Mechanism Of Atrial Flutter Research Articles

Transition mechanisms from atrial flutter to atrial fibrillation during anti-tachycardia pacing therapy.

Atrial anti-tachycardia pacing (aATP) has been shown to be effective for the termination of atrial tachyarrhythmias, but its success rate is still not high enough. The main objective of this study was to investigate the mechanisms of atrial flutter (AFL) termination by aATP and the transition from AFL to atrial fibrillation (AF) during aATP. We developed a multi-scale model of the human atrium based on magnetic resonance images and examined the atrial electrophysiology of AFL during aATP with a ramp protocol. In successful cases of aATP, paced excitation entered the excitable gap and collided with the leading edge of the reentrant wave front. Furthermore, the excitation propagating in the opposite direction collided with the trailing edge of the reentrant wave to terminate AFL. The second collision was made possible by the distribution of the wave propagation velocity in the atria. The detailed analysis revealed that the slowing of propagation velocity occurred at the exit of the sub-Eustachian isthmus, probably due to source-sink mismatch. During the transition from AFL to AF, the excitation collided with the refractory zone of the preceding wave and broke into multiple wave fronts to induce AF. A similar observation was made for the transition from AF to sinus rhythm. In both cases, the complex anatomy of the atria played an essential role. The complex anatomy of atria plays an essential role in the maintenance of stable AFL and its termination by aATP, which were revealed by the realistic three-dimensional simulation model.

Supervised Machine Learning Based Noninvasive Prediction of Atrial Flutter Mechanism from P-to-P Interval Variability under Imbalanced Dataset Conditions.

Atrial flutter (AFL) is a common arrhythmia with two significant mechanisms, namely, focal (FAFL) and macroreentry (MAFL). Discrimination of the AFL mechanism through noninvasive techniques can improve radiofrequency ablation efficacy. This study aims to differentiate the AFL mechanism using a 12-lead surface electrocardiogram. P-P interval series variability is hypothesized to be different in FAFL and MAFL and may be useful for discrimination. 12-lead ECG signals were collected from 46 patients with known AFL mechanisms. Features for a proposed classifier are extracted through descriptive statistics of the interval series. On the other hand, the class ratio of MAFL and FAFL was 41 : 5, respectively, which was highly imbalanced. To resolve this, different data augmentation techniques (SMOTE, modified-SMOTE, and smoothed-bootstrap) have been applied on the interval series to generate synthetic interval series and minimize imbalance. Modification is introduced in the classic SMOTE technique (modified-SMOTE) to properly produce data samples from the original distribution. The characteristics of modified-SMOTE are found closer to the original dataset than the other two techniques based on the four validation criteria. The performance of the proposed model has been evaluated by three linear classifiers, namely, linear discriminant analysis (LDA), logistic regression (LOG), and support vector machine (SVM). Filter and wrapper methods have been used for selecting relevant features. The best average performance was achieved at 400% augmentation of the FAFL interval series (90.24% sensitivity, 49.50% specificity, and 76.88% accuracy) in the LOG classifier. The variation of consecutive P-wave intervals has been shown as an effective concept that differentiates FAFL from MAFL through the 12-lead surface ECG.

Paradoxical delayed capture proved the dual-loop tachycardia mechanism of a cavotricuspid isthmus-dependent atrial flutter

A 37-year-old man underwent catheter ablation for a cavotricuspid isthmus-dependent atrial flutter. Two 20-pole deflectable electrode catheters were placed in a parallel position on the tricuspid annulus and right atrial lateral wall. The dual-loop tachycardia mechanism of the atrial flutter was suggested by paradoxical delayed capture of the lateral wall of the right atrium during entrainment pacing from the lateral tricuspid annulus.

Atrial Flutter Mechanism Detection Using Directed Network Mapping.

