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We report the case of a 8-month-old boy with atrial septal defect associated with congenital atrial flutter. He was operated on for ASD successfully. Atrial flutter in infants has been reported to be uncommon and to have a poor prognosis when associated with underlying cardiac disease. Therefore, early surgical intervention may improve the prognosis.
OBJECTIVE: To evaluate the clinical effects of different catheter ablation strategies in the treatment of typical atrial flutter complicated with paroxysmal atrial fibrillation (PAF). [CTIA, pulmonary vein segmental isolation (PVSI), CTIA + PVI] to the patients coexisted with typical atrial flutter and PAF. METHODS: 66 patients with typical atrial flutter complicated with PAF were divided into 3 groups: Group A (n = 30), undergoing cavotricuspid isthmus ablation, (CTIA), Group B (n = 17), undergoing pulmonary vein segmental isolation, (PVSI), and Group C (n = 19), undergoing CTIA + PVSI. Follow-up was conducted for 30.5 weeks +/- 10.4 weeks. The clinical curative effects, operation safety, and complication were evaluated. RESULTS: The recurrence rate of typical atrial flutter within 12 weeks after operation of Groups A and C were 13.3% and 10.5% respectively, both significantly lower than that of Group B (52.9%, both P < 0.05) without no significant difference between Group A and Group C (P > 0.05). The recurrence rate of typical atrial flutter within 36 weeks after operation of the Groups A, B, and C were 10%, 11.8%, and 10.5% respectively, without significant differences among these 3 groups (all P > 0.05). The recurrence rates of PAF within 12 weeks and 30 weeks after operation of Groups B and C were 29.4% and 31.6%, and 23.5% and 26.3% respectively, all significantly lower than those of Group A (46.7% and 73.3% respectively, all P < 0.05) without significant o differences between Groups B and C. CONCLUSION: In patients with both typical atrial flutter and PAF, pure CTIA has a good effect on typical atrial flutter, whereas the PAF recurrence rate is higher; Pure PVSI has a good control of typical atrial flutter while curing PAF; PVSI + CTIA only reduces the early recurrence of typical atrial flutter, however, has no advantage in long-term follow up.
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 RESULT: 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.
A patient with a surgically repaired double outlet right ventricle developed AF 6 months after successful RF catheter ablation of typical atrial flutter. Guided by a 64-electrode basket catheter, the patient's AF was found to be dependent on an atypical atrial flutter circuit rotating around the fossa ovalis. Successful RF catheter ablation was performed by creating a line of conduction block from the superior vena cava to the fossa ovalis.
BACKGROUND: Atrial flutter is a common arrhythmia which frequently recurs after cardioversion and is relatively difficult to control with antiarrhythmic agents. AIMS: To evaluate the success rate, recurrence rate and safety of radiofrequency, (RF) ablation for atrial flutter in a consecutive series of patients with drug refractory chronic or paroxysmal forms of the arrhythmia. METHODS: Electrophysiologic evaluation of atrial flutter included activation mapping with a 20 electrode halo catheter placed around the tricuspid annulus and entrainment mapping from within the low right atrial isthmus. After confirmation of the arrhythmia mechanism with these techniques, an anatomic approach was used to create a linear lesion between the inferior tricuspid annulus and the eustachian ridge at the anterior margin of the inferior vena cava. In order to demonstrate successful ablation, mapping techniques were employed to show that bi-directional conduction block was present in the low right atrial isthmus. RESULTS: Successful ablation was achieved in 26/27 patients (96%). In one patient with a grossly enlarged right atrium, isthmus block could not be achieved. Of the 26 patients with successful ablation, there has been one recurrence of typical flutter (4%) during a mean follow-up period of 5.5 +/- 2.7 months. This patient underwent a successful repeat ablation procedure. Of eight patients with documented clinical atrial fibrillation (in addition to atrial flutter) prior to the procedure, five continued to have atrial fibrillation following the ablation. There were no procedural complications and all patients had normal AV conduction at the completion of the ablation. CONCLUSIONS: RF ablation is a highly effective and safe procedure for cure of atrial flutter. In patients with chronic or recurrent forms of atrial flutter RF ablation should be considered as a first line therapeutic option.
