Atrial Flutter: Lessons from Surgical Interventions (Musing on Atrial Flutter Mechanism)

We report our experience with seven patients who underwent direct surgical ablation of problematic common flutter. Intraoperative mapping was obtained in four patients. Surgical techniques varied over time. A circular incision of the right atrium was performed in the first patient. Two patients had epicardial cryoablation of the isthmus between the inferior vena cava and the tricuspid valve annulus. Four patients had extensive endocardial cryoablation of the isthmus. There were no immediate postoperative complications. One patient had atrial fibrillation 2 months postoperatively and underwent a corridor operation 1 year later. The other six patients are free of arrhythmias without antiarrhythmic drugs. Surgical ablation confirmed that the common form of atrial flutter is associated with a right atrial macroreentrant circuit. One of our intraoperative endocardial maps suggested that variant reentrant circuits can be associated with variant forms of flutter.     

Atrial tachycardia: mechanisms and management

Atrial tachycardias comprise a heterogeneous group of arrhythmias that include focal atrial tachycardia, typical atrial flutter and atypical atrial flutter. Focal atrial tachyardias arise from automatic, triggered or microreentrant mechanisms, while typical and atypical flutters are macroreentrant in nature. Typical flutter describes a reentrant circuit that is dependant on the cavotricuspid isthmus in the right atrium while atypical flutter includes various lesional and de novo macroreentrant circuits in the right and left atria. Electrocardiographic criteria have been proposed to distinguish these mechanisms of tachycardia, but they are not specific; whereas adenosine often aids in the diagnosis. Management of focal atrial tachyardias and macroreentry centers around rate control, antiarrhythmic therapy, ablation and anticoagulation. Success rates for ablation are highest for typical atrial flutter and higher than antiarrhythmic therapy for most atrial tachycardias.     

Atrial tachycardia: mechanisms and management

Atrial tachycardias comprise a heterogeneous group of arrhythmias that include focal atrial tachycardia, typical atrial flutter and atypical atrial flutter. Focal atrial tachyardias arise from automatic, triggered or microreentrant mechanisms, while typical and atypical flutters are macroreentrant in nature. Typical flutter describes a reentrant circuit that is dependent on the cavotricuspid isthmus in the right atrium while atypical flutter includes various lesional and de novo macroreentrant circuits in the right and left atria. Electrocardiographic criteria have been proposed to distinguish these mechanisms of tachycardia, but they are not specific; whereas adenosine often aids in the diagnosis. Management of focal atrial tachyardias and macroreentry centers around rate control, antiarrhythmic therapy, ablation and anticoagulation. Success rates for ablation are highest for typical atrial flutter and higher than antiarrhythmic therapy for most atrial tachycardias.     

Atrial tachycardias following circumferential pulmonary vein ablation: observations during catheter ablation

Circumferential pulmonary vein ablation performing linear lesions around the ostia of the pulmonary veins has been shown to be effective for the treatment of atrial fibrillation. During the follow-up period, persistent atrial tachycardia may occur as a proarrhythmic complication. Only little information is available about the underlying mechanism. In our study, atrial tachycardia following circumferential pulmonary vein ablation was identified in 13 out of 84 consecutive patients (15.5%), as a transient appearance in four and with recurrences for more than 3 months in nine patients (10.7%). Electrophysiological study and ablation was performed in eight cases, revealing common atrial flutter in two, a focal origin secondary to conduction recovery from the pulmonary vein to the left atrium in two and macro reentrant left atrial flutter in four patients. The electrophysiological characteristics demonstrated by electroanatomic activation mapping (CARTO™) and consecutive ablation therapy with a 100% success rate are described and discussed with regard to the literature.     

