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While Drs. Wolff, Parkinson, and White fully described the syndrome that bears their names in 1930, prior case reports had already described the essentials. Over the ensuing century this syndrome has captivated the interest of anatomists, clinical cardiologists, and cardiac surgeons. Stanley Kent described lateral muscular connections over the atrioventricular (AV) groove, which he felt were the normal AV connections. The normal AV connections were, however, clearly described by His and Tawara. True right-sided AV connections were initially described by Wood et al., while Ohnell first described left free wall pathways. David Scherf is thought to be the first to describe our current understanding of the pathogenesis of the Wolff-Parkinson-White (WPW) syndrome in terms of a reentrant circuit involving both the AV node--His axis as well as the accessory pathway. This hypothesis was not universally accepted and many theories were applied to explain the clinical findings. The basics of our understandings were established by the brilliant work of Pick, Langendorf, and Katz who by using careful deductive analysis of ECGs were able to define the basic pathophysiological processes. Subsequently, Wellens and Durrer applied invasive electrical stimulation to the heart in order to confirm the pathophysiological processes. Sealy and his colleagues at Duke University Medical Center were the first to successfully surgically divide an accessory pathway and ushered in the modern area for curative therapy for these patients. Morady and Scheinman were the first to successfully ablate an accessory pathway (posteroseptal) using high-energy direct-current shocks. Subsequently, Jackman, Kuck, Morady, and a number of groups proved the remarkable safety and efficiency of catheter ablation for pathways in all locations using radiofrequency energy. More recently, Gallob et al. first described the gene responsible for a familial form of WPW. The current ability to cure patients with WPW is due to the splendid contributions of individuals from diverse disciplines from throughout the world.

Introduction: The causes of transcristal conduction (TC) in patients with atrial flutter (AFL) are unknown., Methods and Results: In two groups of patients referred for AFL ablation, 36 had cavotricuspid isthmus (CTI) dependent flutter (Group I) and 24 had lower (n = 21) or upper loop reentry (n = 5) (Group II). After ablation, isthmus block was evaluated by pacing from the coronary sinus (CS) and low lateral right atrium and by alternative techniques, including mapping with electrodes spanning the CTI or electroanatomic mapping. After bidirectional CTI block was verified, 21/36 (58%) in Group I showed TC with CS pacing, including low TC in 16 (including 11 showing "pseudo" CTI conduction), higher TC in 6 and multiple breaks in 3. However, 8 with low TC during CS pacing showed unidirectional block by pacing outside of the CS os. Twelve (50%) in Group II had TC during CS pacing after bidirectional CTI block, with low TC in 5 (2 mimicking residual CTI conduction) and higher breaks in 9. There was no significant difference in the incidence of TC during CS pacing after CTI block between groups. In seven autopsied hearts, the muscle orientation between the proximal CS musculature and Eustachian ridge were examined. Muscular connections between the CS and Eustachian ridge coursing toward the orifice of inferior vena cava were found in one of the hearts., Conclusions: It is concluded that in patients with bidirectional CTI block, pacing from the CS may be associated with TC mimicking a conduction leak through the isthmus. Pacing just outside the CS os helps distinguish pseudo from true isthmus block.

Objectives: We sought to assess the efficacy and safety of ibutilide cardioversion for those with atrial fibrillation (AF) or atrial flutter (AFL) receiving long-term treatmentwith class IC agents., Background: Attenuation of ibutilide-induced QT prolongation has been observed in a small number of patients pretreated with class IC agents. The clinical significance of the interaction between ibutilide and class IC agents is unknown., Methods: Seventy-one patients with AF (n = 48) or AFL (n = 23), receiving propafenone 300 to 900 mg/day (n = 46) or flecainide 100 to 300 mg/day (n = 25), presented for ibutilide (2.0 mg) cardioversion., Results: The mean durations of arrhythmia episode and arrhythmia history were 25 +/- 48 days and 4.4 +/- 6.4 years, respectively. Sixty-five patients (91.5%) had normal left ventricular systolic function. Twenty-three of 48 patients (47.9%; 95% confidence interval, 33.3% to 62.8%) with AF and 17 of 23 patients (73.9%; 95% confidence interval, 51.6% to 89.8%) with AFL converted with mean conversion times of 25 +/- 14 min and 20 +/- 12 min, respectively. There was a small increase in corrected QT interval after ibutilide (from442 +/- 61 ms to 462 +/- 59 ms, p = 0.006). One patient developed non-sustained polymorphous ventricular tachycardia and responded to intravenous magnesium. Another developed sustained torsade de pointes and was treated effectively with direct-current shock and intravenous dopamine., Conclusions: Our observations suggest that the use of ibutilide in patients receiving class IC agents is as successful in restoring sinus rhythm and has a similar incidence of adverse effects as the use of ibutilide alone.

