Inducible Atrioventricular Nodal Reentrant Tachycardia Research Articles

Effects of partial and complete ablation of the slow pathway on fast pathway properties in patients with atrioventricular nodal reentrant tachycardia.

The purpose of this study was to prospectively compare the effects of complete and partial ablation of slow pathway function on the fast pathway effective refractory period (ERP). The subjects were 20 patients (mean age 43 +/- 13 years) with atrioventricular nodal reentrant tachycardia (AVNRT), no structural heart disease, and easily inducible AVNRT. Autonomic blockade was achieved with propranolol (0.2 mg/kg) and atropine (0.04 mg/kg). After elimination of AVNRT and during autonomic blockade, the presence of residual slow pathway function was determined by the presence of a single AV nodal echo and/or dual AV nodal physiology. After autonomic blockade and before ablation, the mean fast pathway ERP was 319 +/- 44 msec and the mean slow pathway ERP was 251 +/- 31 msec. After slow pathway ablation and during autonomic blockade, 7 patients had residual slow pathway function and 13 did not. Complete loss of slow pathway function was associated with a shortening of the fast pathway ERP from 334 +/- 35 msec to 300 +/- 62 msec (P < 0.01), while the fast pathway ERP did not change significantly in patients with residual slow pathway function (291 +/- 29 msec vs 303 +/- 38 msec, respectively; P = 0.08). A shortening of 30 msec or more in the fast pathway ERP was observed in 11 of 13 patients who did not have residual slow pathway function, compared to 0 of 7 patients with residual slow pathway function (P < 0.001). Shortening of the fast pathway ERP after successful ablation of AVNRT is dependent upon complete loss of slow pathway function. This observation is consistent with electrotonic inhibition of the fast pathway by the slow pathway.

Predictors of recurrent atrioventricular nodal reentry after selective slow pathway ablation

Although radiofrequency catheter ablation of the slow atrioventricular (AV) nodal pathway is highly effective for the management of AV nodal reentrant tachycardia (AVNRT), this arrhythmia may recur in some patients after an ablation procedure that initially renders AVNRT noninducible. A retrospective study examined the factors that are associated with the recurrence of AVNRT after selective radiofrequency catheter ablation of the slow pathway. Patients were included in the study if they had initially inducible, typical slow-fast AVNRT that was noninducible at the end of the ablation session. Selective ablation of the slow pathway was performed using radiofrequency energy applied along the tricuspid annulus near the coronary sinus ostium. AVNRT recurred after initially successful slow pathway ablation in 10 of 136 patients (7.4%) over a mean follow-up period of 20.1 ± 5.0 months; the time to recurrence ranged from 1 to 411 days. Despite the absence of inducible AVNRT, dual anterograde AV nodal conduction properties persisted after slow pathway ablation in 10 patients AVNRT recurred in 4 of 10 patients who had evidence of residual slow pathway conduction compared with only 6 of 126 who had no residual slow pathway conduction (p = 0.003). All patients with persistent slow pathway conduction and recurrent AVNRT also had residual AV nodal echo beats. AVNRT recurred in 3 of 6 patients without accelerated junctional tachycardia during radiofrequency application compared with only 7 of 109 with accelerated junctional tachycardia (p = 0.003). Thus, AVNRT infrequently recurs after successful selective radiofrequency ablation of the slow pathway. The presence of residual slow pathway conduction and AV nodal echo beats after ablation is associated with an increased risk of recurrent AVNRT.

Elimination of slow pathway conduction: An accurate indicator of clinical success after radiofrequency atrioventricular node modification

