Time Dependent Changes in Duration of Ventricular Repolarization After AV Node Ablation: Insights into the Possible Mechanism of Postprocedural Sudden Death

DIZON, J., et al. : Time Dependent Changes in Duration of Ventricular Repolarization After AV Node Ablation: Insights into the Possible Mechanism of Postprocedural Sudden Death. Although effective, there is a disturbing incidence of sudden death after AV node ablation. The mechanism may be related to proarrhythmia associated with prolongation in ventricular repolarization from the sudden decrease in heart rate. To examine this issue, we studied 15 patients undergoing complete radiofrequency ablation of the AV node for rapid atrial arrhythmias. Twelve‐lead ECGs of paced rhythms at rates of 60, 80, 100, and 120 beats/min were recorded at time points of 30 minutes, 24 hours, 1 week, and 1 month after ablation. The QT interval was measured in the limb and precordial leads with the best T wave offset. The change in the QT interval (ΔQT) relative to the measurement at 30‐minute postablation was calculated. For comparison, a similar procedure was performed on patients receiving pacemakers for primary bradycardia (n = 5 ). The mean QT interval at 60 beats/min, 30‐minutes postablation was significantly longer than at time points thereafter (482 ± 39 vs 446 ± 28 ms at 1 month, limb leads, for example, P < 0.05 ). Analysis of ΔQT revealed a significant shortening of the QT interval at nearly every paced rate at every time point relative to the value at 30‐minute postablation. The QT intervals shortened and stabilized after 24 hours. Neither the QT interval nor ΔQT changed significantly in patients paced for primary bradycardia. We conclude that there is a relative increase in the duration of ventricular repolarization after AV node ablation, which then decreases and stabilizes after 24 hours. Such changes are not seen in patients being paced for primary bradycardia. This data is consistent with the hypothesis that sudden death after AV node ablation may be related to proarrhythmia from prolonged ventricular repolarization.     

Stability of ventricular repolarization in conscious dogs with chronic atrioventricular dissociation and his-bundle pacing

Following AVN ablation, eight dogs were surgically instrumented for chronic (continuous) HIS-bundle pacing. For data collection, implanted pacemakers were transiently programmed to pace in stepwise ascending ramps at rates from 50 to 200 beats/min in 30-beat/min steps. Each rate was held for 60 seconds. At each rate, ECG signals were collected from conscious dogs for measurements of QT intervals during the last 10 seconds of each paced rate to construct a QT-HR ramp. This QT-HR ramp was repeated twice on each day of study 10 minutes apart. Dogs were randomly assigned to two groups and studied weekly for a minimum of 6 weeks. Group 1 dogs had pacemakers programmed to a rate of 80 beats/min for the duration of the study. Group 2 dogs were paced at 80 beats/min for weeks 1-3, then increased to 140 beats/min for weeks 4-6. The difference between paired QT-HR ramps within 1 day was <3 ms. QT-HR ramps were statistically indistinguishable over the 6-week study for group 1 dogs. Group 2 dogs experienced a slight flattening in the slope of the QT-HR ramps from week 3 to week 6 due to a reduction in QT interval at low HRs (50 and 80 beats/min) only. This conscious HIS-pacing model in dogs is a sensitive, stable, and reproducible method to define ventricular repolarization characteristics over a range of programmable HRs and experimental conditions.     

Polymorphous Ventricular Tachycardia and Atrioventricular Block

Nine patients are presented who had polymorphous ventricular tachycardia (PMVT) occurring during atrioventricular (AV) block. There were five men and four women with a mean age of 80 +/- 9 years. Five patients had organic heart disease and the remaining four had primary conduction disease (bundle branch block). AV block was complete in four patients (2:1 in three, and paroxysmal in two). The mean ventricular cycle length (of the AV block rhythm) was 1567 +/- 203 ms. The mean QT interval was 0.64 +/- 0.09 s and the mean QTc was 0.51 +/- 0.06 s. When compared to a similar control group with AV block but without PMVT, the ventricular cycle length was similar but the QT and QTc were significantly longer. PMVT was usually of short duration (eight beats to 12 s) and in seven of these nine patients, frequent premature ventricular beats (PVBs) were recorded at various times from the occurrence of PMVT. This is in contrast to the control patients in whom PVBs were detected in one patient only. In conclusion, patients with AV block who develop PMVT usually have longer QT intervals and have detectable PVBs on routine ECGs, unlike similar patients with AV block but without PMVT. In a patient with AV block, a QT interval above 0.60 s and PVBs on the ECG seem to indicate an increased risk for the development of PMVT.     

