Electrophysiologic Characteristics and Radiofrequency Catheter Ablation in Atrioventricular Node Reentrant Tachycardia with Second-Degree Atrioventricular Block

Second-Degree AV Block During AVNRT. Introduction : Detailed electrophysiologic study of AV nodal reentrant tachycardia (AVNRT) with 2:1 AV block has been limited.
Methods and Results : Six hundred nine consecutive patients with AVNRT underwent electrophysiologic study and radiofrequency catheter ablation of the slow pathway. Twenty-six patients with 2:1 AV block during AVNRT were designated as group I, und those without this particular finding were designated as group II. The major findings of the present study were: (1) group I patients had better anterograde and retrograde AV nodal function, shorter tachycardia cycle length (during tachycardia with 1:1 conduction) (307 ± 30 vs 360 ± 58 msec, P < 0.001), and higher incidence of transient bundle branch block during tachycardia (18/26 vs 43/609, P < 0.001) than group II patients: (2) 21 (80.8%) group I patients had alternans of AA intervals during AVNRT with 2:1 AV block. Longer AH intervals (264 ± 26 vs 253 ± 27 msec, P = 0.031) were associated with the blocked beats. However, similar HA intervals (51 ± 12 vs 50 ± 12 msec, P = 0.363) and similar HV intervals (53 ± 11 vs 52 ± 12, P = 0.834) were found in the blocked and conducted beats; (3) ventricular extrastimulation before or during the His-bundle refractory period bundle could convert 2:1 AV block to 1:1 AV conduction.
Conclusions : Fast reentrant circuit, rather than underlying impaired conduction of the distal AV node or infranodal area, might account for second-degree AV block during AVNRT. Slow pathway ablation is safe and effective in patients who have AVNRT with 2:1 AV block.     

High variability of retrograde fast pathway sensitivity to adenosine

BACKGROUND: Adenosine is widely used as a tool to assess the effectiveness of radiofrequency ablation of concealed accessory pathways. HYPOTHESIS: The goal of this study was to determine the reliability of this test by studying the retrograde fast pathway sensibility in a large patient population with typical atrioventricular (AV) nodal reentry tachycardias. We sought also to determine whether AV nodal properties were predictive of a retrograde fast pathway sensitivity to adenosine. METHODS: In all, 124 patients with inducible AV nodal reentrant tachycardia were included in this study. All patients received a clinically used standard dose of 12 mg adenosine during ventricular pacing, with 500 ms and a constant ventriculoatrial (VA) conduction via the fast pathway. Electrophysiologic parameters of the AV node were determined in all patients in order to correlate them with the adenosine sensitivity of the retrograde pathway. RESULTS: In 74 patients, the injection of 12 mg adenosine resulted in a transient VA block, whereas no VA block occurred in the remaining 50 patients. In two patients, concealed accessory pathways were unmasked after the injection of adenosine. The adenosine sensitivity of the retrograde fast pathway was associated with longer retrograde conduction times and cycle lengths during AV nodal reentrant tachycardias. CONCLUSION: This study shows a high variability of retrograde fast pathway sensitivity to adenosine. Thus, in 40% of patients the lack of VA block after adenosine injection is not specific for persistent accessory pathway function after radiofrequency ablation. Electrophysiologic properties of patients with AV nodal reentrant tachycardias were different in patients with and without adenosine-sensitive retrograde fast pathways, possibly indicating differential patterns of penetration of the retrograde fast pathway into the compact AV node.     

