心房颤动导管消融术中迷走反射时肺静脉和心房电位周长的变化

目的评价心房颤动(简称房颤)导管消融过程中迷走反射对肺静脉和心房电位周长的影响。方法分析行环肺静脉消融且术中发生迷走反射的12例房颤患者(阵发性房颤10例,持续性房颤2例)心内电生理记录资料。分别测定迷走反射前10s、迷走反射过程中以及迷走反射后60s时的靶肺静脉电位和冠状静脉窦心房电位平均周长(PVCL及CSCL)。结果12例中5例消融时为房颤心律,迷走反射时平均最长RR间期为4025.42±1774.35ms。这5例中,迷走反射时PVCL及CSCL较迷走反射前明显缩短(分别为168.80±47.00msvs174.80±46.41ms;176.80±43.03msvs181.80±40.90ms,P均<0.05)。消融时为窦性心律者中,迷走反射后PVCL及CSCL较迷走反射前明显缩短(分别为882.86±86.74msvs1267.14±214.53ms,880.00±92.92msvs1261.43±209.95ms,P均<0.05)。结论房颤导管消融过程中迷走神经兴奋时,肺静脉和冠状静脉窦心房颤动波周长明显缩短,提示迷走神经兴奋可能在驱动或者加速肺静脉电位传导中起一定作用。     

Frequency analysis in different types of paroxysmal atrial fibrillation.

OBJECTIVES: This study sought to investigate the regional frequency distribution from multiple bi-atrial sites in different types of paroxysmal atrial fibrillation (AF). BACKGROUND: A previous study showed a left atrium (LA) to right atrium (RA) frequency gradient in patients with paroxysmal AF. METHODS: Forty-four patients (age = 60 +/- 16, male patients = 27) with paroxysmal AF originating from the pulmonary veins (PVs) (n = 31) or superior vena cava (SVC) (n = 13) were included. Frequency analysis was performed on the intracardiac electrograms (7 s, 1 kHz/channel) recorded from PV, posterior LA, coronary sinus (CS), posterolateral RA, and SVC. The largest peak frequency was identified as the dominant frequency (DF). RESULTS: In the PV-AF patients, there was a frequency gradient from the PV ostium to the LA, RA, and SVC (8.5 +/- 3.3 Hz vs. 5.9 +/- 1.1 Hz vs. 5.2 +/- 0.85 Hz vs. 5.5 +/- 0.48 Hz, respectively, p < 0.001). The highest DFs were mostly located at the arrhythmogenic PV ostium (58%). The DFs of the arrhythmogenic PV and PV ostium were significantly higher than those of the non-arrhythmogenic PVs and PV ostia (p < 0.05). In the SVC-AF patients, there was a frequency gradient from the SVC to the RA, LA, and PV (8.0 +/- 2.4 Hz vs. 5.9 +/- 1.1 Hz vs. 5.9 +/- 0.7 Hz vs. 5.8 +/- 0.7 Hz, respectively, p = 0.001). The highest DFs were mostly located inside the SVC (77%) instead of the SVC ostium (as compared with PV-AF patients, p = 0.035). CONCLUSIONS: The location of the highest DF depended on the arrhythmogenic PV or SVC. A frequency gradient was present between the arrhythmogenic thoracic vein and atrium in all patients.     

Deterioration of interatrial conduction in patients with paroxysmal atrial fibrillation: Electroanatomic mapping of the right atrium and coronary sinus

OBJECTIVES: The purpose of this study was to analyze the velocities across the coronary sinus ostium (cross-CSo) and within the coronary sinus (intra-CS) in patients with and without paroxysmal atrial (AF) fibrillation and to estimate the interatrial conduction deterioration area in AF patients. BACKGROUND: Interatrial conduction delay in AF patients has been reported. However, localization of the interatrial conduction delay still is not clear. METHODS: Thirteen patients with paroxysmal AF and 10 control patients with AV nodal reentrant tachycardia or ectopic atrial tachycardia were enrolled in the study. Right atrial and CS mapping were performed using the CARTO electroanatomic mapping system during sinus rhythm and during distal CS pacing. The activation times and spatial distances of cross-CSo and intra-CS were measured between paired sites, from which the activation velocities of cross-CSo and intra-CS were obtained. RESULTS: During sinus rhythm, the activation velocities of cross-CSo in the AF group (1.2 +/- 0.2 m/s) were significantly slower than those in the control group (2.9 +/- 1.6 m/s, P < .05). During distal CS pacing, the cross-CSo velocities of the AF group (1.0 +/- 0.5 m/s) also appeared slower than those in the control group (1.4 +/- 0.2 m/s, P = .07). However, no difference was found in intra-CS activation velocities between the two groups (2.8 +/- 1.9 vs 3.2 +/- 2.2 m/s and 1.5 +/- 0.3 vs 1.4 +/- 0.3 m/s, P > .05 during sinus rhythm and distal CS pacing, respectively). CONCLUSIONS: Interatrial conduction at the posteroparaseptal region across the CS ostium was significantly slower in patients with paroxysmal AF than in control patients, further supporting the link between interatrial conduction deterioration and paroxysmal AF.     

