Accessory Atrioventricular Research Articles

Indications for modification of coexisting dual atrioventricular node pathways in patients undergoing surgical ablation of accessory atrioventricular connections

Concomitant susceptibility to atrioventricular (AV) node reentrant tachycardia has been demonstrated in certain patients having reentrant tachycardia utilizing accessory AV connections. For those patients undergoing accessory connection ablation, AV node surgical modification may be warranted during the same operative procedure. To assess indications for a combined operative procedure, this study evaluated potential predictors of subsequent spontaneous AV node reentrant tachycardia in patients undergoing ablation of accessory AV connections.Among 62 consecutive patients undergoing surgical ablation of an accessory AV connection, 13 (21%) manifested dual AV node pathways. The latter were identified preoperatively in five patients (four with concealed and one with bidirectional accessory connections) and postoperatively in seven (all seven with bidirectional accessory connections). In one patient with a bidirectional accessory connection, dual AV node pathways could not be demonstrated preoperatively, but AV node reentrant tachycardia was induced. Operative ablation of an accessory connection was successful in all patients. However, postoperatively, 2 of the 13 patients had inducible AV node reentrant tachycardia, 5 had AV node “echo” beats and 6 had no inducible arrhythmia.During 26 ± 7 months of follow-up study, the two patients with inducible AV node reentrant tachycardia postoperatively had symptomatic AV node reentrant tachycardia. In addition, the one patient with inducible AV node reentrant tachycardia preoperatively had recurrence of this tachycardia 4 months after attempted surgical modification of the AV node. Consequently, although dual AV node pathways appear to be common in patients undergoing surgical ablation of an accessory AV connection (21%), only a small group (3 of 13) of these patients are at risk for subsequent clinical AV node reentrant tachycardia.The presence of dual AV node pathways either alone or in conjunction with AV node echoes does not predict occurrence of AV node reentrant tachycardia. However, induction of sustained AV node reentrant tachycardia appears to be associated with a greater likelihood of spontaneous symptomatic tachycardia and therefore warrants consideration of AV node modification at the time of surgical ablation of an accessory connection.

Electrocardiographic body surface potential mapping in the Wolff-Parkinson-White syndrome. Noninvasive determination of the ventricular insertion sites of accessory atrioventricular connections.

A reliable, noninvasive procedure to determine the location of accessory atrioventricular connections in patients with Wolff-Parkinson-White syndrome would add an important diagnostic tool to the clinical armamentarium. Body surface potential mapping (BSPM) using 180 electrodes in various-sized vests and displayed as a calibrated color map was used to determine the ventricular insertion site of the accessory atrioventricular (AV) connections in 34 patients with Wolff-Parkinson-White syndrome. Attempts were made to determine the 17 ventricular insertion sites described by Guiraudon et al. All 34 patients had an electrophysiologic study (EPS) at cardiac catheterization, and 18 had surgery so the ventricular insertion sites could be accurately located using EPS at surgery. A number of physiologic observations were also made with BSPM. The following conclusions were drawn: 1) BSPM using QRS analysis accurately predicts the ventricular insertion site of accessory AV connections in the presence of a delta wave in the electrocardiogram; 2) the ventricular insertion sites of accessory AV connections determined by BSPM and by EPS at surgery were identical or within one mapping site (1.5 cm or less) in all but four of 18 cases; three of the four exceptions had more than one accessory AV connection, and the other had a very broad ventricular insertion; 3) BSPM and EPS locations of the accessory AV connections correlated very well in the 34 cases despite the fact that BSPM determines the ventricular insertion site and EPS determines the atrial insertion site of the accessory AV connection; 4) as suggested by the three cases of multiple accessory AV connections, EPS and BSPM may be complementary since BSPM identified one pathway and EPS identified the other (in the case with a broad ventricular insertion, BSPM and EPS demonstrated different proportions of that insertion); 5) BSPM using ST-T analysis is very much less accurate in predicting the ventricular insertion site of accessory AV connections unless there is marked preexcitation; 6) standard electrocardiography using the Gallagher grid methodology (but with no attempt at stimulating maximal preexcitation) was not as accurate as QRS analysis of BSPM in predicting the ventricular insertion site of the accessory AV connection; however, exact comparison is hampered by the different number and size of the Gallagher and Guiraudon insertion sites; 7) BSPM using QRS analysis appears to be very accurate in predicting right ventricular versus left ventricular posteroseptal accessory AV connections; 8) typical epicardial right ventricular breakthrough, indicative of conduction via the specialized AV conduction system, occurs in all patients with left ventricular free wall accessory AV connections; 9) epicardial right ventricular breakthrough was not observed in cases with right ventricular free wall or anteroseptal accessory AV connections; 10) epicardial right ventricular breakthrough can occur in the presence of posteroseptal accessory AV connections, whether right or left ventricular; and 11) the delay in epicardial right ventricular breakthrough in cases with left ventricular insertion may provide a marker to estimate the degree of ventricular preexcitation.

