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.     

Pseudo-electrical alternation due to deformation of QRS-T by atrial flutter waves

A case of pseudo-electrical alternation produced by deformation of QRS-T waves by atrial flutter waves is reported. It should be differentiated from the true electrical alternation which has definite diagnostic and prognostic implications.     

Radiofrequency ablation of atrial flutter due to administration of class IC antiarrhythmic drugs for atrial fibrillation

In selected patients, atrial fibrillation (AF) converts to atrial flutter (AFI) due to treatment with class IC antiarrhythmic drugs. In this study, we prospectively investigated the effects of AFI ablation and continuation of drug therapy in patients with AF who developed AFI due to long-term administration of class IC antiarrhythmic drugs. The study population consisted of 187 patients from an AF registry with paroxysmal AF who were orally treated with flecainide (n = 96) or propafenone (n = 91). Twenty-four patients (12.8%) developed AFI during the course of treatment. In 20 of these patients (10.7%), electrophysiologic study revealed typical AFI. These patients underwent radiofrequency ablation of AFI. Ablation failed in 1 patient. All patients continued preexisting drug treatment. Recurrence of AF was assessed by ambulatory Holter monitoring and serial questionnaires. During a mean follow-up of 11 +/- 4 months, the incidence of AF episodes was significantly lower in patients with a combined therapy (2.7 +/- 3.6 per year) than in control subjects with a sole drug treatment (7.8 +/- 9.2 per year, p <0.05) and than before therapy (10.2 +/- 5.4 per year, p <0.001). Subgroup analysis revealed that 7 patients (36.8%) remained symptom free with no evidence of atrial tachyarrhythmia. Eight additional patients (42.1%) had ongoing paroxysmal AF, however, with a significantly lower incidence of AF episodes than before therapy (2.3 +/- 1.6 per year vs 11.5 +/- 5.0 per year, p <0.001). In the remaining 4 patients (14.7%), no beneficial effect of AFI ablation was found. It is concluded that in patients with AF who develop typical AFI due to administration of class IC antiarrhythmic agents, a combined therapy with catheter ablation of AFI and continuation of drug treatment is highly effective in reducing occurrence and duration of atrial tachyarrhythmias.     

Right atrial flutter due to lower loop reentry: mechanism and anatomic substrates

BACKGROUND: The mechanisms of an atrial flutter (AFL) that is more rapid and at times more irregular than typical AFL are unknown. METHODS AND RESULTS: Twenty-nine patients with AFL were studied. Atrial electrograms were recorded from a 20-pole catheter placed against the tricuspid annulus (TA), with its distal electrodes lateral to the isthmus between the TA and the eustachian ridge (ER), and from the His bundle and coronary sinus catheters. Atrial extrastimuli were delivered in the TA-ER isthmus during typical AFL. Episodes of a right atrial flutter rhythm that was different from typical AFL were induced in 3 patients and occurred spontaneously in 3 patients. This sustained AFL, designated as lower-loop reentry (LLR), involved the lower right atrium (RA), as manifested by early breakthrough in the lower RA, wave-front collision in the high lateral RA or septum, and conduction through the TA-ER isthmus. Linear ablation resulting in bidirectional conduction block in the TA-ER isthmus terminated spontaneous LLR in 3 patients and rendered LLR noninducible in all patients. The cycle length of LLR was shorter than that of typical AFL (217+/-32 versus 272+/-40 ms, P<0. 01). Alternating LLR and typical AFL in 1 patient resulted in cycle length oscillation. CONCLUSIONS: LLR is a subtype of right atrial flutter and depends on conduction through the TA-ER isthmus.     

Simulated myocardial infarction and slow atrial flutter due to cerebral embolism from a free left atrial thrombus

The case of a 38-year-old female who suffered a cerebral embolism from a free left atrial thrombus is reported. The clinical picture, including serum enzyme elevations, was consistent with a nontransmural myocardial infarction. Atrial flutter exhibiting very slow (162/min) and tall waves was transiently recorded indicating development of an intra-atrial conduction disturbance.     

