Higher Rate of Recurrent Atrial Flutter and Atrial Fibrillation Following Atrial Flutter Ablation After Cardiac Surgery

Atrial Flutter After Cardiac Surgery . Introduction: Atrial flutter (AFL) is common after cardiac surgery. However, the types of post‐cardiac surgery AFL, its response to catheter‐based radiofrequency ablation, and its relationship to atrial fibrillation (AF) are unknown. Methods and Results: We retrospectively studied all patients who underwent mapping and ablation for AFL after cardiac surgery from January 1990 to July 2004. One hundred randomly selected patients without prior cardiac surgery (PCS) who underwent mapping and ablation of AFL served as the control population. A total of 236 patients formed the study population (mean age 62 + 13 years, 22% female) and 100 patients formed the control population (mean age 60 + 13 years, 25% female). The majority of patients without PCS had cavo‐tricuspid isthmus (CTI)‐dependent AFL when compared to patients with PCS (93% vs 72%, respectively, P < 0.0001). In contrast, scar‐related AFL was more common in patients with PCS as compared to patients without PCS (22% vs 3%, P < 0.0001). Predictors of scar related AFL in multivariable regression analysis included PCS and left‐sided AFL. Acute success rates and complications were similar between the groups. When compared to patients with AFL ablation without PCS, those that had AFL after PCS had higher rates of recurrence of both AFL (1% vs 12%, P < 0.0001; mean time to recurrence 1.85 years) and AF (16% vs 28%, P = 0.02; mean time to recurrence 2.67 years). Conclusion: Despite ablation of AFL, patients with PCS have a higher rate of AFL and AF when compared to patients without PCS who underwent ablation of atrial flutter during long‐term follow‐up. (J Cardiovasc Electrophysiol, Vol. pp. 760‐765, July 2010)     

与肌袖电活动相关的短阵心房扑动的心电图和心内电生理研究

选择体表心电图表现为短阵心房扑动 (简称房扑 )的阵发性心房颤动 (简称房颤 )病例 ,结合心内电生理标测和导管射频消融大静脉肌袖电隔离的结果 ,探讨短阵房扑与心脏大静脉肌袖和房颤的关系。 2 3例阵发性房颤 ,心电图和动态心电图表现为短阵发作的房扑的患者入选本研究 ,2 3例中有 17例进行了心内电生理标测 ,有 14例标测到短阵房扑和房颤 ,其中单纯短阵房扑发作 8例 ,短阵房扑触发房颤 6例 ,均提示短阵房扑为起源于大静脉肌袖的快速电活动所驱动 ,其中肺静脉 10根 ,上腔静脉 4根 ,均进行了相关肌袖的导管射频消融电隔离治疗 ,成功 13例。结论 :短阵房扑的发生机理是大静脉肌袖的快速电活动所驱动 ,这种机制与阵发性房颤的发生有密切关系 ,短阵房扑可能是房颤由肌袖电活动触发的特征性心电图表现 ,导管射频消融电隔离是治疗这一心律失常的有效方法。     

Early versus Late Atrial Fibrillation after Atrial Flutter Ablation

Introduction: Radiofrequency catheter ablation of atrial flutter (AFl) has high initial success with a 10–15% recurrence. Atrial fibrillation (AFib) after radiofrequency catheter ablation of AFl can occur but may be transient (lasting no more than four weeks). Methods: Of one hundred seventeen consecutive patients studied, one hundred and four consecutive patients with sustained, symptomatic AFl, as the predominant rhythm disturbance (some of whom had transient pre-ablation AFib), referred for radiofrequency catheter ablation, had clinical follow-up. All had evidence for successful AFl ablation. Patients were followed prospectively. Results: Over a mean follow-up of 28 months, 28 patients developed AFib after ablation of AFl [12 early AFib (<2 months) and 16 late AFib (>2 months)]. Seven of 12 (58%) patients in the early onset group reverted to normal sinus rhythm; none required long-term antiarrhythmic therapy. Only one (8%) developed permanent AFib. No patient in the late onset group remained in sinus rhythm without an antiarrhythmic drug. Three (19%) developed permanent AFib despite therapy among those with late onset AFib. Two (17%) patients with early onset AFib reverted to normal sinus rhythm with treatment versus 5 (31%) in the late onset group. Finally, only 2 patients (17%) with paroxysmal/persistent episodes of Afib from the early onset group stayed in normal sinus rhythm despite therapy, while 8 patients ( ± %) with paroxysmal/persistent AFib episodes from the late onset group required therapy to maintain normal sinus rhythm. Conclusion: Early onset AFib after ablation of AFl is likely to be transient and self-limited. Late onset AFib after ablation of AFl can persist and require chronic therapy.     