Automaticity from extra nodal accessory pathways appears to be rare. We report the case of a man with the WPW syndrome who presented for repeat electrophysiological study and catheter ablation. After successful ablation of a para-Hisian accessory pathway, an isoproterenol challenge produced an accelerated wide complex rhythm that was dissociated from sinus rhythm and matched the previous pattern of maximal preexcitation. This automatic rhythm was transient and dependent on catecholamine administration. One month after successful ablation, an exercise treadmill test (ETT) did not demonstrate any pre-excitation or ectopy.

Congenital long QT syndrome (LQTS) is a genetic disease that predisposes affected individuals to arrhythmias, syncope, and sudden death. Mutations in several ion channel genes have been discovered in different families with LQTS: KCNQ1 (KVLQT1, LQT1), KCNH2 (HERG, LQT2), SCN5A (LQT3), KCNE1 (minK, LQT5), and KCNE2 (MiRP1, LQT6). Previously, the P448R-KVLQT1 missense mutation has been reported as an LQT1-causing mutation. In this report, we demonstrate the presence of the P448R polymorphism in two, unrelated Chinese LQTS families. Although absent from 500 reference alleles derived from 150 white and 100 African-American subjects, P448R was present in 14% of healthy Chinese volunteers. Given the inconsistencies between the genotype (LQT1) and clinical phenotype (LQT2) in our two LQTS families, together with the finding that the P448R appears to be a common, ethnic-specific polymorphism, mutational analysis was extended to the other LQTS-causing genes resulting in the identification of distinct HERG missense mutations in each of these two families. Heterologous expression of P448R-KVLQT1 yielded normal, wild-type (WT) currents. In contrast, the two unique HERG mutations resulted in dominant-negative suppression of the WT HERG channel. Our study has profound implications for those engaged in genetic research. Importantly, one child of the original proband was initially diagnosed with LQT1 based upon the presence of P448R-KVLQT1 and was treated with beta-blockers. However, he did not possess the subsequently determined LQT2-causing mutation. On the other hand, his untreated P448R-negative brother harbored the true, disease-causing HERG mutation. These findings underscore the importance of distinguishing channel polymorphisms from mutations pathogenic for LQTS and emphasize the importance of using appropriate ethnically matched controls in the genotypic analysis of LQTS.

Numerous drugs have been implicated in causing a prolonged QT interval and Torsades de pointes. However, the association of famotidine and acquired long QT syndrome has rarely been reported. We report 2 cases of famotidine-associated acquired long QT syndrome.

We describe a 53-year-old man with recurrent syncopal events and a malignant family history who was treated for 13 years with sotalol drug therapy with no further occurrence of Brugada syndrome symptoms. Genetic testing revealed that he carried a Brugada syndrome sodium channel SCN5A mutation (4189delT). This finding suggests that sotalol may be of therapeutic benefit in such patients.

To compare usefulness of a ventricular extrastimulus (VES) from the right ventricular (RV) apex versus the RV septum in patients with a septal accessory pathway (AP), VES was applied from the RV apex and the summit of the RV septum in patients with septal APs. A VES from the RV apex and from the summit was diagnostic of the presence of an AP in 13 of 28 patients (83%) and in 10 of 12 patients, respectively (46% p <0.05), and VES proved an AP as a part of the tachycardia circuit in 5 of 28 patients (18%) and 6 of 12 patients, respectively (50%, p <0.05). A VES during His bundle refractoriness from the RV summit increases the diagnostic yield for both the presence of an AP and its participation in the tachycardia circuit with respect to RV apical VES.

There are very limited data on the effects of bundle branch block (BBB) in patients with atrioventricular nodal reentrant tachycardia (AVNRT). Studies in a total of 155 patients with 162 episodes of AVNRT were retrospectively analyzed. A total of 38 patients (25%) developed spontaneous right BBB, whereas 5 (3%) developed left BBB during tachycardia. Five of the 38 (13%) with right BBB showed near identical prolongation of both the ventriculoatrial (VA) (15 +/- 5 ms; 10 to 23) and His to atrial intervals (HA) (14 +/- 4 ms; 10 to 20) with an identical atrial activation sequence for both right BBB or normal QRS tachycardia complexes. In contrast, all 5 patients with left BBB showed a decrease in the VA (-18 +/- 11 ms; 10 to 36) with unchanged HA comparing left BBB to normal QRS patterns during AVNRT. The magnitude of prolongation of the His to ventricular interval (HV) during left BBB (19 +/- 12 ms; 10 to 40) was nearly identical to the decrease in the VA. In conclusion, prolongation of VA and HA with unchanged HV in patients with AVNRT and right BBB suggests that right BBB is due to a block in the fibers in close proximity to the His recording site. The data suggest that fibers in the His bundle are predestined to activate the right bundle branch, and in AVNRT the lower turnaround point may be within the His bundle.

