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PubMed1996

Radiofrequency catheter ablation of atrial flutter circuits.

Common atrial flutter is due to reentrant activation of the right atrium, rotating around anatomic structures and areas of functional block, in counterclockwise direction in the frontal plane. The myocardium between the inferior vena cava and the tricuspid valve is critical to close the activation circuit, and ablation of this isthmus by catheter-delivered radiofrequency can interrupt flutter, and eventually destroy the circuit, preventing recurrence of the arrhythmia. Flutter interruption does not mean complete isthmus ablation, and the procedure endpoint is to attain flutter non-inducibility, and isthmus block. Despite non-inducibility, flutter may recur, and new procedures may be needed for complete ablation. Atrial fibrillation can occur in up to 35% of the cases during follow-up but is generally well controlled with drugs that were ineffective against flutter before ablation. Some atypical atrial flutters show circular right atrial activation, using the same circuit in a clockwise direction, and these can also be interrupted by ablation of the inferior vena cava-tricuspid valve isthmus. Other atypical flutters can have different anatomic substrates in the right or left atrium, and mapping has to define specific isthmuses as ablation targets in each case. Left atrial flutter remains inaccessible to ablation.

Atrial Flutter↗
PubMed1996

Conversion of atrial flutter by ibutilide is associated with increased atrial cycle length variability.

OBJECTIVES: This study was designed to test the hypothesis that conversion of atrial flutter in humans by ibutilide, a new class III antiarrhythmic agent, is characterized by an increase in atrial cycle length variability. BACKGROUND: Conversion of tachyarrhythmias has been associated with increased oscillations of cycle length. METHODS: Electrograms and monophasic action potentials from the right atrium in 35 patients with spontaneous, sustained atrial flutter were recorded before, during and after intravenous ibutilide (0.005 to 0.025 mg/kg body weight, n = 25) or placebo (n = 10). Atrial cycle length, cycle length variability (coefficient of variation), diastolic interval and diastolic interval variability were measured from 10 consecutive cycles at baseline and 3 min before, 1 min before, 30 s before and immediately before conversion. Similar measurements were made in patients who received ibutilide or placebo but did not convert. RESULTS: Ibutilide converted atrial flutter in 14 of 25 patients 25 +/- 16 min (mean +/- SD) after initiation of the infusion, whereas placebo converted no patients. Atrial cycle length was prolonged to the same extent in ibutilide converters and nonconverters (36 +/- 19 vs. 38 +/- 21 ms, p = NS) and was not affected by placebo. Beat-to-beat variability in atrial cycle length (baseline 1.2 +/- 0.7 vs. preconversion 7.3 +/- 4.9, p < 0.01) and diastolic interval (baseline 11 +/- 8 vs. preconversion 33 +/- 23, p < 0.05) increased significantly just before atrial flutter conversion and remained unchanged in ibutilide nonconverters and placebo group patients. CONCLUSIONS: Ibutilide prolongs atrial cycle length, but conversion of atrial flutter by ibutilide is characterized by increased variability in atrial cycle length and diastolic interval.

Aged↗
PubMed2004

Anatomic and electrophysiological differences between chronic and paroxysmal forms of common atrial flutter and comparison with controls:.

