Right septal macroreentrant tachycardia late after mitral valve repair: Importance of surgical access approach

BACKGROUND: Reentrant atrial tachycardias may occur after mitral valve surgery. These usually involve the left atrium or the lateral wall of the right atrium around the atriotomy scar. OBJECTIVE: The purpose of this study was to test whether ablation could eliminate atrial tachycardia after mitral valve repair. METHODS: Three patients (two men, one woman; mean age 57 +/- 12 years) were studied 48 +/- 38 months after mitral valve repair. In all cases, the surgical approach involved a transseptal incision. Tachycardia mapping was performed using multipolar catheters and the three-dimensional electroanatomic mapping system. The mean flutter cycle length was 313 +/- 21 ms. All patients had dual-loop reentry with one circuit around a septal scar and the other circuit around the tricuspid annulus. RESULTS: Successful radiofrequency ablation of the septal circuit was performed between the scar and the superior tricuspid annulus in all three cases. CONCLUSION: After mitral valve repair using a transseptal incision, dual-loop reentry may occur around the septal scar and the tricuspid annulus. Successful ablation may be achieved with an ablation line between the scar and the tricuspid annulus.     

Macroreentrant Atrial Tachycardia in Patients without Previous Atrial Surgery or Catheter Ablation: Clinical and Electrophysiological Characteristics of Scar‐Related Left Atrial Anterior Wall Reentry

Scar‐Related Left Atrial Anterior Wall Reentry. Introduction: Macroreentrant atrial tachycardia (MRAT) has been described most frequently in patients with prior cardiac surgery. Left atrial tachycardia and flutter are common in patients who undergo atrial fibrillation ablation; however, few reports describe left atrial MRAT involving the regions of spontaneous scarring. Here, we describe left atrial MRAT in patients without prior cardiac surgery or catheter ablation (CA) and discuss the clinical and electrophysiological characteristics of tachycardia and outcome of CA. Methods and Results: An electrophysiological study and CA were performed in 6 patients (3 men; age 76 ± 6 years) with MRAT originating from the left atrial anterior wall (LAAW). No patient had a history of cardiac surgery or CA in the left atrium. Spontaneous scars (areas with bipolar voltage ≤ 0.05 mV) were observed in all patients. The activation map showed a figure‐eight circuit with loops around the mitral annulus (4 counterclockwise and 2 clockwise) and a low‐voltage area with LAAW scarring. The mean tachycardia cycle length was 303 ± 49 milliseconds. The conduction velocity was significantly slower in the isthmus between the scar in the LAAW and the mitral annulus than in the lateral mitral annulus (0.17 ± 0.05 m/s vs 0.94 ± 0.35 m/s; P = 0.003). Successful ablation of the isthmus caused interruption of the tachycardia and rendered it noninducible in all patients. Conclusion: Spontaneous LAAW scarring is an unusual cause of MRAT, showing activation patterns with a figure‐eight configuration. Radiofrequency CA is a feasible and effective treatment in such cases. (J Cardiovasc Electrophysiol, Vol. 24, pp. 404‐412, April 2013)     

Dual-loop intra-atrial re-entry tachycardia in a patient with ischaemic cardiomyopathy.

A 65-year-old man with ischaemic cardiomyopathy (three prior coronary artery bypass surgery procedures), underwent catheter ablation for recurrent atrial flutter. Electrophysiological study initially revealed clockwise, tricuspid annulus/inferior vena cava isthmus dependent, atrial flutter. During radiofrequency energy ablation atrial flutter changed into a different atrial tachycardia without change in cycle length or interruption of the tachycardia. The new tachycardia was a right atrial free wall re-entry tachycardia. Thus the two atrial tachycardias formed a dual-loop ('figure-of-eight') re-entry circuit, possibly due to atrial scar tissue from multiple cardiac surgery procedures.     