Atriofascicular pathways supporting antidromic reentrant tachycardia are uncommon, and may be difficult to ablate. Traditional mapping can be associated with traumatic loss of atriofascicular conduction. Atriofascicular fibers can insert into the right bundle and will, therefore, first activate the right ventricle. In contrast to initial activation of the ventricle near the tricuspid annulus that can be seen in patients with right-sided decremental atrioventricular pathways. We used electroanatomic mapping to map and ablate the ventricular insertion of atriofascicular pathways in two patients during sinus rhythm and during atrial pacing. In our 2 cases an atriofascicular potential was recorded from below the tricuspid valve annulus and tagged. At this site, each pathway was ablated with one radiofrequency lesion. We describe 2 cases where electroanatomic mapping of the right ventricle was used to map and ablate atriofascicular pathways.

The purpose of this study was to show that multipolar electrographic recordings along the subeustachian isthmus (SI) can better differentiate slow conduction from complete isthmus block after atrial flutter ablation, leading to a lower incidence of recurrent atrial flutter (Afl). Despite the presence of various techniques to identify bidirectional conduction block (BDB) after isthmus ablation for typical Afl, several studies, including a report from a national registry, suggest that radiofrequency ablation is still associated with a 15% recurrence rate. Thus, techniques that can distinguish slow conduction from complete isthmus block have the potential for reducing long-term recurrences. We evaluated patients who underwent radiofrequency ablation for typical isthmus-dependent Afl. Patients were separated into 2 groups. Group A underwent assessment of BDB with conventional methods. In group B, BDB was assessed by placing a multipolar catheter along the floor of the SI, pacing adjacent to the line of radiofrequency application, and assessing electrographic activation on either side. One hundred thirty-one cases of Afl ablation were analyzed (86 in group A, 45 in group B). Over a mean follow-up period of 17 months, recurrence rates of Afl were 16.5% in group A and 4.3% in group B (p = 0.043). Thus, assessment of BDB by placement of a multipolar catheter across the SI after ablation of typical Afl is associated with a significant reduction in long-term recurrence of Afl.

The purpose of this study was to explore the mechanisms of conversion from atypical atrial flutter (AFL) to atrial fibrillation (AF), and the long-term results of cavotricuspid isthmus ablation in these patients. We retrospectively reviewed the records of 221 patients with typical AFL referred to our hospital for ablation. A total of 25 patients had atypical AFL, and cavotricuspid isthmus ablation was performed in 23 with isthmus-dependent atypical AFL, as well as in 180 patients with typical counterclockwise and/or clockwise AFL. In all, 13 spontaneous transitions from atypical AFL to AF were documented in 11 of 17 patients. Before AF, a pattern of lower loop reentry was observed in 11 of 13 patients (85%) and upper loop reentry in 3 (1 had both). Multiple early breaks along the tricuspid annulus during AFL were noted in 6 of 13 patients (46%). Among the 13 transitions, discrete atrial premature complexes before AF were found in 5 patients with lower loop reentry and in 1 with upper loop reentry (46%). In the remaining patients, a more rapid atrial rhythm was involved in the development of AF with a pulmonary venous focus in 2. In some cases, additional "breaks" in the functional line of block occurred before the development of AF. There was a significant increased incidence of AF (68%) in those with atypical AFL compared with those with typical AFL (38%) (p = 0.004). After a mean follow-up of 28 +/- 9 months for the atypical group and 18 +/- 11 months for the typical group, the AF recurrence rate was similar (57% vs 48%, p = 0.4). Discrete atrial premature complexes or atrial tachycardia may initiate AF either directly or by producing further breaks in lines of functional block. Bidirectional cavotricuspid isthmus block is associated with cure or control of AF in approximately 50% of patients with AFL.

Focal junctional tachycardia (FJT) is characterized by a rapid often irregular narrow complex tachycardia with episodes of atrioventricular (AV) dissociation. This uncommon arrhythmia is most likely due to abnormal automaticity or triggered activity. The patients are often quite symptomatic and if left untreated may develop heart failure particularly if their tachycardia is incessant. In patients refractory to medical management, the role of radiofrequency ablation involves either (1) selective ablation of the tachycardia focus while preserving AV conduction or as a last resort (2) AV junction ablation followed by pacemaker implantation. The clinician should first assess whether ventriculoatrial (VA) conduction is present or absent during tachycardia. If present, radiofrequency ablation should be applied at the site of earliest retrograde atrial activation. In the absence of VA conduction and hence an atrial target site, sequential lesions should be applied in the posterior septum (slow pathway region) followed by lesions applied in midseptum and anteroseptum respectively if tachycardia persists. To further minimize the risk of AV nodal block, some authors delivered radiofrequency energy during atrial overdrive pacing to assess AV conduction during ablation. Others recommended mapping the perinodal region and applying radiofrequency ablation at the site where catheter manipulation resulted in tachycardia termination. Using this ablative approach, the risk of AV block is around 5-10%.

