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Background: Current maneuvers for differentiation of atrioventricular node reentry tachycardia (AVNRT) and atrioventricular reentry tachycardia (AVRT) lack sensitivity and specificity for AVRT circuits located away from the site of pacing. We hypothesized that a premature His complex (PHC) will always perturb AVRT because the His bundle is obligatory to the circuit. Further, AVNRT could not be perturbed by a late PHC (≤20 ms ahead of the His) due to the retrograde His conduction time. Earlier PHCs can advance the AVNRT circuit but only by a quantity less than the prematurity of the PHC., Methods: High-output pacing at the distal His location delivered PHCs. AVRT was predicted when late PHCs perturbed tachycardia or when earlier PHCs led to atrial advancement by an amount equal or greater than the degree of PHC prematurity., Results: Among the 73 supraventricular tachycardias, the test accurately predicted AVRT (n=29) and AVNRT (n=44) in all cases. Late PHC advanced the circuit in all 29 AVRTs and none of the AVNRTs (sensitivity and specificity, 100%). With earlier PHCs, the degree of atrial advancement was equal or greater than the PHC prematurity in 26/29 AVRTs and none of the AVNRTs (90% sensitivity and 100% specificity). The mean prematurity of the PHC required to perturb AVNRT was 48 ms (range, 28-70 ms) and the advancement less than the prematurity of the PHC (mean, 32 ms; range, 18-54 ms)., Conclusions: The responses to PHCs distinguished AVRT and AVNRT with 100% specificity and sensitivity.

Background: Improving health-related quality of life (HRQoL) is an important treatment goal in the management of patients with atrial fibrillation (AF). Uncertainty exists as to whether patients' HRQoL differ when treated with medical rhythm control or rate control. We compared HRQoL between patients treated with rhythm control or rate control in a large observational registry of patients with recent-onset AF., Methods and Results: In the Registry on Cardiac Rhythm Disorders Assessing the Control of Atrial Fibrillation (RECORD-AF), 2439 patients with recent onset (<1 year) AF completed an AF-specific HRQoL questionnaire, the University of Toronto Atrial Fibrillation Severity Scale. HRQoL was assessed by the AF symptom severity score (0-35, with higher scores reflecting more severe AF-related symptoms) at baseline and 1 year. The minimal clinically important difference was defined as a change of ≥3 points. The primary analysis was based on a propensity score-adjusted longitudinal regression analysis which compared the change in AF symptom severity scores between the 2 groups. Over an average follow-up of 1 year, the AF symptom severity scores improved in both groups (rhythm control: -2.82 point [95% confidence interval, -3.22 to -2.41]; rate control: -2.11 point [95% confidence interval, -2.54 to -1.67]; P<0.01 for both groups). The magnitude of improvement was higher in the rhythm control group than the rate control group (unadjusted difference: -0.75 point; 95% confidence interval, -1.31 to -0.19; P=0.01; propensity score-adjusted difference: -0.71 point; 95% confidence interval, -1.31 to -0.11; P=0.02)., Conclusions: In this observational cohort of recent-onset AF patients, treatment with medical rhythm- or rate control over 1 year was associated with an improvement in HRQoL. The magnitude of HRQoL improvement was minimally higher in patients treated with rhythm control than rate control. However, the overall degree of improvement was not large, and its clinical significance was uncertain., (© 2014 American Heart Association, Inc.)

Background: Definitive diagnosis of bilateral bundle-branch delay/block may be made when catheter-induced right bundle-branch block (RBBB) develops in patients with baseline left bundle-branch (LBB) block. We hypothesized that a RBBB pattern with absent S waves in leads I and aVL will identify bilateral bundle-branch delay/block., Methods and Results: Fifty patients developing transient RBBB pattern in lead V1 during right heart catheterization were studied. Patients were grouped according to whether the baseline ECG demonstrated a normal QRS, left fascicular blocks, or LBB block pattern. The RBBB morphologies in each group were compared. The prevalence of bilateral bundle-branch delay/block pattern was examined in our hospital ECG database. All patients with baseline normal QRS complexes (n=30) or left fascicular blocks (4 anterior, 5 posterior) developed a typical RBBB pattern. Among the 11 patients with a baseline LBB block pattern, 7 developed an atypical RBBB pattern with absent S waves in leads I and aVL and the remaining 4 demonstrated a typical RBBB. The absence of S waves in leads I and aVL during RBBB was 100% specific and 64% sensitive for the presence of pre-existing LBB block. Among the consecutive 2253 hospitalized patients with RBBB, 34 (1.5%) had the bilateral bundle-branch delay/block pattern., Conclusions: An ECG pattern of RBBB in lead V1 with absent S wave in leads I and aVL indicates concomitant LBB delay. Pure RBBB and bifascicular blocks are associated with S waves in leads I and aVL., (© 2014 American Heart Association, Inc.)

