典型心房扑动射频消融术后发生心房颤动患者的心房电生理特性

分析典型心房扑动(简称房扑)射频消融术后发生心房颤动(简称房颤)患者的心房电生理特性,探讨心房内传导时间在房颤发生中的意义。56例典型房扑患者,其中19例有器质性心脏病,16例在消融前有房颤发作。所有患者均进行常规的电生理检查及标测,记录消融前后心房的电生理参数。根据消融术后随访是否有房颤的发生分为两组进行分析。结果:56例房扑患者全部消融成功,随访14±12(6～60)个月,中位数14个月。消融术后15例有房颤发作,其中3例进展为慢性房颤。15例有房颤发作患者的年龄较无房颤发作的患者大(57.1±13.6岁vs42.3±11.2岁,P<0.05),消融术前和术后的高右房至冠状窦的传导时间延长(分别为98.4±17.1msvs67.8±16.5ms;93.1±18.4msvs70.2±19.7ms;P均<0.05)。多因素Cox回归分析消融前有房颤发作的病史(危险比2.3,95%CI1.425～4.632,P=0.02)和窦性心律下高右房至冠状窦的传导时间超过90ms(危险比1.7,95%CI1.215～3.758,P=0.03)是预测射频消融术后发生房颤的独立的危险因素。结论:典型房扑射频消融术后发生房颤患者心房内传导延迟,并且房内传导延迟是预测射频消融术后发生房颤的重要电生理指标。     

Catheter ablation of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.

AIMS: Antiarrhythmic drug treatment for atrial fibrillation can cause atrial flutter-like arrhythmias. The aim of this study was to clarify the effect of catheter ablation of the tricuspid annulus-vena cava inferior isthmus on amiodarone-induced atrial flutter and to determine the incidence of atrial fibrillation after catheter ablation of amiodarone-induced atrial flutter in comparison to regular typical flutter. METHODS AND RESULTS: Among 92 consecutive patients with typical atrial flutter who underwent isthmus ablation 28 patients had atrial flutter without a history of previous atrial fibrillation (group I), 10 patients had atrial flutter following the initiation of amiodarone therapy for paroxysmal atrial fibrillation (group II) and 54 patients had atrial flutter and atrial fibrillation (group III). Atrial cycle length during atrial flutter in amiodarone-treated patients (group II) (277+/-24 ms) was significantly longer as compared to the cycle length of atrial flutter in group I (247+/-33 ms) and group III patients (235+/-28 ms). The rate of successful transient entrainment and overdrive stimulation to sinus rhythm was not different between patients with (60%) or without amiodarone therapy (group I: 71%, group III: 53%). Successful isthmus ablation with bidirectional conduction block eliminating right atrial flutter was achieved in 90% of amiodarone-treated patients and 93% of patients without amiodarone therapy. In the amiodarone-treated patient group atrial conduction times during pacing in sinus rhythm were significantly prolonged by 20-30% before and after ablation in all regions of the reentrant circuit. During a mean follow-up of 8+/-3 months post-ablation, atrial fibrillation recurred in two of 10 patients on continued amiodarone therapy after successful isthmus ablation. Thus, successful catheter ablation of atrial flutter due to amiodarone therapy was associated with a markedly lower recurrence rate of paroxysmal atrial fibrillation (20%) as compared to patients with atrial flutter plus preexisting paroxysmal atrial fibrillation (76%) and was similar to the outcome of patients with successful atrial flutter ablation without preexisting atrial fibrillation (25%). CONCLUSION: These data suggest that isthmus ablation with bidirectional block and continuation of amiodarone therapy is an effective therapy for the treatment of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.     