Whether chronic typical atrial flutter differs from paroxysmal atrial flutter regarding electrophysiological properties of reentry pathways and cardiac function remains unknown. If so, can remodeling due to long duration of persistently rapid atrial or ventricular rates explain these changes? The aim of the study was to compare RA local conduction velocities and heart function parameters between three groups: (1) chronic atrial flutter, (2) paroxysmal atrial flutter, and (3) controls. The study evaluated 52 patients undergoing radiofrequency ablation for typical atrial flutter. There were 35 patients with chronic atrial flutter (62.7 +/- 14 years) and 17 patients with paroxysmal atrial flutter (62.7 +/- 10 years). Underlying structural heart disease was present in 20 (57%) of 35 chronic atrial flutter patients and in 7 (41%) of 17 paroxysmal atrial flutter patients (P = 0.1). Chronic atrial flutter duration was 10.9 +/- 17 months and paroxysmal atrial flutter duration was 8.5 +/- 10 (P = 0.06). RA conduction velocity measurements were carried out before ablation during sinus rhythm under pacing (600-ms cycle length) with a 12-pole steerable catheter positioned in the high lateral RA (poles 11-12 [H6]), mid-lateral RA (poles 9-10 [H5]), and along the inferior vena caval tricuspid isthmus (poles 7-8 [H4]; 5-6 [H3]; 3-4 [H2]) with its distal electrode pair at the coronary sinus origin (pole 1-2 [H1]). Counter-clockwise RA conduction velocities were assessed from H6 to H1 and clockwise RA conduction velocities from H1 to H6. After successful ablation, RA and LA areas, LV volumes, LVEF, inferior vena caval tricuspid annulus, and coronary sinus tricuspid annulus (septal isthmus) lengths were measured by two-dimensional echocardiography. The control group included 12 patients without structural heart disease, referred for electrophysiological evaluation of AVN reentry. Counter-clockwise RA conduction velocities at the inferior vena caval tricuspid isthmus were lower in chronic atrial flutter than in paroxysmal atrial flutter (H4, 1.19 +/- 0.4 vs 1.89 +/- 1 m/s, P = 0.0051; H3, 1.14 +/- 0.4 vs 1.6 +/- 0.7 m/s, P = 0.0015; H2, 1.16 +/- 0.4 vs 1.53 +/- 0.5 m/s, P < 0.0056 and H1, 1.2 +/- 0.4 vs 1.5 +/- 0.4 m/s, P = 0.03, respectively). Counter-clockwise RA conduction velocities were identical at the high and mid-lateral RA. Counter-clockwise caval isthmus RA conduction velocities from H3 to H1 were significantly different between chronic atrial flutter and controls (H3, 1.14 +/- 0.4 vs 1.7 +/- 0.3 m/s, P = 0.0014; H2, 1.16 +/- 0.4 vs 1.83 +/- 0.4 m/s, P < 0.0001 and H1, 1.2 +/- 0.4 vs 1.94 +/- 0.4 m/s, P < 0.0001, respectively). A difference was found regarding clockwise isthmus RA conduction velocities between the two groups of atrial flutter and controls but not between chronic atrial flutter and paroxysmal atrial flutter. Respectively, chronic atrial flutter had greater RA and LA areas (24.5 +/- 5 vs 13 +/- 2 cm2; P < 0.0001 and 23 +/- 5 vs 16 +/- 3 cm2, P < 0.0001), LV end-systolic and end-diastolic volumes (50 +/- 25 vs 32 +/- 13 cm3, P = 0.0084 and 112 +/- 40 vs 85 +/- 25 cm3, P = 0.01), septal isthmus length (21 +/- 3 vs 13 +/- 2 mm, P < 0.0001), and inferior vena caval tricuspid isthmus length (39 +/- 6 vs 23 +/- 5 mm; P < 0.0001). Chronic common atrial flutter is characterized by more prolonged counter-clockwise conduction times and larger anatomic conduction pathways than the paroxysmal form, the causal relationship between electrophysiological and anatomic characteristics remains to be demonstrated.

Atrial Flutter↗
PubMed2006

Cryoablation versus radiofrequency ablation in the treatment of atrial flutter trial (CRAAFT).

INTRODUCTION: Atrial flutter is frequently treated with radiofrequency (RF) ablation with excellent results. While RF ablation remains the gold standard for catheter based treatment of atrial flutter, cryoablation has potential advantages including painless ablation and cryoadherence to the myocardium. We performed a prospective randomised trial comparing cryoablation and RF ablation in the treatment of atrial flutter. METHODS AND RESULTS: We randomised 32 consecutive patients with typical atrial flutter to either radiofrequency ablation using an 8 mm tip Blazer II XP catheter (EP Technology, San Jose, USA) or cryoablation using a 9 French 8 mm tip Freezor Max catheter (CryoCath Technologies Inc, Kirkland, QU, Canada). Twenty eight patients were then followed up for a mean of 14.7 months. The procedure was successful in producing isthmus block in all but one patient in the cryoablation group. Cryoablation was associated with a significantly longer procedure (171 vs 99 min) and ablation duration (59 vs 12.7 min), however fluoroscopy exposure was similar (30 vs 29 min). Cryoablation was associated with reduced pain scores compared with RF (mean pain score 0.4 vs 3.5). There were two recurrences of atrial flutter during follow-up, both in the cryoablation group. CONCLUSIONS: Cryoablation has improved patient tolerability compared to RF ablation, however is associated with longer procedure and ablation durations. Further trials are required to confirm whether cryoablation has similar acute and chronic efficacy to RF ablation.

