Antegrade Fast Pathway Research Articles

High-density visualization of antegrade fast pathway activation during atypical fast/slow atrioventricular nodal reentrant tachycardia in two cases.

High-density visualization of antegrade fast pathway activation during atypical fast/slow atrioventricular nodal reentrant tachycardia in two cases.

Evaluation of the input site and characteristics of the antegrade fast pathway based on three-dimensional bi-atrial stimulus-ventricle mapping

PurposePrevious studies examined the right atrial (RA) input site of the antegrade fast pathway (AFp) (AFpI). However, the left atrial (LA) input to the atrioventricular (AV) node has not been extensively evaluated. In this study, we created three-dimensional (3-D) bi-atrial stimulus-ventricle (St-V) maps and analyzed the input site and characteristics of the AFp in both the RA and LA.MethodsForty-four patients diagnosed with atrial fibrillation or WPW syndrome were included in this study. Three-dimensional bi-atrial St-V mapping was performed using an electroanatomical mapping system. Sites exhibiting the minimal St-V interval (MinSt-V) were defined as AFpIs and were classified into seven segments, four in the RA (F, S, M, and I) and three in the LA (M1, M2, and M3). By combining the MinSt-V in the RA and LA, the AFpIs were classified into three types: RA, LA, and bi-atrial (BA) types. The clinical and electrophysiological characteristics were compared.ResultsAFpIs were most frequently observed at site S in the RA (34%) and M2 in the LA (50%), and the BA type was the most common (57%). AFpIs in the LA were recognized in 75% of the patients. There were no clinical or electrophysiological indicators for predicting AFpI sites.ConclusionsThree-dimensional bi-atrial St-V maps could classify AFpIs in both the RA and LA. AFpIs in the LA were frequently recognized. There were no significant clinical or electrophysiological indicators for predicting AFpI sites, and 3-D bi-atrial St-V mapping was the only method to reveal the precise AFp input site.

Visualization of the Antegrade Fast and Slow Pathway Inputs in Patients with Slow‐Fast Atrioventricular Nodal Reentrant Tachycardia

Mapping of the antegrade fast pathway (A-FP) exact sites and antegrade slow pathway (A-SP) input locations has not been well described. In 56 patients with slow-fast atrioventricular nodal reentrant tachycardia (SF-AVNRT), pacing during sinus rhythm and entrainment pacing during SF-AVNRT were performed at various sites in the triangle of Koch and coronary sinus (CS) to identify the A-FP and A-SP inputs. User-defined three-dimensional electro-anatomical mapping of the stimulus-His potential (St-H) interval and anatomical location was performed. The A-FP input was defined as the site of the shortest St-H interval, and A-SP input as the site of the shortest St-H interval and with a postpacing-interval equal to the tachycardia cycle length. The locations of the A-FP and A-SP inputs were mapped as a ratio of the distance between the His bundle (HB) and CS orifice (CSO), and the HB-CSO axis was divided into three zones: superior-, mid-, and inferior septum. The distance between the A-SP and A-FP inputs was calculated using the distance from each input to the HB and HB-CSO axis. Only 30 patients were included in this study because the A-SP mapping failed in 26. The A-SP input was distributed to the superior septum in four, mid- or inferior septum in 25, and CS in one. An A-SP input which was located less than 10 mm from the A-FP input was observed in one of four patients with a superior septum A-SP. An A-SP input at the superior septum seemed to be a potential risk for atrioventricular nodal injury during ablation.

Improvement of atrioventricular conduction following catheter ablation of atrioventricular nodal reentry tachycardia in a patient with a prolonged PR interval

We herein present the case of a 60-year-old male with narrow QRS tachycardia who had a remarkable PR prolongation during sinus rhythm. The tachycardia was diagnosed as a slow-fast atrioventricular nodal reentry tachycardia. Slow pathway ablation was performed after the confirmation of the presence of an antegrade fast pathway. Following the elimination of the slow pathway, the PR and atrio-His intervals became shortened from 470 and 420 to 170 and 120ms, respectively. Moreover, the improvement of atrioventricular conduction after the slow pathway ablation lasted for at least 34months.

