Retrograde Accessory Pathway Conduction Research Articles

Effect of left atrial-coronary sinus musculature connections on the coronary sinus activation pattern via retrograde conduction in patients with WPW syndrome.

Double potential (DP) activation patterns observed in coronary sinus (CS) electrograms recorded during left lateral atrial pacing, were explained by an initial low-frequency left atrial (LA) activation potential and secondary high-frequency CS musculature activation potential in canine hearts. Moreover, the connections between the LA and CS musculature vary greatly in size and location in the human heart. The purpose of this study was to investigate the relationship between the CS activation pattern during retrograde conduction via an accessory pathway (AP) and the location of left-sided APs. Fifty-one patients (31 males, mean age 48.6 years) who underwent radiofrequency catheter ablation of left-sided APs were divided into two groups according to the successful ablation site. The CS electrograms during retrograde AP conduction were classified into 3 types; single, fractionated, and DP activation patterns. A DP pattern was identified in 10 of 12 patients (83.3%) with posteroseptal to posterolateral APs, and in particular, 9 had a divergent sequence. Twenty-six of 39 patients (66.7%) with lateral to anterolateral APs, demonstrated a single pattern. The number of radiofrequency applications was significantly higher in patients with a DP pattern than in those with a single pattern (3.4 +/- 3.3 vs. 7.8 +/- 6.8, p < 0.01). Misleading information obtained when mapping for optimal ablation sites might result from DP patterns with a divergent sequence produced by discrete muscular connections between the LA and CS musculature. Ablation around left posterior APs may require meticulous observation of the CS activation patterns.

Prevalence of retrograde accessory pathway conduction during atrial fibrillation.

Although atrial fibrillation occurs frequently in patients with the preexcitation syndrome, its pathogenesis remains controversial. The purpose of this study was to test the hypothesis that retrograde conduction over the accessory pathway occurs during atrial fibrillation and can serve as an important source of new wavefronts in atrial fibrillation. Eight patients undergoing surgical division of their accessory pathway(s) were studied. A plaque electrode array containing 56 (7 x 8) bipolar electrodes (5-mm resolution) was placed epicardially at the AV junction over the accessory pathway and atrial fibrillation was electrically induced. Excluding one patient who had only preexcited QRS complexes during atrial fibrillation and another whose accessory pathway was outside the mapped region, 4 of the 6 patients studied showed retrograde conduction over the accessory pathway during atrial fibrillation (mean atrial cycle length 157 +/- 59 msec). In these patients, 186 atrial wavefronts near the accessory pathway were analyzed. Among 67 wavefronts immediately following nonpreexcited QRS complexes, 17 originated from retrograde conduction. This constituted 9% (17/186) of total atrial wavefronts near the accessory pathway. Estimated atrial refractory period during atrial fibrillation ranged from 81 to 165 msec. (1) In patients with the preexcitation syndrome and atrial fibrillation, retrograde conduction over the accessory pathway contributed up to 9% of total atrial wavefronts near the accessory pathway. (2) The presence of an excitable gap in human atrial fibrillation was suggested by atrial preexcitation during retrograde conduction.

Demonstration of Retrograde Conduction over an Atriofascicular Accessory Pathway

Absence of retrograde conduction over a right atriofascicular accessory pathway causing reciprocating tachycardia has been considered a hallmark of this clinical entity. This report describes successful catheter ablation in a patient presenting with the distinctive pattern of preexcited left bundle branch block tachycardia utilizing a right atriofascicular accessory pathway. This pathway, however, exhibited the unique capability of ventriculoatrial conduction. Both anterograde and retrograde conduction were characterized by "node-like" properties. Demonstration of retrograde accessory pathway conduction in this particular setting does not exclude the diagnosis of a single, atriofascicular accessory pathway.

Longitudinal clinical and electrophysiological assessment of patients with symptomatic Wolff-Parkinson-White syndrome and atrioventricular node reentrant tachycardia.