Radiofrequency Ablation of Atrial Flutter

RF Ablation of Atrial Flutter. Activation mapping in common atrial flutter has shown circular (reentrant) activation of the right atrium around anatomic structures and areas of functional block. The direction of rotation is counterclockwise (in a frontal view), and in the low right atrium the myocardium between the inferior vena cava (IVC) and the tricuspid valve (TV) is critical to close the activation circle. The circuit can be interrupted by radiofrequency ablation of the myocardium between the TV and the IVC, and, in some cases, by ablation between the coronary sinus and TV. Flutter interruption does not mean complete isthmus ablation, as it may remain inducible, requiring further ablation. Despite attaining noninducibility, flutter may recur, and new procedures may be needed for complete ablation. Atrial fibrillation occurs in up to 30% of the cases during follow-up but is generally well controlled with antiarrhythmic drugs that were ineffective in treating flutter before ablation. Some noncommon atrial flutters show circular right atrial activation in a reversed (clockwise) direction, with the same critical areas in the low right atrium, and in these isthmus ablation is effective. Other noncommon flutters have different substrates in the right or left atrium, and mapping has to define specific critical isthmuses as ablation targets in each case. Left atrial flutter circuits remain inaccessible to ablation.     

非接触心内膜激动标测系统指导房间隔缺损修补术后Ⅱ型心房扑动的射频消融(附一例报道)

评价非接触球囊导管标测系统 (EnSite 30 0 0 )在指导房间隔缺损 (ASD)修补术后心房扑动 (简称房扑 )的射频消融中的临床应用。 1例女性患者 ,41岁 ,ASD修补术后 2 2年开始频繁发作心动过速 ,体表心电图示Ⅱ型房扑。应用EnSite 30 0 0构建右房三维几何模型 ,标测心动过速的折返激动顺序 ,发现手术疤痕与三尖瓣环之间、下腔静脉与三尖瓣环之间为折返环路的关键峡部 ,应用导航系统指导峡部消融 ,成功阻断心动过速 ;消融后通过起搏标测判定峡部已达完全双向阻滞。随访 2 0个月 ,无心动过速复发。结论 :在ASD修补术后房扑的标测和消融中应用EnSite30 0 0系统是安全有效的 ,不仅能确定折返环路的关键峡部 ,而且能准确判断线性损伤的连续性。     

心房内双环折返性心动过速的非接触球囊导管标测及射频消融

目的 阐明心房内双环折返性心动过速的电生理机制及导管射频消融的技术。方法 3例患，均为女性，年龄41-66岁，心动过速病史6个月-10年，例1为先天性心脏病房间隔缺损修补术后，例2为特发性心动过速，例3为扩张型心肌病，经左股静脉置入9F球囊电极至右心房中部并展开，球囊中心位于希氏束和冠状静脉窦口中间，进入球囊时，静脉注射肝素100U/kg，并保持手术过程中活化的血小板凝结时间（ACT）位于250s左右，以后经右股静脉进入8F消融导管构建右心房三维几何构型，构型构建完毕后，经高位右心房诱发心动过速，建立心动过速的腔内等电势图，然后分析心动过速的起源，折返激动的环路，传导方向，关键峡部，由此确定线性消融的部位和起止点，经导航系统引导消融导管至拟订靶点处，每点予以60W，60s,60℃温控消融，直至产生消融线径的双向阻滞。结果 3例患均有心房内双环折返性房性心动过速（房速），折返环分别围绕三尖瓣环和病变组织周围，于各自的峡部行线性消融产生双向阻滞后，心动过速不再诱发，随访分别为3、5和12个月，无心动过速复发，例2术后动态心电图记录有频繁房性早搏，部分房性早搏触发短阵心房颤动。结论 心房内存在病变组织如手术瘢痕，补片及梗死病灶时可产生心房内折返，若合并围绕三尖瓣环折返的典型心房扑动则形成心房内双环折返性房速。双环折返性房速也可发生在无器质性心脏病的患，不同的基础心脏病变决定着不同的折返环路和折返方式，双环折返性房速存在两个关键峡部，需要两次线性消融才可阻止心动过速的发生，非接触球囊导管标测系统（EnSite3000)不同可破译心房内双环折返性心动过速的电生理机制，也为其消融方法提供可靠的策略。     

Dual independent atrial tachycardias after ablation of chronic atrial fibrillation

We report the case of a 71-year-old man with two atrial tachycardias evolving simultaneously and independently in two dissociated regions after extensive ablation for chronic atrial fibrillation. One tachycardia was a focal tachycardia originating from the right inferior pulmonary vein and activating the posterior left atrium with a 2:1 conduction block, while the other tachycardia was an atrial flutter circulating around the tricuspid annulus, activating the right atrium and the anterior wall of the left atrium. These two atrial tachycardias were successfully ablated prior to restoration of sinus rhythm.     