Procainamide and retrograde atrioventricular nodal conduction in man

Recent studies that show a depressant effect of procainamide (PA) on retrograde conduction in patients with atrioventricular (AV) nodal reentrant tachycardia (RT) have suggested possible incorporation of AV nodal bypass tracts. Electrophysiologic effects of i.v. PA, 10 mg/kg, on retrograde AV nodal conduction were examined in 13 patients without RT, demonstrable AV nodal refractory period curves, or accessory pathways. Ventriculoatrial (VA) conduction was recorded before and after PA using intracardiac electrograms, incremental ventricular pacing and extrastimulation. With incremental pacing during the control, VA block occurred at a mean cycle length (CL) of 364.6 +/- 87.9 msec. After PA, VA conduction was abolished in five of 13 patients due to onset of retrograde block in the AV node; in seven of 13, VA block occurred at a longer paced CL after PA (344.2 +/- 51.2 msec vs 477.1 +/- 93.2 msec). In one patient, PA did not affect VA conduction. PA invariably produced prolongation in the VA interval at comparable CL of pacing. With ventricular premature stimulation, the retrograde H2A2 intervals during the control period were short (less than 50 msec) in seven of 13, intermediate (60-100 msec) in three of 13 and long (greater than 100 msec) in three of 13 cases. PA either abolished H2A2 conduction (H2 but no A2) or prolonged the H2A2 intervals by 5-20 msec in most cases in this series. The data suggest that i.v. PA almost uniformly depresses retrograde AV nodal conduction in the intact human heart. This depressant response to PA is not indicative of presence of partial or complete AV nodal bypass tracts.     

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.     

Relation of the Atrial Input Sites to the Dual Atrioventricular Nodal Pathways:

Dual AV Nodal Pathways. Introduction : The usually accepted definition of the dual pathway electrophysiology requires the presence of conduction curves with a discontinuity ("Jump"). However, AV nodal reentrant tachycardia has been ohserved in patients with "smooth" conduction curves, whereas discontinuity of the conduction curve does not guarantee induction of stable reentry. We hypothesize that the duality of AV nodal conduction can be revealed by careful choice of stimulation sites during the generation of AV nodal conduction curves.
Methods and Results : In 21 rabbit heart atrial-AV nodal preparations, programmed electrical stimulation with S1-S2-S3 pacing protocol was applied eitber posteriorly at the crista terminalis input site (CrT) or anteriorly at the lower interatrial septum input site (IAS), or (in 8 preparations with surgically divided input sites) at both. We found tbat in intact preparations with "smooth" conduction curves, pacing at long coupling intervals produced shorter AV nodal conductiim times from the IAS (56 ± 9.8 msec vs 69 ± I 0.1 msec; P < 0.01). At short coupling intervals, in contrast, shorter conduction times were obtained from the CrT (173 ± 21.8 msec vs 188 ± 22.8 msec; P < 0.01). This resulted in a characteristic crossing of the superimposed IAS and CrT conduction curves. After division of the inputs, the IAS site had rapid conduction to the His bundle but a longer refractory period, whereas the CrT site bad long conduction times and sborter refractory periods. Wavefronts entering the AV node from these two inputs can summate, resulting in improved conduction.
Conclusion : Pacing protocols designed to accentuate tbe asymmetry between tbe AV nodal inputs can belp to reveal tbe functional difference between tbe dual pathways and thus to better assess the properties of AV nodal conduction.     

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.     

Effects of acebutolol on paroxysmal atrioventricular reentrant tachycardia in patients with manifest or concealed accessory pathways

Electrophysiologic studies before and after administration of 50 mg of intravenous (IV) acebutolol were performed in 20 patients. Four of the 20 had persistent preexcitation, two had intermittent preexcitation, and 14 had a concealed retrogradely conducting accessory pathway (AP). Acebutolol depressed anterograde AP conduction with loss of preexcitation in one patient and increased the effective refractory period of AP in the remaining three; in most, it depressed anterograde normal pathway conduction. The longest atrial paced cycle length producing atrioventricular (AV) nodal block increased from 290 +/- 7 to 39 +/- 6 msec (mean +/- SEM) after acebutolol (p less than 0.01). Acebutolol had no significant effect on retrograde AP conduction. Sustained AV reentrant tachycardia was inducible in all 20 patients before acebutolol and in 19 after acebutolol. The cycle length of tachycardia increased from 323 +/- 8 to 352 +/- 8 msec after acebutolol (p less than 0.01), reflecting an increment of A-H interval from 148 +/- 8 to 174 +/- 9 msec (p less than 0.01). Electrophysiologic studies were reported after 800 mg of oral acebutolol given in four divided doses at six-hour intervals in eight patients. The results were comparable to those of IV acebutolol. Thus, acebutolol depresses AV nodal conduction and slows the rate of AV reentrant tachycardia, but is generally ineffective in inhibiting the induction of sustained tachycardia. It occasionally depresses anterograde AP conduction.     

