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).     

非器质性心脏病的房室传导裂隙现象分析

了解非器质性心脏病的患者在作食管电生理检查时裂隙现象发生的情况及类型 ,并观察药物及不同刺激方式对裂隙现象的影响。对在我院作食管电生理检查的 2 2 0例患者 ,先采用S1S2 法 ,每次递减 10ms进行反扫 ,直至S1S2 间期小于 2 0 0ms ,并且连续 3次以上的早搏刺激无下传 ;其中 6 2例患者同时作了S1S2 与S1S2 S3 法检查 ,2 6例用异丙肾上腺素前后行早搏刺激 ,观察裂隙现象的发生情况。 2 2 0例患者中 6 9例患者出现裂隙现象 ,总共 83例次 ,8例有双裂隙 ,裂隙带时限 45 .3± 32 .1(10～ 12 0 )ms;裂隙类型有房室结及结下组织形成的裂隙 42例次、房室结与束支形成的裂隙 2 8例次、束支裂隙 11例次、旁道裂隙 2例 ;房室结双径路的裂隙现象发生率高于其他患者 ;S1S2 法的裂隙现象发生率高于S1S2 S3 法 ;用异丙肾上腺素后的裂隙现象发生率高于用药前。裂隙现象是无器质性心脏病的患者作食管电生理检查时常见的电生理现象 ,它的发生与激动传导径路、早搏刺激的方式和用药有关。     

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.     

Differential effects of intravenous magnesium on atrioventricular node conduction in supraventricular tachycardia

Evidence from noninvasive studies suggests magnesium has a differential effect on atrioventricular nodal (AVN) pathways. To further explore the electrophysiologic effects of intravenous magnesium sulfate (MgSO(4)) on supraventricular tachycardia, with particular reference to AVN conduction pathways, we studied 23 patients with supraventricular tachycardia at the time of electrophysiologic study. Tachycardia cycle length; AH, HV, and VA intervals; anterograde and retrograde Wenckebach thresholds; slow and fast pathway effective refractory periods (ERPs); accessory pathway ERP; right atrial and ventricular ERPs; blood pressure; and serum magnesium were evaluated before and after administration of MgSO(4) during sustained tachycardia. AVN reentry was induced in 14 patients and atrioventricular reentry was induced in 9; 1 of the latter had dual AVN physiology with tachycardia using the slow pathway. Serum magnesium level increased from 0.88 +/- 0.11 to 1.79 +/- 0.14 mmol/L (p <0.0001). Magnesium increased tachycardia cycle length to a greater extent in those with dual AVN physiology than those without: 340 +/- 54 to 370 +/- 57 ms versus 347 +/- 29 to 350 +/- 30 ms (p = 0.01). This was associated with greater increase in AH interval in those with dual AVN physiology than in those without: 241 +/- 59 to 270 +/- 60 ms versus 144 +/- 16 to 140 +/- 20 ms (p = 0.003). Presence of dual AVN physiology was more frequently associated with reversion to sinus rhythm: 5 of 15 versus 0 of 8 (p = 0.06). MgSO(4) did not alter other measured parameters. In conclusion, magnesium increases tachycardia cycle length and AH interval in patients with dual AVN physiology through a dominant effect on the slow AVN pathway.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Pseudosimultaneous fast and slow pathway conduction: a common electrophysiologic finding in patients with dual atrioventricular nodal pathways

Two ventricular responses following termination of rapid atrial pacing were noted in 24 of 87 patients with dual atrioventricular (AV) nodal pathways and supraventricular tachycardia. In all 24 patients, the AH intervals of the first and second ventricular responses were comparable with those of the fast and slow pathways, respectively. Careful analysis of the whole pacing sequence revealed that, in 21 patients, this phenomenon resulted from sustained slow pathway conduction with long AH intervals. In these patients, as the AH interval of each paced beat was progressively lengthened during pacing, the corresponding His bundle and ventricular responses were pushed one cycle behind the current atrial paced beat, so that the last paced beat was followed by two His bundle and ventricular responses. In only three patients did double ventricular responses result from simultaneous fast and slow pathway conduction. One of these three patients also showed two ventricular responses resulting from sustained slow pathway conduction. Several factors predispose to the occurrence of this phenomenon in patients with dual AV nodal pathways. These include an ability to sustain slow pathway conduction, a longer slow pathway AH interval, a shorter sinus AH interval (fast pathway) and a shorter atrial paced cycle length that sustains slow pathway conduction. In conclusion, sustained slow pathway conduction with resultant long AH intervals is the mechanism of two ventricular responses following termination of atrial pacing in most patients with dual AV nodal pathways. This phenomenon should be distinguished from the rare occurrence of double ventricular responses to an atrial impulse due to simultaneous fast and slow pathway conduction.     