Background: Although cardiac resynchronization therapy (CRT) can improve left ventricular ejection fraction (LVEF), it is not known whether a specific level of improvement will predict future implantable cardioverter defibrillator (ICD) therapy., Methods and Results: CRT-defibrillator (CRT-D) was implanted in 423 patients at 1 institution between October 2, 2001 and January 19, 2007. A retrospective analysis was performed to evaluate the relationship between post-CRT-D LVEF and ICD therapy for ventricular tachyarrhythmias. A landmark population of 270 patients, with post-CRT-D LVEF measured and no ICD therapy within 1 year of device implantation, was followed for subsequent outcomes. Of these, 22 patients (8.2%) had subsequent appropriate ICD therapy over a median follow-up of 1.5 years. The estimated 2-year risk of appropriate ICD therapy is 3.0% (95% confidence interval [95% CI], 0%-6.3%), 2.1% (95% CI, 0%-5.0%), and 1.5% (95% CI, 0%-3.9%) for post-CRT-D LVEF of 45%, 50%, and 55%, respectively. In patients with a primary prevention indication for CRT-D, the estimated 2-year risk is 3.3% (95% CI, 0%-7.3%), 2.5% (95% CI, 0%-6.1%), and 1.9% (95% CI, 0%-5.1%) for post-CRT-D LVEF of 45%, 50%, and 55%, respectively., Conclusions: When a CRT responder demonstrates near normalization in LVEF to ≥45%, the incidence of ICD therapy for ventricular arrhythmias becomes low. Future studies are needed to determine whether an ICD is still needed in some of these patients at the time of generator replacement.

Background: The aim of this study was to test the electrophysiological effects of continuous enhanced vagal tone on dual atrioventricular (AV) nodal and accessory pathways., Methods and Results: This study included 10 patients with typical, slow-fast AV nodal reentrant tachycardia (AVNRT) and 10 patients with AV reciprocating tachycardia. Electrophysiological data were measured before and during continuous vagal enhancement by using phenylephrine infusion (0.6 to 1.5 microg/kg per min). For patients with AVNRT, during phenylephrine infusion, 1:1 conduction times over the anterograde fast and slow and retrograde fast pathways were prolonged (453+/-64 to 662+/-120 ms, P<0.001; 379+/-53 to 443+/-95 ms, P<0.05; 405+/-112 to 442+/-118 ms, P<0.05). The effective refractory period and functional refractory period of the anterograde fast pathway were prolonged with phenylephrine (394+/-73 to 544+/-128 ms, P<0.001; 454+/-60 to 596+/-118 ms, P<0.001). In contrast, the effective refractory period and functional refractory period of the anterograde slow and retrograde fast were not significantly changed. No significant change was observed in the conduction or refractoriness of the accessory pathways in patients with AV reciprocating tachycardia nor in atrial or ventricular refractoriness., Conclusions: Enhanced vagal tone produces disparate effects on the refractoriness of the slow and fast AV nodal conduction pathways, with the anterograde fast pathway being the most sensitive. These changes are conducive to induction of AVNRT with a premature atrial complex and may explain in part the relatively common occurrence of AVNRT during sleep or other periods of presumed increased parasympathetic tone.

Background: Fifty percent of deaths in patients with coronary disease occur suddenly. Although many factors correlate with increased mortality, there is little information regarding the influence of these factors on mode of death. As such, optimum methods to determine patients most likely to benefit from implantable defibrillator therapy are unclear., Methods and Results: We analyzed the relation of ejection fraction and inducible ventricular tachyarrhythmias to mode of death in all 1791 patients enrolled in the Multicenter Unsustained Tachycardia Trial who did not receive antiarrhythmic therapy. Total mortality and arrhythmic deaths/cardiac arrests occurred more frequently in patients with ejection fraction <30% than in those with ejection fraction of 30% to 40%. The percentage of deaths classified as arrhythmic was similar in patients with ejection fraction <30% or > or =30%. The relative contribution of arrhythmic events to total mortality was significantly higher in patients with inducible tachyarrhythmia (58% of deaths in inducible patients versus 46% in noninducible patients, P=0.004). The higher percentage of events that were arrhythmic among patients with inducible tachyarrhythmia appeared more distinct among patients with an ejection fraction > or =30% (61% of events were arrhythmic among inducible patients with ejection fraction > or =30% and only 42% among noninducible patients, P=0.002)., Conclusions: Both low ejection fraction and inducible tachyarrhythmias identify patients with coronary disease at increased mortality risk. Ejection fraction does not discriminate between modes of death, whereas inducible tachyarrhythmia identifies patients for whom death, if it occurs, is significantly more likely to be arrhythmic, especially if ejection fraction is > or =30%.