Atrial flutter (AFL) is a common atrial arrhythmia typically characterized by electrical activity propagating around specific anatomical regions. It is usually treated with catheter ablation. However, the identification of rotational activities is not straightforward, and requires an intense effort during the first phase of the electrophysiological (EP) study, i.e., the mapping phase, in which an anatomical 3D model is built and electrograms (EGMs) are recorded. In this study, we modeled the electrical propagation pattern of AFL (measured during mapping) using network theory (NT), a well-known field of research from the computer science domain. The main advantage of NT is the large number of available algorithms that can efficiently analyze the network. Using directed network mapping, we employed a cycle-finding algorithm to detect all cycles in the network, resembling the main propagation pattern of AFL. The method was tested on two subjects in sinus rhythm, six in an experimental model of in-silico simulations, and 10 subjects diagnosed with AFL who underwent a catheter ablation. The algorithm correctly detected the electrical propagation of both sinus rhythm cases and in-silico simulations. Regarding the AFL cases, arrhythmia mechanisms were either totally or partially identified in most of the cases (8 out of 10), i.e., cycles around the mitral valve, tricuspid valve and figure-of-eight reentries. The other two cases presented a poor mapping quality or a major complexity related to previous ablations, large areas of fibrotic tissue, etc. Directed network mapping represents an innovative tool that showed promising results in identifying AFL mechanisms in an automatic fashion. Further investigations are needed to assess the reliability of the method in different clinical scenarios.

Non-Invasive Characterization of Atrial Flutter Mechanisms Using Recurrence Quantification Analysis on the ECG: A Computational Study.

Atrial flutter (AFl) is a common arrhythmia that can be categorized according to different self-sustained electrophysiological mechanisms. The non-invasive discrimination of such mechanisms would greatly benefit ablative methods for AFl therapy as the driving mechanisms would be described prior to the invasive procedure, helping to guide ablation. In the present work, we sought to implement recurrence quantification analysis (RQA) on 12-lead ECG signals from a computational framework to discriminate different electrophysiological mechanisms sustaining AFl. 20 different AFl mechanisms were generated in 8 atrial models and were propagated into 8 torso models via forward solution, resulting in 1,256 sets of 12-lead ECG signals. Principal component analysis was applied on the 12-lead ECGs, and six RQA-based features were extracted from the most significant principal component scores in two different approaches: individual component RQA and spatial reduced RQA. In both approaches, RQA-based features were significantly sensitive to the dynamic structures underlying different AFl mechanisms. Hit rate as high as 67.7% was achieved when discriminating the 20 AFl mechanisms. RQA-based features estimated for a clinical sample suggested high agreement with the results found in the computational framework. RQA has been shown an effective method to distinguish different AFl electrophysiological mechanisms in a non-invasive computational framework. A clinical 12-lead ECG used as proof of concept showed the value of both the simulations and the methods. The non-invasive discrimination of AFl mechanisms helps to delineate the ablation strategy, reducing time and resources required to conduct invasive cardiac mapping and ablation procedures.

Neonatal Atrial Flutter: Adenosine Dilemma

Background: Atrial flutter (AFl) is a rare type of neonatal tachyarrhythmia, which is recognized by saw-tooth waves on electrocardiogram (ECG), and an atrial rate of up to 500 beats/minute. The mechanism of AFl is sustained by a macro-reentrant circuit pathway which is limited to the atrial wall, however the atrioventricular (AV) node is not involved of the reentrant circuit. Case Presentation: A 2-day-old, full term, male infant was born to a hypertensive mother, by cesarean section, presented to the pediatric emergency department at Maternity and Children hospital with history of cyanosis and decrease oral intake. At the physical examination, both tachypnea (70/min) and tachycardia (218/bpm) were determined. An electrocardiogram confirmed atrial flutter with 3:1 atrioventricular conduction. AFl didn’t respond to adenosine administration, therefore, electrical cardioversion was required. After conversion to normal sinus rhythm, amiodarone and propranolol therapy were started to maintain sinus rhythm afterward. With no further incidence of AFl or other arrhythmias, the infant was discharged at 9th day of life and in good general state with propranolol therapy, and was followed in the cardiac clinic. Conclusion: Electrical cardioversion with energy of (0.5-1 J/Kg) proved to be the most effective in establishing sinus rhythm, and is safe for neonatal patients. Adenosine doesn’t treat tachycardia of atrial origin, such as AFl. However, adenosine administration may help in identifying AFl, demonstrating the arrhythmia-characteristic saw-tooth waves in the ECG.