射频消融治疗经右心房游离壁切口术后的双环折返性房性心动过速

目的 总结经右心房游离壁切口术后双环折返性房性心动过速（房速）的发生率及射频消融后长期随访的结果.方法 2007年1月至2012年12月共入选48例在南京医科大学第一附属医院心脏科行经右心房游离壁切口治疗先天性心脏病或获得性心脏病后发作房速的患者.双环折返性房速的定义为心房同时存在两个折返环,同时在折返的可能路径上进行多部位拖带均为隐匿性.结果 共观察到8例患者术中存在双环折返性房速,男4例,平均年龄（40.4±22.0）岁.第1次外科术后至房速发作时间为（79.0±65.2）个月,第1次房速发作至第1次消融的时间为（20.8±28.3）个月,所有患者房速均持续发作.所有患者的双环折返性房速均与三尖瓣峡部以及右心房游离壁切口相关.5例患者在消融三尖瓣峡部过程中,心动周期突然变化;1例患者消融三尖瓣峡部时,心动周期无变化,右心房游离壁多部位拖带为右心房游离壁折返性房速,间隔部位拖带证实此部位不在折返环内,可能提示右心房游离壁折返性房速为主导折返环,;1例患者消融过程中心动过速终止,同样行切口致下腔的线性消融;1例患者消融三尖瓣峡部时心动过速无明显变化,但冠状静脉窦的激动有细微变化,拖带标测提示三尖瓣峡部不在折返环内,右心房游离壁多部位拖带提示为围绕右心房切口瘢痕折返的心动过速,行外科切口下部至下腔静脉消融时,房速终止.平均随访（33.6±16.7）个月,3例复发患者均为风湿性心脏病换瓣术后,其中1例复发房速,另外2例复发房颤.结论 经右心房游离壁切口术后双环折返性房速主要与三尖瓣峡部以及切口相关,三尖瓣峡部以及切口至下腔静脉线性消融常能够治疗这类心律失常.     

Pericaval and periannular intra-atrial reentrant tachycardias in patients with congenital heart disease

INTRODUCTION: Intra-atrial reentrant tachycardia (IART) is a frequent late sequel of congenital heart surgery, often involving the cavotricuspid isthmus. In this report, we characterize pericaval reentry, a novel mechanism of isthmus-dependent IART in congenital heart patients, and compare its electrophysiologic characteristics with periannular atrial flutter. METHODS AND RESULTS: Electrophysiologic and electroanatomic mapping data and acute outcomes were reviewed in postoperative patients with congenital heart disease who underwent electrophysiologic study/radiofrequency catheter ablation at The Children's Hospital, Boston between January 1999 and November 2000. The study included all congenital heart patients with IART and who had undergone (1) the Fontan procedure and (2) a biventricular surgical repair other than atrial switch procedures. Thirty-seven IARTs were mapped in 22 Fontan patients. Twelve of 37 IARTs (33%) that revolved about the inferior vena cava (IVC) and involved the isthmus between the IVC and the tricuspid dimple/right-sided AV valve were identified in 12 patients (48%). Mean pericaval IART cycle length was 332 +/- 60 msec (range 240-410). An adjacent or surrounding area of scarring was observed in 10 of 12 IARTs. Slow zones (mean activation latency 39% +/- 11% IART cycle length) were detected in 8 of 12 circuits. The boundaries of the zone of slow conduction were scar-low crista (6) and scar-IVC (2). Periannular IART with CL 289 +/- 65 ms was observed in 14 of 20 patients with 4-chambered hearts. Slow zones (mean activation latency 28 +/- 9% IART cycle length) were found in 8 of 14 circuits. In both forms of IART, the predominant direction of activation of the isthmus was lateral to septal; 83% in pericaval IART and 87% in periannular IART. Radiofrequency catheter ablation successfully terminated 11 of 11 pericaval and 13 of 14 periannular IARTs. CONCLUSION: Pericaval reentry is a novel and ablatable mechanism of IART in patients specific to the Fontan procedure. It is distinguished from periannular atrial reentry by its association with Fontan anatomy, longer cycle lengths, and occurrence of a prominent discrete zone(s) of slow conduction. Both pericaval and periannular reentry show a marked preference for utilization of the isthmus in a lateral-to-septal direction.     