Electrophysiologic Effects and Antiarrhythmic Efficacy of Recainam in Patients with Supraventricular Tachycardia

Recainam is a new antiarrhythmic agent with class Ic properties. To evaluate its electrophysiologic effects and antiarrhythmic efficacy in patients with recurrent supraventricular tachycardia (SVT), programmed electrical stimulation was performed in 10 patients before and after intravenous recainam (loading dose 0.8 mg/kg, infusion 1 mg/kg/h), and in four patients on oral recainam 1,200 mg/day. Five patients had atrioventricular (AV) node reentrant tachycardia; five had AV-reciprocating tachycardia. There were no significant changes in electrocardiographic and intracardiac intervals after either intravenous or oral recainam. After intravenous recainam, the ventricular effective refractory period (ERP) shortened (231 +/- 14-219 +/- 9 ms, p less than 0.05). The antegrade ERP of all three bidirectional accessory pathway markedly prolonged, but the effect on retrograde accessory pathway and AV node ERPs was unremarkable. SVT induction was prevented in three of 10 patients and SVT cycle length increased modestly in seven (357 +/- 44-374 +/- 42 ms, p = 0.07). On oral recainam, an increase in the frequency of spontaneous SVT occurred in two patients. At the doses given, recainam caused less electrophysiologic change than expected, had modest antiarrhythmic efficacy, and might have significant arrhythmogenic potential.

Localization and radiofrequency catheter ablation of accessory AV pathways in Wolff-Parkinson-White syndrome.

Direct catheter recordings of accessory pathway activation were utilized to localize accessory atrioventricular (AV) pathways for radiofrequency catheter ablation in 187 patients with Wolff-ParkinsonWhite syndrome. Closely spaced bipolar catheter electrodes (1.5-2.5 mm center-to-center) were positioned perpendicular to the mitral anulus (orthogonal electrodes placed circumferentially around the catheter) and the tricuspid anulus (conventional ring electrodes), and recordings were obtained at low gain « 1 cm/mV). The small recording range of the close bipolar electrodes minimized the recording of distant atrial or ventricular potentials occurring simultaneously with accessory pathway activation and enabled differentiation of accessory pathway activation potentials from local atrial and ventricular potentials. For ablation, a special large tip electrode (7F, 4 mm long, 27 mrrr' surface area) was positioned against the mitral or tricuspid anulus at a site guided by direct recordings of accessory pathway activation. The large tip electrode was positioned either beneath or above the leaflet, and radiofrequency current (power approximately 30 watts) was delivered for approximately 45 seconds to the large tip electrode using a large skin lead for the return electrode .

Determinants of the ventricular rate during atrial fibrillation

Determinants of the ventricular cycle length during atrial fibrillation were examined in 52 patients. Thirty-three patients had structural heart disease and none had an accessory atrioventricular (AV) connection. The AV node effective and functional refractory periods, the shortest atrial pacing cycle length associated with 1:1 conduction, the AV node conduction time and indexes of concealed conduction in the AV node were measured in the baseline state (36 patients) and after modification of sympathetic tone by infusion of isoproterenol or propranolol (8 patients each). Atrial fibrillation was then induced with rapid atrial pacing, and the mean, shortest and longest ventricular cycle lengths were measured.Variables that correlated most strongly with the mean RR interval during atrial fibrillation were the AV node effective refractory period (r = 0.93; p < 0.001), AV node functional refractory period (r = 0.87; p < 0.001) and shortest atrial pacing cycle length associated with 1:1 conduction (r = 0.91; p < 0.001). The AH interval during sinus rhythm (r = 0.74; p < 0.001) and during atrial pacing at the shortest cycle length with 1:1 conduction (r = 0.52; p < 0.001) had weaker correlations. Measures of concealed conduction did not improve the prediction of the mean or longest ventricular cycle length during atrial fibrillation.In conclusion, the refractory periods and conductivity of the AV node are the best indicators of the potential of the node to transmit atrial impulses to the ventricles during atrial fibrillation. The degree of concealed conduction in the AV node is a less important determinant of the mean ventricular rate during atrial fibrillation.

