in 5 (83%) of 6 patients. CONCLUSION: Most AVNRTs with different VA block patterns were amenable to classic slow pathway ablation. The reentrant circuit could be contained within a functionally protected region around the AV node and posterior nodal extensions, and different VA block patterns resulted from variable conduction at tissues extrinsic to the reentrant circuit.     

"Left-variant" atypical atrioventricular nodal reentrant tachycardia: electrophysiological characteristics and effect of slow pathway ablation within coronary sinus

Introduction: Recent anatomical and electrophysiological studies have demonstrated the presence of leftward posterior nodal extension (LPNE); however, its role in the genesis of atrioventricular nodal reentrant tachycardia (AVNRT) is poorly understood. This study was performed to characterize successful slow pathway (SP) ablation site and to elucidate the role of LPNE in genesis of atypical AVNRT with eccentric activation patterns within the coronary sinus (CS).
Methods and Results: Among 45 patients with atypical AVNRT (slow-slow/fast-slow/both = 20/22/3 patients) with concentric (n = 37, 82%) or eccentric CS activation (n = 8, 18%), successful ablation site was evaluated. Among 35/37 patients (95%) with concentric CS activation, ablation at the conventional SP region outside CS eliminated both retrograde SP conduction and AVNRT inducibility. Among eight patients with eccentric CS activation, the earliest retrograde atrial activation was found at proximal CS 16 ± 4 mm distal to the ostium during AVNRT. The earliest retrograde activation site was located at inferior to inferoseptal mitral annulus, consistent with the presumed location of LPNE. Ablation at the conventional SP region with electroanatomical approach only rendered AVNRT nonsustained without elimination of retrograde SP conduction in seven of eight patients (88%). Ablation targeted to the earliest retrograde atrial activation site within proximal CS (15 ± 4 mm distal to the ostium); however, eliminated retrograde SP conduction and rendered AVNRT noninducible in six of eight patients (75%).
Conclusion: In 75% of "left-variant" atypical AVNRT, ablation within proximal CS was required to eliminate eccentric retrograde SP conduction and render AVNRT noninducible, suggesting LPNE formed retrograde limb of reentrant circuit.     

快速心房起搏时SV间期与SS间期的比值在房室结折返性心动过速慢径消融中的应用

评价快速心房起搏时最快 1∶1房室传导的SV间期 (SV间期 )与 1∶1房室传导的最短S1S1间期 (SS间期 )的比值 (SV/SS)在房室结折返性心动过速 (AVNRT)慢径消融中的应用 ,将AVNRT分为房室结功能曲线连续组 (Ⅰ组 ,10例 )及房室结功能曲线不连续组 (Ⅱ组 ,17例 )测量心房分级递增刺激时的SS间期与SV间期及SV/SS ,并进行消融前、后和组间比较。结果显示 ,两组消融后SV间期较消融前明显缩短 (Ⅰ组 :2 2 1.0± 2 2 .3vs 35 7.0± 43.7ms;Ⅱ组 :2 0 2 .1± 30 .6vs 379.4± 44 .2ms,P均 <0 .0 5 ) ;消融前后SS间期无明显变化 (Ⅰ组 :310 .0± 40 .6vs 30 8.0± 36 .8ms;Ⅱ组 :332 .9± 48.1vs 336 .5± 6 2 .3ms) ;两组中所有患者消融前SV/SS比值均 >1,而消融后SV/SS比值均 <1。结论 :SV/SS可作为慢径消融成功终点的辅助观察指标之一 ,尤其对于房室结传导曲线呈连续性者 ,使用此方法可简便地观察消融终点 ,增加消融的目的性。     

Unmasking of a concealed slow pathway by atrioventricular simultaneous basic pacing

A 71-year-old woman with narrow QRS tachycardia was referred for catheter ablation. The clinical tachycardia was diagnosed as slow/fast form of atrioventricular (AV) nodal reentrant tachycardia (AVNRT) with the upper common pathway. Although neither conventional nor double atrial programmed extrastimulation (APS) showed any evidence of a dual AV nodal pathway, AV simultaneous pacing during basic stimulation preceding APS (AVSP-APS) reproducibly revealed a dual AV nodal pathway as a double ventricular response. The AVSP-APS pacing method may be helpful to unmask a “concealed slow pathway” in patients with AVNRT.     