Functional changes of the accessory AV pathways and dual AV node pathways are very important for patients with Wolff-Parkinson-White syndrome or AV node reentrant tachycardia who refuse to receive long-term medication or radiofrequency catheter ablation. However, no studies of serial clinical and electrophysiological characteristics in these patients have been performed. One hundred thirteen patients with Wolff-Parkinson-White syndrome or AV node reentrant tachycardia were included in this study. The first and second follow-up electrophysiological studies were performed in years 5 and 10 after the baseline study, respectively. Conduction properties of the accessory pathways became poor over time. After a mean follow-up period of 9 +/- 1 years, antegrade ventricular preexcitation and retrograde accessory pathway conduction disappeared in 22.5% and 7.8% (P < .01), respectively; dual AV node pathway physiology persisted and retrograde fast pathway disappeared in 10.8% of the patients. Baseline conduction properties of the antegrade and retrograde accessory pathways and the retrograde fast pathway independently predicted late loss of conduction. Spontaneous disappearance of the original tachyarrhythmias occurred in 10.3% of all patients, and newly developed tachyarrhythmias in 15.2%. The incidence (38.5%) of newly developed atrial fibrillation was significantly higher in patients with manifest accessory pathways. Furthermore, symptom scores and attack frequency increased significantly over time in the patients with accessory pathways and AV node reentrant tachycardia. Disappearance of the original tachycardia and changing patterns of tachycardia, also with an increase in symptom scores and attack frequency, suggested that a detailed evaluation of these events is important and early intervention with radiofrequency ablation would be helpful.

Prevalence of retrograde accessory pathway conduction during atrial fibrillation in the preexcitation syndrome

Prevalence of retrograde accessory pathway conduction during atrial fibrillation in the preexcitation syndrome

Radiofrequency Ablation Therapy in Concealed Left Free Wall Accessory Pathway With Decrementai Conduction

An electrophysiologic study followed by transcatheter radiofrequency ablation therapy was performed in two adult patients with a permanent form of junctional tachycardia. Both patients had no structural heart disease and exhibited a normal resting ECG. The P wave during tachycardia was negative in leads 1, 3, and aVF, biphasic over V6, and positive in V1 and aVL in both patients, while the P-R/R-P interval ratio during tachycardia was 0.82 and 0.36, respectively, in both patients. Both patients displayed an eccentric atrial activation sequence with the earliest atrial activation occurring at the distal coronary sinus and a decremental retrograde conduction property during incremental ventricular pacing, suggesting the presence of a concealed slowly conducting left free wall accessory pathway. The tachycardia used the normal atrioventricular pathway for anterograde conduction and the concealed show left accessory pathway for retrograde conduction. It was terminated following adenosine administration in both patients; termination of tachycardia was due to a block in the retrograde accessory pathway in one patient and due to a block in the atrioventricular node in the other patient. Radiofrequency ablation was performed by the retrograde transaortic approach. The radiofrequency f4p4ent was delivered to the site of the earliest atrial activation during tachycardia at the ventricular aspect of the mitral annulus. The successful ablation site had a ventriculoatrial (VA) interval of 120 and 130 ms, respectively, and was located at the posterolateral and lateral aspects of the mitral annulus. Following ablation, there was no VA conduction; however, conduction through the normal atrioventricular pathway was noted during isoproterenol infusion in both patients. There was no induction of tachycardia. This study demonstrates that the permanent form of junctional tachycardia in adults can incorporate a concealed left free wall accessory pathway with a decremental property. Radiofrequency ablation therapy is effective and safe in this form of arrhythmia.

Fatigue Phenomenon in Accessory Pathways

Fatigue phenomenon is transient failure of conduction following a period of repetitive excitation. Fatigue in accessory pathways is uncommon, and its electrophysiologic characteristics and clinical implications are unknown. Among the 215 patients who underwent electrophysiology studies from July 1992 to December 1993, 4 (2%) were found to exhibit fatigue over accessory pathways. The accessory pathway was posteroseptal in three patients and right free wall in one patient. The mean anterograde effective refractory period of the accessory pathway was 295 +/- 26 msec (range 270 to 330, basic drive cycle length 600 msec). Three patients had neither retrograde accessory pathway conduction nor inducible tachycardia even with infusion of isoproterenol. The fatigue phenomenon was observed after both atrial and ventricular stimulation in three patients and only after ventricular stimulation in one patient. Fatigue was dependent on duration more than rate of stimulation. We conclude that pathways exhibiting fatigue have a low margin of safety for conduction and are unlikely to be clinically problematic.

