Clinical outcome after radiofrequency catheter ablation of focal atrial fibrillation triggers.

INTRODUCTION: Ablative therapy for atrial fibrillation (AF) by targeting initiating triggers, usually in or around the pulmonary veins, has been reported by several centers. Evidence for an overall improvement in quality of life (QOL) and amelioration of symptoms is lacking. METHODS AND RESULTS: Seventy-one patients undergoing attempted ablation of focal AF were followed for 60+/-33 weeks. QOL and symptom questionnaires were completed 1 month before and 6 months after electrophysiologic study. Twenty-three patients (32%) underwent electrophysiologic mapping but no ablation because of either insufficient or multifocal ectopy; the other 48 patients (68%) underwent attempted ablation. Sixteen of 48 patients (33%) undergoing ablation, or 16 (23%) of 71 on an intention-to-treat basis, were found at last follow-up to have persistent sinus rhythm without antiarrhythmic drugs. Patients who underwent mapping without ablation reported no improvements in any QOL or symptom score, whereas patients who had long-term successful ablation had significant improvements in all six QOL measures. Interestingly, patients who developed AF recurrence after ablation still reported significant improvements in 4 of 6 QOL measures. Four of 48 patients (8.3%) undergoing ablation developed pulmonary vein stenosis. CONCLUSION: Paroxysmal AF can be treated successfully in some patients by ablating initiating triggers in the pulmonary veins; however, in our experience the recurrence rate (32/48 [68%]) and risk of pulmonary vein stenosis (8%) after ablation are high. Patients with recurrent AF after ablation of focal AF triggers have significant improvement in QOL and symptoms compared with before ablation. Patients and their physicians should carefully balance the risks and benefits before considering ablation.

Electrocardiographic analysis of ectopic atrial activity obscured by ventricular repolarization: P wave isolation using an automatic 62-lead QRST subtraction algorithm.

INTRODUCTION: Atrial activity on the surface ECG during premature beats and supraventricular arrhythmias frequently is obscured by the superimposed QRST complex of the previous cardiac cycle. This study examines the performance of a newly developed automatic QRST subtraction algorithm to isolate ectopic P waves from the preceding T-U wave. METHODS AND RESULTS: The 62-lead ECG recordings were obtained during (1) sinus rhythm and programmed right atrial stimulation in 12 patients (group A); and (2) sinus rhythm and atrial premature beats, atrial tachycardia, or paroxysmal atrial fibrillation in 5 patients (group B). Pacing in group A patients was conducted at a slow drive cycle length to generate an ectopic P wave not obscured by the previous QRST complex and by delivering single premature extrastimuli at progressively shorter coupling intervals to produce an ectopic P wave obscured by the upsloping (early T-U wave), peak (middle T-U wave), and downsloping component of the T-U wave (late T-U wave). All ectopic P waves in group B patients were concealed by the preceding T-U wave. Automatic QRST subtraction was attained using an adaptive template constructed from averaged QRST complexes (mean 83 +/- 25 complexes) obtained during sinus rhythm (groups A and B) or atrial overdrive pacing (group A). P wave integral maps subsequently were computed, visually compared, and mathematically correlated. A high correspondence in spatial map pattern was observed between integral maps of "nonobscured" and previously "obscured" paced P waves obtained in group A patients (mean r = 0.88 +/- 0.07) as well as between integral maps of two to three previously obscured P waves with the same atrial arrhythmia morphology obtained in group B patients (mean r = 0.94 +/- 0.05). Improved morphologic P wave replication in group A patients was acquired when concealment occurred in the early (mean r = 0.90 +/- 0.08) or late part of the T-U wave (mean r = 0.90 +/- 0.06) as opposed to the middle T-U wave (mean r = 0.85 +/- 0.07) (P = NS and P < 0.05 for early vs middle and late vs middle T-U wave, respectively). CONCLUSION: This novel automatic 62-lead QRST subtraction algorithm enables discrete isolation of T-U wave obscured ectopic atrial activity on the surface ECG while retaining the intricate spatial detail in P wave morphology. Future clinical application of the algorithm may enable improved ECG localization of focal triggers of paroxysmal atrial fibrillation, atrial tachycardia, and the atrial insertion of accessory pathways.