Objectives. The purpose of this study was to determine the optimal end point of radiofrequency atrioventricular (AV) node modification using anatomically guided slow pafhway approaches in patients with AV node reentrant tachycardia.Background. The optimal end point for AV node modification using radiofrequency energy is uncertain, although elimination of inducible AV node reentrant tachycardia has been used.Methods. We followed up 51 consecutive patients (40 women, 11 men, mean age ± SD 41 ± 16 years) with symptomatic AV node reentrant tachycardia for 12 ± 6 months (range 4 to 24) after radiofrequency AV node modification using an anatomically guided slow pathway approach. Inducible AV node reentrant tachycardia was eliminated in all patients, whereas residual slow pathway conduction persisted in 12 patients (24%) after ablation. One study was complicated by complete AV block and two patients were lost to follow-up (one with and one without residual slow pathway conduction).Results. Clinical recurrence of AV node reentrant tachycardia was documented in seven patients (14%) 3 days to 3 months (median 1 month) after ablation. The recurrence rate was significantly higher in patients with than in those without residual slow pathway conduction (6 [55%] of 11 vs. 1 [3%] of 37, p < 0.01). The recurrence rate was not different between patients with only residual slow pathway conduction and those with residual slow pathway conduction and inducible single echo cycles (three [60%] of five in both groups, p = NS). The number of radiofrequency energy applications was not significantly different between those without and those with recurrence (20 ± 17 vs. 16 ± 9, p = NS). Junctional tachycardia during application of radiofrequency energy tended to be more frequently observed in those with a successful outcome (77% vs. 57%, p > 0.05). Of the 22 who underwent modification before 1992, residual slow pathway conduction was present in 9 (41%) of 22 patients. Atrioventricular node reentrant tachycardia recurred in five (56%) of these nine patients. A greater effort made in 1992 to eliminate slow pathway conduction in 29 patients resulted in residual slow pathway conduction in only 3 (11 %) with recurrence in 2 (4%).Conclusions. Complete elimination of slow pathway conduction is feasible in the majority of patients. Elimination of slow pathway conduction is highly predictive of long-term success after AV node modification using an anatomically guided approach.

Experimentally created atrioventricular node reentrant tachycardia in the dog: Evidence of a brake system for nodal reentry in the anterior interatrial septum

Objectives. The purpose of the study was to investigate the hypothesis that nodal approaches of both anterior and posterior atrial input sites of the atrioventricular (AV) node contribute to part of the circuit of AV node reentrant tachycardia. Thus, tachycardia might be elicited by a premature atrial impulse that arrived at the AV node through one input site while blocked at another.Background. Atrioventricular node reentrant tachycardia is the most common supraventricular tachycardia in humans, yet the exact pathway of the reentrant circuit is unknown. Methods. In eight dogs, an operation that blocked atrial impulses from the anterior input site to the AV node was performed through a right thoracotomy with the inflow occlusion method. The right atrial free wall and the anterior atrial septum between the sinoatrial node and the AV node were completely divided, whereas the tissues within the triangle of Koch remained intact. Thus, atrial impulses were blocked from the anterior input site in the right atrium and the atrial septum and were conducted only through the left atrial free wall to the posterior atrial septum into the AV node.Results. In a baseline electrophysiologic study before operation, dual AV conduction pathways were demonstrated in seven of eight dogs, but none of the seven had inducible AV node reentrant tachycardia. A repeat study 1 week postoperatively revealed that 1) both PR and AH intervals were prolonged during sinus rhythm (p < 0.01); 2) anterograde and retrograde conduction of the AV node showed no significant changes; and 3) AV node reentrant tachycardia was induced in four dogs (50%), of which three had sustained tachycardia.Conclusions. These results are compatible with the hypothesis that both nodal approaches of atrial input sites of the AV node contribute to part of the circuit of AV node reentrant tachycardia. They also confirm Moe's hypothesis of the existence of a brake system that prevents sustained AV node reentry. Our data suggest that the brake system is located in the anterior atrial septum.

Association between atrioventricular node reentrant tachycardia and inducible atrial flutter

Objectives. The purpose of this study was to evaluate the inducibility of atrial flutter in patients with atrioventricular (AV) node reentrant tachycardia and to determine the effect of radio-frequency ablation of the slow AV node pathway on the inducibility of atrial flutter.Background. Studies have shown that both AV node reentrant tachycardia and atrial flutter are reentrant arrhythmias having an area of slow conduction that is located in the low posterior right atrium near the ostium of the coronary sinus.Methods. Ninety-one patients were prospectively evaluated using a standardized atrial pacing protocol. Three groups of patients were analyzed: 42 patients with inducible AV node reentrant tachycardia, 13 with a history of spontaneous atrial flutter and 36 control patients. A subgroup of 34 patients with AV node reentrant tachycardia who underwent successful radiofrequency ablation of the slow AV node pathway underwent atrial pacing again after ablation.Results. Atrial flutter was more frequently inducible in patients with AV node reentrant tachycardia (88%) and in those with a history of atrial flutter (92%) than in control patients (36%) (p = 0.0001). There were no differences between the patient groups with respect to atrial effective refractory period, P wave duration or PA interval at the His position. Among the 34 patients with AV node reentrant tachycardia who underwent atriai pacing before and after radiofrequency ablation, there were 30 with atrial flutter and 4 with atriail fibrillation before ablation and 29 with atrial flutter and 5 with atrial fibrillation after ablation (p = NS). There was no difference in the duration of the induced atrial flutter before and after ablation. The mean atrial flutter cycle length before ablation (206 ± 22 ms) was not different from that after ablation (196 ± 20 ms) (p = NS).Conclusions. There is a strong association between AV node reentrant tachycardia and inducible atrial flutter, suggesting that there may be a common area of perinodal atrium participating in the two tachycardia circuits. However, radiofrequency ablation of the slow pathway of the AV node reentrant tachycardia circuit does not influence the inducibility of atrial flutter.

Indications for modification of coexisting dual atrioventricular node pathways in patients undergoing surgical ablation of accessory atrioventricular connections

Concomitant susceptibility to atrioventricular (AV) node reentrant tachycardia has been demonstrated in certain patients having reentrant tachycardia utilizing accessory AV connections. For those patients undergoing accessory connection ablation, AV node surgical modification may be warranted during the same operative procedure. To assess indications for a combined operative procedure, this study evaluated potential predictors of subsequent spontaneous AV node reentrant tachycardia in patients undergoing ablation of accessory AV connections.Among 62 consecutive patients undergoing surgical ablation of an accessory AV connection, 13 (21%) manifested dual AV node pathways. The latter were identified preoperatively in five patients (four with concealed and one with bidirectional accessory connections) and postoperatively in seven (all seven with bidirectional accessory connections). In one patient with a bidirectional accessory connection, dual AV node pathways could not be demonstrated preoperatively, but AV node reentrant tachycardia was induced. Operative ablation of an accessory connection was successful in all patients. However, postoperatively, 2 of the 13 patients had inducible AV node reentrant tachycardia, 5 had AV node “echo” beats and 6 had no inducible arrhythmia.During 26 ± 7 months of follow-up study, the two patients with inducible AV node reentrant tachycardia postoperatively had symptomatic AV node reentrant tachycardia. In addition, the one patient with inducible AV node reentrant tachycardia preoperatively had recurrence of this tachycardia 4 months after attempted surgical modification of the AV node. Consequently, although dual AV node pathways appear to be common in patients undergoing surgical ablation of an accessory AV connection (21%), only a small group (3 of 13) of these patients are at risk for subsequent clinical AV node reentrant tachycardia.The presence of dual AV node pathways either alone or in conjunction with AV node echoes does not predict occurrence of AV node reentrant tachycardia. However, induction of sustained AV node reentrant tachycardia appears to be associated with a greater likelihood of spontaneous symptomatic tachycardia and therefore warrants consideration of AV node modification at the time of surgical ablation of an accessory connection.

Recovery of retrograde fast pathway excitability in the atrioventricular node reentrant circuit after concealed anterograde impulse penetration

The recovery of the retrograde fast pathway excitability in atrioventricular (AV) node reentry has been difficult to assess with ventricular extrastimulation because of difficulty in achieving sufficiently short intranodal coupling intervals and the potential interposition of “lower common pathway” nodal tissue. To circumvent these methodologic obstacles in 10 patients with inducible AV node reentrant tachycardia, a fixed atrial extrastimulus (A2) coupled to a basic atrial drive (A1) at a cycle length of 500 ms was utilized to reproducibly initiate AV node reentrant echoes. A ventricular extrastimulus (V3) was then introduced after A2at progressively shorter coupling intervals (A2V3) in an attempt to pre-excite the retrograde fast pathway after concealed anterograde penetration by A2.In six patients, retrograde fast pathway pre-excitation was achieved at critical A2V3intervals, as evidenced by the appearance of A3by up to 28 ± 6 ms in advance of the expected first AV node reentrant echo. In five of the six cases, the V3A3interval was virtually unaltered (≤5 ms decrease) when A2was omitted. In seven patients, at a critically short A2V3coupling interval (195 ± 27 ms), V3abruptly failed to elicit A3and concomitantly abolished all AV node echoes; yet when A2was omitted, an A3response returned, with V3A3identical to previous values.It is concluded that 1) anterograde concealment by A2in the retrograde fast pathway at onset of reentry car, be demonstrated in a significant proportion of patients with typical AV node reentrant tachycardia; 2) this concealment effect is most often manifested by retrograde block rather than decremental conduction; and (3) after concealed anterograde impulse penetration, the retrograde fast pathway in AV node reentrant tachycardia consists of tissue that, unlike the typical AV node, frequently exhibits an abrupt transition from full excitability to absolute refractoriness.