Persistence of Single Echo Beat Inducibility After Selective Ablation of the Slow Pathway in Patients with Atrioventricular Nodal Reentrant Tachycardia:

Residual Slow Pathway Conduction Effects on AVN Function. Introduction : Residual slow pathway conduction with or without reentrant echo beats has been reported in 25% to 30% of patients undergoing ablation for AV nodal reentrant tachycardia (AVNRT).
Methods and Results : Fifty-eight consecutive patients (aged 45 ± 12 years) with slow-fast AVNRT underwent radiofrequency catheter ablation of the slow AV nodal pathway (SP). Residual slow-fast echo beat was documented in 21 (36%) of 58 patients (group A). The pre-and postablation AH intervals triggering the echo beats were similar (346 ± 8 msec vs 352 ± 6 msec, P = NS), as were the pre-and postablation echo zones (55 ± 6 msec vs 52 ± 5 msec, P = NS) and functional refractory period of the SP. A consistent prolongation of the AV nodal effective refractory period (AVN-ERP; from 265 ± 28 msec to 340 ± 50 msec, P < 0.001) and the Wenckebach cycle length (WBCL; from 298 ± 41 msec to 438 ± 43 msec, P < 0.001) was observed in all patients with abolition of SP conduction (group B). In group A patients, the prolongation of WBCL was less (285 ± 33 msec preablation, and 334 ± 41 msec postablation, P < 0.001). Additional pulses abolished the residual echo in 16 of 21 patients, and further prolongation of the AVN-ERP and WBCL comparable to those found in patients without a residual echo beat was observed. During 19 ± 8 months follow-up, no patient had clinical recurrence of AVNRT.
Conclusion : Residual single echo beat after SP ablation for AVNRT reflects the persistence of some portion of the SP with unchanged functional conduction properties whose prognostic significance is uncertain. A consistent increase of WBCL can be a reliable marker of complete abolition of slow pathway conduction and termination of AVNRT.     

Nonuniform Anisotropy is Responsible for Age-Related Slowing of Atrioventricular Nodal Reentrant Tachycardia

Age-Related Slowing of AVNRT. Introduction : AV nodal reentrant tachycardia cycle length has been shown to he longer in the elderly population. Microfibrosis associated with aging producing nonuniform anisotropic conduction or changes in membrane ionic properties could explain this finding.
Methods and Results : Forty-five patients (33 women and 12 men) with typical AV nodal reentrant tachycardia were studied to analyze the effects of age on electrophysiologic characteristics of the tachycardia using high-density catheter mapping of the triangle of Koch. We classified patients into group A (age ≤ 45 years, mean [± SD] 32.7 ± 8.8, n = 27) and group B (age > 45 years, mean [± SD] 61.1 ± 10.2, n =18). Retrograde atrial activation was recorded during tachycardia by means of a 2-mm decapolar catheter at the His bundle, a quadripolar catheter at the high right atrium, a multipolar catheter (6 to 10 poles) in the coronary sinus, and a deflectable quadripolar catheter at the posterior triangle of Koch. The AH interval at the AV junction as well as HA intervals at several atrial sites were measured during tachycardia. HA intervals at all atrial recording sites except in the posterior triangle of Koch were significantly longer in group B, as well as the tachycardia cycle length (362 vs 329 msec, P = 0.01). The mean AH interval was prolonged by 24 msec in group B, but this difference did not reach statistical significance. A sequential pattern of retrograde atrial activation during tachycardia was more frequently recorded in group B.
Conclusions : Since the delayed activation to the atrium was heterogeneous, transverse nonuniform anisotropic conduction is a likely explanation of these age-related modifications of AV nodal reentrant tachycardia characteristics.     