Usefulness of combined propranolol and verapamil for evaluation of surgical ablation of accessory atrioventricular connections in patients without structural heart disease

Successful surgical ablation of atrioventricular (AV) accessory connections may be confirmed during postoperative electrophysiologic testing by the absence of accessory connection conduction in both the anterograde and retrograde directions. Whereas the former may be readily apparent by examination of the surface electrocardiogram during sinus rhythm or atrial pacing, assessment of the latter may be complicated by the frequent presence of enhanced retrograde AV nodal conduction in the postoperative period. Consequently, availability of interventions that selectively affect AV nodal conduction and refractoriness without concomitant effects on accessory connections may be helpful for assessing the success of the surgical procedure. In this study the effects of combined propranolol and verapamil administration on electrophysiologic properties of the AV node and the accessory AV connection were assessed both pre- and postoperatively in 17 patients (12 men and 5 women, mean age 33 years) undergoing surgical ablation of accessory connections. Preoperatively, electrophysiologic characteristics of all but 1 of the accessory AV connections were unaffected by propranolol and verapamil administration. Postoperatively, on the other hand, propranolol and verapamil significantly prolonged both the retrograde AV node effective refractory period (baseline: 272 ± 34 ms vs after drugs: 384 ± 70 ms [p < 0.0001]) and the shortest cycle length maintaining 1:1 ventriculoatrial conduction (baseline: 357 ± 99 ms vs after drugs: 485 ± 64 ms [p < 0.0001]). Late postoperative electrophysiologic evaluation (7 ± 3 weeks) revealed no evidence of residual accessory AV connection conduction, and all patients remain asymptomatic at 21 ± 10 months follow-up. Thus, thecombined administration of propranolol and verapamil may prove helpful for differentiating between retrograde AV nodal and residual accessory connection conduction during early postoperative assessment of patients undergoing surgery for accessory AV connection ablation.

Effects of resting vagal tone on accessory atrioventricular connections.

The purpose of this study was to determine the effects of resting vagal tone on accessory atrioventricular (AV) connections. Atropine (0.04 mg/kg) was administered to 13 patients with the Wolff-Parkinson-White syndrome and was found to have the following effects on the accessory AV connection: the anterograde block cycle length shortened from 305 +/- 51 to 279 +/- 54 msec (mean +/- SD; p less than 0.001); the retrograde block cycle length shortened from 288 +/- 57 to 251 +/- 50 msec (p less than 0.001); and the effective refractory period measured at a basic drive cycle length of 400 msec shortened from 295 +/- 45 to 265 +/- 47 msec in the anterograde direction (p less than 0.001) and from 283 +/- 18 to 261 +/- 12 msec in the retrograde direction (p less than 0.01). During atrial fibrillation, the mean ventricular cycle length decreased from 434 +/- 88 to 352 +/- 56 msec (p less than 0.001), and the shortest preexcited RR interval decreased from 302 +/- 56 to 256 +/- 43 msec (p less than 0.01). In another seven patients, propranolol (0.2 mg/kg) was administered before atropine, and atropine lengthened the anterograde block cycle length and the effective refractory period of the accessory AV connection; the magnitude of these effects was similar to that in the patients who did not receive propranolol. In conclusion, these data demonstrate that resting vagal tone exerts a direct depressant effect on accessory AV connections that does not require background sympathetic activity to be manifest.

Real‐Time, Automated, Interactive Cardiac Electrophysiology Testing

We describe a new automated interactive system that performs all of the functions required for complete evaluation of the intracardiac conduction system, for inducing, terminating and analyzing tachydysrhythmias, and for locating and characterizing accessory atrioventricular (AV) connections and ectopic foci. In the first year of operation, the system was used to conduct 210 electrophysiology studies. These ranged from simple postoperative evaluation of the conduction system to complete tachycardia studies during pharmacological manipulation of the patient. Patient age at time of catheterization ranged from 6 days to 70 years, with median age of 8 years and 7 months. Advantages accruing from automated electrophysiology testing with this system included great precision and accuracy of timing measurements, flexibility in designing and implementing pacing protocols, and rapid management of induced or spontaneous dysrhythmias. Significant savings of time and labor were achieved by computer generation of reports and graphs as opposed to manual data extraction and plotting. The single most significant advantage is the ability of the system to provide information on a real-time basis, permitting the electrophysiologist to analyze, modify, extend or curtail the procedure.

