Determinants of sustained slow pathway conduction and relation to reentrant tachycardia in patients with dual atrioventricular nodal transmission

In 24 patients with dual atrioventricular (AV) nodal pathways, multiple incremental atrial pacing studies were performed to obtain atrial (A) to His (H) basic driven (A₁ and H₁) and extrastimulus (A₂ and H₂) intervals. Discontinuous A₁-A₂ and H₁-H₂ intervals were analyzed for relations between initial coupling times and subsequent A-H responses, and to examine curves of sequential paced cycle lengths (A-A intervals) versus A-H intervals. Seventeen patients showed sustained slow pathway (SP) conduction with demonstration of discontinuous A-A and A-H curves. Sustained SP conduction occurred at critical atrial paced rates when the first paced beat was blocked in the fast pathway (FP) with conduction via the SP. Eleven of these 17 patients had inducible sustained supraventricular tachycardia (SVT). A-H interval during SVT in these 11 patients was closely related to SP A-H interval during atrial pacing at the paced rate comparable to SVT rate (r = +0.89, p < 0.001). The seven remaining patients showed continuous A-A and A-H curves. In three of these seven patients, sustained SVT was inducible, suggesting ability to sustain SP conduction. All of these three patients had continuous A₁-A₂ and H₁-H₂ curves during sinus rhythm so that the first atrial paced beat could not be blocked in the FP for subsequent SP conduction. In the other four of the remaining seven patients, despite block of the first atrial paced beat in the FP with SP conduction, the second paced beat was blocked in the SP so that all subsequent beats resumed FP conduction. In conclusion, sustalned SP conduction in patients with dual AV nodal pathways requires (1) an initiating beat being blocked in the FP, (2) a critical rate cycle length, and (3) the ability of SP for repetitive conduction at critical rates.     

Usefulness of intravenous diltiazem in predicting subsequent electrophysiologic and clinical responses to oral diltiazem

Diltiazem, 0.25 mg/kg, was given intravenously during induced tachycardias in 6 patients with atrioventricular (AV) nodal reentrant tachycardia (group I) and in 24 patients with AV reentrant tachycardia incorporating a retrogradely conducting accessory pathway (group II). In all 6 group I and in 15 of 24 group II patients, tachycardias terminated within 1 minute after diltiazem administration, with a weak link in the anterograde direction. In 3 other patients in group II, tachycardias were terminated by a premature ventricular complex within 1 minute. In the remaining 6 patients in group II, in whom tachycardias failed to terminate, rates of tachycardias decreased as a result of suppression of anterograde AV nodal conduction by diltiazem. Electrophysiologic studies were performed subsequently 2 hours after the third dose of 90 mg of diltiazem, which was given orally at 8-hour intervals. In 18 responders to intravenous diltiazem who were subjected to oral diltiazem testing, sustained supraventricular tachycardia (SVT) could be induced in only 2. Of the 6 nonresponders, sustained tachycardias could not be induced in 3. Twelve patients, including 11 responders and 1 nonresponder to intravenous diltiazem who responded to oral diltiazem testing, were discharged with oral diltiazem therapy, 90 mg every 8 hours, with follow-up periods of 2 to 13 months (mean 7 +/- 4 [+/- standard deviation]). The frequency of recurrent SVT decreased significantly; 8 patients were free of tachycardias and 4 had occasional recurrences of SVT that required no hospital visit. In conclusion, intravenous diltiazem is effective in terminating SVT. Termination of SVT by intravenous diltiazem predicts subsequent electrophysiologic and clinical responses to oral diltiazem.     