Simultaneous occurrence of atrial fibrillation and atrial flutter

INTRODUCTION: Early reports suggested that some patients with "atrial fibrillation/flutter" might have atrial fibrillation in one atrium and atrial flutter in the other. However, more recent conceptions of atrial fibrillation/flutter postulate that the pattern is due to a relatively organized (type I) form of atrial fibrillation. We report the occurrence and ECG manifestations of simultaneous atrial fibrillation and flutter in patients undergoing attempted catheter ablation of atrial flutter. METHODS AND RESULTS: In patients undergoing radiofrequency ablation for atrial flutter, an attempt was made to entrain atrial flutter by pacing in the right atrium. The arrhythmias observed occurred following attempts at entrainment, or spontaneously in one case. Twelve transient episodes of simultaneous atrial fibrillation and flutter were observed in five patients. The atrial fibrillation was localized to all or a portion of one atrium, during which the other atrium maintained atrial flutter. In each case, the surface 12-lead ECG reflected the right atrial activation pattern. No patients had interatrial or intra-atrial conduction block during sinus rhythm, suggesting functional intra-atrial block as a mechanism for simultaneous atrial fibrillation/flutter. CONCLUSION: In certain patients, the occurrence of transient, simultaneous atrial fibrillation and flutter is possible. In contrast to prior studies in which it was suggested that left atrial or septal activation determines P wave morphology, the results of the present study show that P wave morphology is determined by right atrial activation. Functional interatrial block appears to be a likely mechanism for this phenomenon.     

The role of left atrial muscular bundles in catheter ablation of atrial fibrillation.

OBJECTIVES: We sought to investigate the imaging of the left atrial (LA) muscular bundle and the relationship between the bundle and inducibility of tachyarrhythmia after pulmonary vein isolation (PVI). BACKGROUND: Noninducibility is used as a clinical end point of atrial substrate ablation after PVI. However, little is known about the role of the LA muscular bundles in tachyarrhythmia after PVI. METHODS: Forty-three consecutive patients with paroxysmal atrial fibrillation who underwent catheter ablation were included. Bi-atrial isochronal mapping was performed with the NavX system (St. Jude Medical Inc., St. Paul, Minnesota) during sinus rhythm. After 4 PVI, inducible organized LA flutter with or without transforming to atrial fibrillation (AF) (LA flutter/AF) was ablated with additional lines at the roof and/or mitral isthmus. RESULTS: The existence of bilateral muscular bundles was an independent predictor of LA flutter/AF after PVI (p = 0.02). Patients with LA flutter/AF after PVI had a greater index of the double potentials (5.4 +/- 3.4% vs. 2.8 +/- 1.8%, p = 0.006) and interpotential interval (33 +/- 5 ms vs. 29 +/- 4 ms, p = 0.02) than without LA flutter/AF. The muscular bundles were identified in 28% patients using 16-slice multidetector computed tomography, which were identical to the isochrone map. Patients with noninducible LA flutter/AF after PVI plus the additional linear ablation had a lower recurrence rate as compared with the patients without it (19% vs. 75%, p = 0.02). CONCLUSIONS: Left atrial muscular bundles may provide a conduction block line and barrier, which is important for the formation of LA flutter/AF after PVI. The noninducibility of LA flutter/AF achieved after additional linear ablation may contribute to a better outcome in RF ablation of paroxysmal atrial fibrillation.     

A comparison of P-wave duration and dispersion in patients with short-term and long-term atrial fibrillation

This study compared P-wave duration and dispersion (PD) in patients with short-term (48 hours) atrial fibrillation (AF) after cardioversion. We studied 96 consecutive patients with short-term (group A; n:51, age: 61 +/- 11 years) and long-term AF (group B; n:45, age: 64 +/- 10 years). P-wave measurements were calculated from 12-lead electrocardiogram. There was no difference related to clinical characteristics. Left atrial dimension was significantly higher in group B (P =.003). P maximum (124 +/- 12 vs. 113 +/- 11 ms, P =.001) and PD (57 +/- 8 vs. 49 +/- 9 ms, P =.001) were also significantly longer in group B compared with group A, but P minimum did not. In univariate analysis, PD were related to AF duration (P =.002) and left atrial size (P =.02). This relation remained in multivariate analysis (P =.01, P =.02, respectively). P maximum >112 ms and PD >47 ms had accuracy values of 74% and 83% respectively for separating group B. Our results suggest that P wave duration and dispersion is prolonged in patients with long-term AF compared to short-term AF.     

