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A 59-year-old man presented with atrial flutter and a 2:1 atrioventricular response, which, after intravenous disopyramide, became 1:1. A mechanism of slowed atrial flutter rate and improved atrioventricular nodal conduction, similar to that recognised with quinidine, is suggested.
Endocardial catheter ablation is now considered as the therapy of first choice in highly symptomatic patients with recurrent atrial flutter. Despite of primary success rates between 90 and 100% complete isthmus block is sometimes hard to achieve. We present ablation results of 100 consecutive patients suffering from typical right atrial flutter. After a mean of 18 energy applications persistent bidirectional isthmus block could not be achieved in 16 patients and right atrial angiography was performed in all of them. In 9 patients a large Eustachian valve was detected and considered responsible for failure of endocardial catheter ablation of atrial flutter. Catheter manipulation targeting the anterior region of the Eustachian ridge was successful in all patients after looping the ablation catheter within the right atrium. With a mean of 3 additional RF applications, 6 of the 9 affected patients could be successfully ablated. Large Eustachian ridges are not a rare finding in patients undergoing ablation of typical right atrial flutter. Inversion of the ablation catheter within the right atrium is a simple technique providing excellent tissue contact of the ablation electrode with the anterior region of the Eustachian Ridge. Using this approach, the creation of bidirectional isthmus block is possible in the majority of the respective patients.
BACKGROUND: Atrial flutter (AFL) is a frequent postoperative complication of the classic Fontan operation, which uses an atriopulmonary connection. We hypothesized that the suture lines alone, in the absence of any hemodynamic alterations, provide the necessary electrophysiologic substrates for AFL. The objectives of this study were to determine if the Fontan suture lines alone are sufficient to permit sustained AFL in an acute canine model and to characterize any resulting reentrant circuits to surgically ablate the AFL. METHODS: After cardiopulmonary bypass, adult dogs (n = 18) underwent a simulated classic Fontan operation. This included a longitudinal right atriotomy and an incision from the base of the right atrial appendage toward the dome of the left atrium, representing the atriopulmonary connection. In 6 of 18 dogs, an atrial septal defect was created at the level of the fossa ovalis. Unipolar 253-point biatrial endocardial mapping electrodes were placed via bilateral ventriculotomies. Induction of AFL was attempted by atrial burst pacing. If AFL could not be induced, isoproterenol was administered and pacing repeated. Activation sequence maps of the pathways of atrial reentry were generated. In 8 dogs with inducible AFL, an incision was made from the atriotomy to the atriopulmonary connection and burst pacing repeated. RESULTS: Sustained AFL could not be induced after bypass alone in any case. After the simulated Fontan operation, sustained AFL was reproducibly induced in all 18 dogs, 6 of which required isoproterenol. The mean cycle length of all cases was 177 +/- 20 ms. During AFL, atrial activation sequence maps demonstrated lines of conduction block created by both the atriotomy and the atriopulmonary connection. The isthmus of tissue between these two lines of block was essential for propagation of the reentrant wavefront. Interruption of this isthmus with an incision successfully terminated AFL in 8 of 8 dogs. CONCLUSIONS: In an acute canine model, the Fontan suture lines alone, in the absence of atrial hypertension or stretch, permit the induction of AFL. An essential electrophysiologic substrate is an isthmus of myocardium between the atriotomy and the atriopulmonary connection. Interruption of conduction through this isthmus terminates the AFL in this model and suggests a technique for ablation of AFL in patients who have undergone a classic Fontan operation.
Newer antiarrhythmic agents can control atrial flutter and fibrillation in many patients, although individual episodes may require cardioversion. Catheter ablation is often curative for refractory flutter. Ablation of atrial fibrillation is more difficult, because of its different mechanism. Surgical and catheter-based ablation procedures have been pioneered for fibrillation but remain experimental.