Mechanism of atrial flutter occurring late after orthotopic heart transplantation with atrio-atrial anastomosis

OBJECTIVE: We sought to better define the electrophysiologic mechanism of atrial flutter in patients after heart transplantation. BACKGROUND: Atrial flutter is a recognized problem in the post-cardiac transplant population. The electrophysiologic basis of atrial flutter in this patient population is not completely understood. METHODS: Six patients with cardiac allografts and symptoms related to recurrent atrial flutter underwent diagnostic electrophysiologic study with electroanatomic mapping and radiofrequency catheter ablation. Comparison was made with a control non-transplant population of 11 patients with typical counterclockwise right atrial flutter. RESULTS: In each case, mapping showed typical counterclockwise activation of the donor-derived portion of the right atrium, with concealed entrainment shown upon pacing in the cavotricuspid isthmus (CTI). The anastomotic suture line of the atrio-atrial anastomosis formed the posterior barrier of the reentrant circuit. Ablation of the electrically active, donor-derived portion of the CTI was sufficient to terminate atrial flutter and render it noninducible. Comparison with the control population showed that the electrically active portion of the CTI was significantly shorter in patients with transplant-associated flutter and that ablation was accomplished with the same or fewer radiofrequency lesions. CONCLUSIONS: Atrial flutter in cardiac transplant recipients is a form of typical counterclockwise, isthmus-dependent flutter in which the atrio-atrial anastomotic suture line forms the posterior barrier of the reentrant circuit. Ablation in the donor-derived portion of the CTI is sufficient to create bidirectional conduction block and eliminate this arrhythmia. Ablation or surgical division of the donor CTI at the time of transplantation could prevent this arrhythmia.     

Long-Term Antitachycardia Pacing Experience for Supraventricular Tachycardia

A pacemaker was used to control drug-resistant reentrant supraventricular tachycardia (SVT) in 40 patients. An antitachycardia pacemaker was implanted in 37 for SVT; in one for ventricular tachycardia that could also be used to terminate SVT; in one SVT could be terminated with an activity rate variable pacemaker; and in one a DDD pacemaker was used for prevention and termination of SVT. Twenty patients had AV nodal reentrant tachycardias, eight had tachycardias due to a concealed accessory pathway, eight had a Wolff-Parkinson-White syndrome, three had reentrant atrial tachycardias, and one had atrial flutter. Twenty-two patients were paced from the right atrium, five from the coronary sinus, ten from the right ventricle, and three had a DDD pacemaker. During a total follow-up period of 1,503 (mean 38) months an estimated 16,240 episodes of tachycardia were terminated promptly at home, 58 required several attempts, 57 episodes lasted longer than 30 minutes but did not require medical attention, and 11 required hospital admission. Hospital admission for SVT decreased from one per patient-month (in the 3 months before implantation) to 1 per 137 patient-months after implantation. Additional reentrant tachycardias occurred in 13 patients. Antiarrhythmic drug therapy in combination with a conservative antitachycardia pacing mode was required in four patients paced from the atrium to avoid pacing induced atrial fibrillation. Antiarrhythmic drug therapy was used in 42% of patients to help control SVT. Conclusions: (1) Drug-resistant SVTs can be safely and effectively managed on the long-term with antitachycardia pacemakers. (2) Rapid termination of SVT improved the quality-of-life significantly by avoiding prolonged episodes of tachycardia and repetitive hospital admissions.     

The Role of Catheter Ablation Techniques in the Treatment of Classic (Type 1) Atrial Flutter

Several attempts at circuit interruption of type 1 atrial flutter by means of surgical or catheter techniques have been published. We recently reported the results of a series of patients who underwent catheter fulguration of the low septal right atrium, with a mean follow-up of almost 3 years. True electrophysiological success was observed in 7/14 patients (50%). Clinical success, defined as absence of symptoms, was observed in 8/14 (57%) in this patient population. No serious complications were encountered, but the potential risks of DC shock, and the experience that we gained in right atrial mapping using this approach, led us to reconsider the role of atrial DC ablation in these patients. Additional studies assessing the meaning of fragmented electrograms, and identification of one for of severall slow conduction areas of the reentrant circuit are ongoing.     