Background: Transmural dispersion of repolarization (TDR) may be related to the genesis of torsade de pointes (TdP) in patients with the long-QT (LQT) syndrome. Experimentally, LQT2 models show increased TDR compared with LQT1, and beta-adrenergic stimulation increases TDR in both models. Clinically, LQT1 patients experience symptoms at elevated heart rates, but LQT2 patients do so at lower rates. The interval from T-wave peak to T-wave end (TPE interval) is the clinical counterpart of TDR. We explored the relationship of TPE interval to heart rate and to the presence of symptoms in patients with LQT1 and LQT2., Methods and Results: We reviewed Holter recordings from 90 genotyped subjects, 31 with LQT1, 28 with LQT2, and 31 from unaffected family members, to record TPE intervals by use of an automated computerized program. The median TPE interval was greater in LQT2 (112+/-5 ms) than LQT1 (91+/-2 ms) or unaffected (86+/-3 ms) patients (P<0.001 for all group comparisons), and the maximal TPE values differed as well. LQT1 patients showed abrupt increases in TPE values at RR intervals from 600 to 900 ms, but LQT2 patients did so at RR intervals from 600 to 1400 ms (longest RR studied). Asymptomatic and symptomatic patients showed similar TDRs., Conclusions: TDR is greater in LQT2 than in LQT1 patients. LQT1 patients showed a capacity to increase TDR at elevated heart rates, but LQT2 patients did so at a much wider rate range. The magnitude of TDR is not related to a history of TdP.

Objectives: It was the purpose of this study to define the electrophysiologic (EP) identity of left septal atrial tachycardia (AT)., Background: The clinical and EP characteristics of this particular type of arrhythmia have not been fully described., Methods: A total of 120 patients with AT underwent invasive EP evaluation. Five patients (two men and three women; mean age 49 +/- 15 years) with left septal AT were identified. Mapping of the right and left atrium was performed using conventional electrode catheters (five patients) and a three-dimensional electroanatomic mapping system (three patients) followed by radiofrequency (RF) ablation at the earliest site of local endocardial activation., Results: Five tachycardias with a mean cycle length of 320 +/- 94 ms were mapped, and the earliest endocardial electrogram occurred 22 +/- 10 ms before the onset of the surface P-wave. Three left septal ATs were found to be originating from the left inferoposterior atrial septum and two from the left midseptum. During tachycardia, positive (three patients), biphasic negative-positive deflection (one patient), or isoelectric (one patient) P waves were recorded in lead V(1). The inferior leads demonstrated a positive or biphasic P-wave morphology in four of five patients (80%). Four patients were given both adenosine and verapamil during AT. In three of four patients, verapamil successfully terminated AT after adenosine had failed. Adenosine successfully terminated AT in one of four patients. Successful RF ablation was performed in all patients (mean 2.2 +/- 1.7 RF applications) without affecting atrioventricular conduction properties. No recurrence of AT was observed after a mean follow-up of 14 +/- 8 months., Conclusion: Left septal AT ablation is safe and effective. There was no consistent P-wave morphology associated with this particular type of AT. This arrhythmia appears to be resistant to adenosine and moderately responsive to calcium antagonists.

Background: The efficacy of ibutilide in conversion of atrial fibrillation and flutter (AFL) has been demonstrated. However, its electrophysiological effects on human atria have not been fully studied., Methods and Results: Twelve patients with typical AFL were studied. Electrograms were recorded from the anterolateral right atrium, His bundle position, and coronary sinus. During AFL, we measured the conduction time, CTi, through the isthmus between the tricuspid annulus and eustachian ridge and the conduction time, CTni, through the remainder of the right atrium. Resetting response curves and atrial effective refractory periods were determined with single extrastimuli delivered in the tricuspid annulus-eustachian ridge isthmus. After infusion of ibutilide (2 mg over 15 minutes), AFL cycle length (CL) increased from 260+/-30 to 295+/-39 ms (P<0.0003) because of an increase in either CTi, CTni, or both. Effective refractory periods increased from 149+/-16 to 208+/-26 ms (P<0.001). AFL CL variability increased, with a rightward shift of the resetting response curves and loss of full excitability. In 8 patients, AFL was terminated by atrial overdrive pacing after ibutilide at CLs equal to or longer than those that were not effective at baseline, which was caused by orthodromic block in the tricuspid annulus-eustachian ridge isthmus or was associated with development of transient rapid rhythms around newly formed sites of intra-atrial conduction block., Conclusions: Ibutilide causes prolongation of AFL CL and increased CL variability by abolishment of a fully excitable gap. Ibutilide may facilitate pace termination of AFL by development of new short-lived reentry around functional blocks.