Effect of pulmonary vein isolation on the left-to-right atrial dominant frequency gradient in human atrial fibrillation

BACKGROUND: We previously demonstrated the existence of a left-to-right atrial dominant frequency gradient during paroxysmal but not persistent atrial fibrillation (AF) in humans. One possible mechanism of the left-to-right dominant frequency gradient involves the role of the pulmonary veins (PVs) in AF maintenance. OBJECTIVES: The purpose of this study was to examine the effect of PV isolation on the dominant frequency gradient and outcome after PV isolation. METHODS: Patients with either paroxysmal or persistent AF were studied. Recordings were made from catheters in the coronary sinus (CS), posterior right atrium (RA), and posterior left atrium (LA) during AF before and after PV isolation. Mean left-to-right dominant frequency gradient was measured before and after segmental PV isolation. Patients were followed for AF recurrence after PV isolation. RESULTS: Twenty-seven patients with paroxysmal (n = 15) or persistent (n = 12) AF were studied. In the paroxysmal group, baseline dominant frequency was greatest in the posterior LA with a significant left-to-right atrial dominant frequency gradient (posterior LA = 6.2 +/- 0.9 Hz, CS = 5.8 +/- 0.8 Hz, posterior RA = 5.4 +/- 0.9 Hz; P <.001). After PV isolation, there was no regional difference in dominant frequency (5.9 +/- 0.7 Hz vs 5.7 +/- 0.6 Hz vs 5.7 +/- 0.7 Hz, respectively; P = NS). In the persistent AF group, there was no overall difference in dominant frequency among sites before or after PV isolation (P = NS); however, patients with long-term freedom from AF after PV isolation had a higher left-to-right dominant frequency gradient compared with patients with recurrent AF (0.4 vs 0.1 Hz; P <.05). CONCLUSION: PV isolation results in a loss in the left-to-right dominant frequency gradient in patients with paroxysmal AF. This finding supports the critical role of PVs in the maintenance of ongoing paroxysmal AF. Patients with persistent AF and a baseline left-to-right dominant frequency gradient have a better success rate with PV isolation alone compared with patients without a dominant frequency gradient.     

Role of Right Middle Pulmonary Vein in Patients with Paroxysmal Atrial Fibrillation

INTRODUCTION: Elimination of the ectopic foci from pulmonary veins (PVs) has proved to be a curative therapy for focal atrial fibrillation (AF). However, information about the importance of the right middle PV (RMPV) in initiation of AF and radiofrequency ablation of AF is limited. METHOD AND RESULTS: Forty-three patients (34 men and 9 women; age 65+/-12 years) with drug-refractory paroxysmal AF underwent electrophysiologic study and catheter ablation for treatment of AF. Three-dimensional magnetic resonance angiography (MRA) of the PVs and left atrium (LA) was performed to determine the anatomic patterns of RMPV. Diameter of PV ostium was measured at the junction of the LA and each PV. MRA findings showed the following: (1) 36 (84%) of 43 patients had a discrete RMPV; (2) there are three drainage patterns of RMPV, including joining the proximal part (<1 cm from the ostium) of the right superior PV (RSPV), joining the right inferior PV (RIPV), and a separate RMPV ostium in the LA wall; and (3) the ostial diameter of RMPV was significantly smaller than RSPV and RIPV (P < 0.01). Electrophysiologic studies demonstrated that five AF foci arose from RMPV. The coupling interval between the ectopic beat of AF and sinus beat was longer in RMPV than RSPV (262+/-45 msec vs 212+/-47 msec; P = 0.043). All AFs from RMPV were ablated successfully. PV stenosis or AF recurrence from RMPV was not found during follow-up of 10+/-4 months. CONCLUSION: RMPV was detected by MRA in >80% of paroxysmal AF patients. Ectopy from RMPV can initiate AF, and radiofrequency ablation of RMPV foci is feasible and safe.     

