15,349 research outputs found

    Electrophysiological Mechanisms of Atrial Flutter

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    Atrial flutter (AFL) is a common arrhythmia in clinical practice. Several experimental models such as tricuspid regurgitation model, tricuspid ring model, sterile pericarditis model and atrial crush injury model have provided important information about reentrant circuit and can test the effect of antiarrhythmic drugs. Human atrial flutter has typical and atypical forms. Typical atrial flutter rotates around tricuspid annulus and uses the crista terminalis and sometimes sinus venosa as the boundary. The IVC-tricuspid isthmus is a slow conduction zone and the target of radiofrequency ablation. Atypical atrial flutter may arise from the right or left atrium. Right atrial flutter includes upper loop reentry, free wall reentry and figure of eight reentry. Left atrial flutter includes mitral annular atrial flutter, pulmonary vein-related atrial flutter and left septal atrial flutter. Radiofrequency ablation of the isthmus between the boundaries can eliminate these arrhythmias

    Ablation of Post Transplant Atrial Flutter and Pseudo-fibrillation Using Magnetic Navigation via a Superior Approach.

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    Ablation of cavotricuspid ishtmus flutter and atrial tachycardia in a complex substrate has never been reported using remote navigation via superior approach. Venous access was obtained via right internal jugular for ablation and left subclavian for duodecapolar catheter placement into the coronary sinus. In a posttransplant patient presenting with both regular and irregular tachycardia, both cavotricuspid isthmus flutter in the donor and atrial tachycardia in the recipient was mapped using a two catheter approach. Successful ablation of typical atrial flutter and anastomotic block was achieved. This is the first report of successful ablation of cavotricuspid isthmus flutter and posttransplant atrial tachycardia using magnetic navigation via superior approach. Using only two catheters, this approach is logical and feasible in complex substrates with interrupted inferior venous access

    Atrial fibrillation and its determinants after radiofrequency ablation of chronic common atrial flutter

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    Aim. Atrial fibrillation (AFib) is a major clinical issue and its occurrence is the main problem after catheter ablation of atrial flutter. The long-term occurrence of AFib after common atrial flutter ablation is still matter of debate as it may influence the therapeutic approach. So, the aim of our study was to analyze the determinants and the time course of AFib after radiofrequency catheter ablation of chronic common atrial flutter. Methods and Results. 89 consecutive patients (67.5 ± 12.0 yrs) underwent RF ablation of chronic common atrial flutter. 38.2 % had previous history of paroxysmal AFib. 51% had no underlying structural heart disease. Over a mean follow-up of 38 ± 13 months, the occurrence rate of AFib progressively increased up to 32.9% at the end of follow-up. The median occurrence time for AFib was 8 months. AFib occurrence was significantly associated with previous AFib history (P=0.01) but not with the presence of underlying heart disease (P=n.s.). Of particular interest, in our study, AFib never occurred in patients without previous AFib history. Palpitations after chronic common atrial flutter ablation was mostly related to AFib. Conclusion. In conclusion, after chronic common atrial flutter ablation, AFib incidence progressively increased over the follow-up in all patients. Patients with prior AFib history appeared to be a very high risk group. In these patients, closer monitoring is mandatory and the persistent risk of AFib recurrences may justify prolonged anticoagulation policy

    Isthmus Dependent Atrial Flutter Cycle Length Correlates with Right Atrial Cross-Sectional Area

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    Background: Right atrial flutter cycle length can prolong in the presence of antiarrhythmic drug therapy. We hypothesized that the cycle length of right atrial isthmus dependent flutter would correlate with right atrial cross-sectional area measurements. Methods: 60 patients who underwent ablation for electrophysiologically proven isthmus dependent right atrial flutter, who were not on Class I or Class III antiarrhythmic drugs and had recent 2-dimensional echocardiographic data comprised the study group. Right atrial length and width were measured in the apical four chamber view. Cross-sectional area was estimated by multiplying the length and width. 35 patients had an atrial flutter rate ≥250 bpm (Normal Flutter Group) and 25 patients had an atrial flutter rate < 250 bpm (Slow Flutter Group). Results: Mean atrial flutter rate was 283 bpm in the normal flutter group and 227 bpm in the slow flutter group. Mean atrial flutter cycle length was 213 ms in the Normal Flutter Group and 265 ms in the Slow Flutter Group (p<0.0001). Mean right atrial cross sectional area was 1845 mm2 in the Normal Flutter group and 2378 mm2 in the Slow Flutter Group, (p< 0.0001). Using linear regression, CSA was a significant predictor of cycle length (β =0.014 p = 0.0045). For every 1 mm2 increase in cross-sectional area, cycle length is 0.014 ms longer.Conclusion: In the absence of antiarrhythmic medications, right atrial cross sectional area enlargement correlates with atrial flutter cycle length. These findings provide further evidence that historical rate-related definitions of typical isthmus dependent right atrial are not mechanistically valid