Recognition of inferiorly dislocated fast pathways guided by three-dimensional electro-anatomical mapping

Slow pathway (SP) ablation of atrioventricular (AV) nodal reentrant tachycardia (AVNRT) can be complicated by unexpected AV block even at sites >10 mm inferior to the bundle of His (HB), and one cause is thought to be the inferior dislocation of an antegrade fast pathway (A-FP). We assessed locations of FPs guided by CARTO. Sites of FPs were mapped guided by CARTO before SP ablation in 18 patients with slow-fast AVNRT. The A-FP was defined as the site with the minimum interval between the stimulus and HB potential when pace mapping in the right atrial septum. The A-FP was 7.9 ± 7.5 mm inferior and 2.9 ± 5.0 mm posterior to the HB. In 6 of 18 patients (33%), the A-FP was inferiorly dislocated >10 mm to the HB. SP ablation was successfully performed in all patients at sites >10 mm from both the HB and the A-FP without AV block. In the inferiorly dislocated A-FP group, A-FPs seemed to be positioned much more on atrial sites and sufficiently posterior to SP ablation sites. The A-FP inferiorly dislocated >10 mm to the HB in one third of patients with AVNRT and seemed to be positioned deep on atrial sites. It is again emphasized that SP ablation within the triangle of Koch should be performed at a very ventricular annulus site, particularly in the inferiorly dislocated A-FP group.

Clinical Importance of the Inferiorly Dislocated Fast Pathway in the Patients with Atrioventricular Nodal Reentrant Tachycardia

Backgrounds: In the catheter ablation of atrioventricular nodal reentrant tachycardia (AVNRT), the patients with the inferiorly dislocated fast pathway (IDF) were high risk of the inadvertent atrioventricular block. Objective: The purpose of this study is to show the effects of the IDF on the results of the catheter ablation. Methods: 43 consecutive patients with AVNRT were entered this study. Using the electroanatomical mapping system, the antegrade fast pathway entrance (AF) was detected and divided into 4 groups; outside and posterior to the triangle of Koch (TOK) (group F: n=17) and inside and the upper (group S: n=7), the middle (group M: n=5), and the lower (group I: n=14) third of the TOK. Group M and I were defined as the IDF. In all patients, anatomical slow pathway ablation was performed. Results: The dimension of the TOK was not different in all groups. The success rate of the slow pathway ablation was 100% in group F and S, but 80% in group M and 71% in Group I. During follow-up, no patient in group F, S, and M, but 2 patients in group I had a recurrence of the tachycardia. Conclusion: The patients with the IDF were not only refractory to the conventional slow pathway ablation, but also showed high rate of recurrence.

New Pacing Method for Estimating the Entrance of the Antegrade Fast Pathway

Backgrounds: Catheter ablation of the slow pathway in patients with the inferiorly dislocated fast pathway (IDF) showed high rate of procedure failure and high risk of atrioventricular block. Objective: The purpose of this study is to test the effectiveness of the new pacing method for estimating the antegrade fast pathway entrance (AF). Methods: 30 consecutive patients with PSVT (25 AVNRT, 4 AVRT, 1 AT) were entered this study. Using the electroanatomical mapping system, the AF was detected and divided into 4 groups; outside and posterior to the triangle of Koch (TOK) (group F: n=8) and inside and the upper (group S: n=3), the middle (group M: n=7), and the lower (group I: n=12) third of the TOK. Group M and I were defined as the IDF. During the constant pacing from the Halo catheter at the inferolateral right atrium (Lat) and the coronary sinus ostium (CS), Atrial-His interval at the His bundle recording catheter was measured (A-HLat and A-HCS, respectively). The difference between A-HLat and A-HCS was calculated (δLat-CS) and compared with the AF. Results: The dimension of the TOK was not different in all groups. δLat-CS was significantly larger in the IDF (group F: 2.4±2.3 ms, group S: 2.3±2.1 ms, group M: 11.6±4.8 ms, group I: 25.3±7.4 ms (P<0.0001)). Conclusion: Using new pacing method, we could easily estimate the AF before radiofrequency energy application to the slow pathway.

