Dual Atrioventricular Nodal Pathways Research Articles

Selective blockade of retrograde fast pathway by intravenous disopyramide in paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways.

Electrophysiological effects of 2 to 2.5 mg/kg iv disopyramide were studied in 10 patients with dual nodal pathways who used a slow pathway for anterograde and a fast pathway for retrograde conduction during paroxysmal supraventricular tachycardia (mean cycle length 308.5 +/- 37 ms; range 260-370 ms). Disopyramide terminated the tachycardia in six cases by production of ventriculoatrial block in five and by sinus overdrive in one. In the remaining four patients cycle length of the paroxysmal supraventricular tachycardia increased significantly from 270 +/- 8 ms to 377.5 +/- 28 ms. In all 10 patients disopyramide depressed retrograde fast pathway conduction manifest by an increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 296.5 +/- 25 ms to 358 +/- 60 ms, and increase in retrograde fast pathway effective refractory period from less than or equal to 246 +/- 34 ms to 325 +/- 36 ms; the drug abolished ventriculoatrial conduction in two cases. Anterograde slow pathway and fast pathway conduction properties were unchanged after disopyramide (atrial paced cycle length producing AH block 292 +/- 30 to 306.5 +/- 30 ms; effective refractory period of anterograde fast pathway less than or equal to 274 +/- 56 to 284 +/- 44 ms, before and after the drug, respectively) suggesting that anterograde conduction was not crucial either for sustainment or for failure to initiate paroxysmal supraventricular tachycardia after the drug. Paroxysmal supraventricular tachycardia could not be reinduced in six cases after disopyramide. In the other four the ventricular paced cycle lengths producing ventriculoatrial block (318 +/- 41 ms) and effective refractory period of retrograde fast pathway (320 +/- 28 ms) were shorter than the cycle length of reinduced paroxysmal supraventricular tachycardia (367.5 +/- 35 ms) allowing perpetuation of the tachycardia. We conclude that disopyramide breaks atrioventricular nodal re-entrant tachycardia by specific blockade of the retrograde fast pathway though the effect on anterograde atrioventricular nodal conduction is variable.

Noninvasive Diagnosis of Dual AV Nodal Pathways with Inability to Participate in Reentrant Tachycardia

Noninvasive Diagnosis of Dual AV Nodal Pathways with Inability to Participate in Reentrant Tachycardia

Atrioventricular node reentry: Intravenous verapamil as a method of defining multiple electrophysiologic types

Fourteen patients with recurrent supraventricular tachycardia (SVT) underwent electrophysiological evaluation. Each patient was shown to have reentry confined to the region of the atrioventricular (AV) node. Verapamil, 0.075 to 0.15 mg/kg was administered intravenously to each patient during a stable episode of SVT, resulting in termination in each instance. There was more than one mechanism for termination of SVT. Nine patients showed termination by anterograde AV node block preceded by an increase in conduction time in the anterograde limb of the tachycardia circuit (Ae-H intervals) with no change in the conduction time in the retrograde limb (H-Ae intervals). Three patients showed termination by block in the retrograde limb of the circuit preceded by increases in both Ae-H and H-Ae intervals. An additional example of termination by spontaneous ventricular premature complexes and usurpation by sinus rhythm were also seen. Common features were that verapamil had significant effects on anterograde and retrograde conduction and refractoriness in the AV node. It prolonged the refractory periods of both fast and slow pathways in patients with dual anterograde AV node pathways, and observable effects on retrograde conduction and refractoriness were seen even in patients with constant ventriculoatrial conduction times during incremental ventricular pacing in a control study. However, three distinct groups of patients were identified on the basis of their response to ventricular pacing in a control study and upon verapamil effects recorded during their SVT. An explanation for these latter findings may be that there is a normal variation in the retrograde response of parts of the AV node to ventricular pacing, and a variability in some of the patients' responses to verapamil.

Sudden sinus slowing with junctional escape: a common mode of initiation of juvenile supraventricular tachycardia.

After noting bradycardia-induced supraventricular tachycardia (SVT) in two successive children with SVT, we analyzed Holter monitor recordings done on 66 children with suspected or proved SVT. Ten children had apparent reentry SVT. The most common mode of initiation (eight of 10 patients) was not premature atrial beats, but sudden sinus pause with a junctional escape beat (JEB), usually fused with the delayed sinus P wave, initiating the tachycardia. Electrophysiologic studies in five children who had this mode of initiation showed evidence of reentry in four, possibly by dual atrioventricular nodal (AVN) pathways. Since sudden sinus pause and JEB are relatively uncommon in adults, the disappearance of this phenomenon with age may be the most significant reason why children often have less tachyarrhythmia as they get older. Both propranolol and digoxin significantly increased the numbers of episodes of SVT in the three patients tested with serial Holter monitoring.