Electrophysiological Demonstration of Anterograde Concealed Conduction in Accessory Atrioventricular Pathways Capable Only of Retrograde Conduction

Anterograde concealed conduction into the concealed accessory atrioventricular (AV) pathway has been postulated to be one of the factors preventing the reciprocating process via the accessory pathway in patients with the concealed Wolff-Parkinson-White(WPW) syndrome but its presence has not been documented. To demonstrate the occurrence of anterograde concealment, 12 patients with the concealed WPW syndrome were selected for study. A pacing protocol was designed in which the retrograde conduction of the ventricular extrastimulus over the accessory pathway was assessed during ventricular pacing alone (conventional method) and during the AV simultaneous pacing (simultaneous method); the results were then compared. When the high right atrium was simultaneously paced, the effective refractory period of the concealed accessory pathway shortened as compared with the conventional method in five of 12 patients (from 341.7 +/- 110.8 to 312.5 +/- 108.2 msec, n = 12), whereas, it decreased in all patients studied when the coronary sinus near the accessory pathway was simultaneously paced (from 375.7 +/- 135.0 to 287.1 +/- 116.1 msec, n = 7). These results demonstrate that the AV simultaneous pacing frequently shortens the refractoriness of the concealed accessory AV pathway and such facilitation seems to be well explained by the probable anterograde concealment in it and peeling back of the refractory barrier.

New catheter technique for recording left free-wall accessory atrioventricular pathway activation. Identification of pathway fiber orientation.

The ability to record accessory atrioventricular (AV) pathway activation consistently may be uniquely beneficial in improving pathway localization, identifying anatomic relations, and providing insight into unusual conduction properties. For the purpose of recording left AV accessory pathway activation, an electrode catheter was specially designed for use in the coronary sinus. The orthogonal catheter has three sets of four electrodes spaced evenly around the circumference. Electrograms were recorded at low gain (less than 1 cm/mV) between adjacent electrodes on the same set (interelectrode distance, 1.5 mm, center to center). This provides a recording dipole perpendicular to the atrioventricular groove to enhance recording of accessory pathway activation while minimizing overlapping atrial or ventricular potentials. The orthogonal electrode catheter was used in the electrophysiological study of 48 consecutive patients with 59 left AV accessory pathways. The catheter could be advanced along the coronary sinus beyond the site of earliest retrograde atrial activation in 49 of the 59 accessory pathways. Activation potentials were recorded from 45 of the 49 (92%) accessory pathways accessible to the catheter (5 of 5 anterior, 8 of 8 anterolateral, 15 of 16 lateral, 5 of 5 posterolateral, 5 of 5 posterior, and 7 of 10 posteroseptal). Accessory pathway potentials were validated by dissociating them from both atrial and ventricular activation by programmed-stimulation techniques. During surgery, accessory pathway potentials were identified from orthogonal catheter electrodes in the coronary sinus in 14 of 16 accessory pathways (12 patients). Epicardial mapping confirmed the location of the accessory pathway, and direct pressure over the orthogonal catheter electrode that recorded the accessory pathway potential resulted in transient conduction block in nine of the 14 accessory pathways. Orthogonal electrode maps of the coronary sinus identified an oblique course in 39 of 45 recorded accessory pathways. Thirty-two of 38 left free-wall accessory pathways were oriented with atrial insertion 4-30 mm (median, 14 mm) proximal (posterior) to the ventricular insertion. In the remaining six free-wall accessory pathways, the lateral excursion could not be determined because either only the atrial end of the accessory pathway was recorded or activation of multiple pathway fibers prevented tracking of individual strands. The seven recorded posteroseptal pathways exhibited accessory pathway potentials throughout an 8-18-mm (median, 10 mm) length of the proximal coronary sinus, but fiber orientation was difficult to determine.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of epinephrine in patients with an accessory atrioventricular connection treated with quinidine