By means of highly frequent transoesophageal (left-atrial) atrial stimulation 69 patients with atrial flutter of type I (negative flutter waves in the leads II, III and aVF) and 35 patients with atrial flutter type II (positive flutter waves in the corresponding leads from the extremities) were treated and the results were compared with the results of right-atrial highly frequent stimulation (15 patients with type I atrial flutter, 6 patients with type II atrial flutter). In these cases the atrial flutter of type I nearly without any exception could be influenced by transoesophageal as well as by right-atrial stimulation (transfer into sinus rhythm, atrial fibrillation or atrial flutter of type II). The rate of success of the right-atrial as well as of the transoesophageal (left-atrial) stimulation was clearly lower in the atrial flutter of type II than in the atrial flutter of type I, in which cases are to be discussed as causes the slightly higher frequency of atrial flutter in type II, a smaller reentry circle, a higher rate of mechanisms of focal tachycardia and - in one part of the patients - an origin of tachycardia in the left atrium.
Detection of atrial flutter may be difficult for pacemakers with automatic mode switching algorithms. The Medtronic Kappa 700 device pacemakerfamily offers a dedicated Blanked Flutter Search algorithm specifically designed for the detection of atrial flutter. This report describes how spontaneous atrioventricular conduction, resulting in a sensed QRS complex at a critical time, inhibited the function of the Blanked Flutter Search algorithm to sense "concealed" or "blanked" atrialflutter. This observation underscores the need for further refinement of pacemaker algorithms for the detection of atrial tachyarrhythmias.
Typical atrial flutter is due to a counterclockwise macro-re-entry circuit localized in the right atrium with a surface ECG pattern showing predominantly negative F waves in the inferior leads and positive F waves in V1. Recently it has been proposed to classify atrial flutter on the basis of its cavo-tricuspid isthmus dependence rather than on the ECG pattern. Therefore some atrial flutters are considered typical even if the ECG does not exhibit a typical pattern. This is the case for reverse typical atrial flutter, lower loop re-entry and partial-isthmus-dependent short circuit flutter. The term atypical flutter refers to a non-isthmus dependent flutter. Usually these patients have had previous cardiac surgery with a right or left atriotomy. Flutter involving a spontaneous right atrial scar is not uncommon.
Typical atrial flutter in humans is the consequence of a stable macro-reentrant circuit produced by the unique right atrial architecture providing anatomic barriers and functional blocks to conduction. Mapping studies have indicated that the so-called isthmus between the inferior aspect of the tricuspid annulus and the ostium of the inferior caval vein is a critical zone for maintenance of atrial flutter. An anatomically guided approach with placement of a transmural and contiguous lesion line throughout the isthmus has established as curative treatment of typical atrial flutter. Electrophysical criteria indicating complete bidirectional isthmus conduction block after ablation proved to be superior with respect to redurrences of atrial flutter compared with the noninducibility criterion. The gold standard for prove of complete conduction block is the recording of double potentials along the entire isthmus ablation line. Recently, it proved possible to reduce the period of fluoroscopy during isthmus ablation by using electro-anatomical mapping.
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.
BACKGROUND: Patients who have previously undergone ablation of atrial fibrillation may experience cavotricuspid isthmus (CTI)-dependent atrial flutter during follow-up. The effects of left atrial (LA) ablation on the characteristics of CTI-dependent flutter have not been described. METHODS AND RESULTS: Fifteen patients underwent ablation of CTI-dependent flutter late after LA ablation of AF. The ECG, biatrial activation patterns, and LA voltage maps during flutter were analyzed. Thirty age- and gender-matched patients who underwent ablation of CTI-dependent flutter without prior LA ablation served as control subjects. Among the patients with prior LA ablation, mapping revealed counterclockwise activation around the tricuspid annulus in 12 of 15 patients (80%) and clockwise activation in 3 of 15 patients (20%). The flutter waves in the inferior leads were upright in 9 of the 15 patients (60%) with prior LA ablation and in none of the control subjects (P<0.001). The upright flutter waves in the inferior leads in patients with counterclockwise flutter corresponded to craniocaudal activation of the right atrial free wall. LA activation contributed little to the genesis of the flutter waves in these patients because of a significant reduction in bipolar LA voltage (0.44+/-0.20 versus 1.54+/-0.19 mV in patients with biphasic/negative flutter waves; P<0.001). CONCLUSIONS: CTI-dependent flutter that occurs after LA ablation of atrial fibrillation often has atypical ECG characteristics because of altered LA activation. In patients presenting with atrial flutter after LA ablation, entrainment mapping should be performed at the CTI even if the ECG is uncharacteristic of CTI-dependent flutter.