Acute electrophysiological effects of flecainide acetate on cardiac conduction and refractoriness in man.

The electrophysiological effects of flecainide acetate (2 mg/kg as an intravenous infusion over five minutes) were assessed in 47 patients undergoing electrophysiological study. Seven patients had normal electrophysiology, 16 had a direct accessory atrioventricular pathway, 12 had dual atrioventricular nodal (AH) pathways, five had paroxysmal ventricular tachycardia, six had conduction system disease, and one patient had a left atrial tachycardia. No significant change occurred in sinus cycle length. The PA interval, AH interval, and HV interval were all significantly prolonged. The QRS complex duration increased significantly. The QT interval showed slight prolongation due entirely to the increase in QRS duration. Refractoriness of the atrial and ventricular myocardium was slightly prolonged, but was significant only at ventricular level. No significant change occurred in refractoriness of the normal atrioventricular node. Pronounced prolongation of retrograde "fast" AH pathway refractoriness was observed in those patients with dual AH pathways. Anterograde and retrograde accessory pathway refractoriness were both greatly increased. These electrophysiological properties strongly suggest that flecainide will be useful in the management of a wide variety of cardiac arrhythmias. It should be administered, however, with caution to patients with pre-existing conduction system disease. Because repolarization is not delayed flecainide is unlikely to induce ventricular arrhythmias related to prolongation of the QT interval.

Electrocardiographic Diagnosis of Dual AV Nodal Pathways Complicating the Wolff-Parkinson-White Syndrome

he diagnosis of dual AV nodal pathways compliTcating concealed or manifest preexcitation, is usually made at the time of electrophysiologic study in pa tien ts with recurrent paroxysmal supraventriculax tachycardia. In these patients, electrophysiologic studies demonstrate discontinuous antegrade AV nodal conduction curves (dual AV nodal pathways, fast and slow), as well as a unior bidirectionally conducting anomalous pathway. In some of these patients, one or more tachycardias are induced.14 The tachycardias induced can include a fast AV reentrant tachycardia (antegrade fast pathway and retrograde anomalous pathway), a slow AV reentrant tachycardia (antegrade slow and retrograde anomalous pathway ) , and sometimes the usual variety of AV nodal reentrant paroxysmal tachycardia ( antegrade slow pathway and retrograde fast pathway).' In these cases, one then has to retrospectively examine electrocardiograms in an attempt to correlate induced and clinical tachycardias. In the present study, we report a patient with known Wolff -Parkinson-White syndrome, in whom dual pathways were diagnosed from electrocardiographic findings prior to electmphysiologic study. In this patient, the presence of dual pathways was clinically relevant, in that the patient suffered from two different spontaneous paroxysmal tachycardias.

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).

Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia

Ten patients are described with two discrete discontinulties in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean ± Sd, 48 ± 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion. triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.

Two cases of combined accessory pathway and dual atrio-ventricular nodal pathways

Two cases of combined accessory pathway and dual atrio-ventricular nodal pathways

Dual atrio-ventricular nodal pathways in patients with anomalous bypass tract (Kent bundle)

Dual atrio-ventricular nodal pathways in patients with anomalous bypass tract (Kent bundle)

Sequence of retrograde atrial activation in patients with dual atrioventricular nodal pathways.

To characterize the sequence of retrograde atrial activation in the presence of dual atrioventricular (AV) nodal pathways, we analyzed electrophysiologic data from seven patients in whom discontinuous AV nodal and ventriculoatrial conduction curves could be induced with programmed electrical stimulation. In all patients, electrograms of the high right atrium (HRA), lateral right atrium (LRA), low septal right atrium (SRA) and proximal coronary sinus (PCS) near the coronary sinus ostium were simultaneously recorded at a paper speed of 150-250 mm/sec. During programmed ventricular extrastimulation and incremental ventricular pacing, ventriculoatrial conduction via the fast AV nodal pathway resulted in SRA activation before PCS, HRA and LRA activation. However, the sequence of retrograde atrial activation abruptly changed with a shift from retrograde fast to retrograde slow AV nodal pathway conduction. Characteristically, during ventriculoatrial conduction via the slow AV nodal pathway, activation of the PCS preceded SRA activation by 5-20 msec and was accompanied by an alteration of the temporal relationship between HRA and LRA activation in all patients. These observations suggest that anatomically, the proximal common AV nodal pathway is a broad area that permits the slow AV nodal pathway to have a retrograde exit located posteriorly, inferiorly and to the left of that of the fast AV nodal pathway, and that the retrograde atrial activation sequence recorded during tachyarrhythmias should be determined with caution attempting to differentiate retrograde normal AV pathway from retrograde anomalous bypass tract conduction.