Electrophysiologic properties of pulmonary veins assessed using a multielectrode basket catheter

OBJECTIVES: The purpose of the present study was to evaluate the electrophysiologic properties within the pulmonary vein (PV) and at the PV-left atrial (LA) junction. BACKGROUND: It has been recognized that atrial fibrillation (AF) can originate from PVs. However, the electrophysiologic properties of the PV have not been well characterized. METHODS: Thirty-two bipolar electrograms were recorded simultaneously from a basket catheter placed in 81 PVs of 48 patients with paroxysmal AF. The programmed stimulation was performed in the distal PV and PV-LA junction. Activation maps of PVs were analyzed from episodes of spontaneous onset of AF and initiation of induced AF by a single extrastimulus. RESULTS: The effective refractory period (ERP) of the distal PV was significantly shorter than that of the PV-LA junction (177 +/- 43 vs. 222 +/- 30 ms, p < 0.0001). The conduction delay from the distal PV to the PV-LA junction was significantly longer than that from the PV-LA junction to distal PV (73 +/- 40 vs. 32 +/- 17 ms, p < 0.0001). During initiation of AF, a short coupled extrastimulus or rapid, repetitive focal activities originating from the PV formed a PV-LA reciprocating re-entrant circuit involving exit and entrance breakthrough points at the PV-LA junction. Also, an unstable re-entrant circuit within the PV was observed. CONCLUSIONS: The presence of ERP heterogeneity and anisotropic conduction properties within the PV and at the PV-LA junction may be crucial to promote re-entry formation and thus might play an important role as a substrate for the maintenance of AF.     

Preservation of the anterior fat pad paradoxically decreases the incidence of postoperative atrial fibrillation in humans

OBJECTIVES: The goal of this study was to determine if parasympathetic nerves in the anterior fat pad (FP) can be stimulated at the time of coronary artery bypass surgery (CABG), and if dissection of this FP decreases the incidence of postoperative atrial fibrillation (AF). BACKGROUND: The human anterior epicardial FP contains parasympathetic ganglia and is often dissected during CABG. Changes in parasympathetic tone influence the incidence of AF. METHODS: Fifty-five patients undergoing CABG were randomized to anterior FP preservation (group A) or dissection (group B). Nerve stimulation was applied to the FP before and after surgery. Sinus cycle length (CL) was measured during stimulation. The incidence of postoperative AF was recorded. RESULTS: Of the 55 patients enrolled, 26 patients were randomized to group A, and 29 patients were randomized to group B. In all of the 55 patients, the FP was identified before initiating cardiopulmonary bypass by CL prolongation with stimulation (865.5 +/- 147.9 ms vs. 957.9 +/- 155.1 ms, baseline vs. stimulation, p < 0.001). In group A, stimulation at the conclusion of surgery increased sinus CL (801.8 +/- 166.4 ms vs. 890.9 +/- 178.2 ms, baseline vs. stimulation, p < 0.001). In group B, repeat stimulation failed to increase sinus CL (853.6 +/- 201.6 ms vs. 841.4 +/- 198.4 ms, baseline vs. stimulation, p = NS). The incidence of postoperative AF in group A (7%) was significantly less than that in group B (37%) (p < 0.01). CONCLUSIONS: This is the first study demonstrating that direct stimulation of the human anterior epicardial FP slows sinus CL. This parasympathetic effect is eliminated with FP dissection. Preservation of the human anterior epicardial FP during CABG decreases incidence of postoperative AF.     

Inducibility of atrial fibrillation during atrioventricular pacing with varying intervals: role of atrial electrophysiology and the autonomic nervous system

INTRODUCTION: Patients receiving VVI pacemakers have a higher incidence of paroxysmal atrial fibrillation (AF) than those receiving DDD pacemakers. However, the mechanism behind the difference is not clear. The purpose of this study was to investigate whether atrial electrophysiology and the autonomic nervous system play a role in the occurrence of AF during AV pacing. METHODS AND RESULTS: The study population consisted of 28 patients who had (group I, n = 15) or did not have (group II, n = 13) AF induced by a single extrastimulus during pacing with different AV intervals. Atrial pressure, atrial size, atrial effective refractory periods, and atrial dispersion were evaluated during pacing with different AV intervals. Twenty-four-hour heart rate variability and baroreflex sensitivity also were examined. Atrial pressure, atrial size, effective refractory periods in the right posterolateral atrium and distal coronary sinus, and atrial dispersion increased as the AV interval shortened from 160 to 0 msec. During AV pacing, group I patients had greater minimal (52+/-17 vs 25+/-7 msec; P < 0.005) and maximal (76+/-16 vs 36+/-9 msec; P < 0.005) atrial dispersion than group II patients. The differences in atrial size and atrial dispersion among different AV intervals were greater in patients with AF than in those without AF. Baroreflex sensitivity (6.6+/-1.7 vs 3.9+/-1.0; P < 0.00005), but not heart rate variability, was higher in patients with AF than in those without AF. CONCLUSION: Abnormal atrial electrophysiology and higher vagal reflex activity can play important roles in the genesis of AF in patients receiving pacemakers.     