Recurrent Polymorphic Ventricular Tachycardia Complicating Radiofrequency Catheter Ablation of the Atrioventricular Junction

Recurrent ventricular tachycardia and ventricular fibrillation were observed immediately after RF ablation of the AV junction in a 64-year-old man. This arrhythmia was preceded by ventricular bigeminy and a long-short sequence. It was not associated with prolongation of the QT interval compared to baseline, and recurred 3 months later despite ventricular pacing at 90 beats/min. This is the first reported case of sustained ventricular arrhythmia complicating RF AV junction ablation despite rapid ventricular pacing, and recurring 3 months after discharge. It may explain the rare cases of sudden death complicating this procedure.     

Full Ventricular Capture Indicated by the QT Interval Function

The atrioventricular (AV) interval is critical in dual chamber (DDD) pacing in patients with hypertrophic obstructive cardiomyopathy (HOCM) to obtain full ventricular capture (FVC) with maximal reduction of the left ventricular (LV) outflow gradient and optimal LV diastolic filling. We studied the relationship of FVC, fusion, spontaneous AV conduction, and the QT interval. Methods: 11 patients with various cardiac diseases and stable AV conduction received a QT sensing Diamond (tm) Vitatron, DDD pacemaker. Software was downloaded into the pacemaker. In the DDD pacing mode, with the QT interval measured from the ventricular pacing stimulus to the end of the T wave, the AV interval was shortened from 400 ms, in 20-ms steps, to 90 ms. At 90 ms the stimulation rate was increased by 30 beats/mm and the AV interval was increased stepwise. FVC and fusion was examined on the surface ECG, Results: At 400 ms interval, spontaneous AV conduction inhibited the pacemaker. Shortening the AV interval resulted in pacing with a short QT interval. Further reduction of the AV interval resulted in a longer QT interval up to a point where the QT interval became stable. This point, the bending point in the plot of measured QT interval versus shortened AV intervals, coincided with the point of FVC. The relation of the QT-AV interval plot and the point of fusion was comparable when lengthening the AV interval at a 30 beats/mm faster stimulation rate. Conclusion: The bending point in the QT interval versus AV interval plots showed a good correlation with the FVC and fusion points observed on ECG. The results suggest that automatic discrimination between fusion and full capture using QT interval measurements may be feasible.     

The Ventricular Paced QT Interval—The Effects of Rate and Exercise

Changes in the QT and QTc intervals in 19 patients were studied at a ventricular paced rate difference of 50 beats/min. In all patients the measured QT interval shortened as the pacing rate was increased, from a mean value of 441 ms to 380 ms (p < 0.001), but when correct ed for heart rate the QTc- lengthened from a mean value of 518 ms to 575 ms. In 11 patients the QT in terval was measured at rest and immediately following exercise sufficient to increase the atrial rate by approximately 50 beats/min at identical ventricular paced rates. In all patients exercise-induced QT interval shortening from a mean value of 433 ms to 399 ms (p < 0.001). These results show first that Bazett's formula is unsuitable for correction of QT interval changes induced by ventricular pacing, and second that heart rate and changes in sympathetic tone independently influence the duration of the QT interval. It is suggested that these resuits are relevant to the design of physiological pacemakers in which the duration of the QT interval influences the discharge frequency of the pacemaker and to the consideration of ventricular pacing for the treatment of abnormal repolarization syndromes. (PACE, Vol. 5, May-June, 1982)     

Congestive Heart Failure and VVI Pacing Mode: Dynamic Behavior of the Dispersion of Ventricular Repolarization

Dynamic Behavior of the Dispersion of Ventricular Repolarization. The aim of this study was to evaluate the circadian variation in the spatial dispersion of ventricular repolarization in continuously paced patients with congestive heart failure (CHF). Fourteen patients (10 males, 4 females, aged 65 ± 5 years) with CHF due to dilated cardiomyopathy (DCM) and an echocardiographic ejection fraction of 28%± 3% were studied. All patients underwent AV functional RF ablation and permanent pacemaker implantation for drug refractory chronic atrial fibrillation (AF). Patients were evaluated at 1 month postimplant with a three-channel 24-hour Holter monitor, using the three plane Frank orthogonal leads (X, Y, and Z), in VVI pacing mode at 70 beats/min. For each hour, the mean value of spike-T interval dispersion of the first five beats was measured. The control group consisted of 20 patients without structural heart disease, but with AF and complete AV block, continuously paced in WI mode at 70 beats/min. The dispersion of the spike-T interval had a circadian behavior in the study population, with higher values at night and lower during the daytime. During the daytime, the mean value of spike-T interval dispersion was 39 ± 5 ms and during the nighttime it was 45 ± 7 ms (P = 0.003). Such a difference between day and night was not found in the control group (38 ± 6 ms and 40 ± 8 ms, respectively, P = NS), In the daytime period the mean value of spike-T interval dispersion of our study population was comparable to that of the control group (P = NS), while during the nighttime it was significantly higher (P = 0.0004). In conclusion, by evaluating the dispersion of ventricular repolarization in two dimensions, space and time, a circadian variation was found in paced patients with CHF due to DCM. The increased QT dispersion in these patients during the nighttime period was attributed to different effects of vagal activity in normal and abnormal myocardial areas.     