Determinants of tachycardia induction using ventricular stimulation in dual pathway atrioventricular nodal reentrant tachycardia

Factors determining tachycardia induction using ventricular stimulation in atrioventricular (AV) nodal reentrant tachycardia utilizing the slow pathway for anterograde and the fast pathway for retrograde conduction were analyzed in 53 patients. Sixteen patients had tachycardia induced by ventricular stimulation. In 15, tachycardia was inducible with incremental ventricular pacing. In 4 of these 15 patients, the tachycardia was also induced with V1V2 testing, while in 11 patients, the tachycardia was not induced with V1V2 testing. In 9 of the latter 11 patients, tachycardia could be induced with V1V2V3 testing, suggesting that the retrograde effective refractory period (ERP) of the right bundle (RB) or the relative refractory period of the His-Purkinje system (HPS) was the limiting factor for tachycardia induction during V1V2 testing. In the remaining one patient, tachycardia was induced with V1V2V3 testing, which provoked a premature ventricular beat, leading to tachycardia induction. Tachycardia was not induced by ventricular stimulation in 37 patients. Factors deterring tachycardia induction in these patients may be related to the retrograde ERP or functional refractory period (FRP) of the HPS, the retrograde ERP of the fast pathway, and an insufficient conduction delay of the circuit (retrograde fast and anterograde slow pathway) to allow anterograde conduction of the slow pathway. In conclusion, AV nodal reentrant tachycardia can be induced by ventricular stimulation in approximately 30% of patients with incremental ventricular pacing and/or ventricular extrastimulus testing. Induction of tachycardia with ventricular stimulation, nevertheless, is frequently limited by the retrograde FRP or ERP of the HPS, the retrograde ERP of the fast pathway, and possibly by an insufficient conduction delay of the circuit.     

Retrograde dual atrioventricular nodal pathways

Thirty-one (3.5 percent) of 887 studied patients had retrograde dual atrioventricular (A-V) nodal pathways, as manifested by discontinuous retrograde A-V nodal conduction curves (29 patients) or by two sets of ventriculoatrial (V-A) conduction intervals at the same paced cycle length (2 patients). All patients had A-V nodal reentrant ventricular echoes of the unusual variety induced with ventricular stimulation (25 patients had single, 2 patients had double and 4 patients had more than three ventricular echoes). The weak link of the reentrant circuit was always the retrograde slow pathway. Eleven of the 31 patients also had anterograde dual A-V nodal pathways (bidirectional dual pathways). Eight patients (26 percent) had spontaneous as well as inducible A-V nodal reentrant paroxysmal supraventricular tachycardia (of the unusual type in three and the usual type in five). In addition, three patients (10 percent) had only inducible supraventricular tachycardia (two of the unusual and one of the usual type).Retrograde dual A-V nodal pathways are uncommon. They are associated with the finding of at least single A-V nodal reentrant ventricular echoes (all patients), anterograde dual pathways (one third of patients) and A-V nodal reentrant paroxysmal supraventricular tachycardia of the usual or unusual variety (one third of patients).     

Analysis of anterograde and retrograde fast pathway properties in patients with dual atrioventricular nodal pathways: Observations regarding the pathophysiology of the Lown-Ganong-Levine syndrome

Anterograde and retrograde fast pathway properties were analyzed in 160 patients with anterograde dual atrioventricular (A-V) nodal pathways, with or without A-V nodal reentrant tachycardia. A-H intervals (reflecting anterograde fast pathway conduction) ranged from 46 to 234 ms (mean ± standard deviation 91 ± 30). The longest atrial paced cycle lengths at which block occurred in the anterograde fast pathway ranged from 231 to 857 ms (435 ± 112). Regression analysis of these cycle lengths versus A-H intervals revealed a correlation coefficient (r) value of 0.41 (p < 0.01). Retrograde fast pathway conduction was present (at a ventricular paced cycle length slightly shorter than sinus rhythm) in 84 of 125 patients: 15 of 16 with an A-H interval of less than 60 ms, 44 of 58 with an interval of 60 to 90 ms, 20 of 41 with an interval of 91 to 130 ms and 5 of 10 with an A-H Interval of more than 130 ms (p < 0.01). Retrograde fast pathway conduction was intact at a cycle length of 375 ms in 41 of 124 patients: 11 of 16 with an A-H interval of less than 60 ms, 22 of 57 with an interval of 60 to 90 ms, 7 of 41 with an interval of 91 to 130 ms and 1 of 10 with an A-H interval of more than 130 ms (p <0.01). Sustained A-V nodal reentrant tachycardia could be induced in 51 of 160 patients, being induced in 7 of 17 with an A-H interval of less than 60 ms, 27 of 72 with an interval of 60 to 90 ms, 15 of 59 with an interval of 91 to 130 and 2 of 10 with an interval greater than 130 ms (p < 0.05).In conclusion, in patients with dual A-V nodal pathways, there are relations between the A-H interval and the ability of the fast pathway to sustain sequential anterograde conduction, and between the A-H interval and the ability of the fast pathway to sustain sequential retrograde conduction. Among patients with dual pathways, patients with a shorter A-H interval are more likely to have A-V nodal reentrant tachycardia, because these patients are more likely to have excellent retrograde fast pathway sequential conduction (a requirement for the occurrence of reentrant tachycardia).     

