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.     

Incidence, determinants and significance of fixed retrograde conduction in the region of the atrioventricular node. Evidence for retrograde atrioventricular nodal bypass tracts.

Of 104 consecutive patients studied in our laboratory with His bundle electrograms, atrial and ventricular pacing and the atrial and ventricular extrastimulus techniques, 18 patients in whom the existence and utilization of ventriculoatrial (V-A) bypass tracts were excluded demonstrated evidence for fixed and rapid retrograde conduction in the region of the atrioventricular node (A-V) as suggested by the following: (1) short (36 +/- 2 msec [mean +/- standard error of mean]) and constant retrograde H2-A2 intervals during retrograde refractory period studies; (2) significantly (P less than 0.025) better V-A than A-V conduction; (3) significantly (P less than 0.025) shorter retrograde functional refractory period of the V-A conducting system than of the A-V conduction system; and (4) the retrograde effective refractory period of the A=V nodal region was not attainable in any of the 18 patients. Fourteen of the 18 patients (77 percent) had a history of palpitations and 10 (51 percent) had documented paroxysmal supraventricular tachycardia; in 13 (72 percent) single echoes or sustained reentrant supraventricular tachycardia, or both, could be induced during atrial pacing or atrial premature stimulation studies, or both. During tachycardia all these 13 patients had a short (37 +/- 2.4 msec) and constant conduction time in the retrograde limb (H-Ae interval) of the reentrant circuit that was identical to the H2-A2 interval. In conclusion, fixed and rapid retrograde conduction in the region of the A-V node (1) is seen in approximately 17 percent of patients, (2) is associated with a large incidence of reentrant paroxysmal supraventricular tachycardia, and (3) suggests the presence of A-V nodal bypass tracts (intranodal or extranodal functioning in retrograde manner).     

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.     

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).     

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.     

Effects of propranolol on anomalous pathway refractoriness and circus movement tachycardias in patients with preexcitation

Electrophysiologic effects of intravenous propranolol, 0.1 mg/kg, were evaluated in 18 patients with anomalous pathways utilizing intracardiac stimulation and recording. Fourteen patients had Wolff-Parkinson-White syndrome and four had concealed ventricular preexcitation. Anomalous pathway effective refractory period could be measured during the control period and after propranolol administration in nine patients and was 304 ± 7.5 (mean ± standard error of the mean) and 304 ± 8.3 msec, respectively (difference not significant). Ventricular paced 1:1 ventriculoatrial (V-A) conduction (reflecting retrograde anomalous pathway conduction) measured in 12 patients was intact during both the control period and after propranolol at rates of 170 to 200/min. Sustained paroxysmal supraventricular tachycardia was induced in 14 patients during the control period and in 10 after propranolol (in 4 of whom the tachycardia could not be sustained because of atrioventricular [A-V] nodal refractoriness). Mean cycle length of tachycardia in these 10 patients was 328 ± 18 (control) and 352 ± 19 msec (propranolol) (P < 0.01). The increase in tachycardia cycle length reflected an increase in A-V nodal conduction time (A-H interval).In conclusion: (1) Propranolol has an insignificant effect on both anterograde and retrograde anomalous pathway properties. (2) In most cases, propranolol does not interfere with induction of sustained circus movement tachycardia. However, it does produce a statistically significant but slight slowing of the rate of tachycardia. (3) In a minority of cases, propranolol inhibits induction of sustained paroxysmal supraventricular tachycardia by increasing A-V nodal refractoriness.     

Electrophysiologic effects of ouabain in patients with preexcitation and circus movement tachycardia