Electrophysiological properties of atrial fibrillation with WPW syndrome and the role of procainamide in conversion

Fifty one patients with recurrent episodes of atrial fibrillation associated with WPW syndrome were studied by pre-operative clinical electrophysiogical testing. The results showed that: these patients had an markedly prolonged intra-atrial conduction time (PA intervals: 42.22 +/- 10.93 ms) than the patients only with attack of atrioventricular reentry tachycardia (AVRT) (PA intervals: 17.21 +/- 9.68ms, P less than 0.001). The attack of atrial fibrillation related to an markedly prolonged atrial vulnerable phase and the retrograde conduction of accessory pathway (AP). The clinical results of atrial fibrillation were decided by the antegrade effective refractory period (AERP) of AP. When the shortest R-R (V-V) intervals during attack of atrial fibrillation was shorter than 180ms, the atrial fibrillation spontaneously turned to the ventricular fibrillation. The conversion of atrial fibrillation to sinus rhythm showed that procainamide not only prolonged AERP of AP, which were 248.57 +/- 15.74ms and 388.57 +/- 63.9 ms (P less than 0.001) respectively before and after intravenous procainamide infusion, but also prolonged intra-atrial conduction time significantly, the PA interval before and after intravenous procainamide infusion were 42.22 +/- 10.93 ms and 57.14 +/- 11.12 ms (P less than 0.025) respectively.     

房颤与房扑的射频消融治疗研究

目的 探讨房颤与房扑之间的相互关系，寻找房颤的射频治疗方法。方法 对40例阵发性房颤患者进行了电生理标测及射频消融。结果 40例中有6例患者发生房扑，行右房峡部消融，1例行Halo电极标测示峡部双向阻滞，随访12－30个月房颤消失或次数明显减少。结论 房颤与房扑为两种密切相关的心律失常，消融右房峡部可能对部分房颤患者起到治疗作用。     

Mechanism, localization and cure of atrial arrhythmias occurring after a new intraoperative endocardial radiofrequency ablation procedure for atrial fibrillation

OBJECTIVES: The purpose of this study was to test a new pattern of radiofrequency ablation for atrial fibrillation (AFib) intended to optimize atrial activation, and to demonstrate the usefulness of catheter techniques for mapping and ablation of postoperative atrial arrhythmias. BACKGROUND: Linear radiofrequency lesions have been used to cure AFib, but the optimal pattern of lesions is unknown and postoperative tachyarrhythmias are common. METHODS: A radial pattern of linear radiofrequency lesions (Star) was made using an endocardial open surgical approach in 25 patients. Postoperative arrhythmias were induced and characterized during electrophysiological studies in 15 patients. RESULTS: The AFib was abolished in most patients (91%), but atrial flutter (AFlut) occurred in 96% of patients postoperatively. At postoperative electrophysiological studies, 37 flutter morphologies were studied in 15 patients (46% spontaneous, cycle length [CL] 223 +/- 25 ms). Seven mechanisms (lesions discontinuity, n = 6; focal mechanism, n = 1) of AFlut were characterized in six patients. In these cases, flutter was abolished using further catheter radiofrequency ablation. In the remaining cases, flutter was usually localized to an area involving the interatrial septum, but no critical isthmus was identified for ablation. After 16 +/-10 months, 15 patients (65%) were asymptomatic with (n = 3) or without (n = 12) antiarrhythmic medications. Eight (35%) patients had persistent arrhythmias. Postoperative atrial electrical activation was near physiological. CONCLUSIONS: The AFib maybe abolished using a radial pattern of linear endocardial radiofrequency lesions, but postoperative AFlut is common even when lesions are made under optimal conditions. Endocardial mapping techniques can be used to characterize the flutter mechanisms, thus enabling subsequent successful catheter ablation.     