Effect of adenosine or adenosine triphosphate on antidromic tachycardia

Objectives. This study was designed to determine the effect of adenosine or adenosine triphosphate (ATP) on antidromic tachycardia.Background. Adenosine and adenosine triphosphate are useful for differential diagnosis of wide QRS tachycardia. It has been believed that tachycardia termination caused by these agents is due to the preferential depressive effect on the atrioventricular (AV) node, whereas their effect on accessory pathways is minimal. Methods. We studied the effect of adenosine or ATP on the termination pattern of antidromic tachycardia in 17 patients (10 men, 7 women; mean age [±SD] 32 ± 11 years) with one or more accessory pathways. Adenosine (6 to 12 mg [n = 10]) or ATP (8 to 20 mg [n = 7]) was injected rapidly through a central venous line and followed by 10 ml of saline flush after induction of sustained antidromic tachycardia.Results. Tachycardia was terminated in < 2 min in 14 patients (82%) after the injection and remained unchanged in 3 (18%). Tachycardia termination was due to conduction block in the accessory pathway (anterograde limb) in seven patients (50%) and in the AV node (retrograde limb) in another seven. Adenosine or ATP caused accessory pathway block in seven (88%) of the eight patients lacking retrograde accessory pathway conduction and in none of the nine patients having retrograde accessory pathway conduction (p < 0.01). All five ptients with an atriofascicular accessory pathway and unidirectional anterograde conduction had tachycardia termination due to anterograde accessory pathway block after injection of adenosine or ATP.Conclusions. 1) Adenosine or ATP effectively terminates antidromic tachycardia; 2) the termination is related to block in either the accessory pathway or the AV node; 3) accessory pathway block occurs in patients with a unidirectional, anterogradely conducting accessory pathway, especially an atriofascicular accessory pathway.

Electrophysiologic Effects of Intravenous E-4031, a Novel Class III Antiarrhythmic Agent, in Patients with Supraventricular Tachyarrhythmias

The electrophysiologic effects of intravenous (i.v.) E-4031, a new class III antiarrhythmic drug, were evaluated in 15 patients with supraventricular tachyarrhythmias [11 men, 4 women; mean age 41 +/- 19 (SD) years]. Eleven patients had accessory atrioventricular (AV) pathways, and 4 patients with no accessory pathway had paroxysmal atrial fibrillation. Electrophysiologic studies were performed before and after E-4031 administration (loading infusion 9 micrograms/kg for 5 min + maintenance infusion 0.15 microgram/kg/min). QT and QTc intervals were significantly prolonged by E-4031 from 0.40 +/- 0.03 (mean +/- SD) to 0.46 +/- 0.03 s (p < 0.0001) and from 0.43 +/- 0.03 to 0.49 +/- 0.04 s (p < 0.0001), respectively. No effect was observed on RR interval, PR interval, QRS duration, or AH and HV intervals. The effective refractory periods (ERPs) of the right atrium and ventricle were significantly prolonged from 219 +/- 27 to 236 +/- 26 ms (p < 0.001) and from 230 +/- 12 to 249 +/- 11 ms (p < 0.001), respectively. The ERP of the AV node did not change significantly after E-4031 administration. In patients with ventricular preexcitation, E-4031 significantly prolonged the ERP of the antegrade accessory pathway conduction from 340 +/- 101 to 362 +/- 106 ms (p < 0.001), but not retrograde accessory pathway conduction. AV reentrant tachycardia was induced in 3 of 11 patients with an accessory pathway, and repetitive atrial firing was induced in 3 of 4 patients with paroxysmal atrial fibrillation. E-4031 could prevent repetitive atrial firing in only 1 patient and could not prevent induction of AV reentrant tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Electrophysiologic Effects of Intravenous E-4031, a Novel Class III Antiarrhythmic Agent, in Patients with Supraventricular Tachyarrhythmias

