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Background— There are no reports describing the technique, electrophysiological evaluation, and clinical consequences of complete linear block at roofline joining the superior pulmonary veins (PVs) in patients with paroxysmal atrial fibrillation (AF). Methods and Results— Ninety patients with drug-refractory paroxysmal AF undergoing radiofrequency ablation were prospectively randomized into 2 ablation strategies: (1) PV isolation (n=45) or (2) PV isolation in combination with linear ablation joining the 2 superior PVs (roofline; n=45). In both groups, the cavotricuspid isthmus, fragmented peri-PV-ostial electrograms, and spontaneous non-PV foci were ablated. Roofline ablation was performed at the most cranial part of the left atrium (LA) with complete conduction block demonstrated during LA appendage pacing by the online mapping of continuous double potential and an activation detour propagating around the PVs to activate caudocranially the posterior wall of the LA. The effect of ablation at the LA roof was evaluated by the change in fibrillatory cycle length, termination and noninducibility of AF, and clinical outcome. PV isolation was achieved in all patients with no significant differences in the radiofrequency duration, fluoroscopy, or procedural time between the groups. Roofline ablation required 12±6 (median 11, range 3 to 25) minutes of radiofrequency energy delivery with a fluoroscopic duration of 7±2 minutes and was performed in 19±7 minutes. Complete block was confirmed in 43 patients (96%) and resulted in an activation delay that was shorter circumventing the left than the right PVs during LA appendage pacing (138±15 versus 146±25 ms, respectively; P =0.01). Roofline ablation resulted in a significant increase in the fibrillatory cycle length (198±38 to 217±44 ms; P =0.0005), termination of arrhythmia in 47% (8/17), and subsequent noninducibility of AF in 59% (10/17) of the patients inducible after PV isolation. However, LA flutter, predominantly perimitral, could be induced in 10 patients (22%) after roofline ablation. At 15±4 months, 87% of the roofline group and 69% with PV isolation alone are arrhythmia free without antiarrhythmics ( P =0.04). Conclusions— This prospective randomized study demonstrates the feasibility of achieving complete linear block at the LA roof. Such ablation resulted in the prolongation of the fibrillatory cycle, termination of AF, and subsequent noninducibility and is associated with an improved clinical outcome compared with PV isolation alone.

Background— The modification of atrial fibrillation cycle length (AFCL) during catheter ablation in humans has not been evaluated. Methods and Results— Seventy patients undergoing ablation of prolonged episodes of AF were randomized to pulmonary vein (PV) isolation or additional ablation of the mitral isthmus. Mean AFCL was determined at a distance from the ablated area (coronary sinus) at the following intervals: before ablation, after 2- and 4-PV isolations, and after linear ablation. Inducibility of sustained AF (≥10 minutes) was determined before and after ablation. Spontaneous sustained AF (715±845 minutes) was present in 30 patients and induced in 26 (AFCL, 186±19 ms). PV isolation terminated AF in 75%, with the number of PVs requiring isolation before termination increasing with AF duration ( P =0.018). PV isolation resulted in progressive or abrupt AFCL prolongation to various extents, depending on the PV: to 214±24 ms ( P P =0.002) when AF persisted. The increase in AFCL (30±17 versus 14±11 ms; P =0.005) and the decrease in fragmentation (30.0±26.8% to 10.3±14.5%; P P =0.08). Sustained AF was noninducible in 57% after PV isolation and in 77% after linear ablation. At 7±3 months, 74% with PV isolation and 83% with linear ablation were arrhythmia free without antiarrhythmics, which was significantly associated with noninducibility ( P =0.03) with a recurrence rate of 38% and 13% in patients with and without inducibility, respectively. Conclusions— AF ablation results in a decline in AF frequency, with a magnitude correlating with termination of AF and prevention of inducibility that is predictive of subsequent clinical outcome.