This study assesses the use of 24-hour ambulatory electrocardiographic recordings in distinguishing patients with long-QT1 syndrome (LQT1) from those with LQT2, and for distinguishing affected from unaffected patients. The diagnoses of the congenital LQT syndrome and its most common types LQT1 and LQT2 are made difficult because of the limitations of the electrocardiogram as a diagnostic tool. With an automated computerized program, Holter recordings from 15 LQT1 and 15 LQT2 patients and 43 healthy subjects (training set) were reviewed to select the best criteria using QT duration and rate dependence as well as the difference between QT end and QT apex to separate the 3 groups. Fixed criteria were then applied in blinded fashion to separate a different group of 32 genotyped patients and 16 unaffected subjects (test set). In the training set, the RR interval (100 ms), a slope value for median QT/RR curves of -0.016 separated 25 of 30 (83%) and a minimal QT end - QT apex value of 80 ms, separated 26 of 30 (87%) LQT1 patients from LQT2 patients. When all selected criteria were applied to differentiate LQT1 from LQT2 versus unaffected genotypes in the test set, 38 of 48 cases (79%) were correctly identified, whereas using the electrocardiogram alone, 60% of patients were correctly classified into 3 genotypes (p = 0.03). Combining measures for QT duration, rate dependence, and QT end - QT apex interval, derived from Holter recordings, complements the clinical differentiation between LQT1 versus LQT2 patients and between affected and unaffected persons for genotype screening purposes.

Background: Atrial fibrillation (AF) may cause life-threatening ventricular arrhythmias in patients with Wolff-Parkinson-White syndrome. We prospectively evaluated the effects of ibutilide on the conduction system in patients with accessory pathways (AP)., Methods and Results: In part I, we gave ibutilide to 22 patients (18 men, 31+/-13 years of age) who had AF during electrophysiology study, including 6 pediatric patients

Background: In canine hearts with inducible reentry, the isthmus tends to form along an axis from the area of last to first activity during sinus rhythm. It was hypothesized that this phenomenon could be quantified to predict reentry and the isthmus location., Methods and Results: An in situ canine model of reentrant ventricular tachycardia occurring in the epicardial border zone was used in 54 experiments (25 canine hearts in which primarily long monomorphic runs of figure-8 reentry were inducible, 11 with short monomorphic or polymorphic runs, and 18 lacking inducible reentry). From the sinus rhythm activation map for each experiment, the linear regression coefficient and slope were calculated for the activation times along each of 8 rays extending from the area of last activation. The slope of the regression line for the ray with greatest regression coefficient (called the primary axis) was used to predict whether or not reentry would be inducible (correct prediction in 48 of 54 experiments). For all 36 experiments with reentry, isthmus location and shape were then estimated on the basis of site-to-site differences in sinus rhythm electrogram duration. For long and short runs of reentry, estimated isthmus location and shape partially overlapped the actual isthmus (mean overlap of 71.3% and 43.6%, respectively). On average for all reentry experiments, a linear ablation lesion positioned across the estimated isthmus would have spanned 78.2% of the actual isthmus width., Conclusions: Parameters of sinus rhythm activation provide key information for prediction of reentry inducibility and isthmus location and shape.

Background: The purpose of our study was to define the incidence and mechanisms of atypical right atrial flutter., Methods and Results: A total of 28 (8%) of 372 consecutive patients with atrial flutter (AFL) had 36 episodes of sustained atypical right AFL. Among 24 (67%) of 36 episodes of lower loop reentry (LLR), 13 (54%) of 24 episodes had early breakthrough at the lower lateral tricuspid annulus, whereas 11 (46%) of 24 episodes had early breakthrough at the high lateral tricuspid annulus, and 9 (38%) of 24 episodes showed multiple annular breaks. Bidirectional isthmus block resulted in elimination of LLR. A pattern of posterior breakthrough from the eustachian ridge to the septum was observed in 4 (14%) of 28 patients. Upper loop reentry was observed in 8 (22%) of 36 episodes and was defined as showing a clockwise orientation with early annular break and wave-front collision over the isthmus. Two patients had atypical right AFL around low voltage areas ("scars") in the posterolateral right atrium., Conclusions: Atypical right AFL is most commonly associated with an isthmus-dependent mechanism (ie, LLR or subeustachian isthmus breaks). Non-isthmus-dependent circuits include upper loop reentry or scar-related circuits.

This article contains the results of an attempt by appointed members of the North American Society of Pacing and Electrophysiology to define the research frontier in electrophysiology and suggest areas of study as an aid in setting the research agenda.

Background: Ibutilide is a class III drug that is used for the cardioversion of atrial arrhythmias, but it can cause torsade de pointes. Amiodarone also prolongs the QT interval but rarely causes torsade de pointes. There are no studies in which the concomitant use of the 2 agents was examined. The purpose of the present study was to assess the efficacy and safety of cardioversion with combination therapy in patients with atrial fibrillation or flutter., Methods and Results: The study included 70 patients who were treated with long-term oral amiodarone and were referred for elective cardioversion of atrial fibrillation (57 of 70, 81%) or flutter (13 of 70, 19%). Patients were taking amiodarone (153+/-259 days, mean+/-SD) and were administered 2 mg intravenous ibutilide. Left ventricular ejection fraction was measured with echocardiography. The QT intervals were measured on 12-lead ECG. Fifty-five patients (79%) had structural heart disease. Patients were in arrhythmia for 196+/-508 days before cardioversion, with a left ventricular ejection fraction of 50+/-11%. In patients with atrial fibrillation, 22 (39%) of 57 and 7 (54%) of 13 patients with flutter converted within 30 minutes of infusion. Thirty-nine patients who did not convert after ibutilide were treated with electrical cardioversion, and 35 (90%) of 39 patients were successfully converted. The QT intervals were further prolonged after ibutilide for the group from 371+/-61 to 479+/-92 ms (P:<0.001). There was 1 episode of nonsustained torsade de pointes (1 of 70, 1.4%) after ibutilide., Conclusions: The use of ibutilide converted 54% of patients with atrial flutter and 39% of patients with atrial fibrillation who were treated with long-term amiodarone. Despite QT-interval prolongation after ibutilide, only 1 episode of torsade de pointes occurred. Our observations suggest that combination therapy may be a useful cardioversion method for chronic atrial fibrillation or flutter.