Reversal of electrical remodeling after cardioversion of persistent atrial fibrillation

INTRODUCTION: In animals, atrial fibrillation results in reversible atrial electrical remodeling manifested as shortening of the atrial effective refractory period, slowing of intra-atrial conduction, and prolongation of sinus node recovery time. There is limited information on changes in these parameters after cardioversion in patients with persistent atrial fibrillation. METHODS AND RESULTS: Thirty-eight patients who had been in atrial fibrillation for 1 to 12 months underwent electrophysiologic testing 10 minutes and 1 hour after cardioversion. At 1 week, 19 patients still in sinus rhythm returned for repeat testing. Reverse remodeling of the effective refractory period was not uniform across the three atrial sites tested. At the lateral right atrium, there was a highly significant increase in the effective refractory period between 10 minutes and 1 hour after cardioversion (drive cycle length 400 ms: 204 +/- 17 ms vs 211 +/- 20 ms, drive cycle length 550 ms: 213 +/- 18 ms vs 219 +/- 23 ms, P < 0.001). The effective refractory period at the coronary sinus and distal coronary sinus did not change in the first hour but had increased by 1 week. The corrected sinus node recovery time did not change in the first hour but was shorter at 1 week (606 +/- 311 ms vs 408 +/- 160 ms, P = 0.009). P wave duration also was shorter at 1 week (135 +/- 18 ms vs 129 +/- 13 ms, P = 0.04) consistent with increasing atrial conduction velocity. CONCLUSION: The atrial effective refractory period increases, sinus node function improves, and atrial conduction velocity goes up in the first week after cardioversion of long-standing atrial fibrillation in humans. Reverse electrical remodeling of the effective refractory period occurs at different rates in different regions of the atrium.     

Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: role of the accessory pathway

Clinical and electrophysiologic characteristics associated with spontaneous and inducible atrial fibrillation and ventricular tachyarrhythmia were assessed in 20 consecutive patients with Wolff-Parkinson-White (WPW) syndrome undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. Patients with spontaneous atrial fibrillation were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 +/- 26 vs 303 +/- 109 msec). However, patients with and without spontaneous atrial fibrillation did not differ with respect to prevalence of structural heart disease (3 of 11 vs 2 of 9), intra-atrial conduction time (34 +/- 10 vs 32 +/- 10 msec), or interatrial conduction time (86 +/- 21 vs 88 +/- 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to atrial fibrillation. Among the 20 patients, 10 to 35 beats of nonsustained ventricular tachycardia (seven patients) or ventricular fibrillation (three patients) were induced at electrophysiologic study with one to three programmed extrastimuli. Clinically, a ventricular arrhythmia (ventricular fibrillation during atrial fibrillation) had occurred in only one of these patients. The discordance of these observations was significant (p less than 0.01). Patients with and without inducible ventricular arrhythmias were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 patients. During a mean follow-up of 27 months, atrial fibrillation recurred in two patients with failed ablation procedures and in one patient with left atrial enlargement (despite accessory pathway division) (p = 0.019 vs pre-ablation). Ventricular arrhythmias remained inducible in two patients in whom accessory pathway ablation failed (p = 0.01 vs initial study). However, spontaneous ventricular tachyarrhythmias did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible atrial fibrillation and ventricular tachyarrhythmia in patients with WPW syndrome and no organic heart disease depends primarily on the existence of a functional accessory pathway. These susceptibilities are eliminated by interruption of accessory pathway conduction. Ventricular tachyarrhythmias remain infrequent spontaneous events in the WPW syndrome. Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.     