Abstract 15958: Comparison of In-hospital Outcomes of Patients Undergoing Catheter Ablation for Typical versus Atypical Atrial Flutter

Introduction: Catheter Ablation (CA) is indicated as definitive therapy for patients with atrial flutter (AF) which is unresponsive to medical therapy. While atrial flutter may be typical (TAF) or atypical (AAF), there is a paucity of data regarding in-hospital outcomes of patients undergoing CA. Methods: This retrospective cohort study used the Nationwide Inpatient Sample to identify all patients above 18 years who underwent CA between 2015 and 2017. Individuals were identified using ICD-10-CM/PCS for TAF, AAF and CA. Statistical analysis was performed comparing TAF to AAF. Results: A total of 17,390 patients underwent CA for AF, with 33% having AAF and 67% TAF. Patients with TAF were younger (median 67 years vs. 68 years), with lower proportion of females (29.6% vs. 42.8% p≤0.05 for both) compared to patients with AAF. TAF group had higher rates of emergent admission (85.7% vs. 65.5% p≤0.05). Interestingly, subjects with AAF had earlier interventions than patients with TAF (≤3 days of admission, 76.4% vs. 71% p≤0.05). Patients with TAF have a higher rate of hypertension, diabetes, smoking, heart failure, liver disease, and chronic obstructive pulmonary disease (p≤0.05 for all). However, patients with AAF had increased prior strokes and percutaneous coronary interventions (PCI) (p≤0.05 for both). The mean CHA2DS2-VASc score was found to be 2.3 in AAF compared to 2.1 in TAF (controlled for comorbidities, p≤0.05). Multivariable regression showed a significantly higher proportion of cardiogenic shock, acute coronary syndrome, sepsis, cardiac catheterization, PCI, thromboembolism event, transfusion, and longer length of stay in patients with TAF (p≤0.05 for all). Although we found that patients with AAF have significant higher rates of cardioversion, implantation of cardiac device, pericardial complications, and increased hospital charges (p≤0.05 for all), no significant difference was found in mortality. Conclusion: In this retrospective cohort study, we found higher complication rates in CA of patients with TAF, even when adjusting for pertinent comorbidities, but no difference in in-hospital all-cause mortality. Variation in CA depending upon the mechanism of AF may underlie these differences, and warrant further study.

Atrial flutter: more than just one of a kind.

Since its first description about one century ago, our understanding of atrial flutter (AFL) circuits has considerably evolved. One AFL circuit can have variable electrocardiographic (ECG) manifestations depending on the presence of pre-existing atrial lesions, or impaired atrial substrate. Conversely, different (right sided or even left sided) atrial circuits including different mechanisms (macroreentrant, microreentrant, or focal) can present with a very similar surface ECG manifestation. The development of efficient high-resolution electroanatomical mapping systems has improved our knowledge about AFL mechanisms, as well as facilitated their curative treatment with radiofrequency catheter ablation. This article will review ECG features for typical and atypical flutters, and emphasize the limitations for circuit location from the surface ECG.

Mechanisms of atrial flutter following epicardial high intensity focused ultrasound left atrial ablative procedures during concomitant cardiac surgery