Aged↗
PubMedDate not supplied

Atrial overdrive pacing for conversion of atrial flutter in children.

Atrial flutter (AF) is a potentially dangerous arrhythmia in children, which is difficult to be converted into sinus rhythm by drug therapy alone. In four young patients (3 had history of cardiac surgery, 1 had Ebstein's anomaly), the AF which had failed to medical therapy was converted into sinus rhythm by an intracardiac atrial pacing: In two patients the AF was terminated by atrial pacing alone, and in the other two the AF was converted into sinus rhythm by atrial pacing after procainamide infusion. In all patients an entrainment of AF was observed during the atrial pacing, which favored a reentrant mechanism for the AF in these patients. Evidences of sinus node dysfunction were observed in all three postoperative patients. We conclude that atrial pacing with or without procainamide infusion is an effective method for the conversion of atrial flutter. In addition, for patients with AF and concomitant sinus node dysfunction, this method can ensure the patients' safetiness.

Adolescent↗
PubMed1997

Mechanisms and medical management of patients with atrial flutter.

Type I atrial flutter is due to reentrant excitation, principally in the right atrium. The standard ECG remains the cornerstone for its clinical diagnosis. Acute treatment should be directed at control of the ventricular response rate and, if possible, restoration of sinus rhythm. Radiofrequency catheter ablation therapy provides the best hope of cure, although atrial fibrillation may subsequently occur after an ostensibly successful ablative procedure. Alternatively, antiarrhythmic drug therapy to suppress recurrent atrial flutter episodes may be useful, recognizing that occasional recurrences are common despite therapy. Radiofrequency ablation of the His bundle ablation with placement of an appropriate pacemaker system may be useful in selected patients.

Animals↗
PubMed2002

Prospective randomized comparison of cooled radiofrequency versus standard radiofrequency energy for ablation of typical atrial flutter.

In patients with atrial flutter, conventional RF ablation may not result in complete isthmus block. This prospective, randomized study tested the hypothesis that the cooled RF ablation is safe and facilitates the achievement of isthmus block with fewer RF applications than with standard ablation for typical atrial flutter. Isthmus ablation was performed in 59 patients (40 men, 64 +/- 14 years) with type I atrial flutter using standard RF (n = 31) or cooled RF (n = 28) catheters with crossover after 12 unsuccessful RF applications. The endpoint was bidirectional isthmus block or a total of 24 unsuccessful RF applications. After the first 12 RF applications, 17 (55%) of 31 standard RF and 22 (79%) of 28 cooled RF patients had bidirectional isthmus block (P < 0.05). After the remaining patients crossed over to the alternate RF ablation system and underwent up to 12 more RF applications, bidirectional isthmus block had been demonstrated in 27 (87%) of 31 standard RF and 25 (89%) of 28 cooled RF patients (P = NS). Isthmus block was not achieved within 24 RF applications in four standard and three cooled RF patients. Mean measured tip temperatures for cooled RF were lower than for standard RF (38.5 degrees C +/- 6.98 degrees C vs 57.2 degrees C +/- 7.42 degrees C, P < 0.0001). Peak temperatures were also lower for cooled RF compared to standard RF (45.7 degrees C +/- 22.7 degrees C vs 63.4 degrees C +/- 9.87 degrees C, P < 0.0001). Importantly, mean power delivered was significantly higher for cooled than for standard RF (42.3 +/- 9.48 vs 34.0 +/- 14.0 W, P < 0.0001). There were no serious complications for either ablation system. During a 12.8 +/- 3.76-month follow-up, there were two atrial flutter recurrences in the cooled RF group and four in the standard RF group (P = NS). In patients with type I atrial flutter, ablation with the cooled RF catheter is as safe as, and facilitates creation of bidirectional isthmus block more rapidly than, standard RF ablation.