PR/RR Interval Ratio During Rapid Atrial Pacing:

Method for Confirming Slow Pathway Conduction. Introduction: Although the AV conduction curve in patients with AV nodal reentrant tachycardia (AVNRT) is usually discontinuous, many patients with this arrhythmia do not demonstrate criteria for dual AV nodal pathways. During rapid atrial pacing, the PR interval often exceeds the pacing cycle length when there is anterograde conduction over the slow pathway and AVNRT is induced. The purpose of this prospective study was to determine the diagnostic value of the ratio of the PR interval to the RR interval during rapid atrial pacing as an indicator of anterograde slow pathway conduction in patients undergoing electrophysioiogic testing. Methods and Results: The PR and RR intervals were measured during rapid atrial pacing at the maximum rate with consistent 1:1 AV conduction in four study groups: (1) patients with inducible AV nodal reentry and the classical criterion for dual AV nodal pathways during atrial extrastimulus testing (AVNRT Group 1); (2) patients with inducible AV nodal reentry without dual AV nodal pathways (AVNRT Group 2); (3) control subjects ≤ 60 years of age without inducible AV nodal reentry; and (4) control subjects > 60 years of age without inducible AV nodal reentry. For both groups of patients with inducible AV nodal reentry, AV conduction was assessed before and after radiofrequency ablation of the slow AV nodal pathway. Before slow pathway ablation, the PR/RR ratio exceeded 1.0 in 12 of 13 AVNRT Group 1 patients (mean 1.27 ± 0.21) and 16 of 17 AVNRT Group 2 patients (mean 1.18 ± 0.15, P = NS Group 1 vs Group 2). After slow pathway ablation, the maximum PR/RR ratio was < 1.0 in all AVNRT patients (Group 1 = 0.59 ± 0.08, P < 0. 00001 vs before ablation: Group 2 = 0.67 ± 0.11; P < 0.00001 vs before ablation). Among both groups of control subjects, the PR/RR ratio was > 1.0 in only 3 of 27 patients with no relation to patient age. Conclusion: The ratio of the PR interval to the RR interval during rapid atrial pacing at the maximum rate with consistent 1:1 AV conduction provides a simple and clinically useful method for determining the presence of slow AV nodal pathway conduction. This finding may be particularly useful in patients with inducible AV nodal reentry without dual AV nodal physiology on atrial extrastimulus testing.     

Conversion of typical to "atypical" atrioventricular nodal reentrant tachycardia after radiofrequency catheter modification of the atrioventricular junction.

Typical atrioventricular (AV) nodal reentry tachycardia (AVNRT) is characterized by anterograde activation over a slowly conducting pathway and by retrograde activation through a rapidly conducting pathway. Preliminary reports suggest that radiofrequency catheter modification can eliminate typical AVNRT while preserving anterograde conduction. Radiofrequency catheter modification was used to treat 88 patients with typical AVNRT. After baseline electrophysiologic evaluation, the ablation catheter was positioned proximal and superior to the site of maximal His deflection. Radiofrequency energy was applied until there was significant attenuation of retrograde conduction, and elimination of AVNRT inducibility. Eighty-one patients were successfully treated and form the basis of this report. A new paroxysmal supraventricular tachycardia with RP greater than PR interval was induced at electrophysiologic testing after successful ablation in 9 patients (11%). Mean atrial-His activation time was 140 +/- 31 ms, and the ventriculoatrial activation time was 170 +/- 46 ms. This arrhythmia was induced only with ventricular pacing during isoproterenol infusion and appeared to be mediated by AV nodal reentry. New retrograde dual AV nodal physiology after modification was more frequent in patients with atypical tachycardia than in those without (4 of 9 vs 2 of 72; p less than 0.0001). Although none of the patients were treated, only 1 of 9 had an episode of spontaneous atypical tachycardia during a mean follow-up of 12 months. Results of this study confirm that typical AVNRT can be rendered noninducible without the complete destruction of reentrant pathways. Because induction of "atypical" AVNRT was not predictive of spontaneous arrhythmia recurrence, it should not be an indication for additional ablation sessions or long-term drug therapy.     