AV Block and Pseudo Sinus Exit Block in a Patient with PSVT due to Dual AV Nodal Pathways

AV nodal reentry is the most frequent mechanism of paroxysmal supraventricular tachycardia (PSVT) in man. 1 Wu D Denes P Amat-y-Leon F et al. Clinical, electrocardiographic and electrophysiologic observations in patients with paroxysmal supraventricular tachycardia. Am J Cardiol. 1978; 41: 1045-1051 Abstract Full Text PDF PubMed Scopus (279) Google Scholar In most patients with AV nodal reentrant PSVT, electrophysiologic studies demonstrate discontinuous AV nodal conduction curves suggestive of dual AV nodal pathways. 2 Denes P Wu D Dhingra RC et al. Demonstration of dual AV nodal pathways in patients with paroxysmal supraventricular tachycardia. Circulation. 1973; 48: 549-555 Crossref PubMed Scopus (418) Google Scholar , 3 Denes P Wu D Dhingra RC et al. Dual atrioventricular nodal pathways: A common electrophysiologic response. Br Heart J. 1975; 37: 1069-1076 Crossref PubMed Scopus (177) Google Scholar Measurable slow and fast pathway properties determine the occurrence of single or repetitive reentry. 4 Denes P Wu D Amat-y-Leon F et al. The determinants of atrioventricular nodal re-entrance with premature atrial stimulation in patients with dual AV nodal pathways. Circulation. 1977; 56: 253-259 Crossref PubMed Scopus (70) Google Scholar

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).

Observations on mechanisms of circus movement tachycardia in the Wolff-Parkinson-White syndrome. Role of different tachycardia circuits and sites of block in maintenance of tachycardia.

Different mechanisms of block of impulse propagation in several re-entrant circuits resulted in a major discordance between the "echo-zone" and the "tachycardia-zone" in a patient with intermittent Wolff-Parkinson-White syndrome, dual atrioventricular nodal pathways, and bundle branch re-entry. This case illustrates the delicate balance in electrophysiological properties required between the tissues incorporated in a re-entrant circuit to initiate and sustain the arrhythmia. It also shows how the presence of several reentrant pathways can lead to refractoriness in the circuit responsible for the circus movement tachycardia.

Limitation of tachycardia zone resulting from longitudinal dissociation of the atrioventricular node in concealed pre-excitation.

Two cases with a concealed left-sided accessory atrioventricular bypass tract are described. In both, functional longitudinal dissociation of the atrioventricular node narrowed the range of atrial premature beat coupling intervals which could initiate re-entry using the accessory pathway. In case 1 early premature atrial beats were followed by an atrioventricular nodal re-entrant echo. The atrial echo pre-empted retrograde conduction over the Kent bundle and thus limited the development of paroxysmal supraventricular tachycardia. In case 2 atrioventricular nodal conduction showed typical features ascribed to dual atrioventricular nodal pathways. In addition there was a bradycardia-related retrograde block in the concealed accessory pathway. Early premature atrial beats, because of exclusive "slow pathway" anterograde conduction, arrived at the ventricles during the period of bradycardia-dependent retrograde block and failed to initiate a macro re-entrant tachycardia. This study shows that (1) longitudinal dissociation within the atrioventricular node may limit the ability to initiate tachycardia in patients with concealed pre-excitation; and (2) discontinuous atrioventricular nodal conduction curves occasionally help to reveal bradycardia-related retrograde block in a concealed accessory pathway.

Mechanisms of spontaneous tachycardia termination in a patient with the Wolff-Parkinson-White syndrome and dual atrioventricular nodal pathways.

A patient with the Wolff-Parkinson-White syndrome and recurrent bouts of paroxysmal supraventricular tachycardia under-went electrophysiologic studies. These studies revealed evidence of dual atrioventricular nodal pathways and a septal accessory pathway. The tachycardia circuit involved anterograde conduction over a slow atrioventricular nodal pathway and retrograde conduction over the accessory pathway. Spontaneous tachycardia termination was frequently observed, was almost always abrupt, and was associated with a beat-to-beat decrease in the A-H interval. In this patient, the mechanism for spontaneous tachycardia termination appeared to be an abrupt shift in anterograde conduction from the slow to the fast pathway, advancing the tachycardia so that the block occurred in the accessory pathway (or atrium). To our knowledge, this mechanism of spontaneous tachycardia termination has not been described previously. Use of agents to facilitate fast atrioventricular nodal conduction (i.e., atropine) may be effective in tachycardia termination for these patients.