Prolonged fractionation of paced right atrial electrograms in patients with atrial flutter and fibrillation

OBJECTIVES: This study investigated the extent of fractionation of paced right atrial electrograms in patients with and without paroxysmal atrial flutter (AFL) or atrial fibrillation (AF). BACKGROUND: Slow conduction through nonuniform anisotropic atrial muscles, represented by fractionated electrograms, may favor the generation of atrial tachyarrhythmias. METHODS: This study included 10 control patients (Group 1), 8 patients with documented paroxysmal AFL (Group 2) and 10 patients with documented paroxysmal AF (Group 3). Five electrode catheters were placed in the different sites of the right atrium and one catheter was positioned at the coronary sinus ostium. Atrial pacing from one site was done by a constant drive train with an extrastimulus inserted every fourth beat while recording at the other five sites was performed. The delay of each fractionated potential in the high-pass filtered atrial electrogram in response to extrastimulation was determined and used to construct conduction curves of delay versus the S1S2 interval. RESULTS: The mean increase in electrogram duration between a coupling interval of 350 ms and 10 ms above atrial refractoriness was significantly greater in Groups 2 and 3 compared with that in Group 1 (8.5 +/- 2.5 vs. 11.0 +/- 2.7 vs. 5.9 +/- 2.3 ms, respectively, p < 0.001). The mean S1S2 interval at which delay increased suddenly was also longer in Groups 2 and 3 compared with Group 1 (326 +/- 9 vs. 343 +/- 12 vs. 307 +/- 17 ms, respectively, p < 0.001). CONCLUSIONS: Increased delays in the individual potential of the fractionated atrial electrograms may be related to the development of AFL and AF.     

Chronic atrial dilation, electrical remodeling, and atrial fibrillation in the goat.

OBJECTIVES: This study was designed to investigate the mutual effects of chronic atrial dilation and electrical remodeling on the characteristics of atrial fibrillation (AF). BACKGROUND: Both electrical remodeling and atrial dilation promote the inducibility and perpetuation of AF. METHODS: In seven goats AF was induced during 48 h by burst pacing, both at baseline and after four weeks of slow idioventricular rhythm (total AV block). Atrial size and refractory period (AERP) were monitored together with the duration and cycle length of AF paroxysms (AFCL). After four weeks of total atrioventricular (AV) block, the conduction in both atria was mapped during AF. Six non-instrumented goats served as controls. RESULTS: At baseline, AF-induced electrical remodeling shortened AERP and AFCL to the same extent (from 185 +/- 9 ms to 149 +/- 14 ms [p < 0.05] and from 154 +/- 11 ms to 121 +/- 5 ms [p < 0.05], respectively). After four weeks of AV block the right atrial diameter had increased by 13.2 +/- 3.0% (p < 0.01). Surprisingly, in dilated atria electrical remodeling still shortened the AERP (from 165 +/- 9 ms to 132 +/- 15 ms [p < 0.05]) but failed to shorten the AFCL (140 +/- 19 ms vs. 139 +/- 11 ms [p = 0.98]). Mapping revealed a higher incidence of intra-atrial conduction delays during AF. Histologic analysis showed no atrial fibrosis but did reveal a positive correlation between the size of atrial myocytes and the incidence of intra-atrial conduction block (r = 0.60, p = 0.03). CONCLUSIONS: In a goat model of chronic atrial dilation, AF-induced electrical remodeling was unchanged. However, AFCL no longer shortened during electrical remodeling. Thus, in dilated atria a wider excitable gap exists during AF, probably caused by intra-atrial conduction defects and a higher contribution of anatomically defined re-entrant circuits.     

Heart rate turbulence after atrial premature beats before spontaneous onset of atrial fibrillation