Coexistence of Intracardiac Atrial Flutter and Extracardiac Fibrillation

This report describes the coexistence of fibrillatory activity limited to an isolated left common pulmonary vein trunk with typical counterclockwise isthmus-dependent right atrial flutter in a patient undergoing a pulmonary vein isolation procedure.     

Effects of High-Frequency Atrial Pacing in Atypical Atrial Flutter and Atrial Fibrillation

Atypical atrial flutter has, hitherto, been relatively refractory totermination by rapid atrial pacing. High-frequency pacing (HFP) in theatrium, for termination of atrial flutter or atrial fibrillation (AF), andthe electrophysiologic effects related to it have not been examined. Weexamined the clinical efficacy, safety, and electrophysiologic mechanisms ofHFP using 50-Hz bursts at 10 mA applied at the high right atrium in patientswith atypical atrial flutter (group 1) or AF (group 2), using a prospectiverandomized study protocol. Four burst durations (500, 1000, 2000, and 4000ms) were applied at the high right atrium repetitively in random sequence in22 patients with spontaneous atrial flutter or AF. Local and distant rightand left atrial electrogram recordings were analyzed during and after HFP.HFP resulted in local and distant right and left atrial electrogramacceleration in 8 of 10 patients (80%) in group 1 but caused lessfrequent local atrial electrogram acceleration (6 of 12 patients) and nodistant atrial electrogram effects in group 2 (p < .05 versus group 1).The HFP protocol was effective in arrhythmia termination in 6 of 10patients in group 1 but in no patient in group 2 (p < .05 versus group1). Standard HFP protocol applied at the high right atrium can frequentlyalter atrial activation in both atria and can terminate atypical atrialflutter. Efficacy in AF is limited, probably due to limitedelectrophysiologic actions beyond the local pacing site.     

Nonpharmacologic Approaches to the Treatment of Atrial Fibrillation and Atrial Flutter

Nonpharmacologic Approaches to Atrial Fibrillation and Flutter. The high prevalence of atrial fibrillation, the associated morbidity and mortality, the absence of safe and effective drug therapy, and an increased understanding of the pathophysiologic basis of atrial fibrillation and flutter have collectively led to the development of novel nonpharmacologic treatments for the management of these arrhythmias, including the CORRIDOR and MAZE surgical procedures, catheter-based ablation and modification of AV conduction, catheter-based ablation of atrial flutter and fibrillation, and internal atrial defibrillation. These surgical and catheter-based techniques offer potentially curative therapy while sparing the long-term risks of antiarrhythmic drug therapy. For patients with typical atrial flutter, catheter ablation affords cure rates in excess of 70%. As technological innovations further facilitate identification and ablation of the critical isthmus in the floor of the right atrium, success rates should improve substantially. For patients with atrial fibrillation, AV junction ablation with implantation of a rate-responsive ventricular pacemaker should be considered palliative therapy, as should modification of AV junction conduction. The MAZE procedure offers very high cure rates, but because it currently involves open heart surgery, patient selection is critical. Catheter-based procedures emulating aspects of the MAZE procedure may one day offer cure rates comparable to those of the surgery itself, but additional research and technological development are necessary to further define and refine the minimal effective procedure, and then to facilitate the placement of contiguous, full-thickness lesions in precise three-dimensional configurations. In the interim, the implantable automatic atrial defibrillator may offer a means for rapidly restoring sinus rhythm without the risks of long-term antiarrhythmic drug therapy.     