The usefulness of surface 12-lead electrocardiogram to predict intra-atrial conduction block after successful atrial flutter ablation

Intraatrial conduction block at the inferior vena cava-tricuspid annulus isthmus was shown to predict successful atrial flutter ablation. However, its demonstration requires the use of several electrode catheters. Thus, a simple approach using surface 12-lead ECG to prove the conduction block would be valuable. Twenty-two patients were prospectively studied during low septal and low lateral atrial pacing before and after successful atrial flutter ablation. Creation of the conduction block was confirmed by comparing the sequence of atrial activation using 3 multipolar catheters during atrial pacing before and after ablation. During low septal pacing, there was no significant difference before and after ablation in P-wave width, axis, or morphology. During low lateral atrial pacing, there was a significant P-wave axis rotation towards the right (from -67 +/- 27 degrees to +13 +/- 35 degrees, P <.001), and P-wave polarity in limb lead II changed from predominantly negative to predominantly positive in 21 of 22 patients. There was also an increase in P-wave width (from 136 +/- 32 to 169 +/- 36 ms, P <.001) and stimulus-to-QRS interval (from 268 +/- 61 ms to 343 +/- 95 ms, P <.001) during low lateral pacing that was not observed during low septal pacing. We conclude that creation of a conduction block in the inferior vena cava-tricuspid annulus isthmus modifies surface 12-lead ECG during low lateral atrial pacing only. We also suggest that P-wave polarity in limb lead II during low lateral pacing could be used as a noninvasive marker of unidirectional counter-clockwise conduction block during atrial flutter ablation.     

A novel method of multisite atrial pacing, incorporating Bachmann's bundle area and coronary sinus ostium, for electrical atrial resynchronization in patients with recurrent atrial fibrillation.

AIMS: The aim of the study was to assess efficacy and safety of a novel method of multisite atrial pacing, incorporating Bachmann's bundle (BB) and coronary sinus (CS) ostium pacing, which was implemented for the first time in atrial fibrillation (AF) patients with intra-atrial conduction delay. METHODS AND RESULTS: This follow-up study included 97 patients with drug refractory symptomatic AF, sinus node dysfunction, sinus P-wave > or = 120 ms, and normal atrioventricular conduction. Pacing efficacy was assessed on the basis of two main endpoints: successful rhythm control and the absence of documented or symptomatic AF. During the mean 2.3 +/- 0.7 years of follow-up, the survival rate was 99%, pacing maintenance rate 97%, and the need for re-operation 5%. Rhythm control efficacy was 90%, and 14 patients had no evidence of recurrent AF. After implantation, the mean number of anti-arrhythmic drugs used (P < 0.0001), the need for cardioversion (P < 0.01), and the incidence (P < 0.0001) and duration (P < 0.001) of AF-related hospitalizations decreased. P-wave duration with multisite atrial pacing was shorter than during sinus rhythm, BB, and CS pacing (P < 0.0001). CONCLUSION: A novel method of multisite atrial pacing is safe, provides effective long-term rhythm control, and decreases the necessity for adjunctive therapies in patients with refractory AF and intra-atrial conduction delay.     

Transverse conduction capabilities of the crista terminalis in patients with atrial flutter and atrial fibrillation.