Background: The Multicenter Unsustained Tachycardia Trial (MUSTT) was designed to evaluate an antiarrhythmic treatment strategy, including drugs and implantable defibrillators (ICDs), guided by electrophysiological (EP) testing. We performed several statistical analyses to assess the contribution of defibrillators to the observed treatment benefit., Methods and Results: First, the effects of defibrillators were indirectly examined by comparing the randomized treatment arms (EP-guided therapy versus no antiarrhythmic therapy) within subgroups that varied according to ICD usage. Use of ICDs increased during the trial; hence, the randomized treatments were compared according to date of enrollment. There were also site-specific differences in ICD use; hence, the randomized arms were compared within groups of sites defined by level of ICD use. There was a distinct "dose response" in relation to ICD use. Where ICD use was high, EP-guided therapy produced significant reductions in arrhythmic death or cardiac arrest (P<0.004). Where ICD use was low, there was no benefit of EP-guided therapy. Finally, outcomes of EP-guided therapy patients who received an ICD were directly compared with outcomes of other patients using the Cox proportional hazards model with receipt of an ICD as a time-dependent covariate. Adjusted for other prognostic factors, patients who received an ICD had risk reductions of >70% in arrhythmic death or cardiac arrest and >50% in total mortality (P<0.001 for both end points)., Conclusions: The benefit of EP-guided antiarrhythmic therapy observed in MUSTT was due to improved outcomes among patients who received an ICD but not among patients who received antiarrhythmic drugs.

Sudden cardiac death continues to be a major health problem in the United States, accounting for approximately 400,000 deaths per year. The last 10 yrs have seen major advances in the primary and secondary prevention of this problem. In patients who have survived an episode of cardiac arrest, the AVID study conclusively established the superiority of the implantable cardioverter defibrillator over empiric amiodarone. For patients with recurrent hemodynamically destabilizing ventricular tachycardia and ventricular fibrillation, intravenous amiodarone has emerged as a potent therapeutic agent, especially when other agents such as lidocaine and procainamide have not been effective. Finally, recent work has focused on the risk stratification of patients for sudden cardiac death. Both the MADIT and MUSTT studies suggest that patients with coronary artery disease, reduced ejection fraction, and nonsustained ventricular tachycardia who are inducible to a sustained ventricular arrhythmia at electrophysiology testing have improved survival with an implantable cardioverter defibrillator.

Background: Implantable ventricular cardioverter defibrillator (ICD) shocks can cause atrial fibrillation/flutter (AF). This study investigated the pathogenesis of AF after ICD shocks in a canine model., Methods and Results: The study was conducted in 8 dogs. In 5 dogs (group 1), truncated exponential (8 ms, 78% tilt) monophasic and biphasic shocks were delivered through a bipolar epicardial (patch) or endocardial lead. After the last S1 of atrial pacing at a cycle length of 350 ms, shocks of 0.1 to 7.6 A (0.005 to 27.7 J) were delivered, timed to the atrial effective refractory period (AERP). Ventricular defibrillation thresholds were also determined. In 3 dogs (group 2), the effect of the open versus closed chest technique on AF induction was tested in the endocardial biphasic shock configuration. AF was induced in all 8 dogs and in all waveforms and configurations. Mean AF duration was 11.5+/-6 s, with a mean ventricular rate of 184+/-37 bpm. Ventricular shocks could induce AF only if they were timed between an AERP of -60 to 40 ms, -40 to 60 ms, -40 to 60 ms, and -20 to 60 ms in the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively. The mean+/-SD of the upper limit of vulnerability (ULV) for AF induction (in J) was 5. 2+/-0.6, 3.5+/-0.4, 5.2+/-1.2, and 2.5+/-0.1 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P<0.05). The lower limit of vulnerability (LLV) was 0.8+/-0.1, 0.8+/-0.1, 0.9+/-0, and 0.6+/-0 for the epicardial monophasic, epicardial biphasic, endocardial monophasic, and endocardial biphasic configurations, respectively (P=NS). The ventricular defibrillation threshold (in J) for all wave forms and configurations was higher than the ULV (P<0. 05)., Conclusions: (1) An atrial LLV and ULV exist for ventricular ICD shock-induced AF; (2) the shock-induced AF is related to both shock intensity and its timing to AERP; and (3) avoiding this atrial window of vulnerability may minimize the risk of post-ICD shock AF.