OBJECTIVES: This study was designed to assess the temporal changes in vagal responses to atrial premature beats before spontaneous onset of atrial fibrillation (AF). BACKGROUND: Enhanced vagal activity plays a major role in the onset and perpetuation of experimental AF, but the role of vagal activation in the onset of clinical AF episodes is not so well established. METHODS: We calculated heart rate turbulence after atrial premature impulses occurring 0 to 60 min before the onset of AF ("prior to AF") and compared it with the hourly means of the other hours of the 24-h electrocardiogram recordings ("non-AF hours") in 39 patients with structural heart disease and 29 patients with lone AF. Traditional heart rate variability measurements and approximate entropy (ApEn) were also analyzed. RESULTS: Turbulence onset (TO) was significantly less negative during the 1 h preceding AF than during the non-AF hours (0.71 +/- 1.76 vs. -0.35 +/- 1.46, p < 0.00001). Less negative TO before AF was observed among both the patients with structural heart disease (1.16 +/- 1.73 vs. 0.07 +/- 1.23; p < 0.0001) and those with lone AF (0.17 +/- 1.67 vs. -0.85 +/- 1.56; p < 0.0001). No significant difference was seen in the turbulence slope between the two periods, and none of the traditional frequency and time domain measurements differentiated between the periods; ApEn was significantly lower before AF than during the non-AF hours (p < 0.01). CONCLUSIONS: Altered heart rate dynamics, suggesting transient enhancement of vagal outflow after premature atrial excitation, are temporally related to spontaneous onset of clinical AF.     

Anatomic relationship of the esophagus and left atrium: implication for catheter ablation of atrial fibrillation

STUDY OBJECTIVES: Atrioesophageal fistulas have been reported to be a lethal complication following catheter ablation of atrial fibrillation (AF). The purpose of this study was to investigate the relationship between the esophagus and posterior left atrium (LA) and provide the anatomic information necessary to minimize the risk of esophageal injury during AF ablation. METHODS AND RESULTS: Forty-eight patients (43 men; mean +/- SD age, 59 +/- 12 years) with drug-refractory paroxysmal AF and 32 control subjects (26 men; mean age, 60 +/- 9 years) were included. All underwent a CT scan for delineation of the relationship between the esophagus and posterior LA. In the paroxysmal AF group, two major types of esophageal routes were demonstrated. Type 1 routes were found in 42 patients with the lower portion of esophagus close to the ostium of the left inferior pulmonary vein (LIPV), including three subtypes of courses according to the proximity to the left superior pulmonary vein (PV) and LIPV. Type 2 routes were found in six patients with the lower portion of esophagus close to the ostium of the right inferior pulmonary vein (RIPV), including three subtypes of courses according to the proximity to the right superior PV and RIPVs. The mean shortest distance of the esophagus to the four individual PVs significantly differed between type 1 and type 2: 28.4 +/- 6.1 mm vs 10.5 +/- 5.7 mm (to the right superior), 19.6 +/- 7.0 mm vs 3.7 +/- 3.4 mm (to the right inferior), 10.1 +/- 3.4 mm vs 22.8 +/- 4.2 mm (to the left superior), and 2.8 +/- 2.5 mm vs 18.7 +/- 5.2 mm (to the left inferior), respectively (p < 0.001 for all). Contact of the esophagus and middle part of posterior LA was observed in each patient. However, direct contact of the aorta with the posterior LA wall was more frequent in type 2 than in type 1 (p = 0.001). The clinical characteristics, type of esophageal routes, distance from the esophagus to the four PVs, and diameter of the thoracic cage, LA, and aorta in the control group were similar to those in the AF group (p > 0.05 for all). CONCLUSION: Although the anatomic relationship between the esophagus and LA posterior wall varied widely, two major patterns of esophageal routes could be depicted. This information is important for deciding the location of the ablation lesions around the PV ostia and LA and for avoiding the potential risk of esophageal injury.     

Frequency mapping of the pulmonary veins in paroxysmal versus permanent atrial fibrillation

Introduction: The pulmonary veins (PVs) are a dominant source of triggers initiating atrial fibrillation (AF). While recent evidence implicates these structures in the maintenance of paroxysmal AF, their role in permanent AF is not known. The current study aims to compare the contribution of PV activity to the maintenance of paroxysmal and permanent AF.
Methods and Results: Thirty-four patients with paroxysmal AF (n = 20) or permanent AF (n = 14) undergoing ablation were studied. Prior to ablation, 32 seconds of electrograms were acquired from each PV and the coronary sinus (CS). The frequency of activity of each PV and CS was defined as the highest amplitude frequency on spectral analysis. The effects of ablation on the AF cycle length (AFCL) and frequency and on AF termination were determined. Significant differences were observed between paroxysmal and permanent AF. Paroxysmal AF demonstrates higher frequency PV activity (11.0 ± 3.1 vs 8.8 ± 3.0 Hz; P = 0.0003) but lower CS frequency (5.8 ± 1.2 vs 6.9 ± 1.4 Hz; P = 0.01) and longer AFCL (182 ± 17 vs 158 ± 21 msec; P = 0.002), resulting in greater PV to atrial frequency gradient (7.2 ± 2.2 vs 4.2 ± 2.9 Hz; P = 0.006). PV isolation in paroxysmal AF resulted in a greater decrease in atrial frequency (1.0 ± 0.7 vs −0.05 ± 0.4 Hz; P < 0.0001), greater prolongation of the AFCL (49 ± 35 vs 5 ± 6 msec; P < 0.0001), and more frequent AF termination (11/20 vs 0/14; P = 0.0007) compared to permanent AF.
Conclusion: Paroxysmal AF is associated with higher frequency PV activity and lesser CS frequency compared to permanent AF. Isolation of the PVs had a greater impact on the fibrillatory process in paroxysmal AF compared to permanent AF, suggesting that while the PVs have a role in maintaining paroxysmal AF, these structures independently contribute less to the maintenance of permanent AF.     