Atypical right atrial flutter patterns.

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.

Central clinical research issues in electrophysiology: report of the NASPE Committee.

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.

The role of the crista terminalis in atrial flutter and fibrillation: a computer modeling study.

Although atrial fibrillation is a common arrhythmia, the underlying mechanisms are incompletely understood. Recent studies have determined the role of the crista terminalis in the mechanisms of a simpler arrhythmia, atrial flutter. We hypothesize that as transverse coupling across the crista terminalis increases, the activation pattern that results is less like typical atrial flutter and more like atrial fibrillation. 6480 Van Capelle elements were coupled in an icosahedron, simulating the right atrium. Atrial simulations were created which incorporated no heterogeneity, heterogeneous coupling, heterogeneous effective refractory periods, and both heterogeneous coupling and effective refractory periods. When the entire crista terminalis was uncoupled, typical atrial flutter occurred. When transverse coupling allowed activation to propagate across the crista terminalis, the flutter cycle length decreased (p<0.0001). In addition, when heterogeneity was present, both the coefficient of variation of cycle length and the number of activation wavelets increased (p<0.0001). Thus, a more rapid reentrant circuit in the superior right atrium drove fibrillatory activity in the remainder of the atrium, as predicted by the "mother wavelet hypothesis." While awaiting in vivo validation, our study indicates that transverse coupling along the crista terminalis may play an important role in the development of atrial fibrillation from atrial flutter.

Prevalence of the Brugada sign in idiopathic ventricular fibrillation and healthy controls.

OBJECTIVE: To determine the prevalence of the Brugada sign (right bundle branch block with ST elevation in V1-V3) in idiopathic ventricular fibrillation and in an age matched healthy population. DESIGN: ECGs from 39 consecutive patients with idiopathic ventricular fibrillation and 592 healthy controls were reviewed. They were classified as definite, questionable, and no Brugada sign (according to predetermined criteria) by four investigators blinded to the subjects' status. RESULTS: Eight patients (21%) with idiopathic ventricular fibrillation but none of the 592 controls had a definite Brugada sign (p < 0.005). Thus the estimated 95% confidence limits for the prevalence of a definite Brugada sign among healthy controls was less than 0.5%. A questionable Brugada sign was seen in two patients with idiopathic ventricular fibrillation (5%) but also in five controls (1%) (p < 0.05). Normal ECGs were found following resuscitation and during long term follow up in 31 patients with idiopathic ventricular fibrillation (79%). Patients with idiopathic ventricular fibrillation and a normal ECG and those with the Brugada syndrome were of similar age and had similar spontaneous and inducible arrhythmias. However, the two groups differed in terms of sex, family history, and the incidence of sleep related ventricular fibrillation. CONCLUSIONS: A definite Brugada sign is a specific marker of arrhythmic risk. However, less than obvious ECG abnormalities have little diagnostic value, as a "questionable" Brugada sign was observed in 1% of healthy controls. In this series of consecutive patients with idiopathic ventricular fibrillation, most had normal ECGs.

Body surface mapping of counterclockwise and clockwise typical atrial flutter: a comparative analysis with endocardial activation sequence mapping.

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.

Derivation of an optimal lead set for measuring ectopic atrial activation from the pulmonary veins by using body surface mapping.