Persistent Atrial Flutter in Patients Treated for Atrial Fibrillation with Amiodarone and Propafenone:

INTRODUCTION: Antiarrhythmic drugs have been reported to promote the conversion of atrial fibrillation to atrial flutter in patients with paroxysmal atrial fibrillation. However, information about the electrophysiologic mechanism and response to radiofrequency ablation of these drug-induced atrial flutters is limited. Furthermore, the determinants of the development of persistent atrial flutter in patients treated for atrial fibrillation with antiarrhythmic drugs are still unknown. METHODS AND RESULTS: Among the 136 patients treated for atrial fibrillation with amiodarone (n = 96) or propafenone (n = 40), 15 (11%, mean age 65.5 +/- 12.3 years) were identified to have subsequent development of persistent atrial flutter based on surface ECG characteristics during antiarrhythmic drug treatment. The mean interval between the beginning of drug treatment and the onset of atrial flutter was 5.0 +/- 5.5 months. Intracardiac mapping and entrainment studies revealed that 11 patients had counterclockwise typical atrial flutter, and 4 had clockwise typical atrial flutter. All 15 patients underwent successful ablation with creation of complete bidirectional isthmus conduction block. After a mean follow-up of 12.3 +/- 4.2 months, 14 (93%) of 15 patients who underwent successful ablation and continued taking antiarrhythmic drugs have remained in sinus rhythm. Univariate analysis of clinical variables demonstrated that only atrial enlargement was significantly related to the occurrence of persistent atrial flutter. CONCLUSION: In patients with atrial fibrillation, persistent typical atrial flutter might occur during antiarrhythmic drug treatment, and atrial enlargement was a risk factor for the development of such an arrhythmia. Radiofrequency ablation and continuation of pharmacologic therapy offered a safe and effective means of achieving and maintaining sinus rhythm.     

Atrial Electrograms and Activation Sequences in the Transition Between Atrial Fibrillation and Atrial Flutter

Transition Between Atrial Fibrillation and Flutter. Introduction: The eletrophysiologic mechanism of atrial fibrillation (AF) has a wide spectrum, and it seems that some atrial regions are essential for the occurrence of a particular type of AF. We focused on one type of AF: AF associated with typical atrial flutter (AFI), which was right atrial (RA) arrhythmia, and sought to investigate intra-atrial electrograms and activation sequences in the transition between AF and AFL.
Methods and Results: Intra-atrial electrograms and activation sequences in the R.A free wall and the septum were evaluated in the transition between AF and AFL in seven patients without organic heart disease (all men; mean age 57 ± 11 years). In five episodes of the conversion of AFL into AF, the AFL cycle length was shortened (from 211 ± 6 msec in stable AFL to 190 ± 15 msec before the conversion, P, 0.001). Interruption of the AFL wavefront and an abrupt activation sequential change induced by a premature atrial impulse resulted in fractionation and disorganization of the septal electrograms. During sustained AF, septal electrograms were persistently fractionated with disorganized activation sequences. However, the RA free-wall electrograms were organized, and the activation sequence was predominantly craniocaudal rather than caudocranial throughout AF. In 12 episodes of the conversion of AF into AFL, the AF cycle length measured in the RA free wall increased (from 165 ± 26 msec at the onset of AF to 180 ± 24 msec before the conversion, P, 0.001). AFL resumed when fractionated septal electrograms were separated and organized to the caudocranial direction, despite the RA free-wall electrograms remaining discrete and sharp with an isoelectric line.
Conclusion: Changes of the electrogram and activation sequence in the atrial septum played an important role in the transition between AF and AFL.     

Atrial Appendage Thrombosis Risk Is Lower for Atrial Flutter Compared with Atrial Fibrillation

Background

The risk of stroke and thromboembolism in atrial fibrillation is established. However, the evidence surrounding the risk of thromboembolism in patients with atrial flutter is not as clear. We hypothesized that atrial flutter would have indicators of less risk for thromboembolism compared with atrial fibrillation on transesophageal echocardiography, thereby possibly leading to a lower stroke risk.