Bystander cavo-tricuspid isthmus activation during post-incisional intra-atrial reentrant tachycardia.

We describe a case of post-incisional atrial tachycardia resembling typical atrial flutter on the surface ECG. Typical atrial flutter reentry was ruled out by the results of activation and entrainment mapping. Nevertheless, overdrive pacing from the lateral edge of the cavo-tricuspid isthmus produced tachycardia entrainment with concealed fusion associated with post-pacing and stimulus-to-P wave onset intervals exactly matching the tachycardia cycle length duration and the electrogram-to-P wave onset interval, respectively. Therefore, that site was firstly severed by sequential radiofrequency pulses. However, a transformation of the tachycardia P wave morphology and endocardial activation sequence, not associated with tachycardia termination or cycle length modification occurred. After additional mapping manoeuvres, a relatively small reentrant circuit was identified in the low and mid aspect of the lateral right atrium with the critical isthmus located between the lower border of a cannulation atriotomy and the crista terminalis, close to the inferior vena cava orifice. A single radiofrequency pulse at that site terminated the tachycardia. Both the electrocardiographic pattern and the endocardial mapping data obtained in our case might be explained by a split of the reentrant wavefront into a secondary wavelet which freely propagated through the cavo-tricuspid isthmus without completing the peritricuspid loop. In conclusion, bystander cavo-tricuspid isthmus activation during atrial tachycardia may simulate a typical atrial flutter pattern on the surface ECG. Further studies should evaluate the prevalence of this propagation pattern in post-incisional atrial reentry and atypical atrial flutters, and identify its implications for ablation strategy.     

Invasive Elektrophysiologie: Komplikationen, Alpträume und deren Management

Most minor side effects of ablation in the right atrium and right ventricle relate to femoral venous catheterization but there is a small risk of severe complications including atrioventricular (AV) block, damage of surrounding structures and thromboembolic events. Impairment of AV conduction can occur during ablation of atrioventricular re-entrant tachycardia, ablation of anteroseptal, mid-septal and parahisian accessory pathways, ablation of ectopic atrial tachycardia originating from the vicinity of the atrioventricular node and when ablating the septal isthmus for typical atrial flutter. Damage of the right coronary artery is a very rare complication after inferior isthmus ablation with high energy. The thromboembolic risk during and after cardioversion and ablation of atrial flutter is higher than previously recognized and anticoagulation therapy decreases this risk. The risk of perforation and tamponade during ablation in the right atrium and right ventricle is very low but particular caution is necessary in thin-walled structures such as the coronary sinus and the upper right ventricular outflow tract. Phrenic nerve injury can be avoided by pacing from the mapping electrode before application of radiofrequency energy at the right atrial free wall. Limitation of power output depending on the site of ablation and titration of energy application with continuous control of temperature and impedance should be considered to minimize the risk of complications.     

Ablation of focal atrial arrhythmia in patients with congenital heart defects after surgery: Role of circumscribed areas with heterogeneous conduction