Demonstration of dual atrioventricular nodal pathways in man

Electrophysiologic studies in a patient manifesting two P-R intervals revealed two ranges of atrioventricular (A-V) nodal conduction time (A-H intervals) and two A-V nodal effective and functional refractory periods. Similar demonstrations in patients with paroxysmal supraventricular tachycardia would strongly support the presence of longitudinal A-V nodal dissociation with reentry as a causative mechanism.     

Dual atrioventricular nodal pathways associated with a gap phenomenon in atrioventricular nodal conduction

A 67 year old man underwent electrophysiologic study for evaluation of syncope. During atrial pacing at a basic cycle length of 600 ms, atrial premature stimuli were introduced at progressively shorter coupling intervals. The graph of atrial coupling intervals versus corresponding His bundle responses revealed an abrupt increase in atrioventricular (AV) nodal conduction time with coupling intervals from 320 to 340 ms. In an atrial coupling interval of less than 320 ms, conduction was again rapid until the effective refractory period of the atrium was reached. These unique findings are compatible with dual pathways and a gap phenomenon within the AV node.     

Paroxysmal nonreentrant tachycardias due to simultaneous conduction in dual atrioventricular nodal pathways.

Electrophysiologic studies were performed in a 41 year old man for analysis of paroxysmal tachycardias appearing in various electrocardiographic patterns of supraventricular and ventricular bigeminy, junctional and ventricular tachycardia and atrial fibrillation, among others. All these arrhythmias were due to dual atrioventricular (A-V) nodal pathways with simultaneous dual fast and slow conduction of single atrial beats at a normal basic sinus rate. Moderate changes in sinus rate and in fast or slow pathway conduction times, or both, changed the position of the slowly conducted beats between the neighboring two fast conducted beats and resulted in various electrocardiographic manifestations of the conduction disturbance. Different blocks, such as second degree type 1, 2:1, 3:1 and possibly also type II, in one of the two pathways and occasionally aberrant conduction induced even more unusual tracings. After intravenous injection of 25 mg of ajmaline, unexpected lengthening and shortening of the A-H interval occurred, suggesting variable shifts between fast and slow pathway conduction. The incidence of dual A-V nodal pathways is discussed; it was documented in 17 (4.2 percent) of 405 patients studied. A theoretical model of A-V nodal conduction is proposed to explain its normal properties and abnormal patterns.     

Retrograde block during dual pathway atrioventricular nodal reentrant paroxysmal tachycardia

There are limited reported data regarding the occurrence of retrograde block during dual pathway atrioventricular (A-V) nodal reentrant paroxysmal tachycardia. This study describes two patients with this phenomenon. The first patient had 2:1 and type 1 retrograde ventriculoatrial block during the common variety of A-V nodal reentrance (slow pathway for anterograde and fast pathway for retrograde conduction). Fractionated atrial electrograms suggested that the site of block was within the atria. The second patient had type 1 retrograde block (between the A-V node and the low septal right atrium) during the unusual variety of A-V nodal reentrance (stow pathway for retrograde and fast pathway for anterograde conduction). The abolition of retrograde block by atropine suggested that the site of block was within A-V nodal tissue. Both cases demonstrate that intact retrograde conduction is not necessary for the continuation of A-V nodal reentrant paroxysymal tachycardia. Case 2 supports the hypothesis that the atria are not a requisite part of the A-V nodal reentrant pathway.     