Background: Assessment of myocardial refractoriness and conduction properties, critical to development and propagation of reentrant arrhythmias, is an integral part of the investigation of atrial and ventricular tachycardias through the use of programmed electrical stimulation. Local conduction itself, however, may be affected by myocardial refractoriness., Methods and Results: We studied the effects of changes in myocardial refractoriness on local conduction in right atrial and ventricular myocardium in 19 patients. Changes in effective, functional, and relative refractoriness were accomplished with the use of four pacing protocols, including drive train pacing cycle lengths (PCLs) of 600 and 400 milliseconds (ms) and drive train durations (DTDs) of 8 and 50 stimuli. Unipolar cathodal stimulation was performed from the distal electrode, and unipolar electrograms were recorded from the proximal three poles of quadripolar catheters with 5-mm interelectrode spaces. Atrial and ventricular effective and relative refractory periods (ERPs and RRPs) were significantly shortened by both the reduction in PCL and the increase in DTD. The reduction in the PCL shortened atrial and ventricular refractory periods significantly more than did the increase in the DTD. Changes in ventricular refractory periods were significantly greater compared with atrial refractory periods. The ratio of RRP to ERP was reduced in the atrium but significantly increased in the ventricle with reduction in PCL and increase in DTD. For all premature intervals, the conduction interval from stimulus to the first recording electrode pole was significantly greater than conduction intervals measured between subsequent electrode poles. The greatest increase in conduction interval with closely coupled premature complexes occurred between the stimulus artifact and the first recording electrode pole. Reduction in ventricular but not atrial ERP was associated with significantly increased local conduction interval., Conclusions: First, most of the conduction delay after the stimulus artifact occurs within 5 mm from the pacing site. Second, closely coupled premature complexes delay conduction primarily by prolonging latency in the first 5 mm from the pacing site. Third, fundamental differences occur between the atrium and ventricle regarding changes in local conduction as a function of changes in ERP, suggesting that factors involved in sudden changes in refractoriness (eg, heart rate acceleration) could produce divergent effects on atrial and ventricular arrhythmogenesis.

Background: Autonomic modulation, especially increased sympathetic activity may play a role in the genesis of ventricular arrhythmias. The purpose of this study was to determine whether beta-sympathetic stimulation with isoproterenol would alter sustained ventricular tachycardia (VT) circuits similarly during the drug-free and antiarrhythmic drug-treated states., Methods and Results: Twenty-five patients with repeatedly inducible, hemodynamically stable, sustained VT were evaluated by programmed ventricular stimulation. In the antiarrhythmic drug-free state, isoproterenol (0.03 microgram/kg per minute) shortened the following intervals (in milliseconds; mean +/- SEM; 25 patients; paired t test): sinus cycle length (792 +/- 37 to 568 +/- 18; (p < 0.001), ventricular paced QT interval (386 +/- 8 to 348 +/- 6; p < 0.001), ventricular paced QRS duration (185 +/- 4 to 182 +/- 4; p = 0.014), ventricular effective (238 +/- 5 to 208 +/- 4; p < 0.001) and functional (261 +/- 6 to 227 +/- 5; p < 0.001) refractory periods, and the VT cycle length (VTCL) (311 +/- 9 to 291 +/- 9; p < 0.001). Isoproterenol (0.03 microgram/kg per minute) was administered during 31 antiarrhythmic drug trials (procainamide, n = 18; quinidine, n = 13) in 22 patients. Isoproterenol shortened the sinus cycle length, QT interval during ventricular pacing, and ventricular effective and functional refractory periods before and during procainamide and quinidine therapy (ANOVA; isoproterenol effect, p < or = 0.0002 for all). The amount of decrease in these intervals with isoproterenol was the same before and during procainamide and quinidine therapy (ANOVA interaction, p = NS for all). The QRS duration during ventricular pacing and VTCL were also shortened by isoproterenol before and during procainamide (baseline, n = 17; QRS, 182 +/- 4 to 178 +/- 4 msec; VTCL, n = 18, 314 +/- 11 to 291 +/- 11 msec; during procainamide, QRS, 218 +/- 7 to 197 +/- 6 msec; VTCL, 422 +/- 15 to 359 +/- 11 msec) and quinidine (baseline, n = 13; QRS, 190 +/- 6 to 185 +/- 5 msec; VTCL, n = 12, 298 +/- 10 to 280 +/- 9 msec; during quinidine, QRS, 223 +/- 9 to 208 +/- 8 msec; VTCL, 415 +/- 14 to 355 +/- 10 msec) (isoproterenol effect p < or = 0.0003 for all). However, the amount of decrease in QRS duration and VTCL with isoproterenol was greater during procainamide and quinidine than in the drug-free state (ANOVA interaction, p < or = 0.02 for all). These changes continued to be significant when normalized for the initial QRS duration and VTCL (p < or = 0.03 for all)., Conclusions: Isoproterenol affects presumed reentrant sustained VT circuits less in the absence of antiarrhythmic drugs but markedly attenuates the antiarrhythmic drug-induced slowing of sustained VT. To the extent that the change in QRS duration reflects a change in conduction within the VT circuit, these data imply that the attenuation of drug-induced slowing of VT by isoproterenol is due to a greater change in conduction rather than refractoriness.

