Atrial Tachycardias Following Atrial Fibrillation Ablation

One of the most important proarrhythmic complications after left atrial (LA) ablation is regular atrial tachycardia (AT) or flutter. Those tachycardias that occur after atrial fibrillation (AF) ablation can cause even more severe symptoms than those from the original arrhythmia prior to the index ablation procedure since they are often incessant and associated with rapid ventricular response. Depending on the method and extent of LA ablation and on the electrophysiological properties of underlying LA substrate, the reported incidence of late ATs is variable. To establish the exact mechanism of these tachycardias can be difficult and controversial but correlates with the ablation technique and in the vast majority of cases the mechanism is reentry related to gaps in prior ablation lines. When tachycardias occur, conservative therapy usually is not effective, radiofrequency ablation procedure is mostly successful, but can be challenging, and requires a complex approach.     

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.     

心房颤动患者心房纤维化研究进展

心房颤动的发生和维持与心房重构有关。心房纤维化是心房颤动患者心房结构重构最突出的表现,目前被认为是发生心房颤动的结构基础,是心房颤动发生、维持的一个重要因素。现综述心房颤动患者心房纤维化及其发生机制。通过对心房颤动患者心房纤维化结构改变及肾素-血管紧张素系统、转化生长因子、基质金属蛋白酶等在心房纤维化的发生和心房颤动发生、维持中的作用等的全面阐述,,探讨了心房颤动患者心房纤维化的研究进展。防治心房颤动新的策略取决于对心房纤维化机制更好的理解。     

Atrial Ectopics Prior to Atrial Fibrillation Onset

Background: This study examined the possible role of atrial ectopics and short runs of atrial tachycardia in the initiation of episodes of paroxysmal atrial fibrillation (PAF). Methods: Holter recordings from patients participating in pharmacotherapy trials for the prevention of PAF were examined. Treatment comprised placebo, digoxin, disopyramide, or atenolol. The frequency of atrial ectopic beats during each 30 seconds over the 5 minutes prior to PAF and whether this was also associated with atrial tachycardia (3 or more ectopics in succession) was calculated. Results: The mean number of ectopics was 4.1 in the final minute, but patients receiving disopyramide or atenolol had significantly more ectopics than those on placebo (P > 0.05 for both). Those on digoxin had a similar number of ectopics to placebo patients. There was no relationship between heart rate at PAF onset and ectopic frequency, nor any association between the presence of one or more episodes of atrial tachycardia and ectopic frequency. Conclusion: Atrial ectopics increase in frequency prior to PAF onset, and this study suggests that antiarrhythmic therapy may increase the number of ectopics required to initiate PAF.     

心房有效不应期离散度与心房颤动

心房颤动是临床最常见的心律失常之一,有较高的致残率及致死率,关于心房颤动的机制有较多的学说,目前研究已经证实心房电重构能够促进心房颤动的发生与维持,心房电重构包括心房有效不应期的缩短,心房有效不应期离散度的增加及局部电传导的减慢,现就心房有效不应期离散度与心房颤动的关系及其影响机制做一综述。     

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.

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).     

心房重构--未来心房颤动防治的新靶点

心房重构是心房颤动 (Af)发生和自我持续的核心环节 ,包括电重构、收缩功能重构和结构重构三种形式。以Af作为靶点可能是将来Af治疗的根本性策略。本文综述了该领域研究的最新进展。     

Right Atrial Thrombi and Depressed Right Atrial Appendage Function After Cardioversion of Atrial Fibrillation

BACKGROUND: It has been shown that cardioversion of atrial fibrillation may result in left atrial chamber and appendage dysfunction and cause new thrombi in the left atrium. The aim of this prospective study was to investigate right atrial appendage function and assess the incidence of new right atrial thrombi after electrical cardioversion. METHODS: Transthoracic echocardiography was performed in 25 patients 4 h before and at 24 h and 7 days after electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical cardioversion, n = 9), as assessed by peak A wave velocities derived from the transtricuspid and transmitral velocity profiles. In addition, transesophageal echocardiography was performed 4 h before and 24 h after cardioversion to evaluate postcardioversion thrombus formation in the right and left atrial chambers and to assess right and left atrial appendage function. The degree of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. RESULTS: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 +/- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0.15 vs 0.4 +/- 0.15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardioversion. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m/sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective values for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0.16 m/sec (P = 0.009). No thrombi were found in either the right or left atrium before cardioversion. In two patients, new thrombi in the right atrium were detected 24 h after internal atrial defibrillation. Thrombi were located at the superior rim of the fossa ovalis in both patients with patent foramen ovale. Another patient had developed a thrombus in the left atrial appendage. CONCLUSIONS: Electrical cardioversion may not only cause left atrial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thrombi in the body of the right atrium.     

Atrial Anatomy and Imaging in Atrial Fibrillation Ablation

Catheter ablation of atrial fibrillation (AF) can be a technically challenging procedure, requiring detailed knowledge of the anatomy of the atria and thoracic veins to achieve successful cure of AF with a low complication rate. In this article, we review the anatomy relevant to AF ablation: the intraatrial septum, the pulmonary veins and left atrial antral region, the left atrial vestibule, the right atrium and related veins, and the esophagus. We focus on normal variations of anatomy and the role of the available imaging modalities in facilitating safe and effective ablation of this common and complex arrhythmia.     

Atrial Tachycardia Confined Within the Left Atrial Appendage

AT Confined Within the LAA. Left atrial tachycardias are often seen following catheter ablation of persistent atrial fibrillation (AF). We report here an unusual case where AF was converted to sinus rhythm following catheter ablation, but ongoing atrial tachycardia confined within the left atrial appendage (LAA) was observed. Although the LAA tachycardia was dissociated from the atrium in sinus rhythm, bidirectional conduction between the left atrium and the LAA was, however, demonstrated after tachycardia termination. (J Cardiovasc Electrophysiol, Vol. 21, pp. 933‐935, August 2010)     

心房颤动致心房重构分子机制研究进展

心房颤动是临床上一种常见的心律失常,心房颤动致心房重构是近年来研究发现的一个重要的电生理现象。心房颤动本身能够导致心房电生理、功能和结构的改变。本文综述了心房颤动致心房快速的电生理变化和缓慢的蛋白质表达及其分子改变机制。通过对心房电生理重构、离子重构和蛋白质重构和超微结构及其功能变化等不同方面的全面阐述,探讨了心房重构的分子机制研究进展。防治心房颤动新的策略将取决于心房重构机制更好的理解。     

Inverted Left Atrial Appendage Bonded to Atrial Septum

Inverted left atrial appendage (LAA) is a rare surgical complication. Our patient, a boy aged 2 years, was diagnosed with a partial atrioventricular defect with mild regurgitation of the left atrioventricular valve and a large primum atrial septal defect. Direct postoperative transesophageal echocardiography revealed a new left atrial mass attached to the atrial septum, without left ventricle inflow obstruction. Out of concern about the nature of this mass, we chose surgical direct examination. Intraoperatively, we diagnosed it as an inverted LAA accidentally attached to the atrial septum suture line. Awareness of this condition can avoid unnecessary diagnostic and therapeutic procedures.     

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 dissociation

An electrocardiographic demonstration of atrial dissociation is presented in which the right atrium was controlled by sinus impulses, whereas the left atrium and the ventricles were controlled by a unilateral ectopic rhythm, presumably originating in the left atrium. Postmortem examination showed recent infarction of the interatrial septum.