    A new animal model of atrial flutter

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    A new, simple and reliable model of atrial flutter utilizing postpericardiotomy pericarditis was developed in the dog. Using a sterile technique, the pericardium was opened by way of a right thoracotomy, Teflon-coated, stainless steel wire electrodes were fixed to three selected sites on the atria and exteriorized, the atrial surfaces were generously dusted with talcum powder and a single layer of gauze was placed on the free left and right atrial walls. The dogs were allowed to recover. Subsequently, the inducibility of atrial flutter and selected electrophysiologic properties of the atria were determined by daily programmed atrial stimulation studies with the dogs in the conscious, nonsedated state.Atrial flutter could be induced in 23 of 25 dogs initially studied. It was sustained (that is, lasting ≥5 min) in 17 of the 23. Neither atrial excitability, Intraatrial conduction time nor atrial refractoriness determined by pacing and recording from the three fixed sites predicted the inducibility of atrial flutter. One hundred thirty-nine episodes of atrial flutter induced in these 23 dogs were analyzed. The mean sustained atrial flutter cycle length was 131 ± 20 ms (mean ± SD) (range 100 to 170); the atrial flutter cycle length was 150 ms or more in 23 episodes, between 120 and 150 ms in 64 episodes and 120 ms or less in 52 episodes.In five dogs, the stability of the atrial flutter cycle length during sustained atrial flutter was studied and shown to be remarkably stable in all five until interrupted by rapid atria) pacing 35 to 95 minutes after its induction. Seventeen dogs were submitted to reoperation for epicardial mapping purposes and atrial flutter could be induced in the open chest state in 12. In conclusion, this sterile pericarditis model of atrial flutter in the canine heart proved to be highly reliable, reproducible and easy to create

    Atrial Flutter: Diagnosis and Management strategies

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    Atrial flutter (AFL) is a regular, macro reentrant arrhythmia traditionally defined as a supraventricular tachycardia with an atrial rate of 240–320 beats per minute (bpm). Pathophysiology of atrial flutter and atrial fibrillation (AF) is closely related to the similar risk of stroke and they coexist clinically. Atrial flutter is classified to cavotricuspid isthmus (CTI) dependent (or typical) and non-isthmus dependent (atypical). Isthmus is a distinct structure in the right atrium (RA) through which atrial flutter passes and makes a good target for ablation therapy. Ablation is the primary therapy in atrial flutter, particularly in CTI dependent group, with regard to its safety profile and high success rate of approximately 90%. Three-dimensional electroanatomic mapping is progressively being used to ablate atypical forms of atrial flutter

    Atrial Flutter — Diagnosis, Management and Treatment

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    Atrial flutter and atrial fibrillation are the two most common arrhythmias which originate in the atrium and cause a narrow complex tachycardia which has thromboembolic risk and coexist clinically. Atrial flutter has been traditionally defined as a supraventricular arrhythmia with an atrial rate of 240–360 beats per minute (bpm). It is due to a macro-reentrant atrial activation around an anatomical barrier. Atrial flutter can be described as typical and atypical. Due to recent innovations in technology, catheter ablation has emerged as the most viable option with a success rate of more than 90 %. Three-dimensional electroanatomical mapping is useful in the treatment of atypical atrial flutter

    Characterization of double potentials in human atrial flutter: Studies during transient entrainment