Evidence suggesting dual A-V nodal pathways in patients without supraventricular tachycardias.

Electrophysiologic evidence for dual pathways of conduction through the A-V node is presented in three patients without history of supraventricular tachycardia. In case 1, abrupt spontaneous changes in the PR interval from 0.17 to 0.42 second were seen. His bundle electrographic studies showed two sets of A-H intervals during sinus rhythm and at several atrial pacing rates, although at rates over 100 per minute only the slow pathway conducted. Using the extrastimulus method, different refractory periods for the fast and slow pathways were documented. Cases 2 and 3 underwent His bundle electrography studies to evaluate intraventricular conduction defects. During atrial pacing studies abrupt changes in the A-H interval, from 220 to 470 msec and from 220 to 370 msec, were observed on increasing the pacing rate from 90 to 95 per minute in case 2 and from 120 to 130 per minute in case 3. In these two patients, dual A-V nodal pathways were suggested by the sudden changes in the A-H -interval at critical pacing rates. These findings indicate that evidence suggesting dual pathways of conduction through the A-V node may not be an uncommon finding and may be present without the manifestation of recurrent supraventricular tachycardias.     

Intermittent preexcitation indicates “a low‐risk” accessory pathway: Time for a paradigm shift?

We report three patients with intermittent loss of the preexcitation pattern in the ECG that had undergone an electrophysiological study. Despite apparently poorly conducting accessory pathway (AP), in each case a fast anterograde conduction, either during spontaneous atrial fibrillation or during incremental atrial pacing (on isoproterenol) was documented; shortest preexcited RR intervals of 200–240 ms were observed. We review the literature and conclude that intermittent preexcitation observed on resting 12‐lead ECG lacks sufficient specificity for the diagnosis of an AP with long refractory period and cannot be considered a substitute for electrophysiological study in patients with this electrocardiographical phenomenon.     

Atrioventricular nodal fast pathway modification: mechanism for lack of ventricular rate slowing in atrial fibrillation

OBJECTIVES: Atrioventricular node (AVN) modification is one of the alternatives for ventricular rate control in patients with drug refractory atrial fibrillation (AF). However, the underlying mechanisms, and in particular the role of the dual pathway electrophysiology is not clear. By using a novel index, His electrogram (HE) alternans, we have previously demonstrated in rabbits that both the slow (SP) and the fast pathways (FP) are involved in AVN conduction during AF. This electrophysiological-morphological study was designed to address the role of selective FP ablation on AVN conduction during AF. METHODS AND RESULTS: In 12 rabbit AVN preparations dual pathway conduction was confirmed by HE alternans during A1A2 pacing protocol, as well as during AF. On average 48% of the conducted beats during AF utilized the FP. Selective FP ablation (n=12) guided by HE alternans resulted in only-SP conduction, with longer AVN conduction time at basic beats, but without change of AVN effective refractory period (ERP). Interestingly, despite elimination of all FP-conducted beats during AF, the selective FP ablation allowed previously concealed SP beats to be conducted, resulting in little net effect on the ventricular rate (average His-His interval 199+/-10 ms before versus 201+/-13 ms after FP ablation, p>0.05). Morphological evidence indicated that FP ablation created lesions within the transitional cells of the superior approaches at the junction between the central fibrous body and the AVN. However, extension of FP ablation lesion into the compact AVN domain resulted in non-selective AVN modification and slowing of ventricular rate during AF. CONCLUSIONS: Despite its longer ERP, FP is responsible for a substantial number of ventricular beats during AF. However, selective FP ablation has a minor effect on ventricular rate. The most likely mechanism for this phenomenon is that FP ablation allows previously concealed SP beats to be conducted. On the other hand, ventricular rate slowdown could be achieved if FP ablations caused collateral damage in the compact node. This study highlights the usefulness of HE alternans as a novel tool to monitor dual pathway conduction during AF and to guide AVN modification.     