Background— The left superior vena cava (LSVC) is the embryological precursor of the ligament of Marshall, which has been implicated in the initiation and maintenance of atrial fibrillation (AF). Rarely, the LSVC may persist and has been associated with some organized arrhythmias, though not with AF. We report 5 patients in whom the LSVC was a source of ectopy, initiating AF. Methods and Results— In 5 patients (4 men; age, 46±11 years) with symptomatic drug-refractory AF, ectopy from the LSVC resulting in AF was observed after pulmonary vein isolation. The ectopics were spontaneous in 2 and induced by isoproterenol in the others and preceded P-wave onset by 67±13 ms. During multielectrode or electroanatomic mapping, venous potentials were recorded circumferentially at the proximal LSVC near its junction with the coronary sinus (CS), but at the mid-LSVC level, they were recorded only on part of the circumference. The LSVC was electrically connected to the lateral left atrium (LA) and through the CS to the right atrium, with 4.1±2.3 CS-LSVC and 1.6±0.5 LA-LSVC connections per patient. Catheter ablation in the LSVC targeting these connections resulted in electrical isolation in 4 of the 5 patients without complications. After 15±10 months, the 4 patients with successful isolation, including 1 who had successful reablation for LA flutter, remained in sinus rhythm without drugs. Conclusions— The LSVC can be the arrhythmogenic source of AF with connections to the CS and LA. Ablation of these connections resulted in electrical isolation.

Background— Symptomatic prolonged sinus pauses on termination of atrial fibrillation (AF) are an indication for pacemaker implantation. We evaluated sinus node function and clinical outcome in patients with prolonged sinus pauses on termination of arrhythmia who underwent ablation of paroxysmal AF. Methods and Results— Twenty patients with paroxysmal AF and prolonged sinus pauses (≥3 seconds) on termination of AF underwent ablation between May 1995 and November 2002. Patients with sinus pauses independent of episodes of AF were excluded from the analysis. The procedure included pulmonary vein and linear atrial ablation. After ablation, sinus node function was assessed during the first week and at 1, 3, and 6 months, by 24-hour ambulatory monitoring to determine the mean heart rate and heart rate range, and by exercise testing to determine the maximal heart rate. Corrected sinus node recovery time was determined at the completion of ablation and at 24.0±11.3 months at 600 and 400 ms. After AF ablation, there was a significant improvement of sinus node function, with an increase in the mean heart rate ( P =0.001), maximal heart rate ( P P P =0.016) and 400 ms ( P =0.019). At 26.0±17.6 months, 18 patients (85%) had no recurrence of AF (in the absence of medication), with no symptoms attributable to bradycardia or sinus pauses on ambulatory monitoring. Two patients had infrequent episodes of AF, 1 requiring pacemaker implantation. Conclusion— Prolonged sinus pauses after paroxysms of AF may result from depression of sinus node function that can be eliminated by curative ablation of AF. This is accompanied by improvement in parameters of sinus node function, suggesting reverse remodeling of the sinus node.

Background— The long-QT and Brugada syndromes are important substrates of malignant ventricular arrhythmia. The feasibility of mapping and ablation of ventricular arrhythmias in these conditions has not been reported. Methods and Results— Seven patients (4 men; age, 38±7 years; 4 with long-QT and 3 with Brugada syndrome) with episodes of ventricular fibrillation or polymorphic ventricular tachycardia and frequent isolated or repetitive premature beats were studied. These premature beats were observed to trigger ventricular arrhythmias and were localized by mapping the earliest endocardial activity. In 4 patients, premature beats originated from the peripheral right (1 Brugada) or left (3 long-QT) Purkinje conducting system and were associated with variable Purkinje-to-muscle conduction times (30 to 110 ms). In the remaining 3 patients, premature beats originated from the right ventricular outflow tract, being 25 to 40 ms ahead of the QRS. The accuracy of mapping was confirmed by acute elimination of premature beats after 12±6 minutes of radiofrequency applications. During a follow-up of 17±17 months using ambulatory monitoring and defibrillator memory interrogation, no patients had recurrence of symptomatic ventricular arrhythmia but 1 had persistent premature beats. Conclusion— Triggers from the Purkinje arborization or the right ventricular outflow tract have a crucial role in initiating ventricular fibrillation associated with the long-QT and Brugada syndromes. These can be eliminated by focal radiofrequency ablation.