Induction of Atrioventricular Node Reentrant Tachycardia With Adenosine: Differential Effect of Adenosine on Fast and Slow Atrioventricular Node Pathways

Objectives. This study sought to evaluate the sensitivity of fast and slow atrioventricular (AV) node pathways to incremental doses of adenosine in patients with typical AV node reentrant tachycardia.

Background. Although adenosine is known to depress conduction through the AV node, the relative sensitivity to adenosine of the anterograde fast and slow pathways in patients with dual AV node pathways and typical AV node reentrant tachycardia has not previously been studied.

Methods. Sixteen patients with dual AV node physiology and typical AV node reentrant tachycardia and 10 control patients were given incremental doses of adenosine during atrial pacing.

Results. In 14 of 16 patients with dual-AV node physiology, administration of small doses of adenosine during atrial pacing led consistently to transient block of impulse conduction in the fast pathway before block in the slow pathway, resulting in abrupt prolongation of the AH interval with continued 1:1 AV conduction. The mean (±SD) doses of adenosine required to cause conduction block in the fast and slow pathways were 2.7 ± 3.0 and 7.2 ± 4.7 mg, respectively (p = 0.004). In 9 of 16 patients, administration of low dose adenosine led to initiation of AV node reentrant tachycardia. The control patients showed no abrupt increases in AH interval with administration of adenosine during atrial pacing.

Conclusions. In most patients with dual AV node pathways and typical AV node reentrant tachycardia, the fast pathway is more sensitive than the slow pathway to the effects of adenosine.     

Effects of upright posture on atrioventricular nodal reentry and dual atrioventricular nodal pathways

The electrophysiologic effects of upright posture (45 degrees upright tilt) were studied in 17 patients with dual atrioventricular (AV) nodal pathways, AV nodal reentry or both. Discontinuous AV nodal conduction curves were observed in 16 patients while supine, but in only 11 patients while upright. Fast pathway refractoriness was shortened: the anterograde fast pathway effective refractory period decreased from 360 +/- 22 to 275 +/- 14 ms (mean +/- standard error of the mean), the anterograde fast pathway block cycle length shortened from 448 +/- 28 to 348 +/- 20 ms and the retrograde fast pathway block cycle length shortened from 425 +/- 29 to 338 +/- 24 ms (all p less than 0.01). The anterograde slow pathway block cycle length shortened from 378 +/- 29 to 316 +/- 17 ms (p less than 0.05). AV nodal reentrant tachycardia was induced in 5 patients while supine (2 sustained, 3 nonsustained) and in 6 patients while upright (4 sustained, 2 nonsustained). Tachycardia cycle length shortened during upright posture, from 413 +/- 30 to 345 +/- 22 ms (p less than 0.01), primarily due to shortened anterograde slow pathway conduction time, from 322 +/- 23 to 268 +/- 20 ms (p less than 0.05). Upright posture thus enhances conduction in patients with dual AV nodal pathways, facilitating AV nodal reentry. Electrophysiologic testing in the upright position may yield additional clinical important information in patients with dual AV nodal pathways.     