The case of a patient with recurrent VT and an ICD is reported. After appropriate device discharges, the patient experienced 40 episodes of inappropriate shock therapy due to atrial arrhythmias confirmed as type I atrial flutter. Since programmed stimulation could reliably initiate atrial flutter, catheter ablation was performed. During delivery of RF current, atrial flutter terminated and was no longer inducible. The patient had no further inappropriate device discharges during 12 months of follow-up. In patients with ICDs suffering from recurrences of atrial flutter leading to inappropriate shock therapy, RF catheter ablation is an effective and curative approach.
OBJECTIVES: This study compared the effect of changes in action potential duration versus conduction velocity on atrial flutter cycle length to determine whether there is a fully or partially excitable gap in atrial flutter. BACKGROUND: In an excitable gap reentrant circuit, cycle length is proportional to conduction velocity. Action potential duration is not a direct determinant of cycle length when the gap is fully excitable. METHODS: Right atrial monophasic action potentials were recorded from 41 patients during type I atrial flutter before and during pharmacologic interventions. RESULTS: Adenosine (17 +/- 3 mg [mean +/- SD]) shortened (p < 0.001) action potential duration but did not change cycle length. Edrophonium (10 mg) had no significant effect on action potential duration or cycle length. Isoproterenol (0.03 microgram/kg body weight per min) shortened (p < 0.05) and procainamide (15 mg/kg, then 2 mg/min) prolonged (p < 0.001) action potential duration and cycle length. Alterations in cycle length were not correlated with changes in action potential duration. Procainamide's prolongation of action potential duration was reversed by adenosine without affecting cycle length. Procainamide's prolongation of action potential duration and cycle length was partially reversed by isoproterenol. Adenosine's and isoproterenol's shortening of action potential duration and isoproterenol's shortening of cycle length were enhanced by procainamide. CONCLUSIONS: Atrial flutter cycle length is determined primarily by conduction velocity and does not depend directly on action potential duration. Atrial flutter has a fully excitable gap, and procainamide does not convert the gap from full to partial excitability. Adenosine and isoproterenol interact with procainamide such that their effects are enhanced and procainamide's effects are diminished.
PURPOSE: To verify the efficacy and safety of the creation of a barrier with radiofrequency (RF) in the tricuspid annulus and the vena cava ostium (TA-IVC). METHODS: Nine consecutive patients, 7 males, with age ranging from 36 to 76 years, with paroxysmal (7 patients) or permanent (2) type I atrial flutter (negative P wave in lead II, III and F) were submitted to RF ablation of TA-IVC istmo. One deflectable catheter with 4mm size tip was introduced into the right ventricle apex and pulled back to the inferior vena cava. When the atrial electrogram was detected the RF application was started. The RF was applied (20 watts during 60s) up to the proximity of inferior vena cava ostium. The end point was to stop atrial flutter. Then a vigorous atrial stimulation protocol, including isoproterenol infusion was used. In the next day, patients were submitted to transesophageal stimulation with the same protocol. RESULTS: Atrial flutter was interrupted in all patients (100%) with 4 to 28 (mean 16.7 +/- 7.7) applications. Eight patients (88.8%) with one session and 1 (11.1%) with two sessions. The mean time spent to stop the atrial flutter with one application was 30.5 +/- 18.5s. There were no complications. After a mean follow up of 3 +/- 1.6 month all patients (100%) are asymptomatic. Two of them are taking propranolol to control symptomatic atrial and ventricular ectopic beats. CONCLUSION: RF ablation of the TA-IVC istmo is efficient and safe in a short term follow up to interrupt and prevent re-induction and recurrence of type I atrial flutter.