The results of the NASPE Prospective Voluntary Registry are reported. A total of 3,357 patients were entered. For those undergoing atrioventricular (AV) junctional ablation (646 patients), the success rate was 97.4% and significant complications occurred in 5 patients. A total of 1,197 patients underwent AV nodal modification for AV nodal reentrant tachycardia, which was successful in 96.1% and the only significant complication was development of AV block (1%). Accessory pathway ablation was performed in 654 patients and was successful in 94%. Major complications included cardiac tamponade (7 patients), acute myocardial infarction (1 patient), femoral artery pseudoaneurysm (1 patient), AV block (1 patient), pneumothorax (1 patient), and pericarditis (2 patients). A total of 447 patients underwent atrial flutter ablation and acute success was achieved in 86% of patients. Significant complications included inadvertent AV block (3 patients), significant tricuspid regurgitation (1 patient), cardiac tamponade (1 patient), and pneumothorax (1 patient). Atrial tachycardia was attempted for 216 patients and the success rate was higher for those with right atrial (80%) or left atrial (72%) compared to those with septal foci (52%). A total of 201 patients underwent ablation for ventricular tachycardia. The success rate was higher for those with idiopathic ventricular tachycardia compared to those with ventricular tachycardia due to ischemic heart disease or cardiomyopathy. While the number of AV junction ablation were higher for those > 60 years of age, there was no significant difference in the success rate or incidence of complication comparing patients > or = 60 to those < 60 years of age. In addition, we found no differences in incidence of success or complications comparing large volume centers (> 100 ablation/year) with lower volume centers or between teaching and non-teaching hospitals.

This paper reviews three recent large scale studies on the use of catheter ablation for elderly patients with supraventricular tachycardia. These patients underwent catheter ablation of the atrioventricular junction for control of atrial fibrillation, ablation of the slow atrioventricular nodal pathway for those with atrioventricular nodal, reentry tachycardia, and ablation of the accessary pathway for those with atrioventricular reentry tachycardia. There was a higher incidence of atrioventricular junctional ablation and lesser incidence of junctional tachycardia compared to other series involving younger individuals. There was no significant difference in the incidence of successful procedures comparing the elderly with younger patients. In addition, there was no significant difference in the incidence of adverse effects between the two groups. In summary, catheter ablation appears to be safe and effective for elderly patients and the procedure should not be omitted solely on the basis of patient age. (c) 2000 by CVRR, Inc.

Changes in the retrograde conduction time (ventriculoatrial [VA]) interval during functional bundle branch block (BBB) have been used to separate septal from free wall accessory pathways (APs), but different values of the VA interval prolongation (deltaVA) have been described in different reports. A total of 95 patients with single nondecremental APs who developed BBB during atrioventricular reentrant tachycardia were studied. Free wall APs were found in 60 patients, and 35 had septal APs. For patients with free wall APs, complete and incomplete BBB ipsilateral to the atrial insertion site of APs were observed in 39 of 60 patients (65%) and 31 of 60 patients (52%), respectively. For patients who had both complete (QRS > or = 120 ms) and incomplete (QRS <120 ms) BBB during atrioventricular reentrant tachycardia, deltaVA for patients with complete BBB was significantly greater than in those with incomplete BBB, 59 +/- 19 ms versus 30 +/- 11 ms, p <0.001. For patients with septal APs and complete and incomplete BBB during tachycardia, the mean deltaVA for those with complete BBB was 31 +/- 20 ms and was significantly longer than in patients with incomplete BBB (14 +/- 6 ms), p <0.001. There was no significant difference in deltaVA between those with free wall APs and incomplete BBB compared with those with septal APs and complete BBB. The criteria of QRS > or = 120 ms associated with deltaVA > or =40 ms served to best separate free wall from septal APs with a sensitivity of 88% and a specificity of 89%. Left anterior fascicular block was associated with marked lengthening of deltaVA for those with left free wall APs, whereas a left posterior fascicular block pattern resulted in a marked increase in the deltaVA for patients with posteroseptal APs. In the absence of fascicular block patterns, a deltaVA > or =40 ms provides strong evidence of a free wall AP, with a sensitivity of 95% and a specificity of 100%. The left posterior fascicle appears to provide predominant innervation of the posterior septum.