Atrioventricular Node Reentrant Tachycardia in Patients With a Prolonged AH Interval During Sinus Rhythm: Clinical Features, Electrophysiologic Characteristics and Results of Radiofrequency Ablation

Among a consecutive series of 600 patients who underwent radiofrequency catheter ablation for AV node reentrant tachycardia, 14 patients (age 29-76 years) had a prolonged AH interval during sinus rhythm (172±18 ms, range 140 to 200). Seven of them had unsuccessful ablation during the previous ablation sessions. Eight patients with anterograde dual AV node pathway physiology received anterograde slow pathway ablation, and the other 6 patients without dual-pathway physiology received retrograde fast pathway ablation. All patients had successful elimination of AV nodal reentrant tachycardia after a mean of 4±4 radiofrequency applications, power level 36±6 watts and a pulse duration of 42±4 seconds. The postablation AH interval remained unchanged. During a follow-up period of 25±13 months, one patient who received slow pathway ablation developed 2:1 AV block with syncope. As compared with the other 586 patients without a prolonged AH interval, these 14 patients had significantly poorer anterograde AV nodal function and lower incidence of anterograde dual AV node physiology (P<0.01). We concluded that slow pathway ablation in patients with dual pathway physiology, and retrograde fast pathway ablation in patients without dual pathway physiology were effective and safe in patients with a prolonged AH interval. However, delayed onset of symptomatic AV block is possible and careful follow-up is necessary.     

Radiofrequency Ablation of a Concealed Nodoventricular Mahaim Fiber Guided by a Discrete Potential

INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.     

Atrioventricular nodal reentry tachycardia in children: curative treatment by high frequency catheter ablation

BACKGROUND: Atrioventricular nodal reentrant tachycardia (AVNRT) is one of the most common forms of supraventricular tachycardia in the pediatric population. PATIENTS AND METHODS: 41 children with a mean age of 9.6 (3.7-16) years with recurrent atrioventricular nodal reentrant tachycardia (AVNRT) refractory to medical treatment (n = 38) and recurrent syncope (n = 3) underwent electrophysiologic (EP) study. In all patients dual AV-nodal physiology could be demonstrated during EP study and typical form of AVNRT (mean heart rate 220/min) could be induced by programmed atrial stimulation. A steerable 7 F ablation catheter was placed at the inferoparaseptal region of the tricuspid valve annulus close to the orifice of the coronary sinus with the intention to record a late fractionated local atrial electrogram during sinus rhythm. Starting at this point radiofrequency current (500 kHz) with a target temperature of 70 degrees C was delivered with the intention to ablate the slow pathway. If a slowly accelerated junctional rhythm (< 120/min) occurred during energy discharge, programmed atrial stimulation was repeated. Otherwise radiofrequency current was delivered step by step up to a septal position next to the tricuspid valve annulus. Slow pathway ablation was defined as lack of evidence of dual AV nodal pathways during repeated atrial stimulation. Slow pathway modulation was defined as maximal one atrial echoimpulse after ablation. RESULTS: The number of energy applications ranged from 1-19 (median 6). In 35/41 patients slow pathway ablation could be achieved; in six patients the slow pathway was modulated. In none of the patients permanent high grade AV block was observed. During follow-up (mean 4.1 years) two patients had a recurrent episode of AVNRT after slow pathway modulation. All other patients are still free of AVNRT without medical treatment. CONCLUSION: Selective radiofrequency current ablation/modulation of the slow pathway is a safe and curative treatment of AVNRT in young patients.     

多型房室结折返性心动过速的机制和射频导管消融

目的分析多型房室结折返性心动过速（AVNRT）并存的电生理机制和射频导管消融结果。方法18例经电生理检查后行射频导管消融的多型AVNRT患者。慢快型和慢慢型AVNRT的消融方法为首选消融前传慢径（房室结右侧后延伸）,快慢型AVNRT的消融方法为消融最早慢径逆传心房激动部位。消融成功的标准为消除1：1前传慢径,消除快慢型AVNRT的逆传慢径,不能诱发任何类型AVNRT。结果11例在消融前的电生理检查中诱发出2种类型AVNRT,均在三尖瓣环与冠状静脉窦口之间（房室结右侧后延伸）成功消融。7例在电生理检查中诱发出1种类型,消融此型后又诱发出另外1种类型,其中4例在房室结右侧后延伸进一步消融成功,另3例均经左侧后延伸进一步消融成功。消融术后随访6个月至8年,18例均无复发。结论对于大多数多型AVNRT,房室结右侧后延伸可能为其折返环的主要基质,消融可成功治愈多型AVNRT。在少部分多型AVNRT中,左侧后延伸与右侧后延伸可能分别作为不Ⅻ类型AVNRT折返环的主要基质,需要分别消融才能成功治愈。