OBJECTIVES: This study was designed to localize and characterize the atrial flutter reentrant circuit and the electrophysiologic effects of right atrial crush injury in a new canine model. BACKGROUND: In previous studies sustained atrial flutter was induced in the canine heart by rapid atrial pacing after a linear crush injury was placed in the right atrial free wall. METHODS: Eight dogs (group 1) with three electrode plaques on the right and left atria and Bachmann's bundle and seven dogs (group 2) with a single high density electrode plaque on the right atrium were studied with use of a 64-channel computerized mapping system. RESULTS: At baseline, during sinus rhythm and right and left atrial pacing, activation spread uniformly without areas of slow conduction. Crush injury produced marked conduction delay or complete block during sinus rhythm, increasing the mean difference in activation times across the injury compared with control values (group 1, 31 +/- 4 vs. 14 +/- 5 ms, p less than 0.01; group 2, 28 +/- 10 vs. 7 +/- 2 ms, p less than 0.01). Rapid atrial pacing (S1S1 200 ms) above and below the crush injury revealed a line of complete block across which adjacent electrodes recorded markedly different activation times (33 +/- 5 and 38 +/- 12 ms difference, respectively) and around which activation wave fronts proceeded, colliding opposite the stimulating electrodes. The mean atrial flutter cycle length of 11 episodes induced in group 1 and 14 episodes in group 2 was 157 +/- 16 and 140 +/- 16 ms, respectively (p = NS). Activation mapping revealed a reentrant circuit in the right atrium around the crush injury in all episodes. Although the reentrant circuit did not contain a discrete area of slow conduction, activation time below was longer than that above the crush injury (92 +/- 14 vs. 66 +/- 8 ms and 82 +/- 12 vs. 59 +/- 9 ms in groups 1 and 2, respectively, p less than 0.01 for both). Rapid atrial pacing or premature stimuli produced progressive conduction delay and unidirectional block between the crush injury and the tricuspid anulus, inducing atrial flutter directly in 9 of 25 episodes. In 16 episodes, atrial flutter developed after transient induction of atrial fibrillation. CONCLUSIONS: 1) Atrial flutter in this model is due to reentry in the right atrium; 2) the crush injury functions as an anatomic obstacle around which reentry may occur; and 3) the reentrant circuit does not contain a discrete area of slow conduction but, rather, generally slower conduction below the crush injury.
Eight patients with atrial flutter (AF) and rapid atrial tachycardia (AT) (5 common AF, 1 uncommon AF and 2 AT) were treated with transesophageal atrial pacing (TEAP). In 5 patients no antiarrhythmic agent was used during this study, and in 3 patients procainamide was administrated intravenously. Conversion to sinus rhythm was successfully achieved in 7 patients (5 common AF and 2 AT). Two patients were converted to sinus rhythm immediately after pacing, and transient atrial fibrillation was induced before conversion to sinus rhythm in 5 patients. TEAP failed to terminate the arrhythmia in 1 patient with uncommon AF. Administration of procainamide reduced the atrial rate in 2 common AF and 1 AT, which were successfully converted to sinus rhythm by TEAP, but induced a rapid ventricular response in 2 patients, one of whom also developed hypotension before conversion. No significant complication due to TEAP was observed in this study. In conclusion, TEAP is a noninvasive method with fewer complications and has nearly the same high efficacy for converting AF and rapid AT to sinus rhythm as DC cardioversion or transvenous atrial pacing.
Fourteen patients with atrial flutter (AFL) and rapid atrial tachycardia (AT) (8 AFL type I, 2 AFL type II and 4 AT) were treated with endocavitary atrial pacing (EAP). In 10 patients no antiarrhythmic agent was during this study and in 4 patients digoxin and/or verapamil was administered before. Conversion to sinus rhythm was successfully achieved in 7 patients, 50% (4 AFL type I and 3 AT). Primary success rate (return to sinus rhythm either immediately or after < 10 min of atrial fibrillation) was 71% (5/7) (2 AFL type I and 3 AT); delayed success (conversion to sinus rhythm in > 10 min, but < 24 h) was observed in 2 cases (29%) with AFL type I. At five patients AFL was converted in stable atrial fibrillation (4 AFL type I and 1 AFL type II). EAP failed to terminate the arrhythmia in 1 patient with uncommon AFL (type II) and 1 case with AT. EAP included single extrastimuli, coaction, single decremental atrial extrastimuli and incremental atrial pacing (burst) during AFL or AT. In conclusion, EAP is a method with few complications and has efficacy for converting AFL and rapid AT sinus rhythm or to atrial fibrillation.
BACKGROUND: Atrial mechanical dysfunction and its recovery time course after successful radiofrequency ablation of chronic atrial flutter (AFL) has been largely unknown. We serially evaluated left atrial function by echocardiography after successful ablation of chronic atrial flutter. METHODS: In 13 patients with chronic AFL, mitral E wave A wave, and the ratio of A/E velocity were measured at 1 day, 1 month, 3 months and 6-12 months after successful radiofrequency (RF) ablation. Doppler tissue imaging (DTI) technique was also used to avoid load-dependent variation in the flow velocity pattern. RESULTS: Left atrial mechanical function, assessed by A wave velocity and the annular motion, was depressed at 1 day, but improved significantly at 1 month and maintained through 6-12 months after the ablation. Left atrial size did not change significantly. CONCLUSION: Left atrial mechanical function was depressed immediately after successful RF ablation of chronic AFL, but it improved significantly after 1 month and was maintained over one year.