A prospective, multicenter evaluation of ablating complex fractionated electrograms (CFEs) during atrial fibrillation (AF) identified by an automated mapping algorithm: Acute effects on AF and efficacy as an adjuvant strategy

BACKGROUND: Complex fractionated electrograms (CFEs) are continuous electrograms (EGMs) of very short cycle length (CL) representing substrate for atrial fibrillation (AF) perpetuation. Ablation of CFEs may result in AF slowing, termination, and prevention, but identifying them can be subjective. OBJECTIVE: The purpose of this study was to prospectively assess (1) whether an automated algorithm can identify CFE regions, (2) the acute effects of ablating these regions on AF, and (3) the long-term efficacy as an adjuvant strategy to pulmonary vein antrum isolation (PVAI). METHODS: Thirty-five patients (three centers, 61 +/- 9 years, left atrium [LA] 43 +/- 9 mm, ejection fraction 53% +/- 7%) with symptomatic paroxysmal (n = 21) or persistent (n = 14) AF were studied. A decapolar lasso (2-mm spacing) was used for mapping. A three-dimensional shell of the LA and pulmonary veins (PVs) was created. If not already in AF, AF was induced by burst pacing (with or without isoproterenol). Atrial EGMs during AF were mapped/analyzed using an automated CFE algorithm. The algorithm measures the time between discrete deflections in a local EGM over 5 seconds (based on selectable width and peak-to-peak [>0.03 mV] criteria). The mean CL of the local EGM is projected onto the LA shell as a color-coded display. Regions of CL <120 ms (published criteria) were targeted for ablation/elimination. Atrial fibrillation cycle length (AFCL) and regularity were measured from the CS. After CFE ablation, further ablation was done to achieve complete PVAI. RESULTS: AF was spontaneous (n = 20) or induced (n = 15) in all patients. CFEs were most commonly found along the septum (97%), anterior LA (97%), PV antra (83%), base of appendage (83%), and annulus (71%). CFE ablation alone prolonged the AFCL (171 +/- 27 vs. 304 +/- 41 ms; P = .03) and regularized AF to left/right flutter (AFL) in 74% of patients. CFE ablation terminated AF/AFL in 19 patients (54%)-the other 16 were cardioverted-and AF became noninducible in 77%. CFE ablation alone did not cause PV isolation (0.1 +/- 0.3 PV isolated/patient). After combined CFE and PVAI ablation, the single-procedure, off-drug success rate was 83% (follow-up 13 +/- 4 months) versus 71% in matched controls who had PVAI alone (P = .045). CONCLUSIONS: CFE ablation guided by an automated algorithm resulted in AFCL prolongation, regularization, and noninducibility in most patients. AF terminated in 54% of cases. PVAI with adjuvant CFE ablation has a high efficacy and may be superior to PVAI alone.     

Radiofrequency ablation of atrioventricular junction and pacemaker implantation versus modulation of atrioventricular conduction in drug refractory atrial fibrillation.

Modulation of atrioventricular (AV) node conduction and radiofrequency ablation of AV junction are alternative approaches to control ventricular rate in drug refractory atrial fibrillation (AF). In 2 centers, 120 patients were treated either with AV junction ablation (center 1, group 1, 60 patients [30 men, aged 64 +/- 11 years], paroxysmal AF in 24 patients) or with modulation (group 2, 60 patients [32 men, aged 58 +/- 12 years], paroxysmal AF in 43 patients). In group 1, complete AV block was achieved in all patients. In group 2, the procedure was performed in sinus rhythm (30 patients), prolonging the Wenckebach cycle length from 328 +/- 85 to 466 +/- 80 ms (p <0.01) or during AF (30 patients), decreasing ventricular rate from 178 +/- 35 to 96 +/- 35 beats/min (p <0.01), and to <100 beats/min in 17 patients (61%). Complete AV block was induced in 9 of 60 patients (15%). In groups 1 and 2, at a follow-up of 27 +/- 7 and 26 +/- 6 months, there were 2 deaths (1 cardiac, 1 sudden death) and 1 death for end-stage heart failure, respectively. Hospital readmissions decreased from 3.2 to 0.2 and from 4.2 to 0.2/year; late AF recurrences at of >120 beats/min were documented in 6% and 12%, respectively. Symptom score analysis including effort and rest dyspnea, exercise intolerance, weakness, and palpitation showed a significant improvement in both treatment groups, when acutely effective, in patients with paroxysmal and/or chronic AF. In conclusion, ablation of the AV junction shows a higher acute success rate compared with modulation of the AV node conduction in patients with drug refractory AF. Depending on the acute success, both approaches therefore were similarly effective in achieving long-term ventricular rate control and symptom score improvement.     

Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.     

Paroxysmal Atrial Fibrillation Maintained by Nonpulmonary Vein Sources Can Be Predicted by Dominant Frequency Analysis of Atriopulmonary Electrograms

Introduction: Increasing evidence suggests that high-frequency excitation in the pulmonary vein (PV) plays a dominant role in the maintenance of paroxysmal atrial fibrillation (AF). However, in a certain population of patients, AF remains inducible after PV isolation (PVI). We sought to clarify whether dominant frequency (DF) analysis of atriopulmonary electrograms can predict paroxysmal AF maintained by non-PV sources.
Methods and Results: Sixty-one patients with paroxysmal AF (aged 59 ± 12 years) were studied. Before PVI, bipolar electrograms during AF were recorded simultaneously from three PV ostia, the coronary sinus (CS), and the septum and free wall of the right atrium (RA). DF was obtained by fast Fourier transform (FFT) analysis. AF was rendered noninducible after PVI in 39 of the 61 patients (noninducible group), but was still inducible in the remaining 22 (inducible group). Among the six recording sites, the highest DF was documented in the PV in all of the patients in the noninducible group; the maximum DF among the three PVs (PV-DF_max) was higher than that among the CS and two RA sites (atrial DF_max; 7.2 ± 1.0 Hz vs 5.8 ± 0.7 Hz, P < 0.0001). In contrast, the highest DF was documented in the CS or RA in 45.5% of the patients in the inducible group; PV-DF_max was comparable with atrial DF_max (6.6 ± 0.8 Hz vs 6.6 ± 0.6 Hz). AF inducibility after PVI was predicted by a PV-to-atrial DF_max gradient of <0.5 Hz, with a sensitivity of 90.9% and a specificity of 89.7%.
Conclusion: Paroxysmal AF maintained by non-PV sources can be predicted by the PV-to-atrial DF gradient.     

房室结慢径区域消融对迷走神经功能及心房颤动易感性的影响

目的心房颤动（房颤）与房室结折返性心动过速有着某种程度的关联性,慢径区域消融可能影响了心房自主神经功能而导致窦性心动过速。但慢径区消融对心房自主神经功能的具体影响目前尚不清楚。本文旨在探讨慢径区消融对心房迷走神经调节功能及房颤易感性的影响。方法11条成年杂种犬,全身麻醉下行颈交感一迷走神经干剥离术。经右颈内静脉穿刺放置冠状静脉窦导管,经左股静脉穿刺放置右心室导管及右心房标测电极导管（Halo导管）,经右股静脉穿刺放置消融导管和希氏束导管。静脉应用美托洛尔阻断交感神经活性。测量慢径区域消融前后基础状态及迷走神经刺激下的窦性周长（SCL）及高位右心房（HRA）、低位右心房（IRA）、冠状静脉窦近端（CSp）和冠状静脉窦远端（CSd）的有效不应期（ERP）及心房易感窗口（VW）。结果（1）SCL的变化：消融前后迷走神经刺激导致的SCL缩短值无明显改变[（107±19）次／min对（108±8）次／min,P〉0．05],提示慢径区域消融没有明显改变迷走神经对窦房结的调节作用。（2）ERP的变化：消融前后迷走神经刺激导致的ERP缩短值在HRA分别为[（69±37）ms对（55±34）ms,P〉0．05],CSd分别为[（55±30）ms对（42±32）ms,P=0．08],IRA分别为[（66±24）ms对（19±21）ms,P〈0．001],CSp分别为[（46±24）ms对（7±18）ms,P〈0．001]。提示慢径区域消融对HRA及窦房结区域的迷走神经调节功能无明显影响,对CSd区域的迷走神经调节功能有一定的影响,而导致了IRA及CSp区域去迷走神经效应。（3）心房VW的变化：消融前后基础状态下各个部位刺激均较难诱发房颤（VW接近0）。消融后,HRA迷走神经刺激诱发房颤的能力较消融前没有明显变化[（63±31）ms对（63±25）ms,P〉0．05],CSd的VW有一定程度的降低[（35±37）ms对（57±28）ms,P     

Effects of thyroid hormone on the arrhythmogenic activity of pulmonary vein cardiomyocytes.