Background— Cardiac ion channelopathies are responsible for an ever-increasing number and diversity of familial cardiac arrhythmia syndromes. We describe a new clinical entity that consists of an ST-segment elevation in the right precordial ECG leads, a shorter-than-normal QT interval, and a history of sudden cardiac death. Methods and Results— Eighty-two consecutive probands with Brugada syndrome were screened for ion channel gene mutations with direct sequencing. Site-directed mutagenesis was performed, and CHO-K1 cells were cotransfected with cDNAs encoding wild-type or mutant CACNB2b (Ca vβ2b ), CACNA2D1 (Ca vα2δ1 ), and CACNA1C tagged with enhanced yellow fluorescent protein (Ca v 1.2). Whole-cell patch-clamp studies were performed after 48 to 72 hours. Three probands displaying ST-segment elevation and corrected QT intervals ≤360 ms had mutations in genes encoding the cardiac L-type calcium channel. Corrected QT ranged from 330 to 370 ms among probands and clinically affected family members. Rate adaptation of QT interval was reduced. Quinidine normalized the QT interval and prevented stimulation-induced ventricular tachycardia. Genetic and heterologous expression studies revealed loss-of-function missense mutations in CACNA1C (A39V and G490R) and CACNB2 (S481L) encoding the α 1 - and β 2b -subunits of the L-type calcium channel. Confocal microscopy revealed a defect in trafficking of A39V Ca v 1.2 channels but normal trafficking of channels containing G490R Ca v 1.2 or S481L Ca vβ2b -subunits. Conclusions— This is the first report of loss-of-function mutations in genes encoding the cardiac L-type calcium channel to be associated with a familial sudden cardiac death syndrome in which a Brugada syndrome phenotype is combined with shorter-than-normal QT intervals.

Background— Endocardial mapping of localized sources driving atrial fibrillation (AF) in humans has not been reported. Methods and Results— Fifty patients with AF organized by prior pulmonary vein and linear ablation were studied. AF was considered organized if mapping during AF showed irregular but discrete atrial complexes exhibiting consistent activation sequences for >75% of the time using a 20-pole catheter with 5 radiating spines covering 3.5-cm diameter or sequential conventional mapping. A site or region centrifugally activating the remaining atrial tissue defined a source. During AF with a cycle length of 211±32 ms, activation mapping identified 1 to 3 sources at the origin of atrial wavefronts in 38 patients (76%) predominantly in the left atrium, including the coronary sinus region. Electrograms at the earliest area varied from discrete centrifugal activation to an activity spanning 75% to 100% of the cycle length in 42% of cases, the latter indicating complex local conduction or a reentrant circuit. A gradient of cycle length (>20 ms) to the surrounding atrium was observed in 28%. Local radiofrequency ablation prolonged AF cycle length by 28±22 ms and either terminated AF or changed activation sequence to another organized rhythm. In 4 patients, the driving source was isolated, surrounded by the atrium in sinus rhythm, and still firing at high frequency (228±31 ms) either permanently or in bursts. Conclusions— AF associated with consistent atrial activation sequences after prior ablation emanates mostly from localized sources that can be mapped and ablated. Some sources harbor electrograms suggesting the presence of localized reentry.

