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Atrial Flutter

The Experts below are selected from a list of 297 Experts worldwide ranked by ideXlab platform

Albert L Waldo – 1st expert on this subject based on the ideXlab platform

  • Inter-relationships between Atrial Flutter and Atrial fibrillation.
    Pacing and clinical electrophysiology : PACE, 2020
    Co-Authors: Albert L Waldo

    Abstract:

    It has been appreciated for a long time that Atrial Flutter and Atrial fibrillation have a clinical relationship. Now, with the technological advances that permit more sophisticated electrophysiological studies, especially mapping studies, we have significantly advanced our understanding of this interrelationship. Regarding the relationship at Atrial fibrillation to Atrial Flutter: Atrial fibrillation of variable duration (very brief to prolonged episodes) precedes the onset of Atrial Flutter in most instances. It seems that during the period of Atrial fibrillation, the functional components of the Atrial Flutter reentrant circuit are formed. This is principally a line of block between the venae cavae. If this line of block does not form, classical Atrial Flutter does not form. And if this line of block shortens or disappears, classical Atrial Flutter disappear as well. In fact, it might be said that the major difference in whether classical Atrial Flutter or Atrial fibrillation develops is whether a line of block forms between the venae cavae. Regarding the relationship of Atrial Flutter to Atrial fibrillation: Studies have demonstrated that a driver (a single focus or reentrant circuit of very short cycle length) can be responsible for causing Atrial fibrillation by producing fibrillatory conduction to the rest of the atria. In experimental models and now beginning to be demonstrated in patients, this driver may be a stable reentrant circuit of very short cycle length, i.e., a fast form of Atrial Flutter, if you will. In fact, there is probably a spectrum of these short cycle lengths that depend, in part, on where the reentrant circuit (i.e., “Atrial Flutter“) exists. When the stable reentrant circuit is of sufficiently short cycle length, it will only activate small portions of the atria in a 1 : 1 manner. The rest of the atria will be activated irregularly, resulting in Atrial fibrillation. Unstable reentrant circuits can also do the same thing. In short, it appears that there are several mechanisms of Atrial fibrillation, one of which is due to a form of very rapid Atrial Flutter.

  • The Interrelationship Between Atrial Fibrillation and Atrial Flutter
    Progress in Cardiovascular Diseases, 2005
    Co-Authors: Albert L Waldo

    Abstract:

    Abstract For a long time, it has been known that Atrial fibrillation and Atrial Flutter have a close clinical interrelationship. Recent electrophysiological studies, especially mapping studies, have significantly advanced our understanding of this interrelationship. Regarding the relationship of Atrial fibrillation with Atrial Flutter: Atrial fibrillation of variable duration precedes the onset of Atrial Flutter in almost all instances. During the Atrial fibrillation, the functional components needed to complete the Atrial Flutter reentrant circuit, principally a line of block between the venae cavae, are formed. If this line of block does not form, classical Atrial Flutter does not develop. If this line of block shortens or disappears, classical Atrial Flutter disappears. In fact, it is fair to say that the major determinant of whether Atrial fibrillation persists or classical Atrial Flutter develops is whether a line of block forms between the venae cavae. Regarding the relationship of Atrial Flutter with Atrial fibrillation: Studies in experimental models and now in patients have demonstrated that a driver (a rapidly firing focus or a reentrant circuit of very short cycle length) can cause Atrial fibrillation by producing fibrillatory conduction to the rest of the atria. When the driver is a stable reentrant circuit of very short cycle length, it is, in effect, a very fast form of Atrial Flutter. There probably is a spectrum of reentrant circuits of short cycle length, i.e., “Atrial Flutter,” that depend, in part, on where the reentrant circuit is located. When the cycle length of the reentrant circuit is so short that it will only activate small portions of the atria in a 1:1 manner, the rest of the atria will be activated rapidly but irregularly, i.e., via fibrillatory conduction, resulting in Atrial fibrillation. In short, there are probably several mechanisms of Atrial fibrillation, one of which is due to a very rapid Atrial Flutter circuit causing fibrillatory conduction. In sum, Atrial fibrillation and Atrial Flutter have an important interrelationship.