Atrial Flutter↗
PubMed1996

[Radiofrequency catheter ablation in patients with common atrial flutter].

BACKGROUND: Type 1 atrial flutter is produced by a reentry circuit located in the right atrium that can be interrupted applying radiofrequency in the inferior cava-tricuspid valve isthmus. AIM: To report our experience in the treatment of atrial flutter with radiofrequency ablation. PATIENTS AND METHODS: Nine patients (eight male) whose ages ranged from 6 to 72 years old were studied. Two patients had an operated congenital cardiopathy, two had high blood pressure, one was subjected previously to radiofrequency ablation due to a left paraspecific pathway, one developed a cardiac failure secondary to tachycardia and three did not have evidences of cardiopathy. RESULTS: In two patients, atrial flutter was not interrupted. In the other seven patients, radiofrequency ablation was successful. There were three relapses in the first month after the procedure, of these, two patients were successfully treated again. After a mean follow up of 4.5 months, these patients are asymptomatic and without antiarrhythmic drugs. Analysis of obtained signals, showed that radiofrequency that interrupted atrial flutter always occurred in zones of double potentials. CONCLUSIONS: Radiofrequency ablation is an effective treatment for atrial flutter and the zone of successful ablation is associated to the presence of double atrial potentials.

Adult↗
PubMed2000

Randomized comparison of two targets in typical atrial flutter ablation.

Typical atrial flutter ablation has become anatomically guided to 2 separate sites within the isthmus at the inferior right atrium: (1) between the inferior vena cava and the tricuspid annulus (anterior side of the isthmus [A]), (2) between the eustachian crest, the coronary sinus ostium and tricuspid annulus (posterior side of the isthmus [P]). We prospectively compared ablation results at these sites in 72 consecutive patients. Patients were randomized in group P or A according to the initial target site. If ablation failed at 1 site after 15 radiofrequency (RF) pulses, the other side of the isthmus was targeted. Before 15 RF pulses, complete bidirectional isthmus block was achieved in 30 of 36 group A patients and in 25 of 36 group P patients, with similar mean RF pulses number, procedure time, and fluoroscopy time. After shifting to the other target, success was finally obtained at P in 2 of 6 group A patients, and at A in 8 of 11 group P patients before a maximum of 30 RF pulses. Among successful patients, number of RF pulses, procedure time, and fluoroscopy time were significantly lower in group A (7.2 +/- 5.4 vs 11.0 +/- 8.1 pulses, p = 0.03; 131 +/- 44 vs 163 +/- 66 minutes, p = 0.03; 31 +/- 19 vs 46 +/- 24 minutes, p = 0.01, respectively). Impairment of atrioventricular (AV) nodal conduction occurred in 5 patients only during ablation at P. AV block was transient in 4 patients and permanent in 1. Although atrial flutter ablation is equally effective at P and A, success seems easier to obtain when A is first targeted. Ablation at P is associated with a significant risk of AV block.

Adult↗
PubMed2000

Catheter ablation of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.