Pseudo atrial flutter

Atrial flutter typically has a cycle length of 200 ms (300 cycles/min or 5 Hz); with 4:1 conduction through the AV node, this would lead to a ventricular rate of 75 bpm. We present a case of a patient with a Parkinsonian tremor at a frequency of 300 cycles/min that masqueraded as atrial flutter on the limb leads of a 12-lead ECG. He had presented with a respiratory tract infection and his bedside rhythm monitor appeared to show atrial flutter. This appeared consistent on a printed (lead II) rhythm strip. His intrinsic sinus rate was coincidentally 75 bpm, which added to the confusion in the initial assessment of his rhythm (mistaken to be atrial flutter with 4:1 AV conduction). Advice was sought regarding management of his atrial 'arrhythmia' and the appropriateness of anticoagulation and cardioversion. A 12-lead ECG was performed and assessment of this revealed normal sinus rhythm. He therefore avoided unnecessary therapy.     

Atypical access to typical atrial flutter.

Typical atrial flutter with reentry around the tricuspid valve can easily be cured by ablating the cavotricuspid isthmus. In the reported case, transvenous access to the tricuspid valve was not possible because of a total cavopulmonal connection in congenital mitral atresia. Successful angioplasty of a small fenestration between the total cavopulmonal connection and the genuine right atrium (RA) allowed anterograde transvenous access to the RA. Electroanatomic RA mapping confirmed peritricuspid reentry, and successful ablation was performed.     

Sleep apnea does not predict atrial flutter recurrence after atrial flutter ablation

Purpose  

Sleep apnea (SA) has been associated with atrial fibrillation (AF) and has been found to be a predictor of AF recurrence after successful pulmonary vein isolation. No investigations have been carried out to determine the prevalence of SA in patients with typical atrial flutter (AFL) and the impact of SA on AFL recurrence after AFL ablation. Our aim is to determine if SA is a predictor of recurrence of AFL and/or atrial arrhythmias in patients who have undergone AFL ablation.     

Management of atrial flutter

Typical atrial flutter is a macroreentrant arrhythmia of the right atrium. The isthmus area between the tricuspid annulus, the inferior vena cava, and the ostium of the coronary sinus is a critical zone of the reentry circle. Atrial flutter has been treated with class I and III antiarrhytmic drugs to maintain sinus rhythm, with moderate success. Catheter ablation has been highly successful in treating atrial flutter. A contiguous line of bidirectional electrical block is created in the isthmus area between the tricuspid annulus and the inferior vena cava by application of radiofrequency energy. In patients with both atrial flutter and atrial fibrillation, ablation of the atrial flutter circuit may make the atrial fibrillation more easy to control. Quality of life assessments show improvement after ablation of atrial flutter. With a probability of success of 90%, a recurrence rate of 5% to 15%, and few complications, catheter ablation emerges as the best treatment of recurrent, symptomatic flutter.     

Management of atrial flutter

Atrial flutter is a macroreentrant arrhythmia that is associated with cardiovascular and pulmonary disease. In the United States, 200,000 new cases of atrial flutter can be expected to develop every year with a male to female ratio of over 2:1. This arrhythmia is associated with atrial fibrillation in over half the cases. It is also associated with an increased risk of thromboembolic complications, but less than that is seen with atrial fibrillation. The most common form of atrial flutter involves a large reentrant circuit within the right atrium, encircling the tricuspid annulus. Other, less common forms of atrial flutter may involve other anatomic barriers, atriotomy scars, and infarcted areas of the atria. Treatment of atrial flutter often involves electrical cardioversion and/or antiarrhythmic medications. Type I and Type III antiarrhythmic drugs are often used to terminate or prevent recurrent episodes and Type II (beta-blockers) and Type IV (calcium channel blockers) can be used to control the ventricular rate during atrial flutter. However, antiarrhythmic drugs alone control atrial flutter in only 50% to 60% of patients. Since the early 1990s, radiofrequency catheter ablation has been used to interrupt the reentrant circuit and prevent recurrences of atrial flutter. Radiofrequency ablation is acutely successful in over 90% of cases and avoids the long-term toxicity seen with antiarrhythmic drugs. Advanced mapping techniques and newer methods of delivering the radiofrequency lesions are being used to delineate unusual forms of atrial flutter and to minimize fluoroscopic exposure during the procedure.     

射频消融因心房颤动服用Ⅰc或Ⅲ类抗心律失常药物后的心房扑动

射频导管消融治疗典型心房扑动(房扑)取得了很好的效果，但持续性心房颤动(房颤)的药物或经导管消融治疗的效果目前尚不理想。在部分典型房扑合并房颤或部分持续性房颤的患者中，服用Ⅰc类或Ⅲ类抗心律失常药物过程中，房颤可以转变为典型房扑，本组前瞻性地观察消融典型房扑并继续抗心律失常药物治疗对房颤的影响。