The purpose of this study was to determine whether physiologic doses of epinephrine reverse the electrophysiologic effects of quinidine in patients with an accessory atrioventricular (AV) connection. Eighteen patients with an accessory AV connection who had inducible sustained orthodromic tachycardia underwent an electrophysiologic study in the baseline state and after at least 2 days of treatment with 1.4 to 1.9 g/day of quinidine gluconate. The effects of epinephrine were then determined. Epinephrine infusion rates of 25 and 50 ng/ kg/min were used in 9 patients each because these doses of epinephrine previously have been demonstrated to result in elevated plasma epinephrine concentrations in the range that occurs during a variety of stresses in humans. Quinidine prolonged refractoriness in the atrium and accessory AV connection and slowed conduction through the accessory AV connection. These effects were partially or completely reversed by epinephrine. Among 8 patients in whom quinidine resulted in orthodromic tachycardia becoming noninducible or nonsustained, sustained tachycardia became inducible again in 5 patients after infusion of epinephrine. After quinidine, atrial fibrillation was either non-inducible or nonsustained in 8 patients; however, sustained atrial fibrillation could be induced in 4 of these patients after infusion of epinephrine. The results of this study demonstrate that the therapeutic effect of quinidine in patients who have an accessory AV connection are often reversed by physiologic increases in circulating epinephrine.

Role of extrastimulus site and tachycardia cycle length in inducibility of atrial preexcitation by premature ventricular stimulation during reciprocating tachycardia

Preexcitation of the atria during reciprocating tachycardia (RT) by a premature ventricular complex occurring when the His bundle is refractory provides direct evidence of the presence of accessory atrioventricular (AV) connection. The impact of ventricular stimulation site and RT cycle length on inducibility of atrial preexcitation was assessed in 38 patients with RT utilizing a single accessory AV connection (right free wall in 5 patients, left free wall in 21 and posterior septal/paraseptal in 12). Extrastimuli were inserted at right ventricular (RV) apical, left ventricular (LV) septal and LV free wall sites. Inducibility of and magnitude of atrial preexcitation increased as stimulation site approached accessory AV connection site. Thus, for RV free wall connections, RV extrastimuli preexcited the atria in 5 of 5 patients, LV septal in 1 of 5 and LV free wall in 0 of 4. For LV free wall accessory connections, RV extrastimuli preexcited the atria in only 3 of 21 patients, compared with 12 of 17 with LV septal and 20 of 21 with LV free wall stimulation. Additionally, the magnitude of atria] preexcitation achieved was related to RT cycle length, diminishing as cycle length shortened. Finally, in a few instances both RV apical and LV free wall extrastimuli failed to elicit preexcitation in patients with a posterior septal connection. Thus, ventricular pacing site and RT cycle length contribute importantly to induction of atrial preexcitation by ventricular extrastimulation technique and should be considered during evaluation of patients with RT in whom accessory AV connections may be present.

Sotalol in patients with Wolff-Parkinson-White syndrome.

We evaluated the effects of intravenous and long-term oral sotalol treatment in 17 patients with an accessory atrioventricular (AV) pathway. All patients had a history of symptomatic supraventricular tachycardia. During electrophysiologic study intravenous (1.5 mg/kg body weight) and oral (240 to 320 mg/day) sotalol caused significant increases of sinus cycle length, AV nodal conduction time, and refractory periods of atrial and ventricular myocardium and accessory pathway. AV reciprocating tachycardia, which was inducible and sustained in 15 patients at control, was still inducible after intravenous sotalol in 14 patients, including one in whom it was not inducible at control. However, tachycardia became nonsustained in 10 patients. In seven patients who underwent repeat drug testing while on oral sotalol, results were the same as after intravenous sotalol. Sixteen patients were followed-up for 36 months (median value). Fifteen of them were clinically free of symptoms or experienced marked improvement, despite recurrences of tachycardia in two. In a third patient sotalol had to be withdrawn because of recurrent supraventricular tachycardia. Orthostatic hypotension occurred in five patients and required withdrawal of sotalol in one. To predict the long-term clinical outcome of patients, exercise testing and Holter monitoring were of little or no value. Programmed electrical stimulation predicted clinical outcome in 63% after intravenous and in 86% after oral sotalol. This study shows that long-term treatment with sotalol is highly effective in patients with the Wolff-Parkinson-White syndrome and regular supraventricular tachycardia.