AIMS: Antiarrhythmic drug treatment for atrial fibrillation can cause atrial flutter-like arrhythmias. The aim of this study was to clarify the effect of catheter ablation of the tricuspid annulus-vena cava inferior isthmus on amiodarone-induced atrial flutter and to determine the incidence of atrial fibrillation after catheter ablation of amiodarone-induced atrial flutter in comparison to regular typical flutter. METHODS AND RESULTS: Among 92 consecutive patients with typical atrial flutter who underwent isthmus ablation 28 patients had atrial flutter without a history of previous atrial fibrillation (group I), 10 patients had atrial flutter following the initiation of amiodarone therapy for paroxysmal atrial fibrillation (group II) and 54 patients had atrial flutter and atrial fibrillation (group III). Atrial cycle length during atrial flutter in amiodarone-treated patients (group II) (277+/-24 ms) was significantly longer as compared to the cycle length of atrial flutter in group I (247+/-33 ms) and group III patients (235+/-28 ms). The rate of successful transient entrainment and overdrive stimulation to sinus rhythm was not different between patients with (60%) or without amiodarone therapy (group I: 71%, group III: 53%). Successful isthmus ablation with bidirectional conduction block eliminating right atrial flutter was achieved in 90% of amiodarone-treated patients and 93% of patients without amiodarone therapy. In the amiodarone-treated patient group atrial conduction times during pacing in sinus rhythm were significantly prolonged by 20-30% before and after ablation in all regions of the reentrant circuit. During a mean follow-up of 8+/-3 months post-ablation, atrial fibrillation recurred in two of 10 patients on continued amiodarone therapy after successful isthmus ablation. Thus, successful catheter ablation of atrial flutter due to amiodarone therapy was associated with a markedly lower recurrence rate of paroxysmal atrial fibrillation (20%) as compared to patients with atrial flutter plus preexisting paroxysmal atrial fibrillation (76%) and was similar to the outcome of patients with successful atrial flutter ablation without preexisting atrial fibrillation (25%). CONCLUSION: These data suggest that isthmus ablation with bidirectional block and continuation of amiodarone therapy is an effective therapy for the treatment of atrial flutter due to amiodarone therapy for paroxysmal atrial fibrillation.

Adult↗
PubMedDate not supplied

The interrelationship between atrial fibrillation and atrial flutter.

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.

Animals↗
PubMed1996

The results of atrial flutter ablation in patients with and without a history of atrial fibrillation.

To determine the impact of atrial flutter radiofrequency catheter ablation on recurrence of atrial flutter and atrial fibrillation, 32 patients with atrial flutter (18 with a history of atrial fibrillation) were followed for a mean of 8.6 months; atrial flutter has not recurred after 1 (26 patients) or 2 (5 patients) successful ablation procedures. Atrial flutter did not appear proarrhythmic for atrial fibrillation, with only 1 of 15 patients without a history of atrial fibrillation developing the arrythmia in the absence of an alcohol binge or cocaine use.

Atrial Fibrillation↗
PubMed2002

Electrophysiological evaluation and ablation of atypical right atrial flutter.

Right atrial reentry which does not critically depend upon activation through the cavotricuspid isthmus is considered to be a subtype of atypical flutter. Diagnosis is dependent upon demonstrating the nonparticipation of the cavotricuspid isthmus. Right atrial free wall atriotomy incisions, the superior vena cava, the inferior vena cava, electrically silent or mute areas, incomplete variants of the posterior intercaval crista terminalis line of block and other functional/anisotropic lines of block form the central barriers around which macroreentry occurs. The length, location and orientation of fixed lines of block such as atriotomy incisions are important determinants of their arrhythmogenicity. Successful catheter ablation depends upon delineating the circuit in order to choose the optimal isthmus for ablation and producing complete block across it.

Adult↗
PubMed1997

Factors that influence the development of atrial flutter after the Fontan operation.