  • Inter-relationships between Atrial Flutter and Atrial fibrillation
    Pacing and Clinical Electrophysiology, 2003
    Co-Authors: Albert L Waldo

    Abstract:

    WALDO, A.L.: Inter-Relationships Between Atrial Flutter and Atrial Fibrillation. It has been appreciated for a long time that Atrial Flutter and Atrial fibrillation have a clinical relationship. Now, with the technological advances that permit more sophisticated electrophysiological studies, especially mapping studies, we have significantly advanced our understanding of this interrelationship. Regarding the relationship at Atrial fibrillation to Atrial Flutter: Atrial fibrillation of variable duration (very brief to prolonged episodes) precedes the onset of Atrial Flutter in most instances. It seems that during the period of Atrial fibrillation, the functional components of the Atrial Flutter reentrant circuit are formed. This is principally a line of block between the venae cavae. If this line of block does not form, classical Atrial Flutter does not form. And if this line of block shortens or disappears, classical Atrial Flutter disappear as well. In fact, it might be said that the major difference in whether classical Atrial Flutter or Atrial fibrillation develops is whether a line of block forms between the venae cavae. Regarding the relationship of Atrial Flutter to Atrial fibrillation: Studies have demonstrated that a driver (a single focus or reentrant circuit of very short cycle length) can be responsible for causing Atrial fibrillation by producing fibrillatory conduction to the rest of the atria. In experimental models and now beginning to be demonstrated in patients, this driver may be a stable reentrant circuit of very short cycle length, i.e., a fast form of Atrial Flutter, if you will. In fact, there is probably a spectrum of these short cycle lengths that depend, in part, on where the reentrant circuit (i.e., “Atrial Flutter“) exists. When the stable reentrant circuit is of sufficiently short cycle length, it will only activate small portions of the atria in a 1 : 1 manner. The rest of the atria will be activated irregularly, resulting in Atrial fibrillation. Unstable reentrant circuits can also do the same thing. In short, it appears that there are several mechanisms of Atrial fibrillation, one of which is due to a form of very rapid Atrial Flutter.

Hugh Calkins – 2nd expert on this subject based on the ideXlab platform

  • Catheter ablation of Atrial Flutter and macroreentrant Atrial tachycardia
    Current Opinion in Cardiology, 2020
    Co-Authors: Richard Wu, Ronald D. Berger, Hugh Calkins

    Abstract:

    Catheter ablation has evolved from an experimental technique to first-line therapy for the treatment of Atrial Flutter. Atrial Flutter is characterized by a macroreentrant Atrial tachycardia circuit. Successful ablation of Atrial Flutter involves (1) mapping the Atrial Flutter to define the conducti

  • Catheter Ablation of Atrial Flutter and Atrial Fibrillation
    Management of Cardiac Arrhythmias, 2010
    Co-Authors: Joseph E. Marine, Hugh Calkins

    Abstract:

    Atrial Flutter and Atrial fibrillation are two of the most common arrhythmias seen in clinical practice and the most common indications for referral for catheter ablation. While they are historically grouped together, research over the past 20 years has shown that Atrial Flutter and Atrial fibrillation are distinct arrhythmias with different electrophysiological mechanisms. This review will consider the development of and current approach to catheter ablation of Atrial Flutter and Atrial fibrillation.

  • Results of catheter ablation of typical Atrial Flutter
    American Journal of Cardiology, 2004
    Co-Authors: Hugh Calkins, Robert C. Canby, Raul Weiss, Gregg Taylor, Peter Wells, Larry Chinitz, Simon Milstein, Steven Compton, Kimberly Oleson, Lou Sherfesee

    Abstract:

    Abstract The purpose of this study was to evaluate the safety and efficacy of radiofrequency (RF) ablation of typical Atrial Flutter by using an 8-mm electrode catheter and a 100-W RF power generator. A limitation of previous trials of catheter ablation of Atrial Flutter is that the data were not collected as part of a prospective multicenter clinical trial. The study results associated catheter ablation of typical Atrial Flutter in a cohort of 150 patients with an 88% acute efficacy rate. At 6-month follow-up, recurrent typical Atrial Flutter was observed in 13% of patients. Of the 12 patients with typical Atrial Flutter recurrence, 4 were symptomatic and 8 were asymptomatic. Procedure duration was a significant predictor of typical Atrial Flutter recurrence. The 12-month rate for development of Atrial fibrillation was 30%. Catheter ablation of Atrial Flutter was associated with significant improvements in 5 of 8 domains of the Short Form 36 Survey (quality of life) and significant decreases in 13 of the 16 symptoms of the Symptom Checklist. The device- or procedure-related complication rate was 2.7%. Skin burns occurred at the dispersive pad site due to stronger RF power in 3 patients. Use of a dual dispersive pad system mitigated this problem. Thus, the results of this study associated catheter ablation of Atrial Flutter with high acute efficacy, a small risk of recurrent Atrial Flutter, and an important risk of Atrial fibrillation during follow-up.