BACKGROUND: Several studies have shown that patients undergoing cardioversion of atrial fibrillation have a high prevalence of of atrial thrombus and spontaneous echo contrast and frequently develop atrial stunning after restoration of sinus rhythm. These findings are strongly associated with increased risk of embolism in these patients. However, little is known about the prevalence of these markers of thromboembolism in patients undergoing cardioversion of atrial flutter. METHODS AND RESULTS: We performed transesophageal echocardiography in 47 consecutive, nonanticoagulated patients scheduled for elective cardioversion of atrial flutter. In patients who underwent successful cardioversion, mitral inflow velocity was recorded by transthoracic pulsed Doppler examination immediately after restoration of sinus rhythm. All patients were men (mean age, 65 +/- 10 years). Mean duration of flutter was 4 +/- 9 weeks. Atrial thrombus and/or spontaneous echo contrast were found in 16 patients (34%). Left atrial thrombus was seen in 5 patients (11%), either with (n = 4) or without spontaneous contrast. Of 40 patients with successful cardioversion, atrial mechanical activity was absent in 28% immediately after restoration of sinus rhythm. CONCLUSIONS: Our findings suggest that contrary to traditional teaching, atrial thrombus and spontaneous contrast are not uncommon in patients with atrial flutter and cardioversion may be associated with increased risk of thromboembolism.
AIM: We evaluated the effect of different stimulation protocols on atrial flutter interruption by transoesophageal pacing. METHODS AND RESULTS: Eighty patients with new onset atrial flutter were randomized into four groups. Pacing was attempted under the following conditions: with short bursts (5 s), without treatment (group A) and after oral administration of propafenone 600 mg (group B); with prolonged bursts (30 s), without treatment (group C) and after oral administration of propafenone 600 mg (group D). Pacing interrupted atrial flutter in 20% of patients in A, 55% in B, 50% in C and 85% in D. The use of longer bursts gave better results both in patients without treatment (P < 0.05: C vs A) and in patients with propafenone (P < 0.05: D vs B). Comparing groups with the same stimulation protocol, we observed a better response in patients treated with propafenone (P < 0.05: B vs A and D vs C). In the groups without treatment the use of shorter bursts was associated with a lower induction of stable atrial fibrillation (three vs nine episodes), in the groups on propafenone no differences were observed (one vs one episode). CONCLUSIONS: We conclude that the association of propafenone with long bursts gives the best result for interruption of new onset atrial flutter by transoesophageal pacing.
A double-blind randomized study was performed to compare the efficacy of intravenous verapamil with saline in 28 patients with a rapid ventricular rate and atrial fibrillation or atrial flutter. Conversion of atrial fibrillation to sinus rhythm occurred in none of 14 patients after saline and in 3 of 20 patients (15%) 7 to 160 min after verapamil. The ventricular rate in atrial fibrillation was slowed greater than or equal to 15% in 2 of 14 patients (14%) by saline, in 17 of 20 patients (85%) by 1 dose of verapamil (p less than 0.001), and in 19 of 20 patients (95%) by 1 or 2 doses of verapamil (p less than 0.001). Conversion of atrial flutter to sinus rhythm occurred in none of 4 patients after saline and in 1 of 7 patients (14%) 105 min after verapamil. The ventricular rate in atrial flutter was slowed greater than or equal to 15% in none of 4 patients by saline, in 4 of 7 patients (57%) by 1 dose of verapamil, and in 7 of 7 patients (100%) by 1 or 2 doses of verapamil (p less than 0.001).
PURPOSE: To determine the incidence of thromboembolic complications after cardioversion in patients with atrial flutter. SUBJECTS AND METHODS: We reviewed 615 electrical cardioversions performed electively in 493 patients with atrial flutter. Embolic complications were evaluated during the 30 days after cardioversion. Follow-up data were obtained by follow-up visits and by contacting the treating physician. RESULTS: Anticoagulants had been administered in 415 cardioversions (67%). Cardioversion was successful in 570 procedures (93%). Three embolic events (in 3 patients) occurred in the 30 days after 550 successful cardioversions with completed follow-up (0.6% of successful procedures; 95% confidence interval, 0.1% to 1.6%). Two of the 3 patients had not been anticoagulated, whereas the third patient had subtherapeutic oral anticoagulation. No embolic event occurred in procedures performed with adequate anticoagulation. The incidence of embolism in patients regardless of subtherapeutic anticoagulation was 1% (3 of 303 successful cardioversions). CONCLUSIONS: We observed a low (0.6%) incidence of postcardioversion thromboembolic complications in patients with atrial flutter. Embolic events did not occur in patients with adequate anticoagulation.