Background: Ebstein's anomaly is the most commonly occurring congenital abnormality associated with the Wolff-Parkinson-White (WPW) syndrome. However, the effects of Ebstein's anomaly on the risks and benefits of surgical ablation of accessory pathways in patients with WPW syndrome are unknown., Methods and Results: This study compared the long-term outcome of 38 WPW patients with Ebstein's anomaly undergoing accessory pathway ablation to a reference population of 384 similarly treated patients without the anomaly. Ebstein's anomaly was mild in 21 patients (55%) and moderate-to-severe in 17 patients (45%). Sixteen patients (42%) required tricuspid valve surgery, and 23 (61%) had an atrial septal defect or patent foramen ovale repaired. Baseline clinical characteristics and preoperative clinical arrhythmias were similar in both groups. Ten-year survival was 92.4% and 91.2% for patients with and without Ebstein's anomaly, respectively (p = NS). During a mean follow-up of 6.2 +/- 3.8 and 5.3 +/- 3.6 years, 82% of patients with and 90% without Ebstein's anomaly had either clinically insignificant or no arrhythmias, and 18% versus 10% reported symptoms suggesting arrhythmias lasting longer than 1 minute, respectively. Atrial fibrillation was reduced postoperatively to 9% (p less than 0.001) in patients with and to 4% (p less than 0.001) in those without the anomaly. Fewer hospitalizations were reported postoperatively by 90% versus 96% of patients with and without Ebstein's anomaly; 9.4% versus 6.0% of patients were disabled at follow-up, respectively (p = NS)., Conclusions: Patients with Ebstein's anomaly are improved significantly after accessory pathway ablation. The presence of this anomaly should not preclude accessory pathway ablation in these patients.

Background: Although the anatomic "substrate" for the occurrence of antidromic reciprocating tachycardia (ART) has been previously examined, the underlying physiological substrate for this unusual arrhythmia in patients with the Wolff-Parkinson-White syndrome has not been thoroughly characterized., Methods and Results: The electrophysiological properties of the accessory pathway and normal ventriculoatrial conduction system in 30 patients with ART and a single accessory pathway were compared with those observed in a control group of 36 patients without this arrhythmia to elucidate the critical physiological substrate essential for the development and maintenance of ART. Inducible ART had a mean cycle length of 286 +/- 31 msec. The average retrograde ventriculoatrial conduction system effective refractory period in ART patients was significantly less than that in the control group (244 +/- 32 versus 291 +/- 46 msec, p = 0.0002). All of the ART patients showed retrograde conduction over the normal conduction system at cycle lengths of less than or equal to 360 msec; 23 had 1:1 conduction to less than or equal to 300 msec, and 16 showed 1:1 propagation at cycle lengths of less than or equal to 260 msec. The shortest cycle length accompanied by 1:1 retrograde propagation over the normal conduction system in patients with ART was also significantly less than that observed in the control group (274 +/- 39 versus 347 +/- 73 msec, p less than 0.001). The accessory pathway anterograde ERP in ART patients with 1:1 retrograde conduction over the normal ventriculoatrial conduction system at cycle lengths of less than or equal to 360 was significantly less than that seen in comparable control patients (247 +/- 23 versus 284 +/- 56 msec, p = 0.001), and the accessory pathway location was significantly further from the atrioventricular node in 21 patients with ART undergoing surgery than that in 22 operated control patients (3.8 +/- 0.8 versus 2.9 +/- 0.8 mapping units, p = 0.0025) who also had retrograde ventriculoatrial conduction to cycle lengths of less than or equal to 360 msec. No significant differences in anterograde atrioventricular conduction system properties, retrograde accessory pathway refractoriness, or shortest ventricular pacing cycle lengths maintaining 1:1 conduction via the accessory pathway were observed between groups., Conclusions: This quantitative characterization of the properties of conduction and refractoriness of both the accessory pathway and ventriculoatrial conduction system and the relation between these characteristics and the accessory pathway location in ART patients provides additional insight into the prerequisites for the initiation and maintenance of this rhythm disturbance.