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 supraventricular tachycardia due to simultaneous fast and slow pathway conduction in dual atrioventricular node pathways

Electrophysiologic studies were performed on a 49 year old woman who had paroxysmal nonreentrant supraventricular tachycardia due to simultaneous anterograde conduction through dual atrioventricular (AV) node pathways. Slow pathway conduction was inversely related to the preceding sinus cycle length and fast pathway conduction was determined by the Hs-A interval (measured from the His potential due to slow pathway conduction to the onset of the subsequent atrial electrogram). Major determinants of sustained simultaneous anterograde fast and slow pathway conduction during sinus rhythm were 1) a retrograde unidirectional block in both fast and slow pathways, and 2) a critical conduction delay in the slow pathway and a long enough Hs-A interval to allow sequential conduction of impulse from both pathways. Flecainide was successful in preventing recurrences of the tachycardia by eliminating slow pathway conduction during long-term follow-up.     

Slowing of paroxysmal tachycardia with loss of functional bundle-branch block.

Electrophysiological studies in a patient with paroxysmal supraventricular tachycardia disclosed anterograde dual atrioventricular nodal pathways, and a concealed left-sided anomalous atrioventricular pathway which was used as the retrograde limb of two circus movement tachycardias. Tachycardia No.1, reflecting anterograde fast pathway conduction, was characterised by functional left bundle-branch block and a stable cycle length of 330 ms. Paroxysmal loss of bundle-branch block resulted in tachycardia No.2, which reflected anterograde slow pathway conduction, and was characterised by narrow QRS and a stable cycle length of 355 ms. Tachycardia No.2 had a longer cycle length than tachycardia No.1 because the increment in AH interval (slow pathway instead of fast pathway condition) more than compensated for the decrement in ventriculoatrial interval (narrow QRS instead of bundle-branch block).     

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.     

Variant Preexcitation Syndrome: A True Nodoventricular Mahaim Fiber or an Accessory Atrioventricular Pathway with Decremental Properties?

WPW Variant. Introduction: The differentiation between a nodoventricular fiber and an accessory atrioventricular (AV) pathway with long conduction times and decremental properties could he very difficult even at detailed electrophysiologic study.
Methods and Results: A 20-year-old male with a history of a wide QRS tachycardia underwent electrophysiologic study. Baseline intervals were normal. There was evidence of dual AV pathways, and a sudden increase in AH interval was associated with the emergence of a delta wave. The atrio-delta interval showed a progressive prolongation. The preexcited QRS complex was typical of a posteroseptal pathway, and the earliest ventricular activation site was recorded at the posteroseptal region. Retrograde conduction was exclusively over the normal conduction system. During ventricular extrastimulation, a sudden increase in HA interval was associated with anterograde conduction over the accessory pathway. The intervals between the stimulus artifact and the onset of the delta wave during atrial pacing from two atrial sites (S-Delta) were compared with those between the retrograde atrial electrogram on the His channel and the onset of the delta wave during ventricular pacing (A2_HB-Delta). When pacing from the proximal coronary sinus, the shortest S-Delta interval did become shorter than the longest A2HK-Delta interval (155 vs 170 msec).
Conclusion: The finding that the S-Delta interval could become shorter than the A2_HB-Delta interval provides strong evidence that this accessory pathway was not connected to the AV node hut arose directly from the atrial tissue of the posteroseptal region.     

Time dependent changes in the functional properties of the atrioventricular conduction system in man.

Time dependent changes in the electrophysiological properties of the atrioventricular conducting system (AVCS) were determined at two or more cycle lengths (CL) in 22 patients using bundle of His (H) electrograms, incremental atrial pacing and atrial extrastimulus method. The atrioventricular (A-H interval) and intraventricular (H-V interval) conduction times and refractory periods (RP) of the atrium, the A-V node (AVN) and His-Purkinje system (HPS) were measured during the control period, and repeat measurements were made after a 30 minute interval in eight patients (group A), after a 60 minute interval in nine (group B) and after 30 and 60 minute intervals in five (group C). No statistically significant changes from control values were seen after 30 and 60 minute intervals in any group in sinus rate, A-V nodal conduction time and the onset of A-V nodal Wenckebach block. H-V intervals were identical to the control values in all groups. Insignificant changes from control values occurred in RP of the atrium and HPS. Only the functional refractory period (FRP) of the AVN showed a statistically significant decrease from control values in groups B and C. This decrease could be explained by changes in autonomic tone. These observations in general confirm the reproducibility of electrophysiological properties of AVCS within one hour, and further support the validity of the techniques utilized in this and previously reported studies in the evaluation of cardioactive drugs.     