Atrial Fibrillation/Flutter Induced by Implantable Ventricular Defibrillator Shocks:

Atrial Fibrillation/Flutter Induced by Defibrillator Shocks. Introduction : We evaluated the incidence and energy dependence of atrial fibrillation/flutter (AF) induced by implantable ventricular defibrillator shocks in 63 patients tested in the operating room or electrophysiology laboratory.
Methods and Results : Defibrillator shocks were epicardial monophasic in 32 patients, and through an Endotak® lead endocardial monophasic in 19 and biphasic in 12 patients. The epicardial and endocardial patient groups had similar clinical characteristics. A total of 517 defibrillator shocks were given. The epicardial group received 336 total defibrillator shocks and 10 ± 6 shocks (mean ± SD) per patient compared with the endocardial group, which received 181 total shocks and 6 ± 4 defibrillator shocks per patient (P = 0.004). In the epicardial group, AF occurred in 13 (41 %) patients and in 17 (5%) of the 336 shocks. No AF was induced with endocardial defibrillator shocks. The epicardial mean energy was 16 ± 9 J, lower than the endocardial mean energy of 20 ± 9 J (P < 0.004). In the epicardial monophasic group, energy correlated with AF induction. Each patient received 7 ± 6 defibrillator shocks < 15 J and 4 ± 2 shocks ≥ 15 J, yet AF occurred in only 2.3% versus 9.6% (P < 0.05) of defibrillator shocks < 15 J and ≥ 15 J, respectively. Of note, AF was not induced with energy < 4 J or > 31 J.
Conclusions : In the epicardial configuration, AF induction is energy dependent, with an apparent lower and upper limit of vulnerability. AF induction by defibrillator shocks delivered through an Endotak lead is very rare, possibly related to an apparent upper limit of vulnerability of less energy, avoidance of thoracotomy, or different energy field distribution.     

Induction of Atrial Fibrillation and Flutter in Dogs Using Methacholine

Systemic infusion of methacholine has been used to facilitate induction of atrial fibrillation. However, the dose-response relationship, reproducibility and effect of anesthetic agents on induction are not well understood. The use of methacholine to facilitate electrical induction of sustained (>10 minutes duration) atrial fibrillation or flutter was examined. In 25 dogs induction of atrial arrhythmias was attempted using a series of ten 50 Hz trains of 10 seconds duration delivered via an endocardial catheter in the baseline anaesthetized state and subsequently in the presence of graded doses of intravenous methacholine (maximum 5 µg/kg/min). Studies were repeated in 13 dogs to assess reproducibility. Twelve dogs (48%) had inducible sustained atrial flutter or fibrillation lasting greater than 10 minutes in the baseline state. During infusion of methacholine the remaining 13 (52%) dogs also had inducible sustained atrial flutter or fibrillation (mean infusion rate 1.6 ± 1.9 µg/kg/min). Induction of sustained atrial flutter or fibrillation was reproducible in all but one dog. The type of anesthetic did not significantly affect inducibility. Induction of prolonged atrial fibrillation or flutter is possible in the baseline anaesthetized state in approximately half of dogs using high frequency programmed electrical stimulation. The yield of inducible sustained atrial fibrillation or flutter with programmed stimulation during intravenous infusion of methacholine was increased to 100%. Induction of sustained atrial fibrillation or flutter was highly reproducible.     

Right Atrial Remodeling is More Advanced in Patients with Atrial Flutter Than with Atrial Fibrillation

Atrial Remodeling in Atrial Flutter. Introduction: Atrial fibrillation (AF) and atrial flutter (AFL) are related arrhythmias with common triggers, yet in individual patients either AF or AFL often predominates. We performed detailed electrophysiologic (EP) and electroanatomic (EA) studies of the right atrium (RA) in patients with AF and AFL to determine substrate differences that may explain the preferential expression of AF/AFL in individual patients. Methods: Patients with AF (n = 13) were compared to patients with persistent AFL (n = 10). Detailed studies were performed, and 3‐dimensional electroanatomic mapping studies were created and the RA was divided into 4 segments for regional analysis. Global, septal, lateral, anterior, and posterior segments were compared for analysis of: bipolar voltage; proportion of low‐voltage areas and areas of electrical silence; conduction times; and proportion of abnormal signals (fractionated signals and double potentials). Results: Compared to patients with AF, patients with AFL had (1) lower bipolar voltage and an increase in the proportion of low‐voltage areas; (2) an increase in the proportion of complex signals; and (3) prolongation of activation times. Conclusions: Patients with AFL showed more advanced remodeling than patients with AF with slowed conduction, lower voltage areas with regions of electrical silence, and a greater proportion of complex signals, particularly in the posterior RA. These changes facilitate the stabilization of AFL and may explain why some patients are more likely to develop AFL as a sustained clinical arrhythmia. (J Cardiovasc Electrophysiol, Vol. 23 pp. 1067‐1072, October 2012)