Prolonged QRS duration increases QT dispersion but does not relate to arrhythmias in survivors of acute myocardial infarction

QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2-3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%-15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 +/- 7 vs 78 +/- 1 ms, JT disp 80 +/- 6 vs 79 +/- 2 ms, mean +/- SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction.     

Different Effects of Amiodarone and Quinidine on the Homogeneity of Myocardial Refractoriness in Patients With Intraventricular Conduction Delay

BACKGROUND: Increases in QT and JT dispersion have been suggested as indicative of a proarrhythmic potential as a result of heterogeneity in myocardial refractoriness, the reduction of which by antiarrhythmic agents might be associated with a beneficial effect on the development of serious ventricular arrhythmias. METHODS: To test the hypothesis that amiodarone reduces the heter-ogeneity of ventricular refractoriness to a significantly greater extent than quinidine in patients with intraventricular conduction defects under treatment for ventricular arrhythmias, the corrected and uncorrected QT and JT intervals and dispersions from 12-lead surface electrocardiograms were determined in 120 patients with intraventricular conduction defects with cardiac arrhythmias before and during treatment with amiodarone (n = 60) and quinidine (n = 60). RESULTS: Amiodarone increased QT from 403 +/- 50 ms to 459 +/- 47 ms (P <.001), with a similar increase in the corrected QT interval (QTc) (P <.001). Amiodarone reduced QT dispersion by 40% (P <.001), whereas quinidine increased by 18% (P <.001). The net effects of both drugs were similar for OTc. Amiodarone, but not quinidine, reduced heart rate significantly; amiodarone had no effect on the QRS; but quinidine increased if (P <.001). Quinidine as well as amiodarone increased the JT and JTc intervals significantly, but the effect of quinidine was qualitatively less striking. Amiodarone decreased the JT dispersion by 33% (P <.001) and JTc dispersion by 37% (P <.001). On the other hand, quinidine increased the corresponding values for JT and JTc by 18% (P <.001) and 21% (P <.001), respectively. The overall data on QT and JT dispersion indicate an improvement in the homogeneity of myocardial refractoriness with amiodarone treatment and the converse with quinidine treatment; this observation is consistent with a lower proarrhythmic propensity and mortality with amiodarone than with quinidine. Quinidine increased the QRS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization. CONCLUSIONS: Amiodarone and quinidine both increased the corrected and uncorrected QT and JT intervals; amiodarone decreased and quinidine increased the dispersion of these intervals, and these results suggested an improvement in the homogeneity of myocardial refractoriness as a result of amiodarone treatment and the converse as a result of quinidine treatment. Quinidine increased the QTS interval more than amiodarone, and the data indicate that in patients with intraventricular conduction defects, the monitoring of the JT interval might more accurately reflect changes in myocardial repolarization.     

Paced QT dispersion and QT morphology after radiofrequency atrioventricular junction ablation: impact of left ventricular function

Catheter ablation of the atrioventricular junction (AVJ) is a widely accepted treatment for drug refractory atrial fibrillation. Unfortunately, there have been some reports of pause dependent ventricular arrhythmias associated with QT interval prolongation, mainly in patients with reduced LV function. The present investigation evaluates the association of LV function with QT dispersion in response to a sudden rate drop. ECGs were' recorded on 20 patients (13 with normal LV function) on the day following AVJ ablation while paced at a range of ventricular rates (40-120 beats/min), and during a sudden drop from 80 to 40 beats/min. The maximum QT interval (QTmax), minimum QT interval (QTmin), and QT interval dispersion (QTdisp) were compared. In both groups, the QTmax and QTmin increased at slower paced heart rates while the QTdisp did not change. In response to a sudden rate drop from 80 to 40 beats/min, the QTmax increased in both groups of LV function (trend), while the QTmin increased in those with normal LV function (24 +/- 22 ms), but not in those with reduced LV function (0 +/- 14 ms; P = 0.01). Consequently, the QTdisp increased significantly in those with reduced LV function (31 +/- 23 ms) but not in normal LV function (-5 +/- 29 ms; P = 0.01). Morphological QTU changes developed following the sudden rate drop in 67% of the reduced LV versus 8% of the normal LV (P = 0.02) function groups. Following AVJ ablation, QTdisp increased during a sudden rate drop in patients with reduced LV function, but not in patients with normal LV function.     