Atrial fibrillation is often initiated by atrial premature beats originating in the pulmonary veins. Non-invasive localization of these ectopic beats would be of significant value in guiding therapy. Body surface potential mapping was performed in nine patients undergoing invasive electrophysiologic study. Signals were recorded from 62 electrodes during pace mapping from each of the pulmonary veins. Optimal electrodes for localizing pulmonary vein activation were sequentially chosen. Seven optimal electrodes (6 anterior, 1 posterior) for recording ectopic atrial activation originating in the pulmonary veins were selected. The seven optimal electrode set performed better than the standard 9 electrode ECG at estimating the full body surface map (correlation 97 vs. 95.7%; p < 0.05). Seven optimally selected electrodes can estimate the body surface potential distribution during ectopic atrial activation orignating from the pulmonary veins. The ability of this electrode configuration to discriminate the site of origin of ectopic atrial beats requires prospective evaluation.

The spatial dispersion of atrial refractoriness and atrial fibrillation vulnerability.

The local dispersion of conduction and refractoriness has been considered essential for induction of atrial arrhythmias. This study sought to determine whether a difference of refractoriness and vulnerability for induction of atrial fibrillation between trabeculated and smooth as well as high and low right atrium may contribute to initiation of atrial fibrillation in dogs. In 14 healthy mongrel dogs weighing 22.4 +/- 1 kg, closed-chest endocardial programmed stimulation was performed from four distinct right atrial sites. Atrial refractory periods and vulnerability for induction of atrial fibrillation or premature atrial complexes were determined during a basic cycle length of 400 and 300 ms and an increasing pacing current strength. For a pacing cycle length of 300 ms, atrial refractory periods were longer on the smooth, as compared to the trabeculated right atrium (102 +/- 25 vs. 97 +/- 17 ms, p < 0.05), whereas for a pacing cycle length of 400 ms, there was no significant difference. The duration of the vulnerability zone for induction of atrial fibrillation was longer on the smooth right atrium, for a cycle length of both 400 ms (40 +/- 30 vs. 31 +/- 22 ms; p < 0.05) and 300 ms (33 +/- 25 vs. 23 +/- 21 ms; p < 0. 01). When comparing high and low right atrium, refractory periods were longer on the the low right atrium, for a cycle length of both 400 ms (111 +/- 23 vs. 94 +/- 24 ms; p < 0.01) and 300 ms (104 +/- 20 vs. 96 +/- 23 ms; p < 0.01). For a pacing cycle length of 300 ms, the duration of the atrial fibrillation vulnerability zone was longer for the high, as compared to the low right atrium (34 +/- 22 vs. 22 +/- 22, p < 0.01). Seven dogs with easily inducible episodes of atrial fibrillation demonstrated significantly shorter refractory periods as compared to 7 non-vulnerable dogs, regardless of pacing site and current strength. In conclusion, significant differences in refractoriness and vulnerability for induction of atrial fibrillation can be observed in the area of the crista terminalis in healthy dogs. Thus, local anatomic factors may play a role in the initiation of atrial fibrillation.

An anatomic approach to prevention of atrial fibrillation: pulmonary vein isolation with through-the-balloon ultrasound ablation (TTB-USA).

Our current understanding is that atrial fibrillation (AF) is initiated most often by a focal trigger from the orifice of or within one of the pulmonary veins. Though mapping and ablation of these triggers appears to be curative in most patients with paroxysmal AF, there are a number of limitations to ablating focal triggers via mapping and ablating the earliest site of activation with a "point" radiofrequency lesion. One way to circumvent thesen limitations is an anatomically-guided ablative approach. By electrically isolating one or more pulmonary veins from the left atrium with a circumferential lesion, firing from within those veins would be unable to reach the body of the atrium, and thus could not trigger atrial fibrillation. We have developed a novel over-the-wire catheter design which integrates a cylindrical ultrasound transducer within a saline filled balloon, termed TTB-USA (through-the-balloon ultrasound ablation) in order to produce narrow circumferential zones of hyperthermic tissue death at the pulmonary vein ostia. Animal studies show great promise, and clinical trials will begin soon.

Use of electroanatomic mapping to delineate transseptal atrial conduction in humans.