Effect of Isoproterenol on Accessory Pathways Without Overt Retrograde Conduction

Effect of Isoproterenol on Accessory Pathways. Introduction : Absence of overt retrograde accessory pathway conduction may be related to low resting sympathetic tone in patients with apparent unidirectional anterogradely conducting accessory pathways (UACAP).
Methods and Results : To test this hypothesis, we studied the effect of isoproterenol on accessory pathway function and tachycardia induction in 18 patients (12 men and 6 women, ages 34 ± 16 years [mean ± SD]) with UACAP. After baseline study in the drug-free state, electrophysiologic testing was repeated during infusion of isoproterenol (0.5 to 1.5 μg/min, titrated to increase heart rate by 20%). Isoproterenol shortened the anterograde effective refractory period (398 ± 117 vs 305 ± 63 msec; P < 0.01; basic drive cycle length 600 msec) of the accessory pathway. However, retrograde accessory pathway conduction and atrioventricular reentrant tachycardia were exposed in only 3 (17%) patients by isoproterenol infusion. All 3 patients with retrograde accessory pathway revealed after isoproterenol had clinically documented tachycardia (supraventricular tachycardia in 2, atrial fibrillation in 1) during exercise, while none of the patients with persistent absence of retrograde accessory pathway conduction had this symptom.
Conclusions : We conclude that absence of overt retrograde conduction over accessory pathways may be related to low resting sympathetic tone in some individuals. Restoration of retrograde conduction with isoproterenol is unusual and most likely to be observed in patients with clinically documented paroxysmal supraventricular tachycardia related to exercise.     

New Evidence that AV Node Slow Pathway Conduction Directly Influences Fast Pathway Function

Interaction Between the Slow and Fast Pathway. Introduction: Shortening of the AV node fast pathway effective refractory period (ERP) following successful slow pathway ablation may be a nonspecific effect of energy application at the AV junction or may be due to elimination of a direct effect of slow pathway conduction on the fast pathway.
Methods and Results: Twenty-six consecutive patients (20 women and 6 men; mean age 45 ± 3 years) with typical AV nodal reentrant tachycardia who underwent successful slow pathway ablation (defined as complete elimination of dual AV node physiology) were studied. The fast pathway ERP (at a drive train cycle length of 600 msec) was determined prior to ablation (baseline) and following unsuccessful and successful ablation attempts. Successful slow pathway ablation shortened the fast pathway ERP significantly (317 ± 9 msec; P < 0.001) compared to baseline (386 ± 12 msec), whereas unsuccessful ablations bad no effect (376 ± 11 msec). Sinus cycle length, the AH interval, and blood pressure were unchanged following successful ablation. Shortening of the fast pathway ERP did not correlate with the number of energy applications or with two measures of the proximity between the slow and the fast pathway.
Conclusion: These results support the hypothesis that shortening of the fast pathway ERP following slow pathway ablation is due to elimination of a direct effect of slow pathway conduction on fast pathway function rather than a nonspecific effect of repeated energy delivery at the AV junction.     

Differential Effect of Esmolol on the Fast and Slow AV Nodal Pathways in Patients with AV Nodal Reentrant Tachycardia

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

Depressant effect on the retrograde atrioventricular nodal conduction of beta-adrenergic blockade by propranolol in humans

Propranolol is known to have a depressant effect on anterograde atrioventricular (AV) nodal conduction in normal subjects and in those with AV nodal reentrant tachycardia. Using His bundle recording and programmed ventricular stimulation, the effect of propranolol-induced beta-adrenergic blockade (1 mg/kg intravenously) on retrograde AV nodal conduction was studied in 17 patients without (group I) and nine with (group II) AV nodal reentrant tachycardia. During baseline studies the ventricular pacing cycle length that induced ventriculoatrial block was 338 +/- 60 ms (range 260 to 450 ms) in group I and 305 +/- 39 ms (range 260 to 375 ms) in group II patients (not significant). After injection of propranolol, the ventricular pacing cycle length that induced ventriculoatrial block in group I patients was 416 +/- 97 ms (range 300 to 550 ms) (P less than 0.001, compared to baseline state) in 15 patients, and complete block occurred in two patients. In group II patients ventriculoatrial block occurred at a ventricular pacing cycle length of 375 +/- 97 ms (range 260 to 510 ms) (P less than 0.02 compared to baseline value) in eight patients, and complete block occurred in one patient. Retrograde AV nodal conduction expressed as the H2A2 interval was 75 +/- 33 ms (range 35 to 150 ms) in group I and 49 +/- 16 ms (range 20 to 80 ms) in group II patients (P less than 0.05). Following the administration of propranolol, the H2A2 interval was prolonged in group I patients by 10 to 45 ms in 11 patients, no retrograde AV nodal conduction was observed in three patients, and there was no effect in two patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential effects of adenosine on antegrade fast pathway,antegrade slow pathway,and retrograde fast pathway in atrioventricular nodal reentry