Effects of intravenous ouabain were evaluated in 19 patients with an anomalous conduction pathway (14 with manifest and 5 with concealed preexcitation) utilizing intracardiac stimulation and recording. Anterograde conduction through the anomalous pathway was present in all 14 patients with manifest preexcitation at a maximal atrial paced rate of 140 to 250 beats/min (mean ± standard error of the mean 214 ± 7.2) before and at 150 to 240 beats/min (mean 206 ± 7.1) after ouabain (difference not significant [NS]). The anterograde effective refractory period of the anomalous pathway, measured at an equivalent atrial paced rate in 10 patients, was 250 to 450 ms (mean 309 ± 19.7) before and 260 to 450 ms (mean 300 ± 17.2) after ouabain (NS). Retrograde conduction through the anomalous pathway was possible at maximal ventricular paced rates (17 patients) of 160 to 250 beats/min (mean 222 ± 6.6) before and 190 to 250 beats/min (mean 221 ± 4.4) after ouabain (NS). Sustained atrioventricular (A-V) reentrant paroxysmal supraventricular tachycardia was inducible in all 19 patients before and in 17 patients (89 percent) after ouabain (tachycardia could not be induced in two patients because of increased A-V nodal refractoriness). The mean cycle length of tachycardia in the 17 patients was 320 ± 6.7 ms before and 340 ± 8.1 ms after ouabain (p <0.01).In conclusion, ouabain has no significant effect on either anterograde or retrograde anomalous pathway refractoriness. Although ouabain slightly increases the cycle length of tachycardia, it does not interfere with induction of tachycardia in most patients with preexcitation. Oral cardiac glycosides alone would appear to be of limited value in patients with preexcitation and recurrent supraventricular tachycardia.     

The fast-slow form of atrioventricular nodal reentrant tachycardia in children

An unusual form of atrioventricular (A-V) nodal reentry is described as the underlying mechanism for incessant tachycardia in two children. During tachycardia a fast pathway was utilized for anterograde conduction and a slow pathway for retrograde conduction. This is the reverse of the usual form of A-V nodal reentrant tachycardia, in which the slow pathway is utilized for anterograde conduction and the fast pathway for retrograde conduction. One patient had a smooth ventriculoatrial (V-A) conduction curve demonstrating exclusive utilization of the slow pathway for retrograde conduction. The other had a discontinuous V-A conduction curve demonstrating failure of retrograde fast pathway conduction with resultant slow pathway conduction. In both cases the retrograde effective refractory period of the fast pathway was longer than that of the slow pathway, resulting in the establishment of this unusual reentry circuit. Both patients had a superior P axis with a P-R interval shorter than the R-P interval during tachycardia, features described in a significant number of children with incessant tachycardia. This unusual form of reentrant tachycardia can be suggested by its electrocardiographic pattern and is another mechanism for reentrant tachycardia not previously documented in children.     

Multiple reentrant tachycardias due to retrograde conduction of dual atrioventricular bundles with atrioventricular nodal-like properties.

A patient is presented who had two paroxysmal supraventricular tachycardias, one slow and incessant and the other fast. Both paroxysmal tachycardias appeared to be atrioventricular (A-V) reentrant, with anterograde conduction by way of a normal A-V pathway. Two pathways conducting in retrograde manner were demonstrated, characterized by different conduction times (fast and slow), identical abnormal atrial activation sequence and A-V nodal-like properties (retrograde Wenckebach periodicity with rapid ventricular pacing, and depression with ouabain and propranolol). Thus, there appeared to be two anomalous A-V bundles with nodal-like properties conducting in retrograde fashion. Whether the paroxysmal tachycardia was fast or slow depended on which of these pathways was utilized. Spontaneous cure of incessant paroxysmal tachycardia was observed and coincided with unexplained total loss of ability for ventriculoatrial conduction.     

Quintuple pathways participating in three distinct types of atrioventricular reciprocating tachycardia in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic studies were performed in a patient with recurrent supraventricular tachyarrhythmias. Sinus and paced atrial beats had QRS complexes characteristic of atrioventricular (A-V) conduction through a manifest left lateral accessory pathway (Wolff-Parkinson-White syndrome, type A). Three distinct types of A-V reciprocating tachycardia and three different modes of retrograde atrial activation were demonstrated. Type 1 tachycardia involved the slow A-V nodal pathway and a second (left lateral or left paraseptal) accessory A-V pathway capable of retrograde conduction only. Type 2 tachycardia was of the slow-fast A-V nodal pathway type. Type 3 tachycardia involved a heretofore undescribed circuit in that retrograde conduction occurred through an accessory A-V pathway with long retrograde conduction times and anterograde conduction through both the manifest left lateral accessory A-V pathway and fast A-V nodal pathway. Premature ventricular beats delivered late in the cycle of this tachycardia advanced (but did not change) the retrograde atrial activity without affecting the timing of the corresponding anterograde H deflection. In summary, this patient had five (three accessory and two intranodal) pathways participating in three different types of A-V reciprocating tachycardia; the recurrence of these were prevented with oral amiodarone therapy.     