Role of intravenous isoproterenol in the electrophysiologic induction of atrioventricular node reentrant tachycardia in patients with dual atrioventricular node pathways

To assess the role of intravenous isoproterenol for the facilitation of electrophysiologic induction of atrioventricular (AV) node reentrant tachycardia, 20 patients with dual AV node pathways who lacked inducible AV node reentrant tachycardia at control study had a constant isoproterenol infusion administered and underwent repeat study. Six (30%) of 20 patients (group I) had inducibte AV node reentrant tachycardia during isoproterenol infusion whereas the other 14 (70%) patients (group II) did not. Paroxysmal supraventricular tachycardia was clinically documented in all 6 group I patients compared to 3 (21%) of 14 group II patients (p = 0.002). The sensitivity and specificity of isoproterenol-facilitated induction of AV node reentrant tachycardia were 67 and 100%, respectively. The isoproterenol-facilitated induction of sustained AV node reentry was mediated by resolution of the weak link in anterograde slow pathway in 2 (33%) patients, in retrograde fast pathway in 3 (50%) and in both anterograde stew and retrograde fast pathways in 1 (17%) patient. Four group I patients were given intravenous propranolol, 0.2 mg/kg body weight, and had complete suppression of isoproterenol-facilitated induction of AV node reentry. Thus, intravenous isoproterenol is a rather sensitive and highly specific adjunct to electrophysiologic induction of AV node reentrant tachycardia in patients with dual AV node pathways but without inducible sustained AV node reentry.

Percutaneous catheter modification of the atrioventricular node. A potential cure for atrioventricular nodal reentrant tachycardia.

Our purpose was to describe a technique of atrioventricular (AV) node modification for patients with drug refractory AV nodal reentrant tachycardia (AVNRT). Nine patients (mean age, 45 +/- 20; range, 14-82) with recurrent drug refractory AVNRT (n = 8) or sudden cardiac death thought to be precipitated by AVNRT (n = 1) underwent a percutaneous catheter procedure to modify AV nodal function. The area between the electrode recording the maximal His-bundle electrogram and the ostium of the coronary sinus was divided into three zones. Perinodal direct current shocks of 100-300 J were delivered to one (n = 2), two (n = 3), or three (n = 4) zones without complications. The procedure endpoints were modification of AV conduction (either first degree AV block or complete retrograde ventriculo-atrial [VA] block) and failure to induce AVNRT before or after isoproterenol and/or atropine administration. Six of nine patients (67%) have had no inducible or spontaneous AVNRT over a mean follow-up of 12.3 +/- 4.1 months (range, 4.5-17). One of the six underwent repeat, successful modification, because AVNRT was inducible at restudy 2 days after the initial procedure. AVNRT recurred in three patients (33%), one early (3 days) and two late (3-4 months). Two of these patients underwent complete ablation of the AV junction and permanent pacemaker placement, whereas one is controlled with drug therapy. Therefore, AV nodal modification resulted in tachycardia control without antiarrhythmic drugs in six of nine (67%) and obviated the need for complete AV junctional ablation in seven of nine patients (78%). Elimination of AVNRT appears to result from either block in the retrograde fast pathway or modification of the antegrade slow pathway, such that AVNRT cannot be sustained. Additional findings suggest that an atrio-Hisian accessory connection may not be involved in AVNRT in some of these patients. Percutaneous catheter AV nodal modification appears to be a promising technique for treatment of refractory AVNRT and may obviate need for complete AV junctional ablation in a substantial number of patients with drug/pacemaker refractory AVNRT.

Direct surgical treatment of atrioventricular node reentrant tachycardia

Atrioventricular node reentry tachycardia is a common type of supraventricular tachycardia. Rarely is it incapacitating and refractory to drug therapy, but when it is, the only option in therapy until recently has been atrioventricular node ablation or antitachycardia pacemaker insertion. The purpose of this paper is to review the case histories of four patients in whom we have surgically abolished atrioventricular node reentrant tachycardia while intentionally preserving atrioventricular node conduction. All four patients had atrioventricular node reentrant tachycardia confirmed by electrophysiologic study as diagnosed by established criteria. One patient had a left posterior atrioventricular accessory pathway, in addition to atrioventricular node reentrant tachycardia. All patients underwent intraoperative epicardial and endocardial mapping. Direct surgical dissection of the atrioventricular node node was performed in all four patients during normothermic cardiopulmonary bypass. Early and late postoperative electrophysiologic studies were used to evaluate the success of the surgical dissection. None of the patients had any evidence of dual atrioventricular node pathways or spontaneous or inducible atrioventricular node reentrant tachycardia postoperatively. At last follow-up (15 weeks to 21 months postoperatively), all patients were free from arrhythmias and cardiac medications, all were in normal sinus rhythm, and all had a subjectively improved life-style. This technique of direct surgical dissection of the atrioventricular node during normothermic cardiopulmonary bypass has allowed for complete cure of atrioventricular node reentrant tachycardia, while maintaining normal atrioventricular node function in these four patients.