BACKGROUND: In patients late after surgical repair of congenital heart disease (CHD), areas with abnormal electrophysiologic properties may serve as slow conducting pathways within a macroreentrant circuit or may be the source of focal atrial tachycardia. OBJECTIVES: The purpose of this study was to evaluate the role of abnormal areas during focal atrial tachycardia prior to ablation. METHODS: Electroanatomic activation mapping of 62 atrial tachycardias was performed in 43 consecutive patients (37 +/- 12 years) after surgical repair of CHD. The mechanism of atrial tachycardia was scar related intra-atrial reentry (n = 27), cavotricuspid-related atrial flutter (n = 21), atrial fibrillation (n = 2), or focal atrial tachycardia (n = 10). During intra-atrial reentry, channels of slow conduction could be identified in all patients. Subsequent ablation was directed toward connecting two nonconductive borders. The site of origin during focal atrial tachycardia showed fractionated potentials and/or continuous electrical activity. RESULTS: Ablation directed at isolating the source area resulted in termination of focal atrial tachycardia in all cases. In two patients, ablation of an area showing continuous electrical activity giving rise to fibrillatory conduction resulted in termination of atrial fibrillation. Ablation of intra-atrial reentry was successful in 70%. Atrial flutter and focal atrial tachycardia were successfully ablated in all patients. No complications were observed. CONCLUSION: In patients with surgically corrected CHD, atrial tachycardia most often is caused by a macroreentrant mechanism but in some is the result of a focal mechanism. Areas of abnormal conduction may serve not only as a zone of slow conduction within a macroreentrant circuit but also as the site of origin of a focal atrial arrhythmia. Catheter ablation directed at "source isolation" is effective in eliminating focal atrial tachycardia in patients with CHD.     

Identification and ablation of atypical atrial flutter. Entrainment pacing combined with electroanatomic mapping

Differentiation between typical and atypical atrial flutter solely based upon surface ECG pattern may be limited. However, successful ablation of atrial flutter depends on the exact identification of the responsible re-entrant circuit and its critical isthmus. Between August 2001 and June 2003, we performed conventional entrainment pacing within the cavotricuspid isthmus in 71 patients with sustained atrial flutter. In patients with positive entrainment we considered the arrhythmia as typical flutter and treated them with conventional ablation of the cavotricuspid isthmus. As a consequence of negative entrainment we performed 3D-electroanatomic activation mapping (CARTO trade mark ). Conventional ablation of the right atrial isthmus was successful in all patients (n = 54) with positive entrainment. We performed electroanatomic mapping in the remaining 17 patients (14 male; age 60.9 +/- 16 years) resulting in the identification of 6 cases with typical and 11 cases with atypical flutter. Therefore, entrainment pacing was able to predict the true presence of typical atrial flutter in 91.5%. Atypical flutter was right sided in 4 patients and left sided in 7 cases. Electrically silent ("low voltage") areas probably demonstrating atrial myopathy were identified in all cases with left sided and in 2 patients with right sided flutter. In these patients targets for ablation lines were located between silent areas and anatomic barriers (inferior pulmonary veins, mitral respectively tricuspid annulus, or vena cava inferior). In 1 patient, the investigation was stopped due to variable ECG pattern and atrial cycle lengths. In the remaining cases, ablation was acutely successful. One patient, after surgical closure of a ventricular septal defect, demonstrated a dual-loop intra-atrial reentry tachycardia dependent on two different isthmuses. This arrhythmia required ablation of those distinct isthmuses to be interrupted. After a mean follow-up of 8.8 +/- 3.4 months, there was one patient with a recurrence of left-sided atrial flutter. Another patient developed permanent atrial fibrillation shortly after the procedure. Mean duration time of the procedure was 235.6 +/- 56.4 min (right atrium: 196 +/- 17.3 min; left atrium: 267.2 +/- 59.5 min), and average fluoroscopy time was 21.8 +/- 11.7 min (right atrium: 9.5 +/- 6 min; left atrium: 28.9 +/- 7 min). There was no incidence of serious complications associated with these procedures. In conclusion, conventional pacing in the cavotricuspid isthmus combined with electroanatomic mapping was an effective method to differentiate between typical and atypical atrial flutter. Electroanatomic mapping was a powerful tool both for identification of different atrial re-entrant circuits including their critical isthmuses as well as for effective application of individual ablation line strategies.     

Atrial flutter update

Typical atrial flutter has long been considered a reentrant arrhythmia, but it is only recently that the full structure of the right atrial circuit was understood, leading to de devise of ablation techniques. Recognition of the role of functional block, based on anisotropic conduction was crucial to understanding of the flutter circuit. Anisotropy at the terminal crest creates a line of block that, with the orifices of superior and inferior vena cava, constitutes the posterior boundary of the flutter circuit. The anterior boundary is the tricuspid ring, and the circuit is a ring of myocardium made by the septal and anterior right atrial walls, linked on top by the right atrial roof and inferiorly by the inferior vena cava-tricuspid ring isthmus. This isthmus, a relatively narrow part of the circuit, has become the established target for typical flutter ablation. Complete, bidirectional isthmus block is the final goal of flutter ablation. This has to be assessed, after flutter interruption, by pacing both sides of the ablation line while recording electrogram sequences from the opposite right atrial wall and the isthmus itself. Success is great in terms of prevention of flutter recurrence, however a 30% incidence of atrial fibrillation during follow-up casts a large shadow on long-term prognosis.Understanding of the myocardial abnormalities underlying atrial flutter and fibrillation will be necessary to improve this long-term outlook.     