Effect of Propranolol on Ventricular Rate During Atrial Fibrillation in the Wolff‐Parkinson‐White Syndrome

Atrial fibrillation was induced during an electrophysiology study in 10 patients with the Wolff-Parkinson-White (WPW) syndrome, after determination of baseline properties of the accessory atrioventricular (AV) connection; intravenous propranolol (0.2 mg/kg) was then administered. Atrial fibrillation terminated during the drug infusion in three patients, allowing determination of propranolol's effects on conduction and refractoriness during sinus rhythm, before atrial fibrillation was reinduced. In these three patients propranolol had no effect on refractoriness or conduction properties of the accessory AV connection during sinus rhythm. The mean ventricular rate during atrial fibrillation was slowed by 15-56 beats/min in six patients, had no effect on the mean rate in three patients, and markedly increased the ventricular rate (203 to 267 beats/min) in one patient. In this patient, 54% of QRS complexes during atrial fibrillation were narrow, compared to 0-25% in the other patients. Propranolol reduced the percentage of QRS complexes that were narrow from 13 +/- 16% to 1 +/- 2% (mean +/- standard deviation, p less than 0.05). We conclude that propranolol may slow the ventricular rate during atrial fibrillation in some patients with the WPW syndrome, probably by blocking the effects of adrenergic activation. However, propranolol should not be used in patients with the WPW syndrome who have atrial fibrillation, if most QRS complexes during atrial fibrillation are preexcited. When a large percentage of QRS complexes are narrow, propranolol may increase the ventricular rate, probably by eliminating concealed retrograde conduction in the accessory AV connection.

Follow-up evaluation of infant paroxysmal atrial tachycardia: transesophageal study.

We report results of follow-up transesophageal electrophysiologic studies in 35 infants seven to 27 months old (mean, 12 months) in whom paroxysmal atrial tachycardia (PAT) using an accessory atrioventricular (AV) connection had been previously evaluated by transesophageal study in the first 2 months (mean, 14 days) of life. No infants were receiving antiarrhythmic drug therapy at the time of follow-up study. To evaluate AV conduction and initiate PAT, a standard transesophageal pacing protocol was used: single extrastimuli in sinus rhythm, incremental pacing to second-degree AV block, and burst pacing at cycle lengths near those resulting in second-degree AV block. If PAT was not initiated during the baseline period, the protocol was repeated during the infusion of isoproterenol and after administration of atropine. At follow-up study, PAT was reinitiated in 24 of 35 (68%) infants, six of whom had exhibited recent spontaneous recurrence of PAT. AV nodal function did not differ in those with and those without inducible PAT. However, when initial and follow-up studies were compared, changes in antegrade conduction of the accessory AV connection were observed, since only five of 10 infants with preexcitation at initial study continued to exhibit preexcitation at follow-up study (1/5 infants only after isoproterenol). Additionally, changes in retrograde conduction of the accessory AV connection were observed; the ventriculoatrial interval in PAT induced at follow-up study increased by 20 to 40 msec in eight of 24 infants and by 50 to 80 msec in five of 24 infants compared with the interval at initial study.(ABSTRACT TRUNCATED AT 250 WORDS)

Frequency, diagnosis and clinical characteristics of patients with multiple accessory atrioventricular pathways

Multiple accessory atrioventricular (AV) pathways were documented in 52 of 388 patients (13%) who underwent detailed electrophysiologic evaluation. Multiple AV pathways were identified during intraoperative mapping or electrophysiologic study by (1) different patterns of ventricular preexcitation during atrial fibrillation, flutter or atrial pacing with different delta-wave morphologic and ventricular activation patterns; (2) different sites of atrial activation during right ventricular pacing or orthodromic reciprocating tachycardia; or (3) preexcited reciprocating tachycardia using a second pathway as the retrograde limb of the tachycardia. A logistic model was used to determine which clinical, electrocardiographic and electrophysiologic variables were associated with multiple AV pathways. Right free-wall and posteroseptal accessory AV pathways were more common in patients with multiple AV pathways and were frequently associated. Multivariate logistic regression identified Ebstein's anomaly, and a history of preexcited reciprocating tachycardia as significant variables (p < 0.0001). Pathway location was not subjected to statistical analysis because of confounding variables.