To determine factors affecting the success rate of rapid atrial pacing in converting atrial flutter to sinus rhythm in medically treated patients, we prospectively used this technique for 120 consecutive episodes in a total of 110 patients (94 male, 16 female, mean age 63 +/- 14 years). Structural heart disease was present in 77%, and all patients were receiving antiarrhythmic drugs at the time of the procedure. Atrial flutter type I was present in 92 of 110 patients (84%), and atrial flutter type II in 18 of 110 (16%). Primary success rate (return to sinus rhythm either immediately or after < 10 min of atrial fibrillation) was 70% (71/102) for flutter type I, and 6% (1/18) for flutter type II (p < 0.001). Delayed success (conversion to sinus rhythm in > 10 min but < 24 h) was observed in 15 additional episodes of flutter type I (15%) and in 1 additional episode of flutter type II (6%). The only clinical factors predicting primary success were (a) characteristics of flutter waves on the 12-lead surface electrocardiogram, (b) duration of flutter (primary success rate of 81% if flutter < 1 month vs. 57% if > 1 month, p < 0.05), and (c) flutter rate (primary success rate of 78% if < 260/min vs. 56% if > 260/min, p < 0.05). In 6/71 episodes of flutter type I (8%), prolonged sinus pauses or severe bradyarrhythmias occurred after conversion to sinus rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVE: Total cavopulmonary connection (TCPC) is a routine operation for palliation of children with cardiac anomalies in whom biventricular repair is impossible. The original technique consists of the creation of a semi-prosthetic intercaval tunnel. A substantial proportion of these patients develop atrial flutter. We developed a technique for creating an intercaval tunnel that uses the tissue of the right auricle as intercaval tunnel. This technique avoids suture lines in the neighbourhood of the blood supply of the sinus node and leaves the terminal crest free. Since atrial flutter frequently occurs after Mustard and Senning operations in which suture lines are similar as for creating the lateral tunnel in TCPC we postulated that our technique for creating the intercaval tunnel without prosthetic material might prevent atrial flutter. METHODS: All the children that qualified for a TCPC were included. Whenever possible our operative technique was applied. In the other cases a semi-prosthetic conduit was used for creating the intercaval tunnel. Of 47 consecutive patients 30 (64%) had a tunnel of right auricle tissue, 12 (26%) had a tunnel of prosthetic material. Five patients did not need an intercaval tunnel and were omitted in this study. Only surviving patients were included in this study. Patients that needed more atrial surgery then necessary for TCPC were also omitted. Postoperative ECG's and Holter monitorings were studied. RESULTS: Overall mortality was 7 of 47 patients (14.9% 70% CL 9.4-22.2%). There was no mortality due to rhythm disturbances. Atrial flutter occurred in 3 of 31 included patients (9.7, 70% CL 4.3-18.5%). In the right auricle group 1 of 22 patients (4.5, 70% CL 0.6-14.6%) had atrial flutter compared to 2 of 9 patients (22.2, 70% CL 7.5-45.0%) in the prosthesis group (P=0.13). CONCLUSION: The use of the right auricular technique for creating the intercaval tunnel TCPC is applicable in the majority of patients qualifying for a TCPC. Mortality and morbidity are equal comparing the two techniques. However, markedly less atrial flutter occurs in the group where the right auricle was used as intercaval tunnel. Therefore, we recommend the use of our technique for total cavopulmonary connection.