Relation Between Left Atrial Size and Secondary Atrial Arrhythmias After Successful Catheter Ablation of Common Atrial Flutter

Catheter ablation ptovides an effective cure for patients with typical atrial flutter. However, these patients may have the potential to develop atrial tachyarrhythmias other than common atrial flutter. This study examines clinical and echocardiographic predictors for the occurrence of uncommon atrial flutter or atrial fibrillation after abolition of common atrial flutter. The study population comprised 17 patients (12 men, 5 women, age 32–74 years) who underwent successful radiofrequency catheter ablation of common atrial flutter. Common atrial flutter did not recur in any patient during a median follow-up time of 8 (range 1–25) months. Within a median of 7 (range 1–223) days, however, symptomatic atrial tachyarrhythmias occurred in 8 of 17 patients (47%): uncommon atrial flutter (n = 4); atrial fibrillation (n = 3); and both uncommon atrial flutter and atrial fibrillation in one patient. Preablation left atrial volume was significantly larger in patients who developed secondary arrhythmias compared with patients who remained in sinus rhythm (57.9 ± 15.6 vs 43.7 ± 16.4 cm³, P < 0.05). Enlarged left atrial volume dichotomized at 51 cm³ independently predicted postablation atrial arrhythmias (x²=5.11, rel. risk = 5.3, P < 0.05). On Kaplan-Meier analysis, time to occurrence of postablation atrial arrhythmias was significantly shorter in patietits with enlarged left atrium (P < 0.02). In conclusion, symptomatic uncommon atrial flutter and atrial fibrillation develops in a substantial proportion of patients after successful ablation of common atrial flutter. Out of a series of clinical and echocardiographic parameters, preablation left atrial size is the best predictor for the occurrence of these postablation atrial arrhythmias.     

Neurohumoral and Hemodynamic Mechanisms of Diuresis During Atrioventricular Nodal Reentrant Tachycardia

Thirty-two consecutive patients with paroxysmal supraventricular tachycardias, with previously defined mechanisms of the tachycardias, were interviewed by noninvestigators about whether they experienced symptoms of diuresis during or at the termination of the tachycardias, to test the hypothesis that patients with AV nodal reentrant tachycardia would have a feeling of diuresis, polyuria, or both during or at the termination of the tachycardia. Twelve of the 13 patients with AV nodal reentrant tachycardia (92%), two of the 15 patients with AV reentrant tachycardia (13%), and one of the 4 patients with atrial flutter associated with 2:1 AV conduction (25%) felt diuresis during or at the termination of the tachycardias (AV nodal reentrant tachycardia vs other forms of tachycardia; P < 0.001). In 14 of the 32 patients, the right atrial pressure and plasma atrial natriuretic peptide (ANP) concentration were measured during both the tachycardias and sinus rhythm. The mean right atrial pressure during AV nodal reentrant tachycardia was significantly elevated compared to that during other forms of tachycardia (P < 0.01). The plasma ANP concentration during AV nodal reentrant tachycardia was also elevated significantly compared to that during other forms of tachycardias (P < O.OO1). There were no significant differences in the cycle lengths of the tachycardias, age, left atrial dimensions, or the left ventricular ejection fraction between the AV nodal reentrant tachycardia and the other forms of tachycardia. We concluded that the feeling of diuresis during or at the termination of tachycardia was a more common symptom in patients with AV nodal reentrant tachycardia. The higher secretion of plasma ANP from the right atrium might be involved in the mechanism of this symptom.     

Uncommon Atrial Flutter: Characteristics, Mechanisms, and Results of Ablative Therapy

Thirty-seven patients with atrial flutter were studied with catheter mapping and radiofrequency ablation. Uncommon atrial flutter occurred in 20 out of 37 (54%) patients. Atrial endocardial mapping showed two types of uncommon atrial flutter. In 15 patients (group I) it was characterized by a single clockwise circuit whereas in 5 patients (Group II) it was characterized by the presence of more than one circuit and/or localized atrial fibrillation. RFA ablation was acutely successful in 14 out of 15 patients (93%) in Group I and in 2 oat of 5 (40%) patients in Group II. On long-term follow-up a significantly larger number of patients in Group I versus Group II (86% vs 20%) remained free of atrial flutter recurrence. We conclude that uncommon atrial flutter is a heterogeneous entity involving one or more reentrant circuits. Uncommon atrial flutter with multiple circuits may not be suitable for RFA.     