Objectives: This study was directed at developing spatial 62-lead electrocardiogram (ECG) criteria for classification of counterclockwise (CCW) and clockwise (CW) typical atrial flutter (Fl) in patients with and without structural heart disease., Background: Electrocardiographic classification of CCW and CW typical atrial Fl is frequently hampered by inaccurate and inconclusive scalar waveform analysis of the 12-lead ECG., Methods: Electrocardiogram signals from 62 torso sites and multisite endocardial recordings were obtained during CCW typical atrial Fl (12 patients), CW typical Fl (3 patients), both forms of typical Fl (4 patients) and CCW typical and atypical atrial Fl (1 patient). All the Fl wave episodes were divided into two or three successive time periods showing stable potential distributions from which integral maps were computed., Results: The initial, intermediate and terminal CCW Fl wave map patterns coincided with: 1) caudocranial activation of the right atrial septum and proximal-to-distal coronary sinus activation, 2) craniocaudal activation of the right atrial free wall, and 3) activation of the lateral part of the subeustachian isthmus, respectively. The initial, intermediate and terminal CW Fl wave map patterns corresponded with : 1) craniocaudal right atrial septal activation, 2) activation of the subeustachian isthmus and proximal-to-distal coronary sinus activation, and 3) caudocranial right atrial free wall activation, respectively. A reference set of typical CCW and CW mean integral maps of the three successive Fl wave periods was computed after establishing a high degree of quantitative interpatient integral map pattern correspondence irrespective of the presence or absence of organic heart disease., Conclusions: The 62-lead ECG of CCW and CW typical atrial Fl in man is characterized by a stereotypical spatial voltage distribution that can be directly related to the underlying activation sequence and is highly specific to the direction of Fl wave rotation. The mean CCW and CW Fl wave integral maps present a unique reference set for improved clinical detection and classification of typical atrial Fl.

Introduction: It would be advantageous, for ablation therapy, to localize reentrant circuits causing ventricular tachycardia by quantifying electrograms obtained during sinus rhythm (SR) or ventricular pacing (VP). In this study, adaptive template matching (ATM) was used to localize reentrant circuits by measuring dynamic electrogram shape using SR and VP data., Methods and Results: Four days after coronary occlusion, reentrant ventricular tachycardia was induced in the epicardial border zone of canine hearts by programmed electrical stimulation. Activation maps of circuits were constructed using electrograms recorded from a multichannel array to ascertain block line location. Electrogram recordings obtained during SR/VP then were used for ATM analysis. A template electrogram was matched with electrograms on subsequent cycles by weighting amplitude, vertical shift, duration, and phase lag for optimal overlap. Sites of largest cycle-to-cycle variance in the optimal ATM weights were found to be adjacent to block lines bounding the central isthmus during reentry (mean 61.1% during SR; 63.9% during VP). The distance between the mean center of mass of the ten highest ATM variance peaks and the narrowest isthmus width was determined. For all VP data, the center of mass resided in the isthmus region occurring during reentry., Conclusion: ATM high variance measured from SR/VP data localizes functional block lines forming during reentry. The center of mass of the high variance peaks localizes the narrowest width of the isthmus. Therefore, ATM methodology may guide ablation catheter position without resorting to reentry induction.

Background: The long-QT syndrome is associated with sudden cardiac death. Combination of beta-blocker and pacing therapy has been proposed for treatment of drug-resistant patients. The purpose of this study was to summarize our long-term experience with combined therapy in patients with long-QT syndrome., Methods and Results: A total of 37 patients with idiopathic long-QT syndrome were treated with combined therapy consisting of continuous cardiac pacing and maximally tolerated beta-blocker therapy and followed up for 6.3+/-4. 6 years (mean+/-SD). The group consisted of 32 female and 5 male patients with a mean age of 31.6 years. The mean paced rate was 82+/-7 bpm (range, 60 to 100 bpm). On follow-up, recurrent symptoms caused by pacemaker malfunction were documented in 3 patients. Four patients died during the follow-up period: 2 adolescents stopped beta-blocker therapy, 1 patient died suddenly while treated with combined therapy, and 1 patient died of unrelated causes. In addition, 3 patients had resuscitated cardiac arrest while on combined therapy, and 1 patient had repeated, appropriate implantable cardioverter-defibrillator discharges on follow-up., Conclusions: Because 28 of 37 patients remain without symptoms with beta-blocker therapy and continuous pacing, combined therapy appears to provide reasonable, long-term control for this high-risk group. However, the incidence of sudden death and aborted sudden death (24% in all patients and 17% in compliant patients) strongly suggests the use of a "back-up" defibrillator, particularly in noncompliant adolescent patients. Implantable cardioverter-defibrillator therapy, however, may be associated with recurrent shocks in susceptible patients.