Sequential dual chamber extrastimulation: A novel pacing maneuver to identify the presence of a slowly conducting concealed accessory pathway

BACKGROUND: Transient VA block can be created in the AV node (AVN) when an atrial extrastimulus is delivered at the AVN effective refractory period (ERP) due to anterograde concealed conduction. OBJECTIVE: We hypothesized that ventricular stimulation during pacing-induced AVN refractoriness could identify concealed accessory pathways (APs) that remain hidden with standard maneuvers. METHODS: Patients undergoing electrophysiological study for supraventricular tachycardia were screened for presence of an AP using standard pacing maneuvers and/or V pacing during adenosine infusion. The dual-chamber sequential extrastimulation maneuver consisted of an 8-beat drive train of simultaneous AV pacing at 600 msec, followed by an A2 delivered at AVN ERP, followed by a V2 delivered at the drive train cycle length (600 msec). Repeat drives were then performed with decrements of 10 msec for V2 until VA block was seen. Retrograde AVN and AP ERP were recorded with standard (V1, V2) and dual-chamber extrastimulation (A1/V1, A2, V2). Patients with an AP identified with standard pacing, manifest pre-excitation, or A ERP < AVN ERP were excluded. RESULTS: Fourteen patients with and 19 patients without an AP were studied. In all patients with an AP, exclusive VA conduction over the AP, without fusion, was seen with the described pacing maneuver. In patients without an AP, retrograde AV nodal ERP was extended by a mean of 138 +/- 46 msec (range 50 to 210 msec) with the A2. Anterograde concealed conduction into the AP was also seen in some patients who showed AP conduction during standard V1V2 pacing (mean retrograde extension of ERP 12 +/- 8 msec, range 0 to 20 msec). CONCLUSION: Dual-chamber sequential extrastimulation is a useful maneuver for identifying slowly conducting APs not revealed with standard pacing maneuvers because of an ERP and conduction time similar to the AVN. The maneuver uses anterograde concealed conduction to prolong AVN refractoriness much more than that of a concealed AP, thereby allowing the AP to become manifest with the V2.     

Utilization of Retrograde Right Bundle Branch Block to Differentiate Atrioventricular Nodal from Accessory Pathway Conduction

Introduction: Defining whether retrograde ventriculoatrial (V-A) conduction is via the AV node (AVN) or an accessory pathway (AP) is important during ablation procedures for supraventricular tachycardia (SVT). With the introduction of ventricular extrastimuli (VEST), retrograde right bundle branch block (RBBB) may occur, prolonging the V-H interval, but only when AV node conduction is present. We hypothesized that when AP conduction was present, the V-A interval would increase less than the V-H interval, whereas with retrograde nodal conduction, the V-A interval would increase at least as much as the V-H interval.
Methods and Results: We retrospectively reviewed the electrophysiological studies of patients undergoing ablation for AVN reentrant tachycardia (AVNRT) (55) or AVRT (50), for induction of retrograde RBBB during the introduction of VEST, and the change in the measured V-H and V-A intervals. Results were found to be reproducible between independent observers. Out of 105 patients, 84 had evidence of induced retrograde RBBB. The average V-H interval increase with induction of RBBB was 53.7 ms for patients with AVRT and 54.4 ms for patients with AVNRT (P = NS). The average V-A interval increase with induction of RBBB was 13.6 ms with AVRT and 70.1 ms with AVNRT (P < 0.001). All patients with a greater V-H than V-A interval change had AVRT, and those with a smaller had AVNRT.
Conclusions: Induction of retrograde RBBB during VEST is common during an electrophysiological study for SVT. The relative change in the intervals during induction of RBBB accurately differentiates between retrograde AVN and AP conduction.     

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.     

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.