OBJECTIVES: In this study, the transverse conduction capabilities of the crista terminalis (CT) were determined during pacing in sinus rhythm in patients with atrial flutter and atrial fibrillation. BACKGROUND: It has been demonstrated that the CT is a barrier to transverse conduction during typical atrial flutter. Mapping studies in animal models provide evidence that this is functional. The influence of transverse conduction capabilities of the CT on the development of atrial flutter remains unclear. METHODS: The CT was identified by intracardiac echocardiography. The atrial activation at the CT was determined during programmed stimulation with one extrastimulus at five pacing sites anteriorly to the CT in 10 patients with atrial flutter and 10 patients with atrial fibrillation before and after intravenous administration of 2 mg/kg disopyramide. Subsequently, atrial arrhythmias were reinduced. RESULTS: At baseline, pacing with longer coupling intervals resulted in a transverse pulse propagation across the CT. During shorter coupling intervals, split electrograms and a marked alteration of the activation sequence of its second component were found, indicating a functional conduction block. In patients with atrial flutter, the longest coupling interval that resulted in a complete transverse conduction block at the CT was significantly longer than that in patients with atrial fibrillation (285 +/- 49 ms vs. 221 +/- 28 ms; p < 0.05). After disopyramide administration, a transverse conduction block occurred at longer coupling intervals as compared with baseline (287 +/- 68 ms vs. 250 +/- 52 ms; p < 0.05). Subsequently, a sustained atrial arrhythmia was inducible in 15 of 20 patients. This was atrial flutter in three patients with previously documented atrial fibrillation and in eight patients with history of atrial flutter. Mapping revealed a conduction block at the CT in all of these patients. CONCLUSIONS: It was found that the CT provides transverse conduction capabilities and that the conduction block during atrial flutter is functional. Limited transverse conduction capabilities of the CT seem to contribute to the development of atrial flutter.     

Improved intra-atrial conduction delay after successful ablation for atrial fibrillation by scar homogenization in right atrium

Atrial fibrosis in the right atrium (RA) presenting as a low-voltage zone might be the mechanism of atrial fibrillation (AF) and intra-atrial conduction delay. The impact of scar homogenization in RA on intra-atrial conduction delay is unknown. We describe a patient with paroxysmal AF and significant intra-atrial conduction delay with repetitive atrial flutter, triggered from the lateral free wall in the RA between the significant low-voltage zone and slow conduction area after pulmonary vein isolation. Linear ablation along the trabeculated lateral free wall in the RA to homogenize the scar was successfully performed, and the intra-atrial conduction delay improved ultimately.     

A comparison of 50-J versus 100-J shocks for direct-current cardioversion of atrial flutter

BACKGROUND: Direct-current cardioversion remains the gold standard for restoration of sinus rhythm in patients with atrial flutter. Although an initial energy of 50 J is recommended, the optimal energy settings have not been evaluated in a large series of contemporary patients. METHODS: We compared the outcome of cardioversion with 50 J versus 100 J in 330 consecutive patients with atrial flutter. Initial energy was based on attending physician preference. One hundred sixty patients received 50 J and 170 patients received 100 J. RESULTS: Patients in both groups did not differ significantly in age, sex, weight, body mass index, duration of the arrhythmia, postoperative status, presence and type of structural heart disease, or use of antiarrhythmic drugs. Patients in the 100-J group had more first shock conversion (85% vs 70%; P =. 001), fewer total shocks (1.2 +/- 0.5 vs 1.4 +/- 0.7; P =.001), and less induction of atrial fibrillation (2% vs 11%; P =.002). There were no significant differences in overall restoration of sinus rhythm, cumulative energy delivered, anesthetic dose, and procedure room time. On multivariate analysis, delivery of 100 J was the strongest predictor of first shock success (odds ratio 2.6, 95% confidence interval 2.13 to 3.16; P <.001). CONCLUSION: An initial energy of 100 J is more efficient for restoration of sinus rhythm in patients with atrial flutter.     

Atrial fibrillation is common after ablation of isolated atrial flutter during long-term follow-up