Abstract Introduction Iatrogenic atrial tachyarrhythmias have increased with the widespread application of left atrial ablative procedures to treat atrial fibrillation. Methods and results Entrainment and activation mapping were utilized to study the mechanisms of atrial flutter in two patients who presented with atypical atrial flutter after high intensity focused ultrasound (HIFU) atrial ablation for persistent atrial fibrillation during the course of concomitant cardiac surgery. Case 1: Atrial flutter with CL of 340 ms was demonstrated to be mediated by entry into and exit from the partially isolated posterior left atrium (LA) with conduction delay across at least one of the connections. The exit site was near the left superior pulmonary vein (LSPV) and the entrance site was near the right inferior pulmonary vein (RIPV) as demonstrated by activation and entrainment mapping. Case 2: Entrainment mapping was highly suggestive of inferior exit from the HIFU ablation line between the two inferior pulmonary veins. Flutter terminated during trans-septal procedure and could not be re-induced. Activation mapping of the LA during pacing revealed the inferior exit and left superior entrance site, both of which were successfully ablated, isolating the posterior LA. Conclusions Re-entrant atrial flutter post-HIFU epicor Maze is caused by slow conduction at entry and exit sites from the otherwise isolated posterior LA wall. In both cases, gaps were found close to the LSPV and RIPV which may reflect difficulty in achieving proper contact between the HIFU device and the left atrial wall at these sites. These gaps are amenable to catheter ablation.

GW24-e2233 Mapping, verification and ablation of the recurrence left atrial polycyclic reentry atrial flutter after ablation of persistent atrial fibrillation

ObjectivesIntroduce the method of mapping, verification and ablation the recurrence left atrial polycyclic reentry atrial flutter (AFL) after ablation of persistent atrial fibrillation (PsAF).Methods14 patients (9 men) with left atrial...

Isthmus-dependent right atrial flutter as the leading cause of atrial tachycardias after surgical atrial septal defect repair

The purpose of this study was to evaluate clinical and electrophysiologic characteristics of AT in patients after surgical ASD repair as well as outcome after ablation. Atrial tachycardias (AT) are a common complication after surgical closure of an atrial septal defect (ASD). From a prospective ablation database we analyzed data of patients with a history of ASD repair who presented to our institution for AT ablation. We investigated ECG characteristics and the electrophysiologic mechanism of AT in this collective and analyzed follow-up data. Data of 54 patients (47.3 ± 14.5 years, 35 females) were included. In 30 patients (55.6%) ASD had been closed by direct suture, 24 patients (44.4%) had a patch for ASD repair without significant difference in terms of gender and age at the time of the procedure (p=0.234, p=0.231). In 42 patients (77.8%), electrophysiological studies were performed in AT. All patients had right atrial macro-reentrant AT. The leading mechanism was isthmus-dependent right atrial flutter in 29 patients (69.0%) with clockwise atrial activation in 41%. The mechanism of AT (typical atrial flutter (n=29), atriotomy-dependent flutter (n=7), and double loop flutter (n=5)) did not differ with regard to type of surgery. Only 70.6% of patients with proven isthmus dependent counter-clockwise atrial flutter presented with an ECG morphology typical for this mechanism. However, all clockwise typical atrial flutter patients showed the characteristic positive P-waves in the inferior leads. Of note, 83.3% of clockwise typical flutter ECGs had long isoelectric lines (mean 74.5 ms). Follow-up was complete in 45 of 54 patients. During a mean follow-up of 7.7 ± 3.7 years, 27 patients (60%) remained free of any arrhythmia, two patients had AT recurrence with different mechanisms compared to the first procedure and underwent successful ablation. Five patients (11%) developed atrial fibrillation. Isthmus dependent right atrial flutter is the leading AT mechanism in patients with a history of ASD repair. The mechanism of atrial flutter did not differ in relation to the mode of ASD closure (direct suture versus patch closure). ECG characteristics of the tachycardia may be misleading as they are more often atypical in patients after ASD repair.

Prediction of Atrial Flutter Mechanisms Following Pulmonary Vein Isolation from the Surface Electrocardiogram

Prediction of Atrial Flutter Mechanisms Following Pulmonary Vein Isolation from the Surface Electrocardiogram