INTRODUCTION: Information about temperature and impedance monitoring during radiofrequency catheter linear ablation of atrial flutter has not been reported. We proposed that a radiofrequency catheter ablation system using a closedloop temperature control model could decrease the incidence of coagulum formation and shorten the radiation exposure and procedure times compared with those found in a power control model. METHODS AND RESULTS: Forty patients (8 women and 32 men; mean age 64 +/- 7 years) with atrial flutter were referred for radiofrequency ablation. The patients were randomized into two groups: group I patients underwent radiofrequency catheter linear ablation of atrial flutter using a power control of energy output model; and group II patients underwent the closedloop temperature control model with a target electrode temperature of 70 degrees C. As compared with group II, group I patients had a higher incidence of coagulum formation (12% vs 2%, P < 0.05), temperature shutdown (11% vs 0%, P < 0.01), and impedance shutdown (16% vs 3%, P < 0.01), more radiofrequency applications (7 +/- 3 vs 4 +/- 2, P < 0.01), and longer procedure time (100 +/- 25 vs 75 +/- 23 minutes, P < 0.05) and radiation exposure time (31 +/- 10 vs 20 +/- 7 minutes, P < 0.05) required for successful ablation. Larger deviations of temperature (9.0 degrees +/- 2.4 degrees C vs 5.0 degrees +/- 1.2 degrees C, P < 0.0001) and impedance (9.2 +/- 2.6 omega vs 5.3 +/- 1.6 omega, P < 0.0001) were also found in group I patients compared with those in group II. CONCLUSIONS: This study demonstrated that a closed-loop temperature control model could facilitate the effects of radiofrequency catheter ablation of the atrial flutter circuit by decreasing coagulum formation, temperature and impedance shutdown, and procedure and radiation exposure times.
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.
We describe a case of 1:1 atrial flutter in a patient with coronary disease taking propafenone. In atrial flutter, the atrial rate is usually about 300 beats/min with 2:1 AV conduction and a ventricular rate of 150 beats/min. Class IA antiarrhythmic drugs, especially quinidine and disopyramide, may cause 1:1 AV response because they reduce atrial rate and are vagolytic. However, propafenone is a Class IC agent and has no anticholinergic properties, and the occurrence of 1:1 AV conduction at a rate of about 250 beats/min is an important side effect that, although uncommon, should be recognized.
Sixteen patients presenting on 21 occasions with atrial flutter in association with complex congenital heart disease were treated by intracardiac stimulation techniques combined with activation mapping. Nineteen episodes of atrial flutter were successfully converted to sinus rhythm. In the remaining two episodes atrial fibrillation was induced with spontaneous conversion to sinus rhythm within 12 hours in one episode and immediate DC cardioversion to sinus rhythm in the other. Intracardiac stimulation techniques were highly successful in this group and allowed reliable conversion to sinus rhythm without general anaesthesia and high energy cardioversion. In patients with atrial flutter associated with congenital heart disease intracardiac stimulation techniques should be tried first.
PURPOSE: We conducted a systematic review and meta-analysis of observational studies to assess the risk of thromboembolism associated with atrial flutter. METHODS: MEDLINE, EMBASE, bibliographies, and consultation with clinical experts were used to identify studies that report the risk of thromboembolism associated with attempted cardioversion and longer-term risk in chronic atrial flutter. The review process and data extraction were performed by two reviewers. Study event rates were assessed graphically, and a chi-squared test was used to assess heterogeneity across studies. Meta-regression with weighted logistic regression was used to assess the association between study-level clinical factors and reported thromboembolic event rates. RESULTS: We found 13 studies that reported the risk of thromboembolism associated with cardioversion of atrial flutter. Short-term event rates ranged from 0% to 7.3%. A chi-squared test for heterogeneity was significant (P < 0.001), so results were not pooled. Instead, a meta-regression analysis was performed, which partly explained the heterogeneity across studies. Studies were more likely to report high event rates when they included patients with a prior history of thromboembolism, and to report lower event rates when at least some patients were anticoagulated or if patients underwent echocardiography before cardioversion. Four studies reported the longer-term risk of thromboembolism, and these suggest a yearly event rate of approximately 3% with sustained atrial flutter. CONCLUSION: These findings suggest that atrial flutter is indeed associated with an increased risk of thromboembolism, and that clinical factors account for the low event rates reported in some studies.