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 +/- 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 +/- 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 +/- 0.5, 4.2 +/- 1.6, and 8.5 +/- 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.     

Cure of Incessant Pacemaker Circus Movement Tachycardia by Radiofrequency Catheter Ablation

Ablation of Pacemaker Circus Movement Tachycardia. Introduction : Treatment of pacemaker circus movement tachycardia (PCMT) in patients with very long VA conduction times may present a problem.
Methods and Results : PCMT occurred in a 46-year-old woman with an uncommon AV nodal reentrant tachycardia who developed 2:1 AV block after fast pathway radiofrequency catheter (RF) ablation performed at another institution. Due to the long VA conduction time, PCMT could not be prevented by reprogramming the pacemaker or by the addition of antiarrhythmic drugs. Cure of the PCMT was obtained after selective RF ablation of the slow AV nodal pathway.
Conclusion : RF ablation of the retrograde conduction offers another alternative for treatment of PCMT.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man

Of 42 patients with supraventricular tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). In these patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventriculoatrial (V-A) conduction curves (V₁-V₂, A₁-A₂) were smooth. Ventricular premature beats, being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. In the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). In these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (V₁-V₂, A₁-A₂) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction.The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atrial premature stimulation in two patients. In this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (A₁-A₂, H₁-H₂) were smooth. Atrial premature beats, conducted anterograde over the fast pathway, could activate the slow pathway in a retrograde direction resulting In an atrial echo or sustained fast-slow form of A-V nodal reentrant tachycardia.     

Alternation of Atrioventricular Nodal Conduction Time During Atrioventricular Reentrant Tachycardia:

AV Nodal Conduction Time Alternation. Introduction: Alternation of atrial cycle length and AV nodal conduction time (NCT) is often observed during AV reentrant tachycardia. Both AV nodal dual pathway and rate-dependent function have been postulated to be involved in this phenomenon. This study was designed to determine the respective role of these two mechanisms in the alternation observed in an in vitro model of orthodromic AV reentrant tachycardia. Methods and Results: The tachycardia was produced by detecting each His-bundle activation and stimulating the atrium after a retrograde delay, thereby simulating retrograde pathway conduction, in six isolated rabbit heart preparations. After a 5-minute stabilization period at a fast rate, the retrograde delay was decremented by 2 msec every minute until nodal blocks occurred. We observed a sequential alternation of the cycle length and NCT in four preparations in the short retrograde delay range. The magnitude of the alternation gradually increased as the retrograde delay was decreased and reached 4.6 ± 0.5 msec during 1:1 conduction. The alternation increased further just prior to termination of the tachycardia by an AV nodal block. None of the preparations showed discontinuous AV nodal recovery curves. Moreover, an electrode positioned over the endocardial surface of the node showed that the alternation developed distally to the nodal inputs, which are believed to constitute a major component of dual pathways. A mathematical model predicted the alternation from known characteristics of rate-dependent nodal functional properties. Conclusions: NCT and cycle length alternation can arise during orthodromic AV reentrant tachycardia when the retrograde delay is sufficiently short. The characteristics of the alternation, presence of continuous recovery curves, intranodal location of the alternation, and mathematical modeling suggest that the alternation is predictahle from the known functional properties of the AV node without postulating dual pathway physiology.