Atrial Flutter after Heart Transplantation: Mechanism and Catheter Ablation

Background Atrial flutter is a frequent arrhythmia after heart transplantation, but little is known about its mechanism and treatment. We report the results of an electrophysiologic study in patients with atrial flutter after orthotopic heart transplantation, describing its mechanism and demonstrating the acute and long-term efficacy of catheter ablation for treating this arrhythmia. Methods We included 14 patients with symptomatic atrial flutter after orthotopic heart transplantation. All of them underwent an electrophysiologic study to determine the mechanism of the arrhythmia and catheter ablation when possible. Results Counterclockwise right atrial circuit around the tricuspid annulus involving the cavotricuspid isthmus was demonstrated in 13 patients (86%). Catheter ablation of the isthmus was performed with good acute results in all but 1. During a mean follow-up of 24 ± 17 months, recurrent atrial flutter was documented in 3 patients and atrial fibrillation in 2. In another patient, we demonstrated a left atrial origin. Conclusions The most common mechanism of atrial flutter in heart transplant recipients is a counterclockwise circuit around the tricuspid annulus involving the cavotricuspid isthmus. Catheter ablation of the isthmus between tricuspid annulus and posterior atrial suture line represents an effective treatment in these patients. This condition may be avoided by changing the surgical technique to a bicaval anastomosis.

Atrial Fibrillation–Atrial Flutter Interactions

An appreciation of the article by Moreira et al in the current issue of Circulation 1 requires an understanding of the close interrelationship between atrial fibrillation (AF) and atrial flutter (AFL). These authors have understood this interrelationship and applied it to their data to advance the approach to both AF and AFL ablation. Key to this understanding is the recognition that cavotricuspid isthmus (CTI)–dependent AFL almost always develops from antecedent AF of variable duration.2–5 This is because in almost all instances, it is during the AF that a functional line of block (LoB) necessary for the development of AFL forms between the superior and inferior vena cavae. This LoB acts as a critical lateral boundary that prevents short-circuiting of the AFL reentrant circuit. Thus, in the vast majority of instances, without preceding AF, there can be no AFL. The most recent additional support of this concept comes from the report by Ellis et al,6 which found that of 363 patients who presented with only CTI-dependent AFL and who underwent CTI ablation, long-term follow-up (mean of 39±11 months) demonstrated newly recognized AF in 82%. It also should be noted that, as Moreira et al1 recognize, in some patients, a LoB between the vena cavae may be fixed (ie, anatomic) rather than functional. In such patients, AF may not be required for AFL to develop. Article p 2786 As Moreira et al1 further recognize, their report does not answer all the questions about the interrelationships of AF and AFL as they relate to AF ablation, …

Mechanism of Atrial Flutter Occurring Late After Orthotopic Heart Transplantation with Atrio‐atrial Anastomosis

We sought to better define the electrophysiologic mechanism of atrial flutter in patients after heart transplantation. 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. 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. 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. 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.

Atrial flutter vector loops derived from the surface ECG: does the plane of the loop correspond anatomically to the macroreentrant circuit?

We hypothesized that if the right atrial circuit during isthmus dependent atrial flutter provides the dominant contribution to the surface electrocardiogram (ECG), the three-dimensional vector loop of the flutter waves would primarily be in a plane approximately parallel to the tricuspid ring. Twenty vectorcardiograms of isthmus dependent atrial flutter derived from 12-lead ECGs of 19 patients recorded prior to radiofrequency ablation were analyzed. The plane of each loop, described by azimuth and elevation angles relative to the frontal plane, was estimated with two methods: 1) plane of maximum loop area and 2) plane of best fit. The plane of maximum loop of the loops had mean azimuth of −58 ± 37°. and elevation of 15 ± 15°. The plane of best fit of the loops had mean azimuth of −50 ± 46° and elevation of 15 ± 14°. Thus, clinical implications include the potential to predict atrial flutter mechanisms prior to intracardiac mapping.

Mechanisms of atrial flutter and atrial fibrillation: distinct entities or two sides of a coin?