QT dispersion in children with ventricular arrhythmia and a structurally normal heart

In adults, increased QT dispersion has been shown to predict arrhythmic risk as well as risk of sudden death in several clinical settings. It is not known whether or not QT dispersion is increased in children with idiopathic ventricular arrhythmia. We studied three groups of children: (1) 20 patients with idiopathic VT (aged 3-18 years; mean 11.2 years); (2) 30 patients with benign PVCs (aged 1-20 years; mean 10.5 years); and (3) 30 control subjects (aged 4-17 years; mean 12 years). Standard ECGs were reviewed and the dispersion of both QT and JT intervals was compared. No patient had structural heart disease or long QT syndrome. The QT and QTc dispersion (QT delta, QTc delta) among the three groups did not differ: QTc delta of the VT group was 70 ms +/- 30 ms, QTc delta of PVC patients was 60 ms +/- 30 ms, and the QTc delta of the control group was 65 ms +/- 30 ms. The JTc delta among the three groups did not differ as well: JTc delta of the VT group was 70 ms +/- 30 ms, the JTc delta of the PVC group was 60 msec +/- 25 msec, and the JTc delta of the control group was 70 ms +/- 30 ms. We conclude that QT and JT dispersion are not significantly altered in children with idiopathic VT or benign PVCs when compared to control subjects. QT dispersion is not a reliable marker for arrhythmic risk in children with idiopathic ventricular arrhythmias and structurally normal hearts.     

Cumulative effect of preceding pacing cycle length on ventricular repolarization after a pause

This study was designed to investigate if the components of the QT interval after a pause are influenced by the preceding pacing cycle length. Ten patients (seven women and three men; age 79 +/- 9 years, means +/- SD) with complete atrioventricular block or sick sinus syndrome whose own heart rate was < 40 beats/min were examined. All patients had already undergone implantation of a permanent pacemaker. Ventricular pacing protocol was performed with simultaneous recording of a 12-lead electrocardiogram. One set of regular stimuli for 30 seconds (S1) with a variable cycle length (1,000, 700, and 400 ms) was followed by a single stimulus (S2) with a fixed coupling interval of 1,500 ms. QT intervals in response to the last S1 (S1-QT) and S2 (S2-QT) were measured. The QT interval was divided into two components, the interval from start of Q wave to the peak of T wave (QaT) and that from the peak to end of T wave (Tae). The S2-QT and S1-QT interval shortened in association with a decrease in the S1S1 interval. The abbreviation of S2-QT interval was not associated with a significant change in the Tae interval. The results demonstrated that the QT interval after a pause shortened by reducing the preceding pacing cycle length. This shortening is probably due to a homogenous abbreviation of action potential duration across the ventricular wall.     

Safety of pacemaker implantation prior to radiofrequency ablation of atrioventricular junction in a single session procedure

RF current delivery may cause acute and chronic dysfunction of previously implanted pacemakers. The aim of this study was to assess prospectively the effects of RF energy on Thera I and Kappa pacemakers in 70 consecutive patients (mean age 70 ± 11 years, mean left ventricular ejection fraction 48 ± 15%) who underwent RF ablation of the AV junction for antiarrhythmic drug refractory atrial fibrillation (permanent in 42 patients, paroxysmal in 28). These pacing systems incorporate protection elements to avoid electromagnetic interference. The pacemakers (Thera DR 7960 I in 20 patients, Thera SR 8960 1 in 30, Kappa DR 600–601 in 8, Kappa SR 700–701 in 12) were implanted prior to RF ablation in a single session procedure and were transiently programmed to VVI mode at a rate of 30 beats/min. Capsure SP and Z unibipolar leads were used. During RF application there was continuous monitoring of three ECG leads, endocavitary electrograms, and event markers. Complete AV block was achieved in all cases after 3.6 ± 2.9 RF pulses and 100 ± 75 seconds of RF energy delivery. The mean time of pacemaker implantation and RF ablation was 60 ± 20 minutes. Transient or permanent pacemaker dysfunction including under/oversensing, reversion to a "noise-mode" pacing, pacing inhibition, reprogramming, or recycling were not observed. Leads impedance, sensing, and pacing thresholds remained in the normal range in the acute and long-term phase (average follow-up 18 ± 12 months). In conclusion, Thera I and Kappa pacemakers exhibit excellent protection against interference produced by RF current. The functional integrity of the pacemakers and Capsure leads was observed in the acute and chronic phases. Thus, the implantation of these pacing systems prior to RF ablation of the AV junction can be recommended.     