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 (A 1 and H 1) and extrastimulus (A 2 and H 2) intervals. Discontinuous A 1-A 2 and H 1-H 2 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 A 1-A 2 and H 1-H 2 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.

Clinical, electrocardiographic, and electrophysiological observations of dual A-V nodal pathways.

In 45 (25%) of 182 patients with various cardiac arrhythmias, dual A-V nodal pathways (DPWs) were diagnosed with atrial extrastimulus technique at least at one or more basic cycle lengths and/or after intravenous administration of atropine (1 mg). The jump of discontinuous A1A2, H1H2 curve of these 45 ranged from 25 to 235 (92±56) msec and the jump of A1A2, A2H2 curve ranged from 40 to 260 (107±55) msec. The fast pathway FRP (functional refractory period), slow pathway FRP, fast pathway ERP (effective refractory period) and slow pathway ERP was 464±87 msec, 532±91 msec, 404±96 msec and 328±70 msec, respectively. DPWs were demonstrated in 10 (59%) of 17 patients with paroxysmal supraventricular tachycardia (PSVT), 3 (5%) of 55 with WPW syndrome, 2 (20%) of 10 with paroxysmal atrial fibrillation, 11 (29%) of 38 with sick sinus syndrome, 10 (38%) of 26 with first degree and/or second degree A-V (AH) block, none of 3 with second degree HV block, 3 (27%) of 11 with bundle branch block and 6 (27%) of 22 with the other cardiac arrhythmias. In 17 patients with PSVT, seven demonstrated A-V nodal reentrant tachycardia. Six of these 7 had evidence of DPWs. In the other 7 of the 17, concealed accessory pathway was demonstrated. Three of these 7 had DPWs, which did not constitute the reentrant circuit. Twenty-eight of 45 patients (62%) with DPWs had one or more electrophysiological abnormalities suggesting A-V nodal dysfunction: 1) prolonged AH interval (>130 msec) during sinus rhythm (10 patients), 2) atrial pacing rates of 130 or less inducing A-V nodal Wenckebach periods (24 patients), 3) prolonged A-V nodal ERP or slow pathway ERP (>400 msec) (8 patients), and 4) prolonged A-V nodal FRP or fast pathway FRP (>500 msec) ( 16 patients). However, in most patients, atropine improved A-V nodal dysfunction. We consider that DPWs are a common electrophysiological finding and have a strong association not only with PSVT but also with A-V nodal dysfunction.

Dual atrioventricular nodal pathways in children without supraventricular tachycardia.

Atrioventricular conduction characteristics were examined by atrial extrastimulus technique in 45 children aged 50 days to 14 years following diagnostic cardiac catheterization. None of the patients had a history of supraventricular tachycardia and none had evidence of pre-excitation on routine electrocardiogram. By plotting the A2H2 and H1H2 intervals against corresponding S1S2 intervals 2 types of conduction curve were obtained. Eight of the 45 children (17.7%) showed discontinuous conduction curves, characteristic of dual atrioventricular nodal pathways, whereas 37 patients had continuous curves. Of the 8 patients with discontinuous curves 3 showed unsustained echo beats following extrastimuli, after the effective refractory period of the fast pathway was reached. This study showed that, as in adults, the atrioventricular node was frequently functionally dissociated in children.

Nodoventricular accessory atrioventricular connection associated with dual atrioventricular pathways: A case report and review of the literature

A case is presented of a patient free from tachyarrhythmias or prior evidence of pre-excitation syndrome, in whom electrophysiologic study revealed evidence of dual AV nodal pathways associated with a nodoventricular bypass tract. Programmed atrial extrastimuli testing revealed that conduction through the fast AV nodal pathway was associated with a normal HV interval and normal QRS morphology. Conduction through the slow AV nodal pathway was always associated with a short HV interval and ventricular pre-excitation. No tachyarrhythmias could be induced with atrial extrastimuli or rapid atrial pacing. Previously reported cases of this pre-excitation variant (all of whom were symptomatic from tachyarrhythmias) are reviewed and the features summarized. This pre-excitation syndrome can occur in individuals without clinical evidence of tachyarrhythmias or overt pre-excitation and as such may be more common than previously suspected.