Summary: The electrophysiologic effects of intravenous (i.v.) E-4031, a new class III antiarrhythmic drug, were evaluated in 15 patients with supraventricular tachyar-rhythmias [11 men, 4 women; mean age 41 ± 19 (SD) years]. Eleven patients had accessory atrioventricular (AV) pathways, and 4 patients with no accessory pathway had paroxysmal atrial fibrillation. Electrophysiologic studies were performed before and after E-4031 administration (loading infusion 9 μg/kg for 5 min + maintenance infusion 0.15 μg/kg/min). QT and QTc intervals were significantly prolonged by E-4031 from 0.40 ± 0.03 (mean ± SD) to 0.46 ± 0.03 s (p < 0.0001) and from 0.43 ± 0.03 to 0.49 ± 0.04 s (p < 0.0001), respectively. No effect was observed on RR interval, PR interval, QRS duration, or AH and HV intervals. The effective refractory periods (ERPs) of the right atrium and ventricle were significantly prolonged from 219 ± 27 to 236 ± 26 ms (p < 0.001) and from 230 ± 12 to 249 ± 11 ms (p < 0.001), respectively. The ERP of the AV node did not change significantly after E-4031 administration. In patients with ventricular preexcitation, E-4031 significantly prolonged the ERP of the antegrade accessory pathway conduction from 340 ± 101 to 362 ± 106 ms (p < 0.001), but not retrograde accessory pathway conduction. AV reentrant tachycardia was induced in 3 of 11 patients with an accessory pathway, and repetitive atrial firing was induced in 3 of 4 patients with paroxysmal atrial fibrillation. E-4031 could prevent repetitive atrial firing in only 1 patient and could not prevent induction of AV reentrant tachycardia. Blood pressure (BP) did not change significantly, and no undesirable side effects were associated with E-4031 administration. That E-4031 prolonged the ERP without affecting conduction time indicates that it possesses pure class III antiarrhythmic properties in patients with supraventricular tachyarrhythmias. Further evaluation of the therapeutic potential of this drug using the higher dosage may be needed.

Curative Radiofrequency Catheter Ablation for Permanent Junctional Reciprocating Tachycardia

Two patients with the permanent form of junctional reciprocating tachycardia successfully treated with the radiofrequency catheter ablation technique are described. In both patients a reentrant tachycardia utilizing a concealed slow conducting posterior septal accessory pathway for retrograde conduction was demonstrated. Radiofrequency current was delivered below the coronary sinus orifice. The procedure resulted in ablation of the accessory pathway conduction in both patients. During the follow-up, both patients remained free from tachycardia on no medication. This report demonstrates that the arrhythmogenic substrate of the permanent junctional reciprocating tachycardia can be easily suppressed by means of the radiofrequency catheter technique.

Comparison of the electrophysiologic effects of oral sustained-release and intravenous verapamil in patients with paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous verapamil (0.15 mg/kg) and oral sustained-release verapamil (verapamil-SR) (240 mg once daily for 7 days) were studied in 17 patients with paroxysmal supraventricular tachycardia (SVT). Ten patients had atrioventricular (AV) nodal reentrant tachycardia and 7 had AV reciprocating tachycardia involving an accessory AV pathway. Both preparations significantly prolonged anterograde effective refractory period of the AV node and depressed the retrograde AV nodal conduction system. The sinus cycle length, and atrial and ventricular effective refractory periods were prolonged after oral verapamil-SR. Furthermore, oral verapamil-SR depressed retrograde accessory pathway conduction which was not interfered with by intravenous verapamil. Intravenous verapamil and oral verapamil-SR prevented induction of sustained SVT in 12 of 17 (71%) and 10 of 17 (59%) patients, respectively. Follow-up study with oral verapamil-SR 240 mg once daily in 15 patients for 19 ± 6 months revealed that among the 8 patients without induction of sustained SVT, 7 have been free of symptomatic arrhythmia; only 1 patient had occasional SVT attacks. For the 7 patients with induction of sustained SVT, 3 patients failed to respond to oral verapamil-SR, 1 patient became symptom free, and the remaining 3 patients had less frequent SVT attacks. Thus, immediate intravenous verapamil testing predicts the electrophysiologic results of oral verapamil-SR therapy, and oral verapamil-SR once daily may be used for long-term prophylaxis of SVT with better patient compliance.