Incidence and Mechanism of Dislocated Fast Pathway in Various Forms of Atrioventricular Nodal Reentrant Tachycardia

The incidence and mechanism of the dislocated antegrade fast pathway (A-FP) were examined in various forms of atrioventricular nodal reentrant tachycardia (AVNRT). To localize the A-FP, 5 atrial sites comprising the inferior coronary sinus ostium (CSOS), apex of the triangle of Koch (A-TOK), and 3 equidistant sites on the atrioventricular junction extending from A-TOK to CSOS (site S, M, and I) were pace mapped at 100 beats/min in 71 patients with slow-fast (n=49), fast-slow (n=7) and slow-intermediate (n=15) forms of AVNRT. The site with the shortest interval between the stimulus and His potential recorded at the A-TOK (shortest St-H) was defined as the A-FP site. The A-FP was located at A-TOK in 31 patients (nondislocated group), and inferior to A-TOK in 40 patients (site S in 26, M in 13, and I in one patient; dislocated group). There was no significant difference in the location of the A-FP among the 3 forms of AVNRT. Although the shortest St-H did not differ between groups, the St-H at A-TOK in the dislocated group was significantly longer than that in the nondislocated group. Additionally, the His potential preceding that of the A-TOK was observed more frequently inferior to the A-TOK in the dislocated group than in the nondislocated group, suggesting that the A-FP dislocation was accompanied by displacement of the His bundle. Dislocated A-FP was frequently and uniformly observed among various forms of AVNRT, and is probably caused by inferior displacement of the entire atrioventricular node - His bundle apparatus.

The Different Ablation Effects on Atrioventricular Nodal Reentrant Tachycardia in Children with and without Dual Nodal Pathways

Previous studies in adults have shown a significant shortening of the fast pathway effective refractory period (ERP) after successful slow pathway ablation. However, information on atrioventricular nodal reentrant tachycardia (AVNRT) in children is limited. The purpose of this retrospective study was to investigate the different effects of radiofrequency (RF) catheter ablation in pediatric AVNRT patients between those with and without dual atrioventricular (AV) nodal pathways. From January 1992 to August 2004, a total 67 pediatric patients with AVNRT underwent an electrophysiologic study and RF catheter ablation at our institution. We compared the electrophysiologic characteristics between those obtained before and after ablation in the children with AVNRT with and without dual AV nodal pathways. Dual AV nodal pathways were found in 37 (55%) of 67 children, including 36 (54%) with antegrade and 10 (15%) with retrograde dual AV nodal pathways. The antegrade and retrograde fast pathway ERPs in children with dual AV nodal pathways were both longer than the antegrade and retrograde ERPs in children without dual AV nodal pathways (300 +/- 68 vs 264 +/- 58 ms, P = 0.004; 415 +/- 70 vs 250 +/- 45 ms, P < 0.001) before ablation. In children with antegrade dual AV nodal pathways, the antegrade fast pathway ERP decreased from 300 +/- 68 ms to 258 +/- 62 ms (P = 0.008). The retrograde fast pathway ERP also decreased after successful ablation in the children with retrograde dual AV nodal pathways (415 +/- 70 vs. 358 +/- 72 ms, P = 0.026). The dual AV nodal physiology could not be commonly demonstrated in pediatric patients with inducible AVNRT. After a successful slow pathway ablation, the fast pathway ERP shortened significantly in the children with dual AV nodal pathways.

Differential Effects of Adenosine on Antegrade Fast Pathway, Antegrade Slow Pathway, and Retrograde Fast Pathway in Atrioventricular Nodal Reentry

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

Variable effects of adenosine on retrograde conduction in patients with atrioventricular nodal reentry tachycardia.

Adenosine has been demonstrated to reliably produce transient block of atrioventricular nodal (AVN) conduction, and has been advocated as a method of differentiating retrograde conduction via the atrioventricular node from accessory pathway conduction. However, the response of retrograde AVN to adenosine in patients with typical atrioventricular nodal reentry tachycardia (AVNRT) remains unclear. We evaluated 13 patients (mean age 45 +/- 20 years) with typical AVNRT prior to AVN modification. During right ventricular pacing, a rapid bolus of adenosine (0.2 mg/kg; maximum 18 mg) was administered. Adenosine sensitivity, defined by transient ventriculoatrial block, was observed in six patients, while in seven patients ventriculoatrial conduction was unaffected. An adenosine bolus administered during sinus rhythm or atrial pacing resulted in antegrade atrioventricular block in all the adenosine resistant patients in whom this was performed (n = 6). Comparisons of AVN electrophysiological characteristics between the adenosine sensitive and adenosine resistant patients were performed. There was no difference with respect to ventriculoatrial effective refractory period, ventriculoatrial Wenckebach, AVNRT cycle length, and His to atrial echo interval in AVNRT. However, there was a trend toward a longer antegrade fast pathway ERP in the adenosine sensitive group (P = 0.07). Electrophysiological properties do not predict retrograde AVN adenosine sensitivity. Adenosine does not cause retrograde AVN block in all patients with AVNRT, and therefore cannot reliably distinguish between retrograde conduction via the AVN or an accessory pathway.

Radiofrequency catheter ablation of atrioventricular nodal reentrant tachycardia in children.

Radiofrequency (RF) catheter ablation has been widely used in the treatment of cardiac arrhythmias. In atrioventricular nodal reentrant tachycardia (AVNRT), the experience has been predominantly in adults. The cardiac electrophysiological records of 18 consecutive children undergoing RF catheter AV node modification for AVNRT were reviewed. The patients (10 females, 8 males) were 8.2-17.9 years of age (mean 13.6 +/- 3.0), weight 15.2-88.1 kg (mean 52.2 +/- 20.8), and height 103-190 cm (mean 157.1 +/- 21.7). Thirteen were on antiarrhythmic medications (1-3, average 1.5 drugs/day). All drugs were discontinued 48 hours prior to the ablations. The procedures were performed under sedation and local anesthesia. Pre- and post-AV node modification electrophysiological studies were performed in all procedures. The 18 patients underwent a total of 25 procedures (1.39 +/- 0.61 per patient): the anterior approach aimed at the antegrade fast pathway in the first four patients and the posterior approach aimed at the slow pathway in the remainder. The number of energy applications was 8-54 (19.8 +/- 10.7) per procedure. The maximum energy used in each procedure was 30-50 watts (33.8 +/- 8.4). The average energy was 24-50 watts (33.0 +/- 6.8). The fluoroscopy time was 7.1-73.4 minutes (29.9 +/- 20.0) per procedure, for a total catheterization time of 228-480 minutes (300.3 +/- 59.1). Preablation spontaneous or induced AVNRT (cycle length 310.4 +/- 55.0 msec) was seen in all except one who had the arrhythmia (cycle length 270 msec) on surface ECG.(ABSTRACT TRUNCATED AT 250 WORDS)

Efficacy and Safety of Radiofrequency Catheter Ablation For Paroxysmal Supraventricular Tachycarias

From January 1992 to June 1993, 100 consecutive patients with clinically documented paroxysmal supraventricular tachycardias underwent radiofrequency catheter ablation. Group 1 consisted of 46 patients (male : female= 9 : 37, age: 46±13 years) with slow-fast atrioventricular nodal reentrant tachycardia. Radiofrequency current was aimed at the slow pathway area which was identified by both anatomical and electrophysiological methods. A mean application of 8± 9 was delivered at a mean power of 22±4 watts with a mean duration of 21±3 seconds. Selective ablation of slow pathway conduction was achieved in 28 patients and modification of slow pathway conduction in 12 patients. Antegrade fast pathway conduction was ablated in 3 patients, and retrograde fast pathway conduction in 1. Mean peak CPK was 156±117 IU/L after ablation. Neither AV block nor clinical recurrence was found during 9.7±5.1 months follow up. Group 2 consisted of 54 patients with accessory pathway (AP) mediated atrioventricular reciprocating tachycardia. For 35 patients (M : F21 : 14, age: 40±12 years) who had left-sided accessory pathway, catheter ablation was approached by the retrograde transaortic technique in 33 patients and by the transseptal left atrial approach through patent foramen ovale in 2 patients. The mean energy delivered was 28±5 watts for a duration of 27±12 sec and 9±8 applications. The accessory pathway conduction was successfully ablated in 30 patients (86%). Mean peak CPK was 392±534 lU/L. Cardiac tamponade occurred in 1 patient and transient cerebral ischemia in another, but without mortality. No clinical recurrence was found during 9±4 months follow-up. Nineteen patients (M : F= 7 : 12, age: 36±11 years) had right-sided AP. The mean energy required for successful ablation was 30±4 watts for a duration of 35±15 sec and 12±9 applications. Mean peak CPK was 147±70 lU/L. Clinical recurrence occurred in 3 patients (15.8%), 1 of them had subsequent successive ablation. The overall immediate procedure success rate for right-sided AP was 65%. In conclusion, radiofrequency catheter ablation is a safe and effective treatment modality for patients with paroxysmal supraventricular tachycardias.

Selective radiofrequency catheter ablation of fast and slow pathways in 100 patients with atrioventricular nodal reentrant tachycardia

One hundred patients received selective radiofrequency ablation of retrograde fast pathway (32 patients, group I) or slow pathway (68 patients, group II) to teat drug-refractory atrioventricular nodal reentrant tachycardia. In group I, a mean of 6 ± 3 radiofrequency pulses eliminated the retrograde fast pathway. Thirty patients were free of symptoms and were not receiving antiarrhythmic drugs; two patients had accidental atrioventricular block. One patient had recurrent tachycardia and received a repeated ablation (slow pathway ablation). In group II, a mean of 9 ± 4 radiofrequency pulses eliminated the slow pathway in 68 patients. All patients were free of symptoms and were not receiving antiarrhythmic drugs. One patient had recurrent tachycardia and received a repeated ablation. Serial follow-up electrophysiologic studies (immediate [20 to 30 minutes], early [5 to 7 days], and late [3 to 6 months]) showed that selective ablation of retrograde fast pathway was associated with nonspecific injury on the antegrade fast pathway (increase of AH interval) without effects on the slow pathway. Selective ablation of slow pathway was associated with nonspecific injury on the retrograde fast pathway in 15 patients (22%), but the antegrade fast pathway conduction parameters did not change significantly. Thus retrograde and antegrade fast pathway may be anatomically similar or have different sensitivities to radiofrequency energy, and slow pathway may be anatomically distinct from fast pathway. We conclude that (1) selective radiofrequency ablation of retrograde fast or slow pathway could cure atrioventricular nodal reentrant tachycardia with a high success rate (98%) and a low recurrence rate (2%) during a follow-up period of 6 to 18 months, but fast pathway ablation was associated with accidental atrioventricular block (5%), and (2) serial follow-up electrophysiologic studies elucidated the possible mechanisms of cure in atrioventricular nodal reentrant tachycardia.

Double Response of the Ventricle During Transient Entrainment in a Common Atrioventricular Nodal Reentrant Tachycardia

We report a patient with slow-fast atrioventricular (AV) nodal reentrant tachycardia, in which double ventricular response was demonstrated during rapid pacing at cycle length of 300 msec or less from the high right atrium. The determinants of double ventricular response during transient entrainment in the present case were: (1) a crucial conduction delay in the slow pathway; (2) the collision between the activation via the antegrade fast pathway (antidromically) of the last paced beat and the activation via the antegrade slow pathway (orthodromically) of the previous paced beat, instead of the unidirectional block in the slow pathway; and (3) the enhanced AV nodal conduction over the antegrade fast pathway.

Electrophysiologic effects and efficacy of cibenzoline in patients with supraventricular tachycardia.

Electrophysiologic effects of intravenous (i.v.) cibenzoline were evaluated in 18 patients with accessory pathways or dual atrioventricular (AV) nodal pathways (12 men and 6 women with a mean age of 44 +/- 18 years). Twelve patients had accessory AV pathways, including 6 patients with a manifest accessory pathway. Six patients had AV nodal reentrant tachycardia (AVNRT). Electrophysiologic studies were performed before and after cibenzoline (1.4 mg/kg i.v.) infusion for 5 min. Sinus cycle length did not change significantly after cibenzoline administration. Cibenzoline increased both the AH (85 +/- 20 vs. 91 +/- 21 ms, p less than 0.05) and HV intervals (41 +/- 10 ms vs. 53 +/- 11 ms, p less than 0.001). Neither the atrial nor ventricular effective refractory period (ERP) was altered by cibenzoline. Complete block in the accessory pathway occurred antegradely in 4 patients and retrogradely in 1 patient. Cibenzoline prevented induction of AV reentrant tachycardia (AVRT) in 3 of 8 patients with sustained orthodromic AVRT by abolishing retrograde accessory pathway conduction or prolonging the retrograde accessory pathway ERP. Of 5 patients who continued to have inducible AVRT before and after cibenzoline administration, the tachycardia cycle length was increased in 3, mainly due to the increase in retrograde accessory pathway conduction time. Cibenzoline prevented induction of sustained AVNRT in 4 of 5 patients by prolonging the minimum pacing cycle length, maintaining 1:1 ventriculoatrial (VA) conduction through the retrograde fast AVN pathway or shortening the antegrade fast AVN pathway ERP equal to the slow AVN pathway. In one patient who had an uncommon type of AVNRT, sustained tachycardia was induced by cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)