Atrial Vulnerability and Electrophysiology Determined in Patients With and Without Paroxysmal Atrial Fibrillation

For elucidation of atrial electrophysiology and vulnerability an electrophysiological study was performed in 45 patients with documented paroxysmal atrial fibrillation and a control group (n = 46). Atrial vulnerability was assessed by programmed atrial stimulation with up to two extrastimuli during sinus rhythm and paced cycle lengths of 600 msec, 430 msec and 330 msec. Sustained atrial fibrillation or flutter was induced in 37/45 patients with paroxysmal atrial fibrillation in contrast to 9/46 patients in the control group (P less than 0.001). Left atrial diameter (M-mode echocardiogram), P wave duration, sinus cycle length, sinus node recovery time, and the effective refractory period of the right atrium were not significantly different between the two study groups. Intraatrial conduction time from the high right atrium (HRA) to the basal right atrium (A) and the functional refractory period of the right atrium were significantly longer in patients with paroxysmal atrial fibrillation.     

Change in atrial flutter wave morphology-insight into the sources of electrocardiographic variants in common atrial flutter

Whether the activation sequence of the right or left atrium plays a role in the morphology of the flutter wave in common atrial flutter is not completely understood. We present two patients with common counterclockwise atrial flutter in whom changes in the left atrial activation sequence produced significant changes in flutter wave polarity (+ to - and - to -/+ biphasic) without a change in the activation sequence within the right atrium. These cases highlight the possible role of alterations of the interatrial connections in the genesis of atypical manifestations of common atrial flutter.     

Electrophysiological mechanisms and catheter ablation of complex atrial arrhythmias from crista terminalis:

Paroxysmal atrial fibrillation (PAF) can be initiated by ectopic activation from the crista terminalis. The crista terminalis conduction gap is also a critical isthmus in atrial reentrant arrhythmias like upper and lower loop reentry. The aim of this study was to investigate the mechanism and results of catheter ablation for complex atrial arrhythmias originating from the crista terminalis using the noncontact mapping system (NCM). The study population consisted of six patients (5 men, 1 woman; 70 +/- 9 years) with drug refractory PAF and typical/atypical atrial flutter. NCM identified the earliest ectopic activation originating from the crista terminalis in these six patients. The reentry circuit of atypical atrial flutter propagated around the upper crista terminalis in five patients, and lower crista terminalis in one patient. The reentry circuit of atypical atrial flutter and the initial reentry circuit of AF conducted through the crista terminalis gap in all patients. Radiofrequency applications were delivered on the sites of ectopy, which initiated AF. Substrate modification was also performed over the crista terminalis gap (six patients) and cavotricuspid isthmus (three patients) responsible for the reentry. During a mean follow-up of 9 +/- 5 months (range 5-18 months), five patients were free of AF without antiarrhythmic drugs, and one patient did not have AF or atrial flutter using propafenone. NCM demonstrated the mechanism of crista terminalis ectopy-initiating AF and associated typical/atypical atrial flutter. Catheter ablation of crista terminalis ectopy and substrate for the reentry guided by NCM successfully eliminated these atrial arrhythmias.     