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)

Differential effect of intravenous procainamide on anterograde and retrograde accessory pathway refractoriness

Although procainamide may markedly impair or abolish anterograde conduction over an accessory atrioventricular (AV) pathway, orthodromic AV reentry may remain inducible. This difference may be related to a systemic differential effect of procainamide on anterograde and retrograde accessory pathway refractoriness. To examine this phenomenon, an infusion of procainamide producing five incremental Mood levels over 75 min was administered to 15 patients with the Wolff-Parkinson-White syndrome. At each procainamide level, accessory pathway effective refractory period and accessory pathway block cycle length were determined in the anterograde and retrograde directions.At baseline, there were no significant differences between anterograde and retrograde accessory pathway effective refractory periods (282 ± 7 vs. 266 ± 9 ms, p = 0.08) and block cycle lengths (288 ± 15 vs. 283 ± 9 ms, p = 0.66). The concentration of procainamide resulting in 50% prolongation of accessory pathway refractoriness was less in the anterograde direction than in the retrograde direction (27.5 [log concentration −4.56 ± SE 0.13] vs. 64.6[−4.19 ± 0.11] μmol/liler, p = 0.02). Similarly, the concentration of procainamide resulting in 50% prolongation of accessory pathway block cycle length in the anterograde direction (25.1 [−4.60 ± 0.13) μmol/liter) was less than in the retrograde direction (52.5 [−4.28 ± 0.07] μmol/liter, p = 0.01).The probability of persistence of accessory pathway conduction in the anterograde direction was less than in the retrograde direction by Kaplan-Meier analysis (p = 0.04). By the 3rd procainamide dose (mean procainamide level 32.3 ± 1.36 μmol/ liter) anterograde pre-excitation was no longer present in 6 of the 15 patients, whereas retrograde conduction over the accessory pathway did not disappear in any patient. These results demonstrate that procainamide has more marked effects on anterograde than on retrograde accessory pathway refractoriness. Thus, it may be more efficacious for arrhythmias dependent on anterograde accessory pathway conduction than for arrhythmias dependent on retrograde accessory pathway conduction.

Efficacy and safety of intravenous sotalol for termination of paroxysmal supraventricular tachycardia

A double-blind, placebo-controlled, crossover, multicenter study was conducted to study the efficacy and safety of a single intravenous dose of sotalol (1.5 mg/kg over 10 minutes) in achieving normal sinus rhythm in paroxysmal supraventricular tachycardia (SVT) lasting ≥15 minutes. Patients were randomized to either sotalol or placebo as initial treatment, and if the SVT was not terminated a crossover was performed after 20 minutes. A total of 43 patients were enrolled, 38 of whom with spontaneous (n = 14) or induced (n = 24) SVT were analyzed for sotalol efficacy. Most patients (n = 27) had atrioventricular (AV) nodal reentrant tachycardia, and an important subgroup (n = 11) had circus movement tachycardia, using an accessory pathway for retrograde conduction. The number of patients converting to sinus rhythm as a result of the initial treatment was significantly higher in the sotalol group than in the placebo group, for spontaneous (p < 0.005) as well as for induced tachycardia (p < 0.001). Sinus rhythm was achieved within 30 minutes in 83% of all patients who received sotalol as the first drug, compared with 16% of the patients first receiving placebo (p < 0.0001). For sotalol safety analysis, 42 patients were included. A total of 37 patients received sotalol, 19 as the first treatment, and 18 as the second treatment, while 25 patients received placebo. A total of 15 possible adverse effects were reported, occurring in 10 patients with sotalol versus 4 with placebo. The only severe side effect (hypotension) necessitating termination of drug administration occurred with placebo. No proarrhythmic effects were observed. The intravenous administration of sotalol appears to be safe and effective for acute termination of supraventricular reentrant tachycardia.