Electrophysiological Effects of E 4031, a Drug with Selective Class III Properties, in Man

We studied the electrophysiological effects ofE 4037, given in a dose ascending manner (1.5, 3.0, and 6.0 μg/kg over 5 min followed by 0.1, 0.2, and 0.4 μg/kg per min for 60 min, respectively) to 19 volunteers. There were significant, dose related linear increases in QT and QT_C intervals, in atrial functional and effective refractory periods (ERPs) at a paced cycle length of 400 ms, and in ventricular functional and ERPs at a paced cycle length of 600 ms. There was no significant change in the AH and HV intervals or QRS duration. No significant proarrhythmic or other side effects were encountered during the administration of the drug. E 4031 prolongs atrial and ventricular refractoriness without significantly affecting AV or intraventricular conduction, consistent with selective Class III properties. At the doses used in the present study, intravenous infusion of E 4031 appears to be safe and well tolerated.     

Effects on Cardiac Performance of Atrioventricular Node Catheter Ablation Using Radiofrequency Current for Drug-Refractory Atrial Arrhythmias

Patients with atrial fibrillation or atrial flutter (AF) are candidates for radiofrequency (RF) catheter ablation of the atrioventricular (AV) node with the aim being to control heart rate. As patients wilh AF can have markedly impaired ventricular function, information concerning the hemodynamic effects of AV node ablation using RF current would be valuable. Fourteen consecutive patients (mean age 65 ± 3 years) with drug-resistant AF underwent AV node catheter ablation with RF current and had permanent pacemaker implantation. The mean left ventricular ejection fraction (FFJ by two-dimensional echoeardiography immediately before ablation was 42 ± 3% (range 14%–54%) and their mean exercise time was 4.4 ± 0.4 minutes. Complete AV block was achieved in all 14 patients with 6 ± 2 RF applications (range 1–18). There was no evidence of any acute cardiodepressant effect associated with delivery of RF current, and EF 3 days after ablation was 44 ± 4%. By 6 weeks after ablation, the left ventricular EF was significantly improved compared to baseline (47 ± 4% postablation vs 42 ± 3% preahlation; P < 0.05), and this modest increase in EF was accompanied by an improvement in exercise time (5.4 ± 0.4 min). In conclusion, delivery of RF current for AV node catheter ablation in patients with AF and reduced ventricular function is not associated with any acute cardiodepressant effect. On the contrary, improved control of rapid heart rate following successful AV node ablation is associated with a modest and progressive improvement in cardiac performance.     

Ventricular Fibrillation and Sudden Death After Radiofrequency Catheter Ablation of the Atrioventricular Junction

Two hundred thirty-five patients underwent RF catheter abhtion of AV conduction for symptomatic drug refractoiy AF (84%), atrial flutter (9%), and atrial tachycardia (7%). In the first 100 patients, postahlation pacing was not prospectively set at any specific rate and was always ≤ 70 beats/min. In the next 135 patients, postabiotion pacing was prospectively set at 90 beats/min for 1–3 months. Six of the first 100 patients (6%) had VF or sudden death after the RF procedure and none (0%) of the next 135 patients did (P < 0.05). One of the six patients had recurrent VF 4 days after the ablation. Five patients were successfully resuscitated and one patient died. There were no statistically significant differences between patients with and without (aborted) sudden death or between the first 100 and the next 135 patients with respect to age, sex, underlying heart disease, EF, number of RF applications, or leftor right-sided approach of the procedure. VF mostly occurred during episodes of slow ventricular escape rhythms or during slow ventricular pacing. We conclude that malignant ventricular arrhythmias and sudden death are possible complications of RF ablation of the AV junction. The mechanism of these complications could have a bradycardia dependent nature and it seems that the occurrence of malignant arrhythmias can be prevented by temporarily pacing the heart at relatively fast rates immediately after ablation.     