Time for primary review 23 days. There has been a long recognized clinical interrelationship between atrial flutter and atrial fibrillation. Patients who primarily manifest atrial flutter commonly also experience atrial fibrillation and vice versa [1,2]. Both are very common as a temporary atrial tachyarrhythmia shortly after open heart surgery, and often in the same patient [3]. And some antiarrhythmic agents, notably class IC drugs, IA drugs and amiodarone, used to suppress atrial fibrillation not uncommonly ‘convert’ recurrences of atrial tachyarrhythmia to atrial flutter [4–6]. Are these clinical associations mere coincidences, or do they reflect an important underlying similar pathophysiology and even similar mechanism(s)? Data derived largely from a series of unconnected studies in animal models and patients seemingly point to a clear interrelationship between the two, suggesting, if not indicating, that they are two sides of a coin. Classical atrial flutter, now called typical and reverse typical atrial flutter [7], is well recognized to be due to a macro-reentrant mechanism, in which the reentrant wave front travels up the inter-atrial septum and down the right atrial free wall or vice versa, respectively [1,7]. Critical to the development and maintenance of this reentrant circuit are the lateral boundaries, one being fixed (anatomic), the tricuspid valve annulus, and the other almost always being functional, a line of block between the venae cavae. We shall develop the theme that one of the fundamental features that determines whether an atrial tachyarrhythmia becomes sustained atrial flutter or atrial fibrillation is the development of the line of block between the venae cavae. We shall also develop the theme that another of the fundamental features that determine whether the atrial tachyarrhythmia becomes atrial flutter or atrial fibrillation often will be the atrial flutter cycle length, i.e. the cycle length of a stable … * Tel.: +1-216-844-7690; fax: +1-216-844-7196 alw2{at}po.cwru.edu

Noncontact mapping-guided ablation of atrial flutter and enhanced-density mapping of the inferior vena caval-tricuspid annulus isthmus.

Three-dimensional visualization of cardiac activation has become important in providing further insights into pathophysiological mechanisms of arrhythmias and to increase the efficacy of catheter ablation. The noncontact mapping enables a single beat analysis in a reconstructed geometry of the cardiac chamber. The aim of the study was to describe three-dimensional activation patterns and inferior vena caval-tricuspid annulus (IVC-TA) isthmus conduction characteristics in patients with atrial flutter and the noncontact guidance of the radiofrequency ablation of this arrhythmia. In 34 patients with atrial flutter, the noncontact probe was deployed in the RA. The global three-dimensional activation and the isthmus conduction (enhanced density mapping) were delineated during ongoing a trial flutter and paced rhythms. Ablation was performed nonfluoroscopically based on reconstructed anatomy and conduction patterns. Noncontact mapping was compared and validated with conventional multielectrode technique. IVC-TA isthmus ablation was completed successfully in 33 (97%) of 34 patients. In one patient a lower loop reentry around the inferior vena cava was depicted as a mechanism of atrial flutter. In another patient with positive flutter waves in inferior leads, an activation pattern typical of counterclockwise flutter was demonstrated in propagation maps. During a follow-up of 15.9 +/- 5.9 months, two atrial flutter recurrences occurred (5.8%). A gap of the resumed conduction through the IVC-TA isthmus was delineated as a mechanism of recurrence and ablated with one and three radiofrequency applications. Noncontact mapping allows construction of the global activation patterns in typical and atypical atrial flutter. It enables the nonfluoroscopic guidance of atrial flutter ablation and a comprehensive evaluation of the ablation results.

Historical backround of mechanism of atrial flutter and fibrillation

Historical backround of mechanism of atrial flutter and fibrillation

Atrial flutter: historical background.

For five decades, the mechanism of atrial flutter remained controversial, with protagonists and antagonists of circus movement versus ectopic focus theories. The development of clinical electrophysiology in the 1970s and the observations made by many authors in various canine heart models supported the concept of atrial flutter as a reentrant wave confined to the right atrium. It was established that, in the common type of atrial flutter, the activation wavefront proceeds in a cranial direction over the right atrial septum and descends on the right atrial free wall in the caudal direction. A zone of slow conduction was identified inferiorly and posteriorly in the right atrium, target of the modern ablative techniques. The history of atrial flutter clearly illustrates the bidirectional flow of information and the mutual stimulation between the basic and the clinical levels, leading both to a better understanding of the nature of the arrhythmia and to new therapeutic approaches.