Intermediate septal accessory pathways: Electrocardiographic characteristics, electrophysiologic observations and their surgical implications

Intermediate septal accessory pathways are located in close proximity to the atrioventricular (AV) node and His bundle, have unique features that distinguish them from typical anterior and posterior accessory pathways and have been associated with a high risk for unsuccessful pathway division and the production of complete AV block after surgery. Between July 1986 and May 1990, 4 of 70 patients (3 men and 1 woman; mean age 33 ± 13 years) undergoing surgery for accessory pathway division were found to have an intermediate septal accessory pathway. The presenting arrhythmia was atrial fibrillation with rapid anterograde conduction over the accessory pathway in two patients and recurrent orthodromic reciprocating tachycardia in two patients.In all patients, the delta wave on the electrocardiogram (ECG) was inversed in lead V1, but two patterns of delta wave configuration were observed. In three patients (type 1 intermediate septal accessory pathway), the delta wave was upright in lead II, inverted in lead III and isoelectric in lead aVF; the transition from a negative to an upright delta wave occurred in lead V2. The fourth patient exhibited a different delta wave pattern (type 2 intermediate septal accessory pathway). The delta wave was upright in each of leads II, III and aVF; the transition from a negative to an upright delta wave occurred at lead V3.Intraoperative electrophysiologic study localized the atrial insertion of type 1 pathways to the midpoint of Koch's triangle close to the AV node. In the one patient with a type 1 pathway in which both anterograde and retrograde accessory pathway conduction was present, preoperative catheter mapping demonstrated that earliest retrograde atrial activation occurred near the foramen ovale. Intraoperative mapping during anterograde conduction over the type 1 pathway demonstrated earliest epicardial ventricular activation to occur simultaneously at the crux and the base of the aorta. The atrial insertion of the type 2 intermediate septal accessory pathway was localized to the apex of Koch's triangle in close proximity to the bundle of His. Preoperative catheter mapping revealed that earliest retrograde atrial activation occurred on the His bundle electrogram. Intraoperative mapping during anterograde conduction over the type 2 pathway demonstrated that earliest epicardial ventricular activation occurred anteriorly at the base of the aorta.Intraoperative ablation of the intermediate septal accessory pathway was accomplished by cooling the endocardium at the site of pathway insertion on the atrial side of the tricuspid anulus with a 5 mm cryoprobe. Patients with a type 1 intermediate septal accessory pathway had preservation of AV conduction, but the patient with the type 2 pathway did not and required permanent pacing. At late follow-up study, no patient has had return of intermediate septal accessory pathway conduction. Distinguishing an intermediate septal accessory pathway close to the AV node (type 1) from one close to the His bundle (type 2) is useful to predict both surgical success and success without the production of permanent complete AV block.

Differential effects of procainamide on anterograde and retrograde accessory pathway conduction

Differential effects of procainamide on anterograde and retrograde accessory pathway conduction

Electrophysiologic effects of isoproterenol in patients with atrioventricular reentrant tachycardia treated with flecainide

The electrophysiologic effects of isoproterenol in patients treated with flecainide for atrioventricular (AV) reentrant tachycardia were studied to evaluate the mechanism of tachycardia inducibility after isoproterenol and the value of isoproterenol challenge as a predictor of spontaneous arrhythmia recurrence. Seventeen patients underwent electrophysiologic study before and after oral flecainide administration and after the addition of isoproterenol to flecainide. No patient had inducible sustained supraventricular tachycardia after flecainide alone. Two patients had inducible sustained and six had inducible nonsustained tachycardia after isoproterenol was added to flecainide. The patients were then followed up on the same flecainide dose they received at the time of the electrophysiologic study.Findings:1) Flecainide treatment prolonged HV and VA intervals, and the addition of isoproterenol did not affect these variables. 2) Isoproterenol shortened anterograde and retrograde block cycle length and the refractory period of the accessory pathway and the AV node. It also decreased the tachycardia cycle length, an effect that was due solely to shortening of AV node conduction time. 3) Flecainide treatment prevented tachycardia induction by affecting retrograde conduction over the accessory pathway. Isoproterenol allowed for tachycardia induction and for more sustained episodes of tachycardia by reversing the effect of flecainide on retrograde accessory pathway conduction. 4) Tachycardia recurred during follow-up in all three patients in whom tachycardia of ≥ 10 s duration was induced after isoprottrenol but in no patient who had no or shorter episodes of induced tachyrardia (and who did not have a change in medical regimen).Conclusions:1) Isoproterenol reverses flecainide-induced prolongation of block cycle length and refractory periods of the accessory pathway and AV node. 2) Isoproterenol reverses flecainide-induced prevention of tachycardia induction through reversal of the effects of flecainide on the retrograde accessory pathway. 3) The addition of isoproterenol during flecainide restudy is valuable in predicting long-term drug efficacy.