Antiarrhythmic drugs may be used as primary therapy to prevent recurrent cardiac arrest or as adjunctive treatment in patients given an implantable cardioverter defibrillator. In the latter instance, drugs are given to suppress nonlethal arrhythmias that are capable of initiating defibrillator discharge or to slow and/or decrease the number of episodes of sustained ventricular tachyarrhythmias. When used as primary therapy, drug efficacy should be judged by nonempirical methods, preferably serial electrophysiological testing. Although no study has compared noninvasive with invasive testing to determine antiarrhythmic drug effectiveness in a substantial number of cardiac arrest survivors, several investigations have demonstrated that electrophysiological testing is useful for this purpose. One important limitation of serial electrophysiological testing is that nearly 40% of cardiac arrest survivors do not have a sustained ventricular tachyarrhythmia initiated at baseline study; nonpharmacological treatment would appear preferable in these patients. Further, since a relatively high arrhythmic recurrence rate has been noted in individuals with suppressible sustained ventricular tachycardia/fibrillation during drug therapy and a left ventricular ejection fraction less than 30%, we recommend serial electrophysiological/pharmacological testing primarily for patients with inducible sustained ventricular tachyarrhythmias with an ejection fraction greater than or equal to 30%.

A constant intravenous infusion of phenylephrine (0.74 +/- 0.41 micrograms/kg/min) was given to 10 patients to cause a continuous augmentation in reflex vagal tone. After the infusion, the diastolic blood pressure increased from 76 +/- 7 to 89 +/- 11 mm Hg (p less than 0.01). The sinus cycle length and atrial-His (AH) interval were measured, and incremental atrial pacing was performed before and during phenylephrine infusion until atrioventricular (AV) nodal block was achieved. For each patient, the AV nodal function curve (i.e., the AH interval plotted as a function of the atrial pacing cycle length) was compared during both the control state and phenylephrine infusion; the AH intervals during each condition at chosen short (AHS) and long (AHL) cycle lengths were compared. The sinus cycle length increased during phenylephrine infusion from 941 +/- 294 to 1,115 +/- 347 msec (p = 0.013). The AH interval during sinus rhythm was not significantly prolonged (77 versus 82 msec, p = NS). The shortest atrial pacing cycle length yielding 1:1 AV nodal conduction increased during phenylephrine infusion from 412 +/- 120 to 575 +/- 211 msec (p less than 0.01). Of note, the degree of sinus cycle length prolongation did not correlate with the degree of prolongation in the shortest atrial pacing cycle length yielding 1:1 AV nodal conduction. The AV nodal function curve was shifted markedly to the right and only slightly upward.(ABSTRACT TRUNCATED AT 250 WORDS)