Determination of the earliest site of ventricular activation in Wolff-Parkinson-White syndrome: Application of digital continuous loop two-dimensional echocardiography

Surgical and transcatheter ablation of accessory atrioventricular (AV) connections (Wolff-Parkinson-White syndrome) requires accurate localization of the accessory pathway. In a canine model of endocardial pacing, a continuous loop two-dimensional echocardiographic technique was developed for determining the earliest site of ventricular activation. This technique was then used to localize accessory AV connections in patients. Echocardiographic images were acquired on videotape and converted to a digital continuous loop format, from which the earliest site of systolic motion was determined. In six dogs, using six distinct endocardial sites, two blinded observers accurately identified the earliest site of ventricular activation in 31 (86%) of 36 and 32 (89%) of 36 locations. Determination of the earliest site of ventricular activation with the continuous loop digital technique was superior to standard analog analysis in overall accuracy (p less than 0.02) and in intraobserver variability (p less than 0.004). After validation of this technique, 21 patients with 22 accessory AV connections with anterograde conduction were studied. The earliest site of mechanical activity was determined during sinus (10 patients) or atrial paced (11 patients) rhythms by two blinded observers and compared with electrophysiologic mapping and surface electrocardiograms. Digitally processed echocardiograms correctly localized the earliest site of ventricular activation in 18 of 22 connections and predicted an adjacent location in the remaining 4.(ABSTRACT TRUNCATED AT 250 WORDS)

Spontaneous termination of reciprocating tachycardia owing to interaction of dual atrioventricular nodal pathways in patients with an accessory pathway

Retrospective analysis of the electrophysiologic recordings from 125 consecutive patients with reciprocating tachycardia involving an accessory atrioventricular (AV) pathway suggested, by the mode of spontaneous termination of reciprocating tachycardia, the coexistence of dual AV nodal pathways in 7 patients. Three different modes of spontaneous tachycardia termination were observed. In 2 patients with antidromic tachycardia, termination was a result of AV nodal reentry, preceded by a decrease in retrograde AV nodal conduction. In 3 other patients with antidromic tachycardia, termination occurred after a sudden switch from a slow to a fast AV nodal pathway, leading to conduction block in either the accessory pathway or the His-Purkinje system. In 2 patients with orthodromic tachycardia, termination was caused by a sudden change of anterograde conduction from a fast to a slow AV nodal pathway, eliciting an AV nodal echo beat. The interaction of dual AV nodal pathways within the reentry circuit incorporating the accessory pathway always inhibited sustained reciprocating tachycardia.

Verapamil-induced retrograde conduction block in a concealed atrioventricular bypass tract

Reentrant supraventricular tachycardia (SVT) using a concealed bypass tract is a relatively common cause of narrow QRS complex tachycardia, accounting for 15 to 30% of cases in patients without evidence of preexcitation on the surface electrocardiogram. 1 The slow channel-blocking agent, verapamil, has been effective in the termination of such tachyarrhythmias, primarily through its actions on the atrioventricular node, with little effect on accessory atrioventricular (AV) pathways. 2–4 This report describes a patient with refractory SVT and a left-sided concealed bypass tract, in whom intravenous verapamil caused retrograde conduction block in the bypass tract.

Paradoxical delay in accessory pathway conduction during long R-P′ tachycardia after interpolated ventricular premature complexes

The introduction of a ventricular premature complex (VPC) into reciprocating tachycardia is a technique used to confirm the presence of an accessory atrioventricular (AV) pathway. 1–3 Retrograde atrial preexcitation after a VPC introduced during reciprocating tachycardia when the His bundle is refractory to retrograde conduction is evidence that an accessory pathway is present. 3 The failure of an appropriately timed VPC to alter the timing of atrial activation implies that either an accessory pathway conducting in the retrograde direction is not present or that the accessory pathway is relatively far from the site of premature stimulation. 3 This latter possibility can occur when VPCs are inserted into the right ventricular apex in patients with a left lateral accessory pathway. The finding that an accessory pathway can show a paradoxical delay in retrograde atrial activation during reciprocating tachycardia with this maneuver has not been described. We report a patient with a posterior septal accessory pathway with decremental conduction properties characteristic of the “permanent form of junctional reciprocating tachycardia.” Paradoxical delay in retrograde atrial activation was observed after the introduction of a VPC into reciprocating tachycardia when the His bundle was refractory.