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。     

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.     

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.     

心房起搏时PR与RR间期比值对阵发性室上性心动过速鉴别诊断的意义

为探讨快速心房起搏最短１∶１房室传导时最大ＰＲ间期（ＰＲｍａｘ）与ＲＲ间期比值（ＰＲｍａｘ／ＲＲ）在鉴别阵发性室上性心动过速中的意义，分析比较了２０例房室结折返性心动过速（ＡＶＮＲＴ，有房室结前传跳跃现象者１２例、无跳跃现象者８例）和２０例房室折返性心动过速（ＡＶＲＴ）患者消融前、后快速心房起搏时最短１∶１房室传导的ＰＲｍａｘ／ＲＲ。ＡＶＮＲＴ组消融前、后心房快速起搏时最短１∶１房室传导的ＰＲｍａｘ／ＲＲ为１．１２±０．１２和０．４２±０．０７，两者比较差异有高度显著性，Ｐ＜０．０１；ＡＶＲＴ组为０．５２±０．１６和０．５１±０．１８，两者比较差异无显著性，Ｐ＞０．０５。消融前，ＡＶＮＲＴ组ＰＲｍａｘ／ＲＲ与ＡＶＲＴ组相比有显著性差异（１．１２±０．１２ｖｓ０．５２±０．１６，Ｐ＜０．０１）。ＰＲｍａｘ／ＲＲ＞１诊断ＡＶＮＲＴ的敏感性为９０％、特异性９１％。提示ＰＲｍａｘ／ＲＲ＞１在消融前可用来鉴别ＡＶＮＲＴ与ＡＶＲＴ；对无房室结前传跳跃的ＡＶＮＲＴ，消融后ＰＲｍａｘ／ＲＲ＜１可作为慢径消融成功的指标     

Use of adenosine as a diagnostic tool for dual atrioventricular nodal pathways: response of control patients to incremental doses of adenosine

BACKGROUND: Adenosine at low doses preferentially blocks fast over slow pathway conduction in patients with dual atrioventricular (AV) nodal physiology and typical AV nodal reentrant tachycardia (AVNRT). During atrial pacing, this effect is manifested as an abrupt increase in the AH interval with low doses of adenosine. This demonstration of dual AV nodal physiology may be useful as a diagnostic tool during electrophysiologic studies in patients with supraventricular tachycardia who are not easily inducible, as clear demonstration of dual AV nodal pathways may indicate that AVNRT is a likely diagnosis and that further attempts at arrhythmia induction should be tailored in that direction. However, to be a useful test, adenosine should not cause an abrupt increase in AH interval in patients without dual AV nodal physiology. HYPOTHESIS: This study was designed to investigate the prevalence of dual AV nodal pathways with administration of adenosine in patients with no history suggestive of AVNRT. METHODS: Thirty-seven patients who had no prior history of AVNRT and were undergoing electrophysiologic study for standard indications were enrolled. Baseline Wenckebach cycle length (WCL) and AV nodal effective refractory periods were measured at atrial pacing cycle lengths of 400 and 600 ms. The atrium was then paced at WCL + 50 ms, and WCL + 100 ms, while incrementally larger doses of intravenous adenosine were administered until AV nodal block occurred. RESULTS: The mean (+/- standard deviation) doses of adenosine required to cause AV nodal block while pacing at WCL + 50 ms and WCL + 100 ms were 7.1 +/- 3.9 and 7.4 +/- 4.5 mg, respectively. In 1 of 37 patients (2.7%, 95% confidence interval 0-8%), an abrupt prolongation of the AH interval was seen with the administration of adenosine during atrial pacing as well as during the atrial refractory period determination. In all other patients, no dual AV nodal physiology was demonstrated during the refractory period determination, and there were only gradual changes in the AH interval with atrial pacing during administration of adenosine. CONCLUSION: Among patients with no history suggestive of AV nodal reentrant tachycardia, only 2.7% have clinically silent dual AV nodal pathways using this method. Incremental adenosine infusion during electrophysiologic study can be used as a highly specific diagnostic tool for patients with dual AV nodal pathways.     

Dependence of electrogram duration in right posteroseptal atrium and atrium-pulmonary vein junction on pacing site: mechanism and implications regarding atrioventricular nodal reentrant tachycardia and paroxysmal atrial fibrillation

INTRODUCTION: The fractionated atrial electrogram, a signal helpful in identifying the target site for radiofrequency catheter ablation of the slow AV nodal pathway, is considered to arise from nonuniform anisotropic electrical activity. However, the effects of pacing sites and radiofrequency ablation on these electrograms are not clear. Similarly, the nature of the fractionated atrial electrogram in the atrium-pulmonary vein junction has yet to be determined. METHODS AND RESULTS: Two experiments were performed in this study. Experiment 1 evaluated the fractionated atrial electrogram at target sites before and after slow AV nodal pathway ablation during sinus rhythm or during pacing from different sites. Group 1A consisted of 16 patients with dual AV nodal pathway physiology and AV nodal reentrant tachycardia who underwent successful ablation without residual slow AV nodal pathway. Group 1B consisted of 7 patients who underwent successful elimination of AV nodal reentry but with residual dual AV nodal pathway physiology. Group 1C consisted of 6 patients who still had AV nodal reentrant tachycardia after two applications of radiofrequency energy. In group 1D, there were 16 patients with dual AV nodal pathway physiology, but without inducible AV nodal reentrant tachycardia. In group 1E, there were 15 patients without dual AV nodal pathway physiology. Experiment 2 investigated the fractionated atrial electrogram in the ostium of the left and right superior pulmonary veins in 18 patients with paroxysmal atrial fibrillation (2A) and in 8 patients without paroxysmal atrial fibrillation (2B). Before radiofrequency ablation, electrogram duration in the right posteroseptal atrium during pacing from the middle coronary sinus or the right posterolateral atrium was shorter than that during pacing from the high right atrium (HRA) in all group 1 patients. After the successful elimination of the slow AV nodal pathway conduction in group 1A, atrial electrogram duration during HRA pacing was shorter than that before ablation. In experiment 2 patients, electrogram duration during pacing from the proximal or distal coronary sinus was shorter than that during pacing from HRA or sinus rhythm. CONCLUSION: These findings suggest that the fractionated atrial electrograms in the right posteroseptal atrium and ostium of left or right superior pulmonary veins are potentially consistent with nonuniform anisotropic propagation. Alternations of electrogram characteristics after successful radiofrequency ablation of the slow AV nodal pathway may arise from the changes of nonuniform anisotropic activity in the right posteroseptal atrium.     

The Electrophysiologic Characteristics in Patients with Only Ventricular-Pacing Inducible Slow–Fast Form Atrioventricular Nodal Reentrant Tachycardia

Background: Atrioventricular nodal reentrant tachycardia (AVNRT) can be usually induced by atrial pacing or extrastimulation. However, it is less commonly induced only by ventricular pacing or extrastimulation. Objective: The purpose of this retrospective study was to investigate the electrophysiologic characteristics in patients with slow–fast form AVNRT that could be induced only by ventricular pacing or extrastimulation. Methods: The total population was 1497 patients associated with AVNRT. There were 1373 (91.7%) patients who had slow–fast form AVNRT included in our study. Group 1 (n = 45) could be induced only by ventricular pacing or extrastimulation, and Group 2 (n = 1328) could be induced by only atrial stimulation or both atrial and ventricular stimulation. The electrophysiologic characteristics of the group 1 and group 2 patients were compared. Results: Group 1 patients had a significantly lower incidence of both antegrade and retrograde dual AV nodal pathways. The pacing cycle length (CL) of the antegrade 1:1 fast pathway (FP) and antegrade ERP of the FP were both significantly shorter in Group 1 patients. Mean antegrade FRP of the fast and slow pathways were significantly shorter in Group 1 patients. The differences of pacing CL of 1:1 antegrade conduction, antegrade ERP and FRP were much longer in Group 2 patients. Conclusion: This study demonstrated the patients with slow–fast form AVNRT that could be induced only by ventricular stimulation had a lower incidence of dual AV nodal pathways and the different electrophysiologic characteristics (shorter pacing CL of the antegrade 1:1 FP, antegrade ERP of the FP and the differences of pacing CL of 1:1 antegrade conduction, antegrade ERP and FRP) from the other patients. The specific electrophysiologic characteristics in such patients could be the reason that could be induced only by ventricular stimulation.     

Single Radiofrequency Application to Cure Atrioventricular Nodal Reentry: Arguments for the Slow Pathway Origin of the High-Low Frequency Slow Potentials

Background: High-low frequency slow potentials are thought to be related to the slow AV pathway conduction. Their use was proposed to guide radiofrequency (RF) ablation of atrioventricular nodal reentrant tachycardia (AVNRT). The present study was designed to determine the prospective value of these high-low frequency slow potentials to guide AVNRT ablation using a single RF application. Single RF application could indeed reduce the size of the lesion created in the viciny of the specialized AV conduction system and shorten the radiation exposure and the overall duration of the procedure.Results: Forty-one patients (14 men, 27 women, 45&plusmn;16 years old) with AVNRT underwent slow pathway RF ablation guided by high-low frequency slow potentials. High-low frequency slow potentials were found in all patients along the tricuspid annulus and above the coronary sinus. Ablation was always performed in the posterior part of Koch's triangle. The mean A/V amplitude ratio of the successful site was 0.43&plusmn;0.59. In 32 patients (78%) AVNRT was no longer inducible after a single RF application. Procedure and radiation times were 35&plusmn;31 and 13&plusmn;12 min respectively. Five patients required 2, 3 patients 3, and 1 patient 6 RF applications. The mean number of RF applications was 1.4&plusmn;0.9 (median &equals; 1). In the 32 patients who required only one RF application, 24 (75%) had an obvious dual AV nodal pathways with a jump before ablation, wich completely disappeared in 18 of them (75%) after ablation. In the 6 remaining patients, who still had a jump after 1 RF application, there was no significant change in either conduction times or refractory periods concerning both the anterograde and retrograde AV conduction. No patient had PR interval purlongation. After a mean follow up of 11&plusmn;5 months, recurrence was observed in a single patient who received 2 discontinued RF applications.Conclusion: Catheter-mediated ablation of AVNRT using high-low frequency slow potentials to localize the slow AV pathway is feasible and safe. Using this technique, a single RF application was successfull in 78% of patients, and slow pathway characteristics were completely eliminated in 75% of patients. The radiation time and the procedure duration were short. This suggest that, in patients with AVNRT, the choice of an appropriate RF target can reduce procedural duration.     

Ablation for atrioventricular nodal reentrant tachycardia with a prolonged PR interval during sinus rhythm: the risk of delayed higher-degree atrioventricular block

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

Atrioventricular Nodal Reentry Tachycardia in Patients with Sinus Node Dysfunction: Electrophysiologic Characteristics, Clinical Presentation, and Results of Slow Pathway Ablation

AVNRT and Sinus Node Dysfunction. Introduction: Sinus node dysfunction (SND) is frequently associated with impaired AV conduction. This study investigated the electrophysiologic properties of dual AV nodal pathways in patients suffering from both SND and AV nodal reentrant tachycardia (AVNRT). Methods and Results: Two groups of patients with slow-fast AVNRT underwent invasive electrophysiologic testing and catheter ablation of the slow pathway. Group A comprised 10 patients with SND (age 70 ± 8 years), (Group B included 10 age-matched patients without SND (age 69 ± 7 years; P = NS) who served as controls. Patients of group A exhibited prolongation of the anterograde Wenckebach cycle lengths (WBCLs) of both the fast pathway (559 ± 96 vs 361 ± 38 msec; P < 0.01) and the slow pathway (409 ± 57 vs 339 ± 32 ms; P < 0.01). However, the delta between the WBCLs of the fast and the slow pathways was larger in patients of group A (150 ± 80 vs 22 ± 20 msec; P < 0.01). Retrograde fast pathway conduction was well preserved with no difference in WBCLs (356 ± 42 vs 330 ± 47 msec; P = NS). Cycle lengths of AVNRT were longer in group A (468 ± 46 vs 363 ± 37 msec; P < 0.01). Clinically, all patients of group A suffered from multiple episodes of AVNRT per week, which was not the case in any patient of group B (P < 0.01). Catheter ablation of the slow pathway eliminated AVNRT in all patients without complications. Conclusions: Patients with AVNRT and SND exhibit characteristic electrophysiologic alterations of both AV nodal pathways. Clinically, this results in significantly more frequent episodes of tachycardia. Slow pathway ablation appears to be safe and effective in these patients.     

Maturational atrioventricular nodal physiology in the mouse

INTRODUCTION: Dual AV nodal physiology is characterized by discontinuous conduction from the atrium to His bundle during programmed atrial extrastimulus testing (A2V2 conduction curves), AV nodal echo beats, and induction of AV nodal reentry tachycardia (AVNRT). The purpose of this study was to characterize in vivo murine maturational AV nodal conduction properties and determine the frequency of dual AV nodal physiology and inducible AVNRT. METHODS AND RESULTS: A complete transvenous in vivo electrophysiologic study was performed on 30 immature and 19 mature mice. Assessment of AV nodal conduction included (1) surface ECG and intracardiac atrial and ventricular electrograms; (2) decremental atrial pacing to the point of Wenckebach block and 2:1 conduction; and (3) programmed premature atrial extrastimuli to determine AV effective refractory periods (AVERP), construct A2V2 conduction curves, and attempt arrhythmia induction. The mean Wenckebach block interval was 73 +/- 12 msec, 2:1 block pacing cycle length was 61 +/- 11 msec, and mean AVERP100 was 54 +/- 11 msec. The frequency of dual AV nodal physiology increased with chronologic age, with discontinuous A2V2 conduction curves or AV nodal echo beats in 27% of young mice < 8 weeks and 58% in adult mice (P = 0.03). CONCLUSION: These data suggest that mice, similar to humans, have maturation of AV nodal physiology, but they do not have inducible AVNRT. Characterization of murine electrophysiology may be of value in studying genetically modified animals with AV conduction abnormalities. Furthermore, extrapolation to humans may help explain the relative rarity of AVNRT in the younger pediatric population.     

Concealed conduction and dual pathway physiology of the atrioventricular node

INTRODUCTION: Both concealed conduction and dual pathway physiology are important electrophysiologic characteristics of the AV node. The interaction of AV nodal concealment and duality, however, is not clearly understood. METHODS AND RESULTS: The properties of AV conduction curves in the presence and absence of a conditioning blocked impulse were prospectively studied during premature atrial stimulation in 20 patients with AV nodal reentrant tachycardia before and after slow pathway ablation and in 14 control patients. AV nodal duality in the control conduction curve in the absence of a conditioning impulse was observed in 19 (95%) of 20 patients with AV nodal reentrant tachycardia. However, AV nodal duality in the modulated conduction curve in the presence of a blocked impulse was only identified in 2 (10%) of 20 patients (2/20 vs 19/20, P < 0.0001). The modulated curve was characterized by a significantly longer AV nodal effective and functional refractory periods compared to the control curve (P < 0.0001) in both patients with and without AV nodal reentry and in AV nodal reentry patients after successful slow pathway ablation. The maximum AH interval (AH(max)) of the modulated curve was significantly shorter than the control curve in both patients with (217 +/- 74 ms vs 347 +/- 55 ms, P < 0.0001) and without AV nodal reentry (178 +/- 50 ms vs 214 +/- 54 ms, P = 0.02). AH(max) of the control curve was significantly longer in AV nodal reentry patients than in controls (P < 0.0001). AH(max) of the modulated curve, however, was not significantly different between the two groups. After slow pathway ablation, AH(max) of the control curve was significantly reduced (347 +/- 55 ms vs 191 +/- 40 ms, P < 0.0001). Significant reduction in AH(max) of the modulated curve was not observed. CONCLUSION: An interaction of AV nodal concealed conduction and dual pathway physiology was demonstrated by our data. Slow pathway conduction of the AV node was prevented by the concealed beat in both patients with and without AV nodal reentry.     