Brian Olshansky – 3rd expert on this subject based on the ideXlab platform

  • Thromboembolism in chronic Atrial Flutter : Is the risk underestimated?
    Journal of the American College of Cardiology, 1997
    Co-Authors: Charles Lanzarotti, Brian Olshansky

    Abstract:

    Abstract Objectives. We sought to evaluate the risk of thromboembolic events in the presence of chronic Atrial Flutter and to determine the impact of anticoagulation therapy, if any, on this risk. Background. Thromboembolic events are thought to be rare after cardioversion of Atrial Flutter. Methods. This study was a retrospective analysis of 110 consecutive patients referred to the electrophysiology laboratory for cardioversion of chronic Atrial Flutter from 1986 to 1996. Atrial Flutter was present for at least 6 months. Of the 110 patients reviewed, 100 had adequate information available regarding the effectiveness of anticoagulation (mean age 64 years, range 27 to 86; 75 men, 25 women; mean left ventricular ejection fraction 42%). Results. Thirteen patients (13%) had a thromboembolic event. Of these, seven were attributable to causes other than Atrial Flutter. In the remaining six patients (6%), thromboembolic events occurred during a rhythm of Atrial Flutter or after cardioversion to sinus rhythm. Other causes of thromboembolism were excluded. Effective anticoagulation was associated with a decreased risk of thromboembolism (p = 0.026). Conclusions. Patients with chronic Atrial Flutter are at an increased risk of thromboembolic events. Effective anticoagulation may decrease this risk.

  • Atrial Flutter—Update on the Mechanism and Treatment
    Pacing and Clinical Electrophysiology, 1992
    Co-Authors: Brian Olshansky, David J. Wilber, Robert J. Hariman

    Abstract:

    Atrial Flutter is a common and usually benign but symptomatic supraventricular tachycardia. There is a striking similarity between patients with Atrial Flutter suggesting a common substrate despite the presence or absence of underlying heart disease. In man, the mechanism is a single reentrant circuit originating in the right atrium whose center appears to be functional within the anatomical constraints of the right atrium. The reentrant circuit of Atrial Flutter contains an area of slow conduction in the inferior right atrium but the size and exact location is uncertain. Drug therapy directed at terminating and preventing Atrial Flutter has been available for many years. The efficacy and safety of this therapy is not as well tested as is the same therapy for Atrial fibrillation. The most effective way to terminate Atrial Flutter is a nonpharmacological approach. Several nonpharmacological methods provide new treatment options in the management of patients with drug resistant or hemodynamically unstable Atrial Flutter. The use of anticoagularion for this disorder is still evolving. There is a risk of clinically apparent thromboemboli in some patients with Atrial Flutter although the risk appears less than that for utrial fibrillation. In the future, refinements and improvements in therapy for Atrial Flutter will likely be derived from a better understanding of its mechanism.

  • demonstration of an area of slow conduction in Atrial Flutter
    Journal of the American College of Cardiology, 1990
    Co-Authors: Albert L Waldo, Brian Olshansky, Ken Okumura, Paul G Hess

    Abstract:

    Abstract Ten patients with chronic Atrial Flutter were studied prospectively using electrophysiologic mapping and pacing techniques to assess the mechanism of Atrial Flutter and the presence of an area of slow conduction in the atria. Electrograms recorded from ≥30 right Atrial sites for each patient during Atrial Flutter demonstrated that right Atrial free wall activation was craniocaudal and that the interAtrial septum activation was caudocranial, consistent with a reentrant circuit involving the right atrium. In six patients, slow conduction occurred during Atrial Flutter in the inferior right atrium and was spatially associated with fractionated electrographic recordings. In the other four patients, a “missing” interval of electrical activity occurred in the inferior right atrium for an average of 40% of the Atrial Flutter cycle. Transient entrainment criteria were demonstrated in each patient during rapid high right Atrial pacing. The mean activation time from the high right Atrial pacing site to the coronary sinus (inferior left Atrial) recording site was long (228 ms) and consistent with activation through an area of slow conduction. During rapid pacing of Atrial Flutter from the coronary sinus site, no transient entrainment criteria could be demonstrated. The mean activation time from the coronary sinus pacing site to the high right Atrial recording site was relatively short (134 ms) and consistent with orthodromic activation of the high right atrium not through an area of slow conduction. High right Atrial pacing during sinus rhythm at rates similar to Atrial Flutter demonstrated a short activation time to the coronary sinus and low right Atrial sites (mean 169 and 88 ms, respectively), indicating activation that did not traverse an area of slow conduction. Coronary sinus pacing during sinus rhythm demonstrated the same phenomena. Low right Atrial electrograms recorded during sinus rhythm and during rapid pacing of sinus rhythm were not fractionated, although they were during Atrial Flutter. Thus, Atrial mapping and pacing data were complementary, indicating that human Atrial Flutter in the patients studied was generated by a reentrant circuit in the right atrium, with an area of slow conduction in the low right atrium present only during Atrial Flutter.