致心律失常性右室心肌病心房重塑及其临床特征分析

目的：致心律失常性右室心肌病（ARVC）是一种少见的遗传性器质性心肌病,既往认为ARVC主要累及左右心室,对心房重塑的影响尚不明确。本横断面研究旨在明确ARVC中心房重塑的发生率及临床特征。方法：本研究纳入2016-2020年我院诊断明确的ARVC患者40例,详细收集所有患者临床资料、心超结果,其中17例患者完善了心脏磁共振检查。分析患者心超及心脏磁共振相关心室、心房功能和结构参数。结果：本研究发现26例发生了右房增大(65%),15例发生了左房增大(37.5%),14例发生了双房增大(35%)。其中6例患者发生了房颤(15%),2例发生了房扑(5%)。心房重塑在ARVC患者中较为常见,心房重塑的ARVC患者房性心律失常事件发生率显著增加。右心房重塑常常伴随右心室扩张、心脏功能不全,右心室心外膜脂肪及MACE事件增加。结论：本研究提示ARVC不仅累及左右心室,对左右心房亦有影响,心房重塑可能作为ARVC的重要病理环节参与ARVC的进展及预后。     

The Upper Link of Human Common Atrial Flutter Circuit Definition by Multiple Endocardial Recordings during Entrainment

Common atrial flutter is due to a macroreentry circuit in the right atrium, but the cranial path of the circuit has not been defined. The objectives of this article are to determine the cranial turning point of flutter activation in relation to a hypothetic obstacle, the superior vena cava opening, by examining the changes in activation sequence produced by entrainment from different points. In 13 cases of common atrial flutter with typical counter-clockwise right atrial circuits confirmed by endocardial mapping the atrium was paced from the high posterior and mid-septal walls. Entrainment was confirmed by simultaneous recordings of 6–7 right atrial electrograms. Changes in sequence of electrograms from high septum and high anterolateral walls was sought. Electrogram sequence and morphology did not change with entrainment at the posterior wall with respect to the basal flutter or mid-septal wall entrainment. Pacing "below" the superior vena cava did not advance the anterior wall electrogram in relation to the septal electrogram. These findings suppport the concept that common Putter activation turned around (cranial and anterior to) the superior vena cava opening, and not around the free end of a line of block below the superior vena cava in the posterior wall. Common atrial flutter activation rotates cranial (and anterior) to the superior vena cava opening, through the "right atrial roof" The line of functional block should span from inferior to superior vena cava openings.     

A Clinical Study of the Application of Endocardial Fulguration in the Treatment of Recurrent Atrial Flutter

Endocardial catheter fulguration has been recently proposed for treatment of arrhythmias originating within the right atrium. In this study the authors attempted to use this technique in eight patients with paroxysmal common atrial gutter. Numerous antiarrhythmic agents failed to prevent recurrences of the episodes, which occurred frequently over periods of at least 4 months. In every procedure, we used a 7F quadripolar catheter electrode introduced via the subclavian vein into the lower part of the right atrium. The two distal electrodes allowed the recording of bipolar double potentials where the critical slow pathway of the reentrant circuit was localized. A unipolar electrogram recording by the tip electrode gave us the location of the area to be ablated when this electrogram was in complete concordance with a small step in the descending part of the F waves in II, III and aVF. This step corresponded to the very depolarization of the reentry area. A DC shock of 100 to 120 J was delivered between the tip electrode and a paddle applied to the left chest wall. Sinus rhythm resumed instantaneously. No mechanical or electrical complications were noted. Three patients are free of relapses without antiarrhythmic drugs (follow-up: 14 to 17 months); three others are also free of relapses, but antiarrhythmic agents were required for treatment of other supraventricular dysrhythmias (follow-up: 3 to 17 months); atrial flutter recurred within several days and persisted in spite of two more procedures in two patients. We conclude that endocardial catheter fulguration of paroxysmal and recurrent atrial flutter seems to be effective therapy. Nevertheless, more experience is required in order to confirm these results.     

Inappropriate detection of supraventricular arrhythmias by implantable dual chamber defibrillators: a comparison of four different algorithms

Inappropriate therapy of supraventricular tachyarrhythmias by an ICD is still a common problem. Dual chamber (DDD) ICDs provide additional atrial sensing and should result in higher specificity for detection of supraventricular tachyarrhythmias. However, a direct comparison of different dual chamber algorithms has not been reported. The detection algorithms of four different DDD ICDs were tested: Phylax AV, Defender IV, Ventak AV III DR, and Gem DR 7271. Based on arrhythmias recorded from patients undergoing invasive electrophysiological studies and in many cases of catheter ablation at our institution, a library consisting of 71 supraventricular and 15 ventricular tachyarrhythmias was created. The library consists of episodes of atrial fibrillation, atrial flutter with different AV conduction, typical and atypical AV nodal reentrant tachycardia, AV reentrant tachycardia, sinus tachycardia, and ventricular tachycardia with and without ventriculoatrial conduction. Atrial fibrillation was appropriately classified by all four algorithms. However, the specificity for detection of other supraventricular tachyarrhythmias achieved by the Biotronik (12%) and the Guidant (11%) devices was significantly lower compared to the specificity of the ELA (28%) and the Medtronic DDD ICD (20%). This is due to the fact that the Biotronik and the Guidant algorithm classified all supraventricular tachyarrhythmias resulting in a stable ventricular rate as ventricular tachycardia, whereas the ELA and Medtronic algorithms performed a more detailed analysis by assessment of PR association, atrial onset, or timing of the atrial event relative to the ventricular event, respectively. Atrial fibrillation, the most common supraventricular tachyarrhythmia in patients with ICD, was detected by all devices.     

Tachycardia Recognition and Diagnosis from Changes in Right Atrial Pressure Waveform—A Feasibility Study

Implantable defibrillators either monitor heart rate or use a probability density function to detect ventricular fibrillation/tachycardia. As a result, they are unable to discriminate sinus tachycardia and atrial arrhythmias from malignant ventricular rhythms. We have assessed high fidelity fiber-optic pressure recordings in the right atrium during cardiac arrhythmias in 23 patients (mean age 44 years, 11 females) undergoing electrophysiological study. The unfiltered pressure signal was amplified and recorded on paper. During sinus rhythm, a constant amplitude deflection occurred during atrial systole (a wave). A characteristic waveform pattern was observed during each of the studied tachyarrhythmias, which included atrial flutter and fibrillation, atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and ventricular tachycardia with and without ventriculoatrial conduction. The waveform pattern allowed clear visual discrimination of the underlying arrhythmia. Mean atrial pressure was increased during all arrhythmias and did not allow discrimination of the nature of the tachycardia. High fidelity pressure recordings produced characteristic appearances for pattern recognition of each arrhythmia studied. They allowed determination of the temporal relation between electrical and mechanical cardiac events and may have potential in the detection and recognition of cardiac arrhythmias.     

Atrial Flutter Mapping and Ablation I

Endocardial mapping has led to a detailed knowledge of reentry mechanisms in atrial flutter. Multipolar and deflecting tip catheters allow recording local electrograms from multiple areas of the right atrium, and from the coronary sinus. In common flutter, with the typical "sawtooth" pattern, there is circular activation of the right atrium in a "counterclockwise" direction, descending in the anterior and lateral walls, and ascending in the septum and posterior wall. Superior and inferior vena cava, linked by a "line" of functional block in the posterolateral wall, make the central obstacle for circular activation. The cranial and caudal turning points are the atrial "roof," and the isthmus between the inferior vena cava and the tricuspid valve. Complex conduction patterns, probably including slow conduction are detectable in the low septal area, around the coronary sinus. Atypical flutter, without the sharp negative deflections of common flutter, sometimes shows circular activation in the right atrium, rotating in the opposite direction of common flutter (clockwise). Other atypical flutters show no circular right atrial activation, and only partial data from coronary sinus activation, combined with the response to atrial stimulation (entrainment) allow the diagnosis of left atrial reentry, without a precise delimitation of the circuits. In patients having undergone cardiac surgery, atypical flutter may be based on reentry around surgical scars. To our knowledge, the mechanism of type II flutter has not been disclosed in humans.