The present investigation evaluates the ability of several electrocardiographic (ECG) and electrophysiologic methods to identify multiple accessory pathways in 47 patients in whom the presence and sites of multiple accessory pathways were confirmed intraoperatively. To establish ECG features that suggested the presence of multiple accessory pathways in these patients, we initially studied the 12-lead ECG during maximal preexcitation in 101 patients with single accessory pathways. Distinctive 12-lead ECG patterns were noted for six defined anatomic areas around the right and left atrioventricular groove. Multiple preexcited QRS morphologies, each typical for a separate accessory pathway, and atypical preexcited QRS morphologies were recorded during atrial fibrillation in 31 of 47 (66%) patients with multiple accessory pathways. By comparison, the ECG during sinus rhythm and rapid atrial pacing identified 14 (32%) and 26 (55%) of the patients, respectively. In 12 (26%) patients in whom evidence for multiple accessory pathways was absent from endocardial mapping data, atrial fibrillation provided the diagnosis. In five (11%) patients, atrial fibrillation was the only method that demonstrated the presence of multiple accessory pathways. A combination of ECG findings during atrial fibrillation and rapid atrial pacing plus endocardial mapping data identified 43 (91%) of the patients with multiple accessory pathways. There were two unique fusion patterns on the 12-lead ECG that were characteristic of specific multiple accessory pathway combinations.(ABSTRACT TRUNCATED AT 250 WORDS)

We followed 11 patients for 5 to 27 months (mean 14.9) after implantation of a permanent transvenous low-energy synchronized cardioverter to evaluate both long-term reproducibility of ventricular tachycardia (VT) induction via noninvasive programmed electrical stimulation with the cardioverter and efficacy of cardioversion. Induction and termination of VT were attempted at implantation and approximately every 3 months thereafter. All patients had coronary artery disease and were receiving antiarrhythmic drug therapy (amiodarone in eight). VT cycle length, morphology, and mode of induction were reproducible on multiple occasions in nine patients; clinical VT was induced inconsistently in two patients. Multiple VT episodes in five patients had one morphology, whereas two morphologies occurred in six patients. Synchronization of the shock within the QRS complex and right ventricular effective refractory periods determined via the cardioverter remained constant over the follow-up period. VT was terminated on every occasion in nine patients and on eight of nine occasions in one patient. Tachycardia was accelerated on three of five occasions in one patient. Consistently effective cardioversion energy (0.2 to 2.0 J) increased modestly in four patients. We conclude that patients with inducible monomorphic VT usually have sustained VT with similar characteristics inducible over a period of time and cardioversion and sensing functions of the cardioverter remain relatively stable over time.

We performed electrophysiologic studies in 19 patients with accessory pathways before and during encainide therapy with a mean daily dose of 197 mg. Fourteen patients had manifest accessory atrioventricular connections, and five patients had concealed accessory atrioventricular connections. The patients had recurrent atrioventricular reentrant tachycardia for a mean of 15.8 years and had received a mean of 3.6 drug trials without successful suppression of recurrent arrhythmias. Encainide caused complete antegrade conduction block in the accessory pathway in eight of 14 patients with manifest accessory atrioventricular connections. The shortest atrial pacing cycle length maintaining 1:1 conduction over the accessory pathway at control study w3as 328 +/- 66 msec in patients in whom antegrade conduction block occurred, and it was 247 +/- 21 msec (p less than .01) in patients in whom conduction remained during encainide therapy. Retrograde conduction over accessory atrioventricular connections could be evaluated in 14 patients, and complete block occurred in seven patients during encainide therapy. There was no correlation between control retrograde effective refractory period or conduction of the accessory pathway and subsequent development of conduction block with encainide therapy. It should be noted that five patients who developed drug-related retrograde block over the accessory pathway had initial retrograde effective refractory periods for the accessory pathway less than 270 msec. Nineteen patients had atrioventricular reentrant tachycardia initiated at control electrophysiologic study. Encainide prevented induction of tachycardia in 10 patients, and in the other nine patients, cycle length of tachycardia increased during drug treatment from 313.9 +/- 53.1 to 418.3 +/- 80.9 msec (p less than .001), primarily due to an increase in ventriculoatrial conduction time from 162.2 +/- 43.8 to 238.3 +/- 87.9 msec (p less than .01). Fifteen patients continued encainide treatment for a mean of 18 months (range 7 to 38), and all but one patient remain asymptomatic. Encainide is well tolerated and prevents recurrence of reentrant tachycardia in patients with Wolff-Parkinson-White syndrome very effectively.