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.     

Ventricular tachycardia as a complication of atrial flutter ablation

A 61-year-old woman with dilated cardiomyopathy, who previously underwent successful radiofrequency catheter ablation for atrial flutter, developed monomorphic ventricular tachycardia (VT). The site of VT origin was the inferobasal right ventricle adjacent to the previous atrial isthmus ablation area. The most likely mechanism for the VT was scar-related reentry, the scar being the result of previous radiofrequency lesions in the atrial isthmus. The VT was successfully ablated.     

Electrophysiologic basis of catheter ablation in atrial flutter

A reentrant mechanism is believed to be responsible for atrial flutter. The recent development of the entrainment criteria further supports this theory, and there is a general consensus that circus movement is the underlying abnormality that supports this arrhythmia. In most clinical studies, abnormal fragmented (or double spike) electrograms, suggesting the presence of areas of localized slowing of conduction or block, have been reported. They are almost always recorded in the lower and posterior portion of the right interatrial septum, but also frequently in the high lateral portion of the right atrium. The determination of their involvement in the reentry pathway is important for designing curative procedures such as surgery or ablation. The low atrial septal area surrounding the mouth of the coronary sinus was suspected as being the critical area of slow conduction in atrial flutter. Rapid pacing at that site can yield a surface electrocardiographic pattern similar to the clinically occuring arrhythmias. Additionally, the flutter circuit can be accelerated during atrial pacing at fixed and slightly faster rates than the intrinsic tachycardia rate—the so-called entrainment phenomenon. When entrainment criteria are fulfilled, tachycardla termination being by definition ruled out, any concomitant recorded local type II block identifies an area that must be outside the circuit. Such local block may be recorded either spontaneously or during entrainment and therefore helps in identifying atrial slow conduction areas that do not belong to the reentrant path. This approach was applied to identify the optimal ablation site in 8 patients with long-standing drug resistant atrial flutter. In 7 of 8 patients, we were able to identify a fragmented potential in the low posteroseptal area during sustained atrial flutter. Fulguration shocks were delivered at this site without complications, and after a mean follow-up of SSA weeks atrial flutter was controlled in 5 of 8 patients without the need of His bundle atrioventricular node ablation.     

Ablation of Ventricular Tachycardia Due to a Postinfarct Ventricular Septal Defect:

Outer Loop Tachycardia. Introduction : Ventricular tachycardia (VT) alter postinfarct ventricular septal defect (VSD) repair has not been well characterized.
Methods and Results: A 55-year-old man developed refractory VT after inferior wall infarction and VSD repair. Entrainment demonstrated a broad reentry circuit path (outer loop) between the tricuspid annulus and VSD patch. A series of radiofrequency (RF) lesions transected this path, abolishing VI' and producing conduction block between the inferior and superior aspects of the basal right ventricular septum.
Conclusion: Some VTs have broad reentry loops requiring ablation by a series of RF lesions across the path to create a line of block. This approach is analogous to that for atrial flutter.     

Electrophysiologic characteristics and ablation of an atypical atrial flutter in the right atrium

Subeustachian isthmus-dependent typical atrial flutter has been well studied. We demonstrate a case with atypical atrial flutter involving only the base of the right atrium around the inferior vena cava. Entrainment pacing and mapping studies documented a distinct circuit traversing the subeustachian isthmus, propagating through the posterobasal right atrium, and skirting the inferior vena cava. Successful radiofrequency ablation of the arrhythmia was accomplished by creating a linear lesion at the subeustachian isthmus. Mapping of the inferior vena cava region and the demonstration of concealed entrainment are essential steps in establishing the mechanism of the atypical atrial flutter.