Background— The identification of sites of dominant activation frequency during atrial fibrillation (AF) in humans and the effect of ablation at these sites have not been reported. Methods and Results— Thirty-two patients undergoing AF ablation (19 paroxysmal, 13 permanent) during ongoing arrhythmia were studied. Electroanatomic mapping was performed, acquiring 126±13 points per patient throughout both atria and coronary sinus. At each point, 5-second electrograms were obtained to determine the highest-amplitude frequency on spectral analysis and to construct 3D dominant frequency (DF) maps. The temporal stability of the recording interval was confirmed in a subset. Ablation was performed with the operator blinded to the DF maps. The effect of ablation at sites with or without high-frequency DF sites (maximal frequencies surrounded by a decreasing frequency gradient ≥20%) was evaluated by determining the change in AF cycle length (AFCL) and the termination and inducibility of AF. The spatial distribution of the DF sites was different in patients with paroxysmal and permanent AF; paroxysmal AF patients were more likely to harbor the DF site within the pulmonary vein, whereas in permanent AF, atrial DF sites were more prevalent. Ablation at a DF site resulted in significant prolongation of the AFCL (180±30 to 198±40 ms; P P =0.4). AF terminated during ablation in 17 of 19 patients with paroxysmal and 0 of 13 with permanent AF ( P P =0.3) and ablated (1.9±1.0 versus 2.4±1.0; P =0.3) in those with and without AF termination. The duration of radiofrequency ablation to achieve termination was significantly shorter than that delivered in those with persisting AF (34.8±24.0 versus 73.5±22.9 minutes; P =0.0002). All patients with persisting AF had additional DF sites outside the ablated zones. Conclusions— Spectral analysis and frequency mapping identify localized sites of high-frequency activity during AF in humans with different distributions in paroxysmal and permanent AF. Ablation at these sites results in prolongation of the AFCL and termination of paroxysmal AF, indicating their role in the maintenance of AF.

Background— This prospective clinical study evaluates the feasibility and efficacy of combined linear mitral isthmus ablation and pulmonary vein (PV) isolation in patients with paroxysmal atrial fibrillation (AF). Methods and Results— One hundred consecutive patients (13 women; age 55±10 years) with drug-refractory, symptomatic paroxysmal AF underwent PV isolation and linear ablation of the cavotricuspid isthmus and the mitral isthmus (lateral mitral annulus to the left inferior PV). They were compared with 100 consecutive patients (14 women; age, 52±10 years) undergoing PV isolation and cavotricuspid ablation without mitral isthmus ablation. Bidirectional mitral isthmus block was confirmed by demonstrating (1) a parallel corridor of double potentials during coronary sinus (CS) pacing, (2) an activation detour by pacing either side of the line, and (3) differential pacing techniques. Isolation of all PVs and cavotricuspid isthmus ablation were performed successfully in all. Mitral isthmus block was achieved in 92 patients after 20±10 minutes of endocardial radiofrequency application and an additional 5±4 minutes of epicardial radiofrequency application from within the CS in 68, resulting in a conduction delay of 151±26 ms during CS pacing. Thirty-two patients with mitral isthmus ablation compared with 49 without had recurrent atrial arrhythmia ( P =0.02) requiring further ablation. At 1 year after the last procedure, 87 patients with mitral isthmus ablation and 69 without ( P =0.002) were arrhythmia free without antiarrhythmic drugs, mitral isthmus ablation being the only factor associated with long-term success (RR for AF recurrence, 0.2; CI, 0.1 to 0.4; P Conclusions— Catheter ablation of the mitral isthmus results consistently in demonstrable conduction block and is associated with a high cure rate for paroxysmal AF.

A 59-year-old man underwent radiofrequency catheter ablation for symptomatic drug refractory atrial fibrillation (AF). Prior ablations for AF had included pulmonary vein (PV) electrical isolation and additional substrate modification involving linear ablation joining the 2 superior PVs (roofline) and the anterior mitral annulus with the roofline (anterior line). Despite significant clinical improvement, further mapping and ablation was performed because of recurrent arrhythmia. At the time of the procedure, the ECG demonstrated AF with intermittent termination that was followed by immediate re-initiations, …

Pulmonary vein isolation for treatment of atrial fibrillation sometimes requires extensive use of fluoroscopy, with inherent risk to the patient, operator, and laboratory staff. The LocaLisa system (Medtronic) is a nonfluoroscopic, noncontact mapping system that uses regular catheters as sensors for a high-frequency thoracic electrical field generated by the system to create a real-time, 3D image. The Data Supplement Movie demonstrates the utility of LocaLisa during a pulmonary vein disconnection procedure. The left screen is the LocaLisa system display, and the right screen shows the intracardiac recordings. The LocaLisa screen shows the Lasso (Biosense Webster)and ablation catheter in the right superior pulmonary vein as if viewed from within …