Exercise-related QT interval shortening with a peaked T wave in a healthy boy with a family history of sudden cardiac death

An asymptomatic 15-year-old boy, who had a family history of sudden cardiac death, was referred for screening for cardiac disease. The 12-lead electrocardiogram at rest showed a short QT/QTc(Bazett)/QTc(Fredericia) interval of 320/388/364 ms, but the intervals were further shortened to 200/339/284 ms after the treadmill test concomitant with appearance of a peaked T wave. Other conventional cardiac examinations were normal, but effective refractory period was less than 180 ms in both ventricles, and double ventricular extrastimulation reproducibly induced nonsustained polymorphic ventricular tachycardia. Intravenous administration of epinephrine also induced a short QT interval and a peaked T wave, and a hump was manifested on the T wave of the first postpacing beat with a longer preceding R-R interval. Furthermore, a couple of premature ventricular complexes originated from a similar timing as the hump. Genetic analysis did not show the mutation in KCNQ1, KCNH2, KCNE1, KCNE2, KCNJ2, SCN5A genes but revealed single nucleotide polymorphism (C5457T) in SCN5A gene.     

A Direct Midseptal Approach to Slow Atrioventricular Nodal Pathway Ablation

Objectives: The purpose of this study was to describe a midseptal approach to selective slow pathway ablation for the treatment of AV nodal reentrant tachycardia (AVNRT). In addition, predictors of success and recurrence were evaluated. Methods: Selective ablation of the slow AV nodal pathway utilizing radiofrequency (RF) energy and a midseptal approach was attempted in 60 consecutive patients with inducible AVNRT. Results: Successful slow pathway ablation or modification was achieved in 59 of 60 patients (98%) during a single procedure. One patient developed inadvertent complete AV block (1.6%). A mean of 2,7 ±1.4 RF applications were required with mean total procedure, ablation, and fluoroscopic times of 191± 6.3, 22.8 ± 2.3, and 28.2 ±1.8 minutes, respectively. The PR and AH intervals, as well as the antegrade and retrograde AV node block cycle length, were unchanged. However, the fast pathway effective refractory period was significantly shortened following ablation (354± 13 msec vs 298 ± 12 msec; P= 0.008). The A/V ratio at successful ablation sites were no different than those at unsuccessful sites (0.22 ± 0.04 vs 0.23± 0.03). Junctional tachycardia was observed during all successful and 60 of 122 (49%) unsuccessful RF applications (P < 0.0001). A residual AV nodal reentrant echo was present in 15 of 59 (25%) patients, During a mean follow-up of 20.1± 0.6 months (11.5–28 months) there were four recurrences (5%), 4 of 15 (27%) in patients with and none of 44 patients without residual slow pathway conduction (P = 0.002). Conclusions: A direct midseptal approach to selective ablation of the slow pathway is a safe, efficacious, and efficient technique. Junctional tachycardia during RF energy application was a highly sensitive but not specific predictor of success and residual slow pathway conduction was associated with a high rate of recurrence.     

JT Dispersion in Wolff-Parkinson-White Syndrome: Effect of Eccentric Ventricular Depolarization on the Dispersion of Repolarization

There is much interest in QT dispersion for noninvasive risk stratification of patients at risk of arrhythmias. However, little is known about the genesis of abnormal QT dispersion. In particular, whether eccentric ventricular depolarization, as seen in preexcitation, can lead to abnormal dispersion of repolarization is unknown. We studied 24 children aged 1–19 years (mean ± SD, 11 ± 5 years) with manifest preexcitation due to Wolff-Parkinson-White syndrome who had successful catheter ablation. Standard ECGs done preablation, early postablation (< 1 week), mid postablation (> 1 week, < 2 months), and late postablation (> 2 months) were reviewed. The QRS duration prior to ablation ranged from 90–160 ms (mean ± SD, 123 ±21 ms). On the preablation ECG, the JT and JTc dispersions showed no relationship to the QRS duration (r = 0.04 and 0.07, respectively). There was no change in JT dispersion when the preablation (42 ±15 ms) ECG was compared to early (43 ±15 ms), mid (44 ±13 ms), and late postablation (48 ± 19 ms) ECGs. There was no significant change in JTc dispersion as well. Thus, JT dispersion is unrelated to QRS duration and unaffected by catheter ablation in patients with Wolff-Parkinson-White syndrome. Eccentric ventricular depolarization does not lead to abnormal dispersion of repolarization.