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    AbstractDouble potentials, defined as atrial electrograms with two discrete deflections per beat separated by an isoelectric interval or a low amplitude baseline, have been observed during right atrial endocardial mapping of human atrial flutter. In this study, bipolar atrial electrograms were recorded during atrial flutter (mean cycle length 235 ± 27 ms [± SEM]) from the high Right atrium, the His bundle region, the coronary sinus and at least 30 right atrial endocardial napping sites in 10 patients. Double potentials were recorded from the right atrium in all patients during atrial flutter.Double potentials were evaluated during transient entrainment of atrial flutter by rapid high right atrial pacing in 5 of the 10 patients. In four of these five patients during such transient entrainment 1) one deflection of the double potential was captured with a relatively short activation time (mean interval 89 ± 45 ms) and the other deflection was captured with a relatively long activation time (mean interval 233 ± 24 ms), producing a paradoxical decrease in the short interdeflection interval from a mean of 75 ± 20 ms to a mean of 59 ± 24 ms; and 2) the configuration of the double potential remained similar to that observed during spontaneous atrial flutter. On pacing termination 1) the two double potential deflections were found to be associated with two different atrial flutter complexes in the electrocardiogram (ECG); 2) the previous double potential deflection relation resumed; and 3) when sinus rhythm was present, the double potentials were replaced by a broad, low amplitude electrogram recording at the same site. These functional double potentials probably represent collision of activation wave fronts in a functional center of the artial flutter reentrant circuit and therefore may serve as a marker for an area of functional block. In one of the five patients, double potentials were recorded from the site during transient entrainment of atrial flutter, during spontaneous atrial flutter and during sinus rhythm. These were called persistent double potentials and were associated with the same atrial flutter complex in the ECG, indicating that not all double potentials recorded during atrial flutter represent the same phenomenon

    Characterisation of atrial flutter variants based on the analysis of spatial vectorcardiographic trajectory from standard ECG

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    After atrial fibrillation, atrial flutter is the most common atrial tachyarrhythmia. Its diagnosis relies on the twelve lead electrocadriogram analysis of the distinctive waves in several leads. Nonetheless, the accurate identification of the type of atrial flutter still requires an invasive procedure. The maneuver for healing atrial flutter consists on ablating a section of the anatomy of the atria, to stop the macroreentrant circuit to keep happening, allowing the signal to travel to the ventricles in stead of staying at the atria. The region to ablate directly depends on the place at which the macroreentrant circuit is located, which at the same time depends on the type of atrial flutter. Being able to noninvasively detect the atrial flutter variant would produce a great advantage when healing this illness. The hypothesis stated at this dissertation is based on the slow conduction regions as the key factor to distinguish the atrial flutter class. This and unveiling further relations between cardiac illnesses and their signal’s alter ego are the purpose of this research project. With such aim, different methods are developed based on the vectorcardiographic representation of electrocardiograms from patients suffering from different atrial flutter types. These methods consist on the characterisation of vectorcardiographic signals from different standpoints. Besides, a mathematical model is implemented to create a large database with synthetic vectorcardiographic signals allowing to test the validity of the utilised methods. The results prove the importance of slow regions in the vectorcardiographic representation of the patient’s signals to characterise the atrial flutter type non-invasively. Furthermore, the analysis of the outcome of the different methods reveal a wide variety of features relating characteristics of the vectorcardiographic signal to the anatomy and physiology of this cardiac disease. Hence, not only results supporting the hypothesis were successful (taking into account some limitations), but also a variegated assortment of results unmasked remarkable relations among the vectorcardiographic signal and the characteristics of the atrial flutter disease.Ingeniería Biomédic

    An Approach to Catheter Ablation of Cavotricuspid Isthmus Dependent Atrial Flutter

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    Much of our understanding of the mechanisms of macro re-entrant atrial tachycardia comes from study of cavotricuspid isthmus (CTI) dependent atrial flutter. In the majority of cases, the diagnosis can be made from simple analysis of the surface ECG. Endocardial mapping during tachycardia allows confirmation of the macro re-entrant circuit within the right atrium while, at the same time, permitting curative catheter ablation targeting the critical isthmus of tissue located between the tricuspid annulus and the inferior vena cava. The procedure is short, safe and by demonstration of an electrophysiological endpoint - bidirectional conduction block across the CTI - is associated with an excellent outcome following ablation. It is now fair to say that catheter ablation should be considered as a first line therapy for patients with documented CTI-dependent atrial flutter
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