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.
BACKGROUND: Typical atrial flutter (AFL) is a macroreentrant arrhythmia characterized by a counterclockwise circuit that passes through the cavotricuspid isthmus with passive depolarization of the left atrium. These electrical events are thought to be responsible for the classic "sawtooth" wave of atrial flutter seen on the surface electrocardiogram characterized by a gradual downward deflection followed by a sharp negative deflection. It has been suggested that the negative flutter wave is a result of passive depolarization of the left atrium. We hypothesized that interruption of the circuit within the isthmus would prevent the reentrant wave from depolarizing the left atrium thus eliminating the component of the electrocardiogram reflecting left atrial depolarization. METHODS: We examined 100 cases of atrial flutter with the typical "sawtooth" pattern referred for radiofrequency ablation. Ninety-seven of the 100 were successfully ablated. All cases were reviewed for termination of atrial flutter with the last intracardiac electrogram just lateral to the site of linear ablation and surface flutter wave at the moment of termination not obscured by the QRS segment or the T-wave. Seventeen of the 97 met these criteria. RESULTS: Seventeen of the 17 cases demonstrated a gradual negative deflection as the last discernible wave of atrial activity followed by an isoelectric period and resumption of normal sinus rhythm. The last generated wave lacked the sharp negative downstroke. CONCLUSION: These results suggest that the sharp negative deflection of flutter waves likely correlates with the wavefront's penetration of the interatrial septum and passive depolarization of the left atrium.
BACKGROUND: Moricizine is said to have potent effects on cardiac conduction but little or no effect on cardiac refractoriness. METHODS AND RESULTS: The effects of moricizine (2 mg/kg IV) on induced atrial flutter were studied 2 to 4 days after the creation of sterile pericarditis in 11 dogs. Ten episodes of stable atrial flutter before and after the administration of moricizine were studied in 9 dogs in the conscious, nonsedated state, and 7 episodes were studied in 6 dogs in the anesthetized, open chest state. In the conscious state, the effects of moricizine on atrial excitability, atrial effective refractory period, and intra-atrial conduction times were studied by recording during overdrive pacing of sinus rhythm from epicardial electrodes placed at selected atrial sites. Moricizine prolonged the atrial flutter cycle length in all the episodes, from a mean of 133 +/- 9 to 172 +/- 27 milliseconds (P < .001), and then terminated 7 of the 10 episodes. Moricizine increased the atrial threshold of excitability from a mean of 2.3 +/- 1.4 to 3.3 +/- 2.2 mA (P < .01) and prolonged intra-atrial conduction times (measured from the sulcus terminalis to the posteroinferior left atrium) from a mean of 58 +/- 6 to 64 +/- 5 milliseconds (P < .005). Prolongation of the atrial effective refractory period from 166 +/- 20 to 174 +/- 24 milliseconds (P < .05) was observed only at the sulcus terminalis site. In the open chest studies, administration of moricizine prolonged the atrial flutter cycle length from a mean of 150 +/- 15 to 216 +/- 30 milliseconds (P < .001) and then terminated the atrial flutter in all 7 episodes. As demonstrated by simultaneous multisite mapping from 95 bipolar sites on the right atrial free wall, the atrial flutter cycle length prolongation was either due to further slowing of conduction in an area of slow conduction in the reentrant circuit of the atrial flutter (5 episodes) or further slowing of conduction in an area of slow conduction plus the development of a second area of slow conduction (2 episodes). The change in conduction times in the rest of the reentrant circuit was negligible (10.9 +/- 8.7% of the total change). In all 7 episodes, the last circulating reentrant wave front blocked in an area of slow conduction. CONCLUSIONS: Moricizine (1) prolongs the atrial flutter cycle length, primarily by slowing conduction in an area of slow conduction in the reentrant circuit, (2) terminates atrial flutter by causing block of the circulating reentrant wave front in an area of slow conduction of the reentrant circuit, and (3) effectively interrupts otherwise stable atrial flutter in this canine model. The reason for these effects of moricizine are not readily explained by its effects on global atrial conduction times and refractoriness studied during sinus rhythm. Local changes in conduction in an area(s) of slow conduction are responsible for both cycle length prolongation and atrial flutter termination rather than the traditional wavelength concept of head-tail interaction.