Atrioventricular nodal gap conduction as a manifestation of dual nodal pathways

Electrophysiologic studies were performed in a 76 year old patient for evaluation of sinus bradycardia. Atrial extrastimuli were induced during sinus rhythm at progressively decreasing coupling (A1-A2) intervals. At an A1-A2 interval of 420 msec, right bundle branch block developed, and at 370 msec conduction failed below the His bundle. When the interval was reduced to 320 msec, conduction resumed with a normal QRS pattern with an abrupt increase in A-H intervals from 165 to 305 msec. These findings are interpreted as type I or atrioventricular (A-V) nodal gap conduction physiologically related to conversion from a rapid to a slow A-V nodal conduction mode.     

Dual atrioventricular nodal pathways: A benign finding in arrhythmia-free children with heart disease

The incidence and significance of dual atrioventricular (A-V) nodal pathways are described in 78 children with associated congenital or acquired heart disease. None of these patients had clinical or electrocardiographic evidence of arrhythmia. Dual A-V nodal pathways were observed in 35 percent of the preoperative group and in 33 percent of the postoperative group. Despite this substrate for A-V nodal reentry, supraventricular tachycardia was neither induced during electrophysiologic evaluation nor did it develop clinically over a follow-up period of 1 month to 15 years. It is concluded that dual A-V nodal pathways are common and may be a benign finding in arrhythmia-free children with heart disease.     

Echocardiographic study of cardiac abnormalities in families of patients with Marfan's syndrome

Twelve patients (5 male and 7 female; mean age 17.7 +/- 12.3 years, range 5 to 42) with Marfan's syndrome and 48 of their first degree relatives (16 male and 22 female; mean age 29.8 +/- 17.3 years, range 4 to 60) were evaluated for cardiac abnormalities by echocardiography. Of the patients with Marfan's syndrome, aortic valve prolapse was present in 1, tricuspid valve prolapse in 4, mitral valve prolapse in 12 and aortic root dilation in 10. Of the 48 first degree relatives of these 12 patients, tricuspid valve prolapse was diagnosed in 3, mitral valve prolapse in 15 and aortic root dilation in 12; aortic valve prolapse was not observed in any of these subjects. Of the 60 persons studied in these 12 kindreds, 28 (47%) had cardiac involvement. Among the 28 with cardiac involvement, aortic valve prolapse was observed in 1 (3.5%), tricuspid valve prolapse in 7 (25%), mitral valve prolapse in 27 (96%) and aortic root dilation in 22 (79%). Mitral valve prolapse was also present in the seven subjects with tricuspid valve prolapse and one with aortic valve prolapse. In 32 of the 60 persons studied in the 12 families, at least one abnormality of the cardiac, skeletal or ophthalmologic system was observed. Nineteen subjects were younger than 18 years of age; all had cardiac involvement associated with Marfan's syndrome. The notably earlier presentation of cardiac involvement in young persons may be responsible for a shorter life span in this group.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Clinical efficacy and electrophysiologic effects of intravenous and oral encainide in patients with accessory atrioventricular pathways and supraventricular arrhythmias