We studied the effect of drive train duration on human right bundle branch refractoriness. Seven patients with a QRS duration of 0.10 sec or less and no preexcitation had functional right bundle branch block induced reproducibly with premature atrial stimulation. Refractoriness of the right bundle branch was defined as the longest H1H2 interval resulting in right bundle branch block and was determined in each patient at a constant pacing cycle length but at five to seven different atrial drive train durations varying from four to 99 complexes. In all seven patients, right bundle branch refractoriness decreased with increasing drive train duration (mean 15 msec). One-third of this decrease (5.0 msec) occurred between drive train durations of four and eight complexes, and close to two-thirds (9.3 msec) occurred between drive train durations of eight and 64 complexes. Very little further decrease (0.7 msec) occurred between 64 and 99 complexes. We conclude that right bundle branch refractoriness shortens progressively as the preceding drive train duration increases. This phenomenon may in part explain the disappearance of functional right bundle branch block during supraventricular tachycardia after a variable number of complexes without a change in cycle length of tachycardia.

We evaluated the electrophysiologic effects of disopyramide phosphate in 12 patients with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed during a control period and after administering i.v. disopyramide (four bolus doses of 9.5 mg/kg over 40 minutes superimposed on a continuous infusion at 1.0 mg/kg/hour). All patients were then restudied after 3 days on oral medication in doses of 800-1200 mg/day. In all patients we tried to induce reciprocating tachycardia and atrial fibrillation. The cycle length during reciprocating tachycardia was not changed by i.v. disopyramide, but increased after oral disopyramide, from 331 +/- 53 (+/- SD) to 370 +/- 68 msec (p less than 0.01). This increase occurred predominantly as a result of prolongation of retrograde conduction time in the accessory pathway. Despite prolonging cycle length during reciprocating tachycardia, disopyramide did not prevent its induction. The shortest and mean RR intervals during atrial fibrillation were used to assess antegrade refractoriness of the accessory pathway. Intravenous disopyramide prolonged the shortest RR from 169 +/- 18 to 226 +/- 24 msec (p less than 0.0001) and the mean RR from 255 +/- 58 to 329 +/- 62 msec (p less than 0.005). Oral disopyramide prolonged the shortest RR interval from 169 +/- 18 to 248 +/- 36 msec (p less than 0.0001) and the mean RR from 255 +/- 58 to 360 +/- 93 msec (p less than 0.001). After oral disopyramide, the episodes of atrial fibrillation were shorter and self-terminating. No acute hemodynamic side effects were observed, but five patients developed gastrointestinal or anticholinergic side effects on oral disopyramide. Seven patients elected to have surgical interruption of their accessory pathways and five have been successfully treated with oral disopyramide for 14-33 months. Disopyramide appears to have beneficial electrophysiologic effects in patients with Wolff-Parkinson-White syndrome. Prolongation of refractoriness in the accessory pathway markedly slows the ventricular response during atrial fibrillation and therefore prevents the development of life-threatening arrhythmias.

The purpose of this study was to ascertain the origin of the atrial electrogram recorded on the esophageal lead. The atria and esophagus were mapped during reciprocating tachycardia in 11 patients with the Wolff-Parkinson-White syndrome and one patient with atrioventricular nodal reentry, and during right ventricular pacing in four additional patients. The esophagus was mapped by recording atrial electrograms at 1-cm intervals throughout the esophagus beginning at the most distal area where atrial depolarization was seen. The retrograde atrial activation time recorded on the esophageal lead in its distal position occurred at the same time as atrial septal depolarization in all patients. In 14 of 16 patients, the distal esophageal ventriculoatrial (VA) conduction time was also the shortest esophageal VA conduction time recorded. In two of five patients with left lateral accessory pathways, the shortest esophageal VA conduction time was noted during pullback of the lead from the esophagus instead of at the most distal area. The most likely explanation for this was an unusual anatomic relationship between the esophagus and left atrium in these two patients. We conclude that 1) the most distal esophageal atrial electrogram probably records posterior paraseptal atrial depolarization; 2) it is unusual to record clearly identifiable left atrial activation in the esophagus; and 3) the esophageal lead is not useful in locating left-sided accessory pathways.

Patterns of ventriculoatrial conduction have been used to distinguish retrograde conduction over an accessory atrioventricular pathway from that over the normal atrioventricular conduction system. Ventriculoatrial conduction at a constant interval during incremental ventricular pacing and during progressive prematurity of ventricular extrastimuli has been considered characteristic of conduction over an accessory pathway. We describe three patients with the Wolff-Parkinson-White syndrome who had progressive or sudden increments in ventriculoatrial conduction over an accessory pathway during fixed-rate ventricular pacing or during introduction of ventricular extrastimuli. Such properties have been considered characteristic of conduction over the normal atrioventricular conduction system. We conclude that retrograde conduction over accessory pathways may resemble conduction over the normal atrioventricular conduction system.