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.

Low-power radiofrequency application and intracardiac echocardiography for creation of continuous left atrial linear lesions.

INTRODUCTION: Continuity of radiofrequency (RF) lesions for a catheter-based cure of atrial fibrillation is essential in order to avoid reentrant tachycardias. In the present study, we assessed the value of intracardiac echocardiography and preablation electrode-tissue interface parameters for creation of left atrial linear lesions. METHODS AND RESULTS: In six healthy dogs, two left atrial linear lesions (lesion 1, along the inferior posterior left atrium; lesion 2, from the appendage to the left atrial roof) were attempted via a transseptal approach using a deflectable catheter with six 7-mm coil electrodes. In a randomized fashion, one lesion was performed under echocardiographic guidance and one with blinded echocardiographic monitoring. The following preablation parameters were assessed for every coil electrode: (1) mean atrial electrogram amplitude of six consecutive sinus beats; (2) diastolic pacing threshold; and (3) temperature response to application of 5 W for 10 seconds. After ablation (target temperature 70 degrees C, maximum power 50 W, duration 60 sec), the excised left atrium was examined macroscopically and histologically for lesion length, continuity, and presence or absence of lesions associated with each coil. Out of 12 attempted RF lesions, 7 were continuous (length, 47+/-5 mm, lesion 2, n = 6) and 5 were discontinuous (lesion 1, n = 5). Fifty-two of 70 coil electrodes (74%) had pathologic evidence of lesion creation. Intracardiac echocardiography was superior to fluoroscopy with respect to the actual number of coil electrodes creating lesions, and lesion continuity was correctly predicted in 9 of 12 lesions. Intracardiac echocardiography was 85% sensitive and 54% specific in predicting lesions created by individual coils. The correlation between the mean 60-second ablation temperature and the preablation parameters was 0.45 for the electrogram amplitude, -0.67 for the pacing threshold, and 0.81 for the temperature response to low-power application. Sensitivity and specificity for prediction of lesions created by individual coils, respectively, were 84% and 48% for the electrogram amplitude, 90% and 68% for the pacing threshold, and 96% and 76% for the low-power RF application. CONCLUSION: Long linear lesions can be safely and effectively performed in the canine left atrium, using a tip-deflectable multielectrode catheter. Intracardiac echocardiography may be helpful for positioning the ablation catheter in some parts of the left atrium, and preablation parameters, especially a nontraumatic low-power RF application, are able to predict ultimate lesion creation with high accuracy.

What is the relationship of atrial flutter and fibrillation?

Animal models and human studies of atrial activation mapping and entrainment have considerably enhanced our understanding of the anatomical substrate for atrial flutter and created the basis for a definite cure with radiofrequency catheter ablation. As atrial flutter has now become a curable arrhythmia, emphasis is shifting to understand the most common arrhythmia: atrial fibrillation. Furthermore, from clinical observation, it is apparent that there is a relationship between atrial fibrillation and atrial flutter in patients with atrial arrhythmias. Techniques that have informed our understanding of the anatomical basis of atrial flutter may also be useful in understanding the relationship between atrial fibrillation and flutter, including animal models, clinical endocardial mapping, and intracardiac anatomical imaging. Thus, atrial anatomy and its relationship to electrophysiological findings, and the role of partial or complete conduction barriers around which reentry can and cannot occur, may be of importance for atrial fibrillation as well. Ultimately, the relationship between atrial fibrillation and atrial flutter may inform our understanding of the mechanisms of atrial fibrillation itself, and help to develop new approaches to device, catheter-based, and pharmacological therapy for atrial fibrillation.

Autonomic nervous system tone measured by baroreflex sensitivity is depressed in patients with end-stage liver disease.

