Identification of left atrial origin of ectopic tachycardia during right atrial mapping: analysis of double potentials at the posteromedial right atrium

INTRODUCTION: The high posteromedial right atrium is adjacent to the left atrium near the right superior pulmonary vein. We hypothesized that analysis of electrograms at this site could distinguish left from right atrial tachycardia. METHODS AND RESULTS: Atrial mapping was performed in 16 patients with left atrial origin ectopic tachycardia (11 patients with right superior pulmonary vein origin and 5 patients with other left atrial tachycardias). During left atrial tachycardia, earliest right atrial activation was recorded at the high posterior right atrium in 14 of 16 patients. At all of these 14 early sites, double potentials were recorded during tachycardia. The first potential was a far-field signal from left atrium as indicated by the following: (1) during sinus beats, the timing of the two potentials reversed such that the left atrial one was late; (2) ablation at the right atrial site did not decrease the amplitude of the first potential, but did decrease the amplitude of the second potential; and (3) the timing of activation at the adjacent left atrium agreed with that of the first potential. In the 11 right superior pulmonary vein tachycardias, the first potential was markedly earlier than the p wave onset, but in left atrial tachycardias with other origins it was later. In a control group of six patients with pacing to simulate right atrial tachycardia, double potentials were recorded in the posterior right atrium, but the timing of components did not reverse during sinus rhythm. CONCLUSION: For some left atrial ectopic tachycardias, particularly those originating from the right superior pulmonary vein, recognition of left versus right atrial origin can be accomplished during right atrial mapping by analysis of double potentials in the posteromedial right atrium.     

心房颤动环肺静脉口外线性消融术后二次消融的电生理发现及随访结果

目的介绍三维导航下环肺静脉口外线性消融治疗心房颤动（房颤）术后快速房性心律失常及房颤复发患者二次消融时的电生理发现、消融策略及随访结果。方法2004年4月至2006年5月,采用左心房线性消融治疗房颤共91例。术后4例患者因心动过速反复发作或无休止发作于2周内行二次消融术。随访3个月后,25例患者有快速性心律失常发作,其中15例接受二次消融术。在所有接受二次消融的19例患者中,第一次消融前房颇为阵发性者11例,持续性2例,永久性6例,其中男性17例,女性2例,年龄25～65（53±12）岁。所有患者术中均使用环状电极行肺静脉电位探查。结果5例患者发现窦律下左侧肺静脉延迟电位,1例出现右侧肺静脉延迟电位,2例患者双侧同时出现延迟肺静脉电位;此类患者于环状电极指导下标测原消融线径的传导“缺口”并再次隔离成功。3例患者左侧肺静脉内颤动样节律,递减传导至左心房出现不规则房性心动过速;此类患者再次于三维标测指导下行左侧环状消融隔离成功;1例患者左侧肺静脉心动过速并1：1传导至左心房,经终止心动过速后隔离成功。4例患者肺静脉探查未发现肺静脉电位,但诱发出其他心动过速,包括右房瘢痕性房性心动过速、隐匿性旁路介导的室上性心动过速、右后间隔局灶性房性心动过速及三尖瓣峡部依赖的心房扑动。此4例患者在常规标测和三维标测指导下,心动过速均被成功消融。术中呈房颤节律者3例,再次于三维标测指导下行环肺静脉线性消融获成功。平均随访4～26（11．5±8．5）个月,16例患者无快速性心律失常发作,1例有频繁房性早搏,1例永久性房颤患者仍呈房颤节律,另1例永久性房颤患者转为阵发性房颤。结论肺静脉与左心房之间电传导恢复是消融术后出现快速房性心律失常的主要因素。肺静脉以外的心动过速在左心房线性消融术后可以表现为独立的心动过速,也可以触发房颤;环肺静脉口外线性消融不足以完全改良永久性房颤的维持基质。     

Focal atrial tachycardia originating from the musculature of the coronary sinus

Focal atrial tachycardias originate predominantly from the right atrium along the crista terminalis and less commonly from the left atrium. Successful catheter ablation usually can be performed via an endocardial approach. We report the case of a 34-year-old patient in whom a focal atrial tachycardia was successfully ablated 4 cm within the coronary sinus after extensive mapping of the left atrial endocardium and coronary sinus using the three-dimensional CARTO mapping system. Rarely, atrial tachycardia can originate from the coronary sinus musculature and require ablation inside the coronary sinus.     

Mechanistic significance of intermittent pulmonary vein tachycardia in patients with atrial fibrillation

INTRODUCTION: The significance of intermittent tachycardia within a pulmonary vein (PV) during an episode of atrial fibrillation (AF) is unclear. The aim of this study was to determine the role that intermittent PV tachycardias play in AF. METHODS AND RESULTS: In 56 patients with AF, segmental ostial ablation guided by PV potentials was performed to isolate the PVs. The characteristics of intermittent PV tachycardias and the inducibility of AF before and after PV isolation were analyzed prospectively. During AF, a PV tachycardia (mean cycle length 130 +/- 30 msec) with exit block to the left atrium was present in 93% of left superior, 80% of left inferior, 73% of right superior, and 7% of right inferior PVs. The site of shortest cycle length during AF alternated between the PVs and left atrium 1 to 13 times per minute. Complete isolation was achieved in 168 (94%) of 178 targeted PVs. In 99% of PVs, tachycardia resolved upon isolation. AF was persistent before and after PV isolation in 100% and 27% of patients, respectively (P < 0.001). CONCLUSION: Intermittent bursts of tachycardia are observed within multiple PVs during persistent AF in a majority of patients. After PV isolation, PV tachycardias almost always resolve, and AF is less likely to be inducible or persistent. These observations suggest a dynamic interplay between the atria and PVs, with intermittent bursts of PV tachycardia being dependent on left atrial input and with the probability of persistent AF diminishing when PV tachycardias are eliminated by PV isolation.     

Acute effects of left atrial radiofrequency ablation on atrial fibrillation

INTRODