Supraventricular tachyarrhythmias: Drug therapy versus catheter ablation

Until recently, the only options available for treatment of supraventricular arrhythmias involved the use of drug therapy or cardiac surgery. However, over the past several years with the introduction of radiofrequency energy sources as well as steerable catheters, the clinician has a variety of additional nonpharmacologic options. This article reviews the use of pharmacologic therapy versus catheter ablation for the treatment of reentrant supraventricular arrhythmias, involving the atrioventricular junction and/or accessory atrioventricular connection, as well as arrhythmias emanating from the atria such as atrial fibrillation, atrial flutter, and atrial tachycardia.     

Radiofrequency Current Catheter Ablation for Control of Supraventricular Arrhythmias

Radiofrequency Catheter Ablation in SVT. With the advent of radiofrequency energy, catheter ablation techniques have become an accepted form of treatment for a variety of Supraventricular arrhythmias. The ablation of the atrioventricular (AV) node was performed first and is now widely used in patients with refractory atrial fibrillation or flutter. Ablation has also replaced surgery in patients with preexcitation syndromes, and as the complication rate in experienced centers is low, it has become the first line of treatment in these institutions. The results of catheter ablation in AV nodal reentrant tachycardia are excellent as well, although there is still debate about whether "slow" pathway ablation is superior to "fast" pathway ablation. Radiofrequency current ablation has also contributed to a better understanding of the pathophysiology of AV nodal reentrant tachycardia, as it has provided evidence for atrial participation in the reentrant circuit. Experience with atrial tachycardias and tachycardias due to Mahaim fibers remains limited. The ideal source of energy for specific arrhythmias is still unknown and improvement in catheter technology is needed.     

Use of Propafenone in Patients With Supraventricular Tachycardia

Propafenone prolongs refractoriness and slows conduction of the atrium, atrioventricular node, and accessory atrioventricular pathway. By interfering with conduction in locations necessary to support supraventricular tachycardia, propafenone effectively treats several mechanisms of rhythm disturbance. Early experience shows that propafenone, when administered in the electrophysiology laboratory, effectively terminates or prevents reinduction of paroxysmal supraventricular reentrant tachycardia in 50% to 75% of patients. The most effective dose associated with the fewest side effects has been 2 mg/kg infused over 10 minutes. Long-term success with propafenone has been demonstrated in patients with paroxysmal atrial fibrillation, paroxysmal atrial flutter, atrioventricular node reentrant tachycardia, atrioventricular reentrant tachycardia using a concealed accessory pathway, and tachycardias associated with the Wolff-Parkinson-White syndrome, including paroxysmal atrial fibrillation and atrioventricular reentrant tachycardia. In 67% (range, 27% to 89%) of patients receiving long-term therapy with propafenone, episodes of supraventricular tachycardia have been either eliminated or significantly reduced in frequency and treatment has not had to be stopped because of side effects. The effective daily dose for longterm therapy has been 550 to 750 mg administered in three or four divided doses. Although the number of patients reported in the literature at this time is small, propafenone appears to be an effective agent for treating supraventricular tachycardia due to one of several mechanisms.     

Laser catheter ablation of atrial flutter and of atrioventricular nodal reentrant tachycardia in a single session

This report describes an adolescent with refractory atrial flutter(AF) and atrioventricular (AV) nodal reentrant tachycardia whowas cured by Nd: YAG, 1064 nm, laser application. Two impactsof 30 s each (power 30 W and irradiated spot diameter 2.0–2.5mm), applied via a novel laser catheter system, abolished bothAF and AV nodal reentrant tachycardia. The procedure was withoutcomplications or recurrent arrhythmias.     

Pathological Findings Following Slow Pathway Ablation for AV Nodal Reentrant Tachycardia

Pathology of Slow Pathway Ablation. Introduction : AV nodal reentrant tachycardia is routinely cured using radiofrequency catheter ablation techniques. However, there remains controversy as to whether the reentrant circuit for this tachycardia exists solely in the AV node or whether perinodal atrial tissues are vital to the circuit. In addition, the effects of radiofrequency ablation of the slow pathway of AV nodal reentrant tachycardia on the AV node are not known. We examined an autopsy specimen to determine the anatomical location and extent of AV nodal damage of radiofrequency slow pathway ablation for cure of AV nodal reentrant tachycardia.
Methods and Results : A 64-year-old woman with confirmed AV nodal reentrant tachycardia underwent a successful "slow pathway" AV modification with a single radiofrequency application. Five months after the procedure, the patient died from a spontaneous intracranial hemorrhage. Postmortem gross pathological examination of the heart was performed. The heart was then sectioned and stained for histologic examination. On gross examination, a pale lesion 0.5 cm in diameter was seen on the endocardial surface adjacent to the tricuspid annulus. approximately 0.85 cm anterior to the coronary sinus os and 1.15 cm from the apex of the triangle of Koch where the AV node resides. Histologic examination revealed a right atrial lesion composed of connective tissue and fat. The compact AV node and surrounding transitional cells were unaffected histologically, with normal atrial cells lying between the AV node and the lesion.
Conclusion : Ablation of the slow pathway to cure AV nodal reentrant tachycardia does not produce any gross or histologic damage to the AV node, suggesting that the AV nodal reentrant circuit does not exist in its entirety in the AV node.     

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.     

Elimination of AV Nodal Reentrant Tachycardia with 2:1 VA Block by Posteroseptal Ablation

AV Nodal Reentrant Tachycardia. AV nodal reentry capable of VA block during tachycardia was successfully eliminated using a posteroseptal ablation pulse delivered well away from the site of earliest atrial activation during tachycardia. A possible explanation is that the arrhythmia represented typical AV nodal reentrant tachycardia with transient intra atrial conduction block during tachycardia.     

NASPE Plenary Lecture 2001. Catheter ablation: a personal perspective

Catheter ablation for control of cardiac arrhythmias was introduced 20 years ago. Since then, this technique has been applied successfully to virtually all cardiac rhythm disturbances. In this essay, some of the newer applications of ablative techniques for patients with AV nodal reentrant tachycardia, atrial flutter, and atrial fibrillation are emphasized. "AV nodal reentrant tachycardia" may involve a nodofascicular tract. A new classification of atrial flutter is proposed and various causes of atrial fibrillation are discussed.     

Double Retrograde Atrial Response After Radiofrequency Ablation of Typical AV Nodal Reentrant Tachycardia

Double Atrial Response. This case report describes a patient in whom a single ventricular depolarization resulted in a double atrial response and the initiation of atypical A V nodal reentrant tachycardia after successful radiofrequency ablation of typical AV nodal reentrant tachycardia using the slow pathway approach. (J Cardiovasc Electrophysiol, Vol. 4, pp. 695–701, December 1993)     

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.     

AV nodal reentrant tachycardia using three different AV nodal pathways

In a patient with frequent paroxysmal supraventricular tachycardia, an electrophysiologic study was performed. Although by programmed atrial stimulation only double AV nodal pathways could be documented, three distinct forms of AV nodal reentrant tachycardia could be induced. By programmed atrial stimulation a typical AV nodal reentrant tachycardia was initiated, by programmed ventricular stimulation, an AV nodal reentrant tachycardia was induced with an antegrade conduction time of 215 ms and a retrograde conduction time of 160 ms. Furthermore, a third form of tachycardia was induced with alternating cycle length due to two different antegrade conduction times, whereas retrograde conduction time was almost identical, irrespective of the antegrade conduction time. The patient received betaxolol (20 mg day-1); during a second electrophysiologic study, the tachycardia could not be induced, and it did not occur spontaneously during a follow-up period of 14 months.     

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.     

Typical atrioventricular nodal reentrant tachycardia in a patient with fasciculoventricular pathway

We report a 34-year-old female patient with preexcitation electrocardiogram and recurrent paroxysmal palpitations. Standard 12-lead electrocardiogram showed minimal preexcitation with normal PR interval and normal frontal QRS axis. The electrophysiologic study showed normal AH intervals, short HV intervals, and no change in the degree of preexcitation by rapid atrial pacing. These findings were compatible with the fasciculoventricular pathway. Typical atrioventricular nodal reentrant tachycardia with narrow QRS complex and normal HV interval was induced reproducibly by programmed electrical stimulation. Slow pathway was ablated successfully with radiofrequency catheter ablation, and then the patient remained asymptomatic during a follow-up of 12 months. Although the fasciculoventricular pathway is rare and supraventricular tachycardia in a patient with fasciculoventricular pathway may mimic Wolff-Parkinson-White syndrome, possibility of typical atrioventricular nodal reentrant tachycardia with fasciculoventricular pathway should be considered as a mechanism of supraventricular tachycardia in a patient showing preexcitation electrocardiogram.     

Atypical Atrioventricular Nodal Reentry Tachycardia with Atrioventricular Block Mimicking Atrial Tachycardia:

AVNRT Mimicking Atrial Tachycardia, Introduction : Fast-intermediate form AV nodal reentry tachycardia (AVNRT) sometimes may mimic atrial tachycardia or atrial flutter and render the diagnosis difficult when the tachycardia rate is fast and AV block occurs during tachycardia.
Methods and Results : A 45-year-old woman with paroxysmal supraventricular tachycardia was referred to this institution. Initially, the tachycardia was thought to be an atrial tachycardia because of: (1) a short cycle length of the tachycardia with 2:1 and Wenckebach AV block; (2) a difference in the atrial activation sequence during tachycardia and during ventricular pacing; and (3) failure of burst ventricular pacing to affect the atrial rate and the atrial activation sequence during tachycardia. An accurate diagnosis of fast-intermediate form AVNRT was subsequently made based on the finding that the tachycardia was induced following delivery of a third ventricular extrastimulus, which showed a sequence of V-A-H and a change on atrial activation sequence of the induced beat. Successful radiofrequency ablation was achieved only after accurate diagnosis of the tachycardia was made.
Conclusion : Fast-intermediate form AVNRT sometimes may masquerade as atrial tachycardia. Accurate diagnosis is mandatory for successful ablation therapy.     

食管心房调搏对室上性心动过速诊断的准确性评价

评价食管电生理检查对室上性心动过速诊断的准确性。方法 比较102例室上性心动过速经心内和食管电生理检查的结果。结果 102例室上性心动过速101例分型诊断一致：房室折返性心运过速（AVRT）58例,房室结折返性心运过速（AVNRT）37例,房内折返性心动过速（IART）5例,窦房结折返性心动过速（SART）1例,房性自律性心动过速（AAT）1例。6例房性心动过速（IART5例,AAT1例）起源于右房还是左房和57例房室折返性心动过速的旁路位于右侧还是左侧,两种检查结果完全一致。结论 食管心房调搏对室上性心动过速的分型诊断和初步定位诊断具有很高的准确性,这对选择射频消融术病例和简化消融术程序具有重要意义。     

食管心房调搏诊断室上性心动过速的临床研究

为探讨食管心房调搏揭示室上性心动过速发生机制的价值和局限性,回顾性分析成功射频导管消融的１３８例隐匿性单房室旁道参与的顺向型房室折返性心动过速和１００例单一类型房室结折返性心动过速的食管心房调搏结果。结果显示：前１３８例中,３例前间隔旁道引起者食管心房调搏均诊断为房室结折返性心动过速余为左右侧其它部位的旁道,诊断正确。后１００例中,５例为慢－慢型,２例为快－慢型,食管心房调搏均诊断为房室折返性心动     

Incidence and clinical significance of inducible atrial tachycardia in patients with atrioventricular nodal reentrant tachycardia

INTRODUCTION: The purpose of this prospective study was to determine the prevalence and clinical significance of inducible atrial tachycardia in patients undergoing slow pathway ablation for AV nodal reentrant tachycardia who did not have clinically documented episodes of atrial tachycardia. METHODS AND RESULTS: Twenty-seven (15%) of 176 consecutive patients who underwent slow pathway ablation for AV nodal reentrant tachycardia were found to have inducible atrial tachycardia with a mean cycle length of 351+/-95 msec. The atrial tachycardia was sustained in 7 (26%) of 27 patients and was isoproterenol dependent in 20 patients (74%). The atrial tachycardia was not ablated or treated with medications, and the patients were followed for 9.7+/-5.8 months. Six (22%) of the 27 patients experienced recurrent palpitations during follow-up. In one patient each, the palpitations were found to be due to sustained atrial tachycardia, nonsustained atrial tachycardia, recurrence of AV nodal reentrant tachycardia, paroxysmal atrial fibrillation, sinus tachycardia, and frequent atrial premature depolarizations. Thus, only 2 (7%) of 27 patients with inducible atrial tachycardia later developed symptoms attributable to atrial tachycardia. CONCLUSION: Atrial tachycardia may be induced by atrial pacing in 15% of patients with AV nodal reentrant tachycardia. Because the vast majority of patients do not experience symptomatic atrial tachycardia during follow-up, treatment for atrial tachycardia should be deferred and limited to the occasional patient who later develops symptomatic atrial tachycardia.     

Atrioventricular junctional reentrant tachycardia utilizing multiple retrograde fibers during ablation of the slow pathway

This report deals with a patient with atrioventricular (AV) reentrant junctional tachycardia who, during radiofrequency ablation of her slow pathway, developed both anterior and posterior type of slow-fast atrioventricular nodal reentry; in both tachycardias different fibers were alternately utilized for retrograde conduction, thus resulting in alternating tachycardia cycle lengths. This observation provides further evidence in favor of the multifiber structure of the AV node in patients with AV reentrant junctional tachycardia.     

Paroxysmal supraventricular tachycardia with persistent ventriculoatrial block

We report the case of a 64-year-old patient with paroxysmal supraventricular tachycardia and persistent VA block. Induction and maintenance of tachycardia occurred without apparent activation of the atria. Diagnostic characteristics were most compatible with AV nodal reentrant tachycardia (AVNRT). Automatic junctional tachycardia and orthodromic nodoventricular or nodofascicular reentry tachycardia were considered in the differential diagnosis. Upper common pathway block during AVNRT may be explained by either intra-atrial conduction block or purely intranodal confined AVNRT. The arrhythmia was cured by a typical posteroseptal ablation approach guided by slow pathway potentials.