Cycle length in atrioventricular nodal reentrant paroxysmal tachycardia with observations on the lown-ganong-levine syndrome

Sixty-five patients with dual pathway atrioventrlcular (A-V) nodal reentrant paroxysmal tachycardia were studied. Of these 65 patients, 11 (17 percent) had a short P-R interval (0.12 second or less) and 3 (5 percent) had a short A-H interval (53 ms or less) during sinus rhythm, suggesting the Lown-Ganong-Levine syndrome. Frequency distribution analyses of P-R and A-H intervals In the 65 patients demonstrated continuous unimodal functions, suggesting a continuum of A-V nodal properties. Regression analyses of P-R and A-H (fast pathway) intervals versus cycle length of paroxysmal tachycardia revealed an r value of 0.11 and 0.10, respectively (not significant). The cycle length of paroxysmal tachycardia did not differ between the 11 patients with a short P-R Interval (370 ± 20 ms) and the 54 patients without a short P-R interval (382 ±11 ms). Regression analysis of the slow pathway A-H interval versus cycle length of paroxysmal tachycardia revealed an r value of 0.68 (p <0.001).

The cycle length of dual pathway A-V nodal reentrant paroxysmal tachycardia is a function of the slow pathway A-H Interval and not the P-R or A-H Interval during sinus rhythm. Identification of short P-R intervals in patients with A-V nodal reentrant paroxysmal tachycardia has little significance.     

A technique for the rapid diagnosis of atrial tachycardia in the electrophysiology laboratory

OBJECTIVE: The purpose of this study was to determine if the atrial response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during paroxysmal supraventricular tachycardia is a useful diagnostic maneuver in the electrophysiology laboratory. BACKGROUND: Despite various maneuvers, it can be difficult to differentiate atrial tachycardia from other forms of paroxysmal supraventricular tachycardia. METHODS: The response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction was studied during four types of tachycardia: 1) atrioventricular nodal reentry (n = 102), 2) orthodromic reciprocating tachycardia (n = 43), 3) atrial tachycardia (n = 19) and 4) atrial tachycardia simulated by demand atrial pacing in patients with inducible atrioventricular nodal reentry or orthodromic reciprocating tachycardia (n = 32). The electrogram sequence upon cessation of ventricular pacing was, categorized as "atrial-ventricular" (A-V) or "atrial-atrial-ventricular" (A-A-V). RESULTS: The A-V response was observed in all cases of atrioventricular nodal reentrant and orthodromic reciprocating tachycardia. In contrast, the A-A-V response was observed in all cases of atrial tachycardia and simulated atrial tachycardia, even in the presence of dual atrioventricular nodal pathways or a concealed accessory atrioventricular pathway. CONCLUSIONS: In conclusion, an A-A-V response upon cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction is highly sensitive and specific for the identification of atrial tachycardia in the electrophysiology laboratory.     

Electrophysiologic evidence for selective retrograde utilization of a specialized conducting system in atrioventricular nodal reentrant tachycardia.

In 12 patients with atrioventricular (A-V) nodal reentrant tachycardia, the existence and utilization of retrograde ventriculoatrial bypass tracts in the reentrant process were excluded, and the characteristics of the anterograde and retrograde limbs of the reentrant circuits were studied using His bundle electrograms, incremental atrial and ventricular pacing and atrial and ventricular extrastimulus techniques before and after the administration of 0.01 mg/kg of intravenous ouabain. Similar studies were also performed in five control patients without tachycardia. Paroxysmal supraventricular tachycardia could be induced in all 12 patients during atrial pacing-induced A-V nodal Wenckebach periods or premature atrial stimulation, or both. On the basis of conduction time in the retrograde limb during tachycardia and during retrograde studies, two groups were identified. Group I (seven patients) had (1) short (39 ± 10 msec) and constant conduction time in the retrogarde limb measured from the anterograde His bundle deflection to the retrograde atrial echo response (H-Ae interval), (2) no change in ventriculoatrial conduction time up to maximal ventricular pacing rates, (3) H₂-A₂ intervals during retrograde refractory period studies that were identical to the H-Ae intervals and that did not increase with decreasing V₁-V₂ intervals, and (4) increased conduction time of the anterograde limb (Ae-H intervals) after the administration of ouabain without any effect on retrograde limb conduction (H-Ae and H₂-A₂ intervals) and refractoriness. Group II (five patients) had (1) long and variable H-Ae intervals (60 to 180 msec), (2) a progressive increase in ventriculoatrial intervals during incremental ventricular pacing, (3) an increase in H₂-A₂ intervals in response to decreasing V₁-V₂ intervals, and (4) increased anterograde (Ae-H interval) and retrograde limb (H-Ae and H₂-A₂ intervals) conduction and refractoriness after the administration of ouabain. Changes in the H₂-A₂ interval corresponded to the changes in four of the five control patients. These findings suggest that (1) in group I the anterograde limb was the A-V node, whereas the retrograde limb was an A-V nodal bypass tract or an insulated intranodal tract physiologically unlike the A-V node; and (2) in group II the A-V node comprised both the anterograde and retrograde limbs of the reentrant circuit.     

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.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

Electrophysiological effects of intravenous propafenone for treating atrial-ventricular nodal dual pathways reentrant tachycardia]

The acute electrophysiological effects of intravenous propafenone were studied through programmed electrical stimulation in 9 patients with atrio-ventricular nodal dual pathways reentrant tachycardia (AVNDP-RT). The results showed that propafenone prolonged significantly the effective refractory period of atrial ventricular nodal fast pathway (AVN-FP) in retrograde conduction and might further terminate the paroxysmal supraventricular tachycardia (PSVT). It is an effective drug for treating AVNDP-RT. Neither blood pressure dropping nor other side effects were observed.     

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.     

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.     

Electrophysiological effects and clinical efficacy of propafenone in children with recurrent paroxysmal supraventricular tachycardia

Twenty-four patients aged 10.1 +/- 4.5 (mean +/- SD) years with recurrent paroxysmal supraventricular tachycardia underwent an electrophysiological study. Eleven patients had an overt and seven had a concealed accessory connection; six patients had no accessory connection. An orthodromic reciprocating tachycardia was inducible in 17 of 18 patients with an accessory connection, and an atrioventricular nodal reentrant tachycardia was inducible in four of six patients without accessory connection. After administration of propafenone, the sinus cycle length decreased. Intra-arterial, intranodal, and His-ventricle intervals and QRS duration increased. The atrial and ventricular effective refractory periods and anterograde and retrograde effective refractory periods of the atrioventricular node increased. The cycle length at which nodal second-degree block occurred increased. Of 18 patients with accessory connection, propafenone prolonged retrograde conduction in all, blocked anterograde conduction in five, and prolonged it in six. The drug terminated the orthodromic reciprocating tachycardia in all 17 patients and the atrioventricular nodal reentrant tachycardia in three of four patients. In three of four patients with atrioventricular nodal reentrant tachycardia and in 15 of 17 patients with orthodromic reciprocating tachycardia, the tachycardia was no longer inducible or nonsustained after propafenone. A follow-up of 26 +/- 10 months revealed that the drug when orally administered to all patients prevented recurrences of tachycardia in 15 of 18 patients with and in four of six patients without accessory connection. The results of short-term drug testing with propafenone predict the response to long-term oral therapy with this drug.     

Electrophysiologic effects and clinical efficacy of flecainide in children with recurrent paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous flecainide were evaluated in 16 patients aged 9 +/- 4 years: 15 with recurrent paroxysmal supraventricular tachycardia (SVT) and 1 with overt accessory pathway and history of syncope. Eleven patients had an accessory pathway; it was concealed in 2, overt in 9 and in 10 of these patients an orthodromic atrioventricular reentrant tachycardia was induced. Five patients without accessory pathway had an atrioventricular nodal reentrant tachycardia. After intravenous flecainide (1.5 mg/kg) the effective refractory period of the atrium and ventricle increased significantly; the anterograde and retrograde effective refractory periods of the atrioventricular node did not. Flecainide blocked retrograde conduction in the accessory pathway in 4 patients (effective refractory period 245 +/- 41 ms) and anterograde conduction in 8 of 9 patients (effective refractory period 284 +/- 57 ms). The mean cycle length of orthodromic reciprocating tachycardia and atrioventricular nodal reentrant tachycardia increased significantly. After flecainide tachycardia was noninducible in 6 patients with orthodromic reciprocating tachycardia and in 1 with atrioventricular nodal reentrant tachycardia. It was inducible but nonsustained (less than or equal to 30 seconds) in 1 patient with orthodromic reciprocating tachycardia and in 3 with atrioventricular nodal reentrant tachycardia. Fifteen patients continued oral flecainide treatment for 19 +/- 11 months.(ABSTRACT TRUNCATED AT 250 WORDS)