房室结折返性心动过速患者房室结功能曲线连续性的电生理分析

分析房室结折返性心动过速 (AVNRT)中房室结功能曲线呈连续性者的电生理特点。将AVNRT分为房室结功能曲线连续组 (Ⅰ组 )及房室结功能曲线不连续组 (Ⅱ组 ) ,行慢径消融 ,进行消融前后和组间的电生理比较 ,分析房室结功能曲线呈连续性者的特点。结果 :I组心房程序刺激对AVNRT的诱发率仅 42 % (5 / 12 ) ,低于Ⅱ组的 6 6 %(2 3/ 35 )。Ⅰ组房室结前传有效不应期 (ERP AVN)消融前后无显著变化 (2 18.2± 2 9.3msvs 2 5 3.3± 80 .3ms,P >0 .0 5 ) ;心房程序刺激最长A2 H2 间期 (AHmax)消融前后无显著变化 (2 2 5 .8± 71.8msvs 175 .4± 41.9ms,P >0 .0 5 )。Ⅱ组ERP AVN消融后显著延长 (2 78.9± 5 8.9msvs 2 35 .8± 39.6ms,P <0 .0 5 ) ;AHmax消融后显著缩短 (172 .0± 6 7.1msvs 331.6± 86 .6ms ,P <0 .0 5 ) ;消融后房室结快径前传有效不应期 (ERP FP)显著缩短 (2 78.9± 5 8.9msvs 330 .0±5 5 .3ms,P <0 .0 5 )。消融前Ⅰ组AHmax短于Ⅱ组 (P <0 .0 5 ) ,Ⅰ组心动过速时A2 H2 间期 (AHSVT)与消融前AHmax比较差异无显著性 (P >0 .0 5 ) ;Ⅱ组AHSVT短于消融前AHmax(P <0 .0 5 )。结论 :房室结功能曲线连续性者较难经常规心房程序刺激诱发心动过速 ;慢径消融后曲线“尾巴”消失可作为消融终点的一项指     

Effects of Slow Pathway Ablation on Fast Pathway Function in Patients with Atrioventricular Nodal Reentrant Tachycardia

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

Cryoablation in pediatric atrioventricular nodal reentry: Electrophysiologic effects on atrioventricular nodal conduction

BACKGROUND: Cryoablation for treatment of atrioventricular nodal reentrant tachycardia (AVNRT) is safe and efficacious. Information on the effects of cryoablation on atrioventricular (AV) nodal conduction is limited. OBJECTIVES: The purpose of this study was to evaluate the effects of cryoablation on AV nodal conduction in pediatric patients with AVNRT. METHODS: We retrospectively analyzed electrophysiologic studies before and after successful cryoablation. Patients were divided into two groups: group 1 (n = 22, age 14 +/- 3 years) had baseline discontinuous atrial-to-His interval (AH) conduction curves; and group 2 (n = 13, age 12 +/- 4 years, P = .054) had continuous curves. RESULTS: At baseline, group 1 had longer measurements of maximal AH with A1A2, AV nodal effective refractory period, and AV block cycle length. Postcryoablation, both group 1 and group 2 showed decreases in maximal AH with A1A2 pacing or atrial overdrive pacing and in the finding of PR > or = RR with atrial overdrive pacing (group 1: 55% vs 5%, P < .001; group 2: 69% vs 0%, P < .001). A significant increase in overall AV effective refractory period and a decrease in AV block cycle length were found in group 1 but not group 2. Fifty percent of group 1 patients had complete abolition of slow pathway conduction. CONCLUSION: Successful cryoablation for treatment of AVNRT is associated with a reduction in PR > or = RR and with decreases in maximal AH with A1A2 pacing or atrial overdrive pacing. Further study is needed to determine the usefulness of these parameters for assessment of ablation efficacy or as proxies for AVNRT inducibility.     