BACKGROUND: Previous studies have shown that the incidence of atrial fibrillation after atrial flutter ablation is approximately 20% among patients presenting with typical atrial flutter and no history of fibrillation. However, studies involving this population have been small, with follow-up typically less than 2 years. OBJECTIVE: The purpose of this study was to provide a more accurate perspective on the long-term risk of atrial fibrillation in patients presenting with isolated typical flutter. METHODS: Clinical records of consecutive patients who had flutter ablations at Presbyterian Medical Center between 1999 and 2004 were assessed (n = 254). Patients with no apparent history of atrial fibrillation before their flutter ablation were identified. Retrospective follow-up data on these patients were obtained by review of medical records from our institution, from patients' cardiologists and primary care physicians, and by direct patient questionnaires. Postablation atrial fibrillation and other arrhythmias were identified by electrocardiography, Holter monitoring, and subsequent clinical records. RESULTS: Postablation atrial fibrillation was identified in 40 (50%) of 80 patients, and an additional three patients presented with atypical atrial flutter, after a mean follow-up of 29.6 +/- 21.7 months. The incidence of atrial fibrillation was progressive, with 49% occurring after 2 years. There was no difference in age, left atrial size, hypertension, structural heart disease, or left ventricular dysfunction in patients who developed atrial fibrillation compared with those who did not. CONCLUSION: Atrial fibrillation occurs in over half of patients who present with isolated typical flutter after cavotricuspid isthmus ablation. Asymptomatic patients should be screened for recurrent arrhythmias indefinitely after ablation. In certain patients, atrial fibrillation and flutter may be different expressions of the same electrical disease, and eradication of the flutter circuit will not prevent the eventual manifestation of atrial fibrillation.     

Factors associated with early atrial fibrillation after ablation of common atrial flutter. A single centre prospective study.

BACKGROUND: The occurrence of early atrial fibrillation (< or = 6 months) after ablation of common atrial flutter is of clinical significance. Variables predicting this evolution in ablated patients without a previous atrial fibrillation history have not been fully investigated. OBJECTIVES: The aim of the present study was: (1) to identify predictive factors of early atrial fibrillation (< or = 6 months) in the overall population following atrial flutter catheter ablation; (2) to identify predictive variables of early atrial fibrillation following (< or = 6 months) atrial flutter catheter ablation within a subgroup of patients without documented prior atrial fibrillation. METHODS: This study prospectively included 96 consecutive patients (age 65 +/- 13 years; 18 women) over a 12-month period. Their counterclockwise flutter was ablated by radiofrequency, by the same operator, with an 8-mm-tip catheter. Clinical, electrophysiological and echocardiographic data were collected and 27 variables were retained for analysis: age; gender; type of atrial flutter (permanent vs paroxysmal); symptom duration (months +/- SD); pre-ablation history of atrial fibrillation; structural heart disease; left ventricular ejection fraction (%); left atrial size (mm); cava--tricuspid isthmus dimension; septal isthmus dimension; systolic pulmonary pressure > or < or = 30 mmHg; right atrial area; left atrial area; isthmus block; number of radiofrequency applications (+/- SD); antiarrhythmic drugs at discharge; left ventricular diastolic diameter; left ventricular systolic diameter; left ventricular telediastolic volume; left ventricular telesystolic volume; A-wave velocity (cm . s(-1)); E-wave velocity (cm . s(-1)); E/A; isovolumetric relaxation time; E-wave deceleration time; significant mitral regurgitation and flutter cycle length (ms). RESULTS: Of the 96 consecutive ablated patients, early atrial fibrillation was documented in 16 patients (17%). Atrial fibrillation occurred 30 +/- 46 days (range 1 to 171 days) after ablation. Univariate analysis associated an early occurrence of atrial fibrillation with: atrial fibrillation history, left ventricular ejection fraction, left atrial size, left ventricular telesystolic volume, A-wave velocity, significant mitral regurgitation and flutter cycle length. Multivariate analysis using a Cox model found that the only independent predictors of early atrial fibrillation were left ventricular ejection fraction and pre-ablation history of atrial fibrillation. In the subgroup without prior atrial fibrillation history (n=63; 66%), the only independent predictor of early atrial fibrillation was the presence of a significant mitral regurgitation. CONCLUSIONS: In a subgroup of patients without atrial fibrillation history, 8% of patients revealed an early atrial fibrillation. Mitral regurgitation is a strong predictive factor of early atrial fibrillation occurrence with 80% sensitivity, 78% specificity and 98% negative predictive value. These data should be considered in post-ablation management.     

Incidence and clinical significance of transformation of atrial fibrillation to atrial flutter in patients undergoing long-term antiarrhythmic drug treatment.