OBJECTIVES: This study was conducted to investigate the effects of thyroid hormone on the electrophysiological characteristics of pulmonary vein (PV) cardiomyocytes. BACKGROUND: Hyperthyroidism is an important etiology of paroxysmal atrial fibrillation (AF). Pulmonary veins are known to initiate paroxysmal AF. METHODS: The action potential and ionic currents were investigated in single rabbit PV and atrial cardiomyocytes with (hyperthyroid) and without (control) incubation of L-triiodothyronine using the whole-cell clamp technique. RESULTS: Compared with the control cardiomyocytes, hyperthyroid PV and atrial cardiomyocytes had shorter action potential duration. Hyperthyroid PV cardiomyocytes had faster beating rates (1.82 +/- 0.13 Hz vs. 1.03 +/- 0.15 Hz, p < 0.005) and a higher incidence of delayed after depolarization (beating: 92% vs. 6%, p < 0.0001; non-beating: 45% vs. 3%, p < 0.005). However, only hyperthyroid PV beating cardiomyocytes had a higher incidence of early after depolarization (46% vs. 0%, p < 0.0001). The ionic current experiments showed that hyperthyroid PV beating cardiomyocytes had larger densities of overall slow inward (2.72 +/- 0.21 pA/pF vs. 2.07 +/- 0.19 pA/pF, p < 0.05), overall transient outward (1.39 +/- 0.21 pA/pF vs. 0.48 +/- 0.08 pA/pF, p < 0.001) and steady state outward currents (0.78 +/- 0.06 pA/pF vs. 0.58 +/- 0.04 pA/pF, p < 0.05) on depolarization and larger transient inward (0.021 +/- 0.004 pA/pF vs. 0.005 +/- 0.001 pA/pF, p < 0.001) on repolarization. By contrast, the hyperthyroid PV non-beating cardiomyocytes had larger densities of overall transient outward (1.01 +/- 0.14 pA/pF vs. 0.37 +/- 0.07 pA/pF, p < 0.001), steady state outward (0.61 +/- 0.06 pA/pF vs. 0.44 +/- 0.04 pA/pF, p < 0.05) and transient inward currents (0.011 +/- 0.002 pA/pF vs. 0.003 +/- 0.001 pA/pF, p < 0.05). CONCLUSIONS: Thyroid hormone changes the electrophysiological activity of the PV cardiomyocytes. Increased automaticity and enhanced triggered activity may increase the arrhythmogenic activity of PVs in hyperthyroidism.     

Stimulation of the intrinsic cardiac autonomic nervous system results in a gradient of fibrillatory cycle length shortening across the atria during atrial fibrillation in humans

Autonomic Stimulation Promotes AFCL Gradients in AF. Introduction: The intrinsic cardiac autonomic nervous system (ANS) is implicated in atrial fibrillation (AF) but little is known about its role in maintenance of the electrophysiological substrate during AF in humans. We hypothesized that ANS activation by high‐frequency stimulation (HFS) of ganglionated plexi (GP) increases dispersion of atrial AF cycle lengths (AFCLs) via a parasympathetic effect. Methods and Results: During AF in 25 patients, HFS was delivered to presumed GP sites to provoke a bradycardic vagal response and AFCL was continuously monitored from catheters placed in the pulmonary vein (PV), coronary sinus (CS), and high right atrium (HRA). A total of 163 vagal responses were identified from 271 HFS episodes. With a vagal response, the greatest reduction in AFCL was seen in the PV adjacent to the site of HFS (16% reduction, 166 ± 28 to 139 ± 26 ms, P < 0.0001) followed by the PV‐atrial junction (9% reduction, 173 ± 21 to 158 ± 20 ms, P < 0.0001), followed by the rest of the atrium (3–7% reduction recorded in HRA and CS). Without a vagal response, AFCL changes were not observed. In 10 patients, atropine was administered in between HFS episodes. Before atropine administration, HFS led to a vagal response and a reduction in PV AFCL (164 ± 28 to 147 ± 26 ms, P < 0.0001). Following atropine, HFS at the same GP sites no longer provoked a vagal response, and the PV AFCL remained unchanged (164 ± 30 to 166 ± 33 ms, P = 0.34). Conclusions: Activation of the parasympathetic component of the cardiac ANS may cause heterogenous changes in atrial AFCL that might promote PV drivers. (J Cardiovasc Electrophysiol, Vol. pp. 1‐8)