Background: Interaction between wave fronts in the right and left atrium may be important for maintenance of atrial fibrillation, but little is known about electrophysiological properties and preferential routes of transseptal conduction., Methods and Results: Eighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroanatomic mapping during pacing from the distal coronary sinus (CS) or the posterior left atrium. During distal CS pacing, 9 patients demonstrated a single transseptal breakthrough near the CS os, 1 patient in the high right atrium near the presumed insertion of Bachmann's bundle and 1 patient near the fossa ovalis. The mean activation time from stimulus to CS os was 48+/-15 ms compared with 86+/-15 ms to Bachmann's bundle insertion (P<0.01) and 59+/-23 ms to the fossa ovalis (P=NS and P<0.01, respectively). During left atrial pacing, the earliest right atrial activation was near Bachmann's bundle in 5 and near the fossa ovalis in 4 patients. The activation time from stimulus to CS os was 70+/-15 ms compared with 47+/-16 ms to Bachmann's bundle (P<0.01) and 59+/-25 ms to the fossa ovalis (P=NS). Whereas the total septal activation time was not significantly different during CS pacing compared with left atrial pacing (41+/-16 versus 33+/-17 ms), the total right atrial activation time was longer during CS pacing (117+/-49 versus 79+/-15 ms; P<0.05)., Conclusions: Three distinct sites of early right atrial activation may be demonstrated during left atrial pacing. These sites are in accord with anatomic muscle bundles and may have relevance for maintenance of atrial flutter or fibrillation.

Background: The mechanisms of an atrial flutter (AFL) that is more rapid and at times more irregular than typical AFL are unknown., Methods and Results: Twenty-nine patients with AFL were studied. Atrial electrograms were recorded from a 20-pole catheter placed against the tricuspid annulus (TA), with its distal electrodes lateral to the isthmus between the TA and the eustachian ridge (ER), and from the His bundle and coronary sinus catheters. Atrial extrastimuli were delivered in the TA-ER isthmus during typical AFL. Episodes of a right atrial flutter rhythm that was different from typical AFL were induced in 3 patients and occurred spontaneously in 3 patients. This sustained AFL, designated as lower-loop reentry (LLR), involved the lower right atrium (RA), as manifested by early breakthrough in the lower RA, wave-front collision in the high lateral RA or septum, and conduction through the TA-ER isthmus. Linear ablation resulting in bidirectional conduction block in the TA-ER isthmus terminated spontaneous LLR in 3 patients and rendered LLR noninducible in all patients. The cycle length of LLR was shorter than that of typical AFL (217+/-32 versus 272+/-40 ms, P<0. 01). Alternating LLR and typical AFL in 1 patient resulted in cycle length oscillation., Conclusions: LLR is a subtype of right atrial flutter and depends on conduction through the TA-ER isthmus.

Background: We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT)., Methods and Results: Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was only observed in AT patients (27%) or IST (30%). Patients with IST showed atrial cycle length increases after adenosine (P<0.05) with little change in activation sequence. The incidence of atrial fibrillation after adenosine was higher for those with AVRT (15%) compared with typical AVNRT (0%) P<0.001, or atypical AVNRT (0%) but similar to those with AT (11%) and PJRT (17%)., Conclusions: The EP response to adenosine proved of limited value to identify the location of AT or SVT mechanisms. Features favoring AT were the presence of AV block or marked shortening of atrial cycle length before tachycardia suppression. Atrial fibrillation was more common after adenosine in patients with AVRT, PJRT, or AT. Patients with IST showed increases in cycle length with little change in atrial activation sequence after adenosine.

A patient with a right atriofascicular (Mahaim) tachycardia was found to have inducible antidromic supraventricular tachycardia, but atrial premature beats from the right atrial free wall failed to reset the tachycardia. An interesting transition from AV nodal reentry tachycardia to Mahaim tachycardia is also presented.

Introduction: Fractionated, low-amplitude or long-duration electrograms have limited specificity for locating reentrant circuits causing ventricular tachycardia (VT). In this study a new method is described, adaptive template matching (ATM), based on the quantification of beat-to-beat changes in electrograms, for locating functional reentrant circuits that are relatively stable and cause monomorphic VT., Methods and Results: Monomorphic VTs were induced in 4-day-old infarcted canine hearts by programmed stimulation and reentrant circuits mapped in the epicardial border zone with a 196 or 312 bipolar electrode array. For ATM analysis, a template electrogram from each electrode, during an early cycle, was matched with all subsequent (input) electrograms at the same site by weighting the inputs of amplitude, duration, average baseline, and phase lag. The mean square error (MSE) between template and input was the criterion used to adapt the weights, and was also a measure of changes in electrogram shape that occur from cycle to cycle. The variance of each of the weighting parameters at all electrode sites were plotted on a representation of the electrode array, and the location of the functional lines of block bounding the central common pathway of reentrant circuits with figure-of-eight characteristics, overlaid on the ATM map. Peaks of high variance were found to be coincident with functional lines of block during all tachycardia episodes., Conclusion: Specific beat-to-beat changes in electrograms occur at functional lines of block in reentrant circuits that can be quantified by ATM analysis, suggesting that these regions might be located without activation mapping. The method might be useful to guide ablation catheter position.