AIMS: To investigate the rate of transformation of atrial fibrillation to atrial flutter in patients taking antiarrhythmic drugs for the prophylaxis of atrial fibrillation, we retrospectively analysed data from 305 consecutive patients with paroxysmal atrial fibrillation (155 male; mean age 63 +/- 11 years) treated with ventricular rate controlling drugs, antiarrhythmic drugs, or without drugs. METHODS AND RESULTS: At a mean follow-up of 9 months (range 1-24) all patients experienced recurrence of arrhythmia: 48 (14.6%, Group A) suffered Type 1 atrial flutter, and 257 (85.4%, Group B) atrial fibrillation. The relative rate of recurrence of atrial flutter vs atrial fibrillation was similar in patients without treatment or with ventricular rate controlling drugs (from 6.8% to 14.6%, P=ns). However, recurrence was higher (25%) in patients administered antiarrhythmic drug therapy. The relative risk in these patients was 3.02 times greater, compared with patients without treatment, or treated with rate controlling drugs (P<0.001). There were no differences between groups concerning the baseline clinical characteristics and the clinical consequences of the recurrence; patients with atrial flutter had a lower rate of conversion to sinus rhythm (42% vs 64%) and a higher rate of hospital admission (69% vs 36%) compared with those with atrial fibrillation. Six patients (8.5%) experienced 1:1 atrioventricular conduction during atrial flutter with a ventricular rate of 240-280 beats x min(-1). CONCLUSION: Our data suggest that the use of antiarrhythmic drugs for the prophylaxis of atrial fibrillation is associated with a threefold increase in the probability of Type 1 atrial flutter recurrence, as opposed to atrial fibrillation, which may have important clinical consequences, but which did not in our study.     

Prevalence of pulmonary vein disconnection after anatomical ablation for atrial fibrillation: consequences of wide atrial encircling of the pulmonary veins.

AIMS: Anatomical and wide atrial encircling of the pulmonary veins (PVs) has been proposed as a cure of atrial fibrillation (AF). We evaluated the acute achievement of electrical PV isolation using this approach. In addition, the consequences of wide encircling of the PVs with isolation were assessed. METHODS AND RESULTS: Twenty patients with paroxysmal AF were studied. Anatomically guided ablation was performed utilizing the CARTO system to deliver coalescent lesions circumferentially around each PV to produce a voltage reduction to <0.1 mV, with the operator blinded to recordings of circumferential PV mapping. After achieving the anatomical endpoint, the incidence of residual conduction and the amplitude and conduction delay of residual PV potentials were determined. Electrical isolation of the PV was then performed and the residual far-field potentials evaluated. Individual PV ablation was performed in all PVs. Anatomically guided PV ablation was performed for 47.3+/-11 min, after which 44 (55%) PVs were electrically isolated. In the remaining 45%, despite abolition of the local potential at the ablation site, PV potentials [amplitude 0.2 mV (range 0.09-0.75) and delay of 50.3+/-12.6 ms] were identified by circumferential mapping. After electrical isolation (12.2+/-11.7 min ablation), 55 (69%) PVs demonstrated far-field potentials; with a greater incidence (P=0.015) and amplitude (P=0.021) on the left compared with the right PVs. At 13.2+/-8.3 months follow-up, 13 patients (65%) remained arrhythmia-free without anti-arrhythmics. In four patients (20%), spontaneous sustained left atrial macrore-entry required re-mapping and ablation. Macrore-entry was observed to utilize regions around or bordering the previous ablation as its substrate. CONCLUSION: Anatomically guided circumferential PV ablation results in apparently coalescent but electrically incomplete lesions with residual conduction in 45% of PVs. Wide encircling of the PVs was associated with left atrial macrore-entry in 20% of patients.     

Activation patterns in experimental canine atrial flutter produced by right atrial crush injury.

OBJECTIVES. This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND. In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS. Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS. At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS. 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.