The electrophysiologic effects and clinical efficacy of intravenous (i.v.) and oral encainide were studied in 13 patients with accessory atrioventricular (AV) pathways (7 overt, 1 intermittent and 5 concealed) and drug-resistant Supraventricular arrhythmias (5 paroxysmal atrial fibrillation, 1 atrial tachycardia and 7 with orthodromic circus movement tachycardia). Previously, therapy had failed with a mean of 3 conventional antiarrhythmic agents. In 5 patients, amiodarone administration had also been unsuccessful. All patients underwent programmed electrical stimulation of the heart before and after 1.5 mg/kg of i.v. encainide. Seven patients were restudied during oral encainide therapy (mean 155.8 ± 54.2 mg/day) 3 days to 6 weeks (average 21 days) later. Anterograde conduction over the accessory AV pathway blocked in 4 of 7 patients after i.v. encainide. Oral encainide blocked anterograde conduction over the accessory pathway or prolonged the refractory period of the accessory pathway in 3 of 4 patients. This change in anterograde conduction was independent of the predrug value for the anterograde refractory period of the accessory AV pathway. Intravenous and oral encainide had minimal effects on retrograde conduction over the accessory AV pathway. The clinical effect of oral encainide was studied in 12 patients. Four patients responded to oral encainide and have been free of arrhythmia or side effects for 2 to 20 months (average 10.5). Encainide failed to prevent the clinical arrhythmia in 2 patients. In 4 patients with atrial arrhythmias, circus movement tachycardia developed during oral encainide therapy. In 1 patient the frequency of circus movement tachycardia increased with oral encainide treatment. Five of the previous 7 patients also suffered from central nervous system side effects, and in 1 patient serious central nervous system effects led to withdrawal of encainide. In conclusion, encainide has a marked effect on anterograde conduction and a minimal effect on retrograde conduction over the accessory AV pathway. Oral encainide was effective in controlling Supraventricular arrhythmia in 4 of 12 of this selected group of patients with accessory AV pathways. Failure to control the initial arrhythmia, facilitation of circus movement tachycardia and central nervous system side effects led to discontinuation of oral encainide in the other patients.     

Simultaneous dual fast and slow pathway conduction upon induction of typical atrioventricular nodal reentrant tachycardia: electrophysiologic characteristics in a series of patients

INTRODUCTION: Simultaneous dual atrioventricular nodal conduction (SDNC) through slow (SP) and fast pathway (FP) is a rare phenomenon observed upon the induction of atrioventricular nodal reciprocating tachycardia (AVNRT). The aim of this study is to report the electrophysiological features of patients showing typical AVNRT induced through SDNC. METHODS AND RESULTS: Among 461 consecutive patients with typical AVNRT submitted to radiofrequency catheter ablation (RFCA), seven patients (1.5%) with SDNC at tachycardia onset (group I: 6 female; age 60-72 years, mean 65.2 +/- 3.8 years) and 118 age-matched controls (group II: 60 female; age 60-88 years, mean 68.4 +/- 6.8 years) were considered. Controls were further subdivided into two subgroups according to age: subgroup A (94 patients, age 60-75 years) and subgroup B (24 patients, age >75 years). The value of the following parameters was significantly higher in group I than in group II and in subgroup A: A-H interval [113 +/- 26 vs. 89 +/- 27 (P < 0.01) vs. 84 +/- 19 (P < 0.001)], ventriculoatrial conduction effective refractory period [355 +/- 85 vs. 293 +/- 87 (P < 0.05) vs. 281 +/- 82 (P < 0.05)], SP conduction time upon AVNRT induction [444 +/- 104 vs. 350 +/- 72 (P < 0.01); vs. 345 +/- 67 (P < 0.001)], AVNRT cycle length [484 +/- 103 vs. 396 +/- 71 ms (P < 0.05); vs. 384 +/- 69 (P < 0.05)], and rate of AVNRT induction from ventricle [71% vs. 10% (P = 0.001); vs. 6% (P = 0.001)]. Differences were mostly not significant between group I and subgroup B. SP location and RFCA success rate were similar in all groups. CONCLUSION: In a population of AVNRT patients, SDNC at AVNRT induction is infrequent and it prevails beyond the fifth decade of life and in females. SDNC is associated with peculiar AVN conduction features, which resemble the age-related modifications of AVN conduction.