OBJECTIVES: Atrial flutter is a frequent, potentially fatal complication of the Fontan operation, but risk factors for its development are ill defined. We evaluated clinical features that might predict the development of atrial flutter in patients who had a Fontan operation. METHODS: We evaluated 334 early survivors of a Fontan operation done between April 1973 and July 1991 (mean follow-up, 5.0 +/- 3.8 years). Evaluation included electrocardiography, Holter monitor recordings, and chart review. Modifications of the Fontan operation included an extracardiac conduit (n = 43), an atriopulmonary anastomosis (n = 117), or a total cavopulmonary anastomosis (n = 174). Patient, time, and procedure-related variables were analyzed with respect to the development of atrial flutter. RESULTS: Atrial flutter was identified in 54 (16%) patients at a mean of 5.3 +/- 4.7 years (range 0 to 19.7 years) after Fontan operation. Atrial flutter developed sooner and was more likely to occur in patients who were older at the time of Fontan operation (12.4 +/- 7.6 vs 6.3 +/- 5.2 years; p < 0.001), had a longer follow-up interval (8.7 +/- 3.9 vs 4.4 +/- 3.4 years; p < 0.001), had a prior atrial septectomy or pulmonary artery reconstruction (p < 0.01), and had worse New York Heart Association class symptoms (p < 0.02). The presence of sinus node dysfunction was associated with a higher incidence of atrial flutter (p < 0.001). Although there was a lower prevalence of atrial flutter in those patients with a total cavopulmonary anastomosis, the follow-up for this group was shorter. Anatomic diagnoses, perioperative hemodynamics, and other previous palliative operations were not associated with an increased incidence of atrial flutter. Multivariate analysis identified age at operation, duration of follow-up, extensive atrial baffling, and type of repair as factors associated with the development of atrial flutter after Fontan operation. CONCLUSION: Atrial flutter continues to develop with time after the Fontan operation. Further follow-up is necessary to determine whether a total cavopulmonary anastomosis reduces the incidence of atrial flutter.

Atrial Flutter↗
PubMed2005

Atrial flutter after surgical radiofrequency ablation of the left atrium for atrial fibrillation.

BACKGROUND: Left atrial radiofrequency ablation is the most common technique for the treatment of atrial fibrillation during mitral valve surgery. Reported failure rates range between 15% and 30%, with some patients remaining in atrial fibrillation and others experiencing atrial flutter. The incidence and nature of the postoperative atrial flutter is not yet well defined. METHODS: The study group consisted of 50 patients with atrial fibrillation who underwent mitral valve surgery combined with left atrial radiofrequency ablation, and were followed for a mean period of 15 +/- 7 months. The majority of patients (39; 78%) had persistent or permanent atrial fibrillation. Placement of the ablation lines was as follows: encircling the pulmonary veins, isolating the base of the left atrial appendage, and bridging the lateral or posterior mitral annulus and the margin of the pulmonary vein or the appendage-encircling ablation lines. RESULTS: There were three hospital deaths (6%). Thirty-four (72%) patients were free of any atrial tachyarrhythmia events, and 37 (79%) patients were in sinus rhythm by the end of the study's follow-up. During the follow-up, 6 patients (12.7%) experienced atrial flutter and 1 patient had atrial tachycardia. Electrophysiologic study was performed in 5 of 6 patients with postoperative atrial flutter. In 4 of them, the study findings were consistent with left atrial flutter. One patient with typical isthmus-dependent right atrial flutter underwent successful ablation. CONCLUSIONS: Left atrial surgical radiofrequency ablation is associated with a high rate of postoperative atrial flutters that appear to be predominantly of left-sided origin.

Adult↗
PubMed2005

Typical atrial flutter ablation and the risk of postablation atrial fibrillation.

Typical atrial flutter is readily abolished by creating a line of block along the isthmus between the tricuspid annulus and the inferior vena cava. However, postablation atrial fibrillation occurs frequently, and its occurrence increases during the follow-up. Preablation atrial fibrillation is the most important risk factor for postablation atrial fibrillation occurrence. Among patients with preablation atrial fibrillation, patients with drug-induced atrial flutter present a lower risk of postablation atrial fibrillation than patients with spontaneous preablation atrial fibrillation. Patients with preablation lone atrial flutter also present a significant risk of atrial fibrillation development as time passes. Hence, they must be advised of the risk of recurrent symptoms and late atrial fibrillation, and closely followed up despite successful transisthmic ablation. Patients with atrial fibrillation after transcatheter isthmus ablation should be offered catheter-based pulmonary vein isolation, particularly if atrial fibrillation occurs despite continuation of antiarrhythmic drug therapy.

Atrial Fibrillation↗
PubMed2005

Mechanism of atrial flutter occurring late after orthotopic heart transplantation with atrio-atrial anastomosis.

OBJECTIVE: We sought to better define the electrophysiologic mechanism of atrial flutter in patients after heart transplantation. BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Adult↗