OBJECTIVES: Chronic liver disease is often associated with impairment of autonomic nervous system (ANS) reflexes. Baroreflex sensitivity (BRS) testing is an inexpensive, relatively noninvasive test that can be used to assess ANS tone. The aims of the present study were to determine the prevalence of ANS dysfunction in cirrhotics who are being considered for liver transplantation and to explore the potential use of BRS as a prognostic tool in identifying patients awaiting transplantation who are at increased risk for death. METHODS: We studied nine cirrhotics who were awaiting liver transplantation and seven controls without liver disease. BRS (ms/mm Hg) was measured using the phenylephrine method. RESULTS: BRS (mean +/- SEM) (ms/mm Hg) was significantly lower in cirrhotics compared with controls (4.2 +/- 0.9 vs 21.1 +/- 3.8 ms/mm Hg; p < 0.05). Furthermore, BRS was lower in cirrhotics with hepatic encephalopathy compared with those without (2.6 +/- 0.9 vs 6.1 +/- 1.0 ms/mm Hg; p < 0.05) and there was a trend toward lower BRS values in Child-Pugh class C patients as compared with class B (3.8 +/- 1.3 vs 5.3 +/- 1.2 ms/mm Hg; p = 0.3). At follow-up (9 months), one patient had died and one underwent liver transplantation. These two patients also had the most severely impaired vagal tone (BRS = 0 and 1.2 ms/mm Hg, respectively). CONCLUSIONS: Vagal tone, as assessed by BRS, is markedly depressed in cirrhotic patients awaiting liver transplantation.

Electrophysiologic effects of adenosine in patients with supraventricular tachycardia.

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.

Catheter-ablative techniques for the treatment of atrial fibrillation.

Atrial fibrillation is the most commonly encountered arrhythmia in clinical practice and is associated with significant morbidity and mortality. Pharmacologic therapy, although useful for rate control, has proven much less effective in the long term maintenance of sinus rhythm. The utility of implantable atrial defibrillators or pacing to prevent atrial fibrillation remains largely untested. This article describes four catheter-based therapies for atrial fibrillation: His ablation, atrioventricular nodal modification, the Maze procedure, and the ablation of pulmonary vein foci which initiate the arrhythmia. Whereas the first two procedures are largely palliative and recommended for patients with symptomatic, drug-refractory atrial fibrillation, the latter two offer the potential for a curative intervention.

Electrophysiologic effects of selective right versus left atrial linear lesions in a canine model of chronic atrial fibrillation.

INTRODUCTION: Long linear lesions have been shown to eliminate atrial fibrillation in animal models, but little is known about the electrophysiologic response in one atrium to lesions in the contralateral atrium. METHODS AND RESULTS: Twelve dogs with chronic atrial fibrillation were randomized to either right atrial ablation (n = 4), left atrial ablation first (n = 4), or a sham procedure (n = 4). Simultaneous biatrial endocardial mapping was performed before and after three linear lesions were applied at specific points in either atrium, using an expandable ablation catheter. Atrial fibrillation was reinducible after single atrial ablation in each dog and no longer inducible after biatrial ablation in five dogs. At baseline, the mean atrial fibrillation cycle length was longer on the trabeculated (117+/-15 msec) compared with the smooth right (101+/-16 msec) or left atrium (88+/-10 msec; P < 0.01). Single right and left atrial ablation caused a significant cycle length increase in the ablated atrium. Left atrial ablation increased the cycle length on both the trabeculated (121+/-18 msec vs 137+/-11 msec; P < 0.05) and smooth right atrium (108+/-12 msec vs 124+/-9 msec; P < 0.05). Right atrial ablation, however, had no significant effect on left atrial fibrillation cycle length (82+/-8 msec vs 86+/-7 msec). CONCLUSION: Left atrial linear lesions affect right atrial endocardial activation, whereas right atrial lesions do not affect left atrial activation in a canine model of atrial fibrillation. These findings suggest that the left atrium is the driver during chronic atrial fibrillation in this animal model and may explain the limited success of right atrial ablation alone in human atrial fibrillation.