Slowing of the Ventricular Rate During Atrial Fibrillation by Ablation of the Slow Pathway of AV Nodal Reentrant Tachycardia

Influence of Slow Pathway Ablation on Atrial Fibrillation. Introduction : The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well-defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.
Methods and Results : In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P < 0.01), 673 ± 161 (P < 0.01), and 535 ± 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P < 0.05) immediately and to 400 ± 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P < 0.05), respectively.
Conclusion : This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node.     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

Differential Effects of Atropine and Isoproterenol on Inducibility of Atrioventricular Nodal Reentrant Tachycardia

Background: 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. Methods: 80 patients (57 women, 23 men, age 50±14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01mg/kg atropine or 0.5-1.0g/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. Results: 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±48ms vs. 374±113ms, P=0.012). Conclusion: 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 in children: effect of slow pathway ablation on fast pathway function

INTRODUCTION: Prior studies in adults have shown significant shortening of the fast pathway effective refractory period after successful slow pathway ablation. As differences between adults and children exist in other characteristics of AV nodal reentrant tachycardia (AVNRT), we sought to characterize the effect of slow pathway ablation or modification in a multicenter study of pediatric patients. METHODS AND RESULTS: Data from procedures in pediatric patients were gathered retrospectively from five institutions. Entry criteria were age <21 years, typical AVNRT inducible with/without isoproterenol infusion, and attempted slow pathway ablation or modification. Dual AV nodal pathways were defined as those with > or =50 msec jump in A2-H2 with a 10-msec decrease in A1-A2. Successful ablation was defined as elimination of AVNRT inducibility. A total of 159 patients (age 4.4 to 21 years, mean 13.1) were studied and had attempted slow pathway ablation. AVNRT was inducible in the baseline state in 74 (47%) of 159 patients and with isoproterenol in the remainder. Dual AV nodal pathways were noted in 98 (62%) of 159 patients in the baseline state. Ablation was successful in 154 (97%) of 159 patients. In patients with dual AV nodal pathways and successful slow pathway ablation, the mean fast pathway effective refractory period was 343+/-68 msec before ablation and 263+/-64 msec after ablation. Mean decrease in the fast pathway effective refractory period was 81+/-82 msec (P < 0.0001) and was not explained by changes in autonomic tone, as measured by changes in sinus cycle length during the ablation procedure. Electrophysiologic measurements were correlated with age. Fast pathway effective refractory period was related to age both before (P = 0.0044) and after ablation (P < 0.0001). AV block cycle length was related to age both before (P = 0.0005) and after ablation (P < 0.0001). However, in dual AV nodal pathway patients, the magnitude of change in the fast pathway effective refractory period after ablation was not related to age. CONCLUSION: Lack of clear dual AV node physiology is common in pediatric patients with inducible AVNRT (38%). Fast pathway effective refractory period shortens substantially in response to slow pathway ablation. The magnitude of change is large compared with adult reports and is not completely explained by changes in autonomic tone. Prospective studies in children using autonomic blockade are needed.     

程控刺激不能诱发的房室结折返性心动过速慢径消融的临床疗效评估

目的　评价程控刺激不能诱发的房室结折返性心动过速 (AVNRT)射频消融慢径的临床疗效。方法　 6 1例有心动过速病史且心电图疑诊为AVNRT的病人 ,电生理检查有房室结双径(DAVNP)但不能诱发AVNRT ,随机分为两组。A组 30例不消融而进行临床随访 ,当心动过速复发且经心电图证实为窄QRS心动过速者接受射频消融阻断慢径。B组 31例接受射频消融以阻断慢径 ,术后临床随访。结果　A、B两组分别有 2 4例和 2 7例病人完成随访。A组 2 4例随访中分别在 1年内发作心动过速 ,再次接受消融阻断慢径后随访 (12 .1± 12 .2 )个月 ,仅 1例复发心动过速 (4.2 % ) ,与消融前比较差异有显著性 (P <0 .0 0 0 1)。B组 2 7例平均随访 (2 4 .2± 17.6 )个月 ,1例复发心动过速 (3.7% ) ,与A组病人消融前相比差异有显著性 (P <0 .0 0 0 1) ,而与其消融后比较差异无显著性 (P >0 .0 5 )。结论　有阵发性心动过速病史且心电图疑诊为AVNRT的病人 ,电生理检查有DAVNP而不能诱发心动过速者 ,射频消融阻断慢径具有良好的临床疗效。