Prognostic value of electrophysiology testing in asymptomatic patients with Wolff-Parkinson-White pattern.

The prognostic value of electrophysiology testing was studied in 75 asymptomatic patients with the Wolff-Parkinson-White electrocardiographic pattern. All patients underwent electrophysiology testing at entry to the study and were followed up annually for a total of 348 patient-years (median, 4.3 years). There were 44 male and 31 female patients, and age at enrollment ranged from 7 to 77 years (mean, 34 +/- 14 years). The median effective refractory period of the accessory pathway was 293 msec (interquartile range, 280-310 msec), and the median shortest RR interval between preexcited beats during atrial fibrillation (SRR) [corrected] was 274 msec (240-320 msec). Twenty-three patients had an SRR of 250 msec or less and eight patients had a median shortest SRR interval of 200 msec or less. Twelve patients had inducible sustained reciprocating tachycardia, 10 patients had inducible nonsustained reciprocating tachycardia, and 23 patients had inducible sustained atrial fibrillation. Twenty patients (27%) lacked retrograde conduction over the accessory pathway. No patient died suddenly during a median follow-up of 4.3 years. Six patients (8%) became symptomatic with documented supraventricular tachycardia, of whom two underwent operative ablation of their accessory pathways. No patient with absent retrograde accessory pathway conduction during the electrophysiology study became symptomatic. Inducible sustained or nonsustained reciprocating tachycardia at electrophysiology study did not predict the development of subsequent symptomatic supraventricular tachycardia. Nine patients lost preexcitation during follow-up. Age at enrollment (relative risk/decade, 1.4; 95% confidence interval, 1.0-1.8) and anterograde accessory pathway refractory period (relative risk, 1.06/10 msec; 95% confidence interval, 1.0-1.12) were independent predictors of loss of preexcitation.(ABSTRACT TRUNCATED AT 250 WORDS)

Sites of conduction block in accessory atrioventricular pathways. Basis for concealed accessory pathways.

Catheter recordings of accessory pathway (AP) activation were used to identify the site of antegrade and retrograde AP conduction block in 126 consecutive patients undergoing electrophysiological testing. Activation was recorded from 89 of 121 left free-wall and posteroseptal pathways (left APs) and from 12 of 24 right free-wall, midseptal, and anteroseptal pathways (right APs). The recorded APs were further subdivided into those exhibiting consistent antegrade conduction during sinus rhythm (overt APs: 50 left APs, eight right APs), those exhibiting intermittent antegrade conduction (intermittent APs: six left APs, two right APs), and those exhibiting only retrograde conduction (concealed APs: 33 left APs, two right APs). The sites of block were recorded during decremental atrial and ventricular stimulation. The sites of both antegrade and retrograde block were determined in 40 of 50 overt left APs and six of eight overt right APs. Antegrade and retrograde block occurred at or near the AP-ventricular (AP-V) interface in 37 of 40 overt left APs and two of six overt right APs and at the atrial-AP (A-AP) interface in one of 40 overt left APs and four of six overt right APs. In three of three overt left APs with no retrograde conduction, retrograde block occurred at or near the AP-V interface. The site of antegrade and retrograde block differed in only two of 58 overt pathways. There was no difference between overt APs limited at the A-AP or the AP-V interface in the shortest atrial or ventricular pacing cycle length maintaining 1:1 antegrade or retrograde AP conduction, respectively. Both antegrade and retrograde block occurred near the AP-V interface in four of six intermittent left APs and zero of two intermittent right APs and near the A-AP interface in two of six intermittent left APs and one of two intermittent right APs. The sites of both antegrade and retrograde block were determined in 28 of 33 concealed left APs, and both occurred at or near the AP-V interface in 26 and A-AP interface in two APs. In two of two concealed right APs, antegrade block occurred at the AP-V interface. These findings suggest that both antegrade and retrograde conduction are limited by factors operating near the AP-V interface in overt left APs and at the A-AP or AP-V interface in overt right APs. Factors limiting antegrade conduction in concealed APs appear to be located almost always near the AP-V interface.