Conduction Properties of the Antegrade Fast and Slow AV Nodal Pathways Associated with AV Nodal Reentrant Tachycardia.

To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500 msec, p less than 0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.

Salutary effects of intravenous ajmaline in patients with paroxysmal supraventricular tachycardia mediated by dual atrioventricular nodal pathways: blockade of the retrograde fast pathway.

Electrophysiologic effects of 50 mg iv ajmaline were evaluated in 10 patients with atrioventricular nodal reentrant paroxysmal supraventricular tachycardia (PSVT) utilizing the slow pathway for antegrade and the fast pathway for retrograde conduction. Ajmaline terminated the PSVT in all 10 patients in 17 to 165 sec (mean 94 +/- 49 sec): by ventriculoatrial block in eight, AH block in one, and intra-atrial reentry in one patient. The predrug mean PSVT cycle length of 289 +/- 44 msec (range 240 to 350) increased significantly to 373.5 +/- 60 msec (range 263 to 464; p less than .01) before the tachycardia was terminated. The increase in cycle length was a function of both AH and HA prolongation. In all 10 patients ajmaline depressed conduction through the retrograde fast pathway, as evidenced by the increase in mean ventricular paced cycle length producing ventriculoatrial block from less than or equal to 280 +/- 40 to 438 +/- 93 msec (p less than .001), and the increase in the effective refractory period of the ventriculoatrial conduction system from less than or equal to 241 +/- 42 to less than or equal to 298 +/- 62 msec (p less than .05); the drug abolished ventriculoatrial conduction in four cases. The effective refractory period of the antegrade fast pathway was unchanged after ajmaline (less than or equal to 281 +/- 31 vs less than or equal to 275 +/- 38 msec; p = NS), but conduction through the antegrade slow pathway was depressed (atrial paced cycle length producing AH block 269 +/- 30 msec before and 312 +/- 44 msec after drug; p less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Effects of procainamide on atrioventricular nodal re-entrant paroxysmal tachycardia.

Electrophysiological effects of 750 mg i.v. procainamide were studied in 14 patients with dual pathway atrioventricular (A-V) nodal re-entrant paroxysmal tachycardia (PSVT). All patients utilized an A-V nodal slow pathway for antegrade and an A-V nodal fast pathway for retrograde conduction during PSVT. In all 14 patients, procainamide depressed retrograde fast pathway conduction, manifest by increase in mean ± SEM ventricular paced cycle length (CL) producing V-A block from 5 295 ± 25 to 385 ± 17 msec (P < 0.001). Antegrade fast and slow pathway properties were unchanged with procainamide. Eleven of the 14 patients had induction of sustained PSVT before procainamide. Eight of these lost ability to induce or sustain PSVT after procainamide, reflecting depression of retrograde fast pathway conduction with either absence of atrial echoes (4 pts) or induction of nonsustained PSVT, with termination of PSVT occurring after QRS (retrograde block in fast pathway) (4 pts). In three of these 11 patients, sustained PSVT was inducible before and after procainamide (mean CL of 395 ± 38 and 395 ± 40 respectively) (NS). Three patients had induction of nonsustained PSVT before procainamide. In two, induction of sustained PSVT occurred after procainamide due to enhanced antegrade slow pathway conduction, while in the other PSVT remained nonsustained. In conclusion, procainamide inhibited induction of sustained A-V nodal re-entrant PSVT in most patients, reflecting selective depression of retrograde A-V nodal fast pathway conduction. In a minorityof patients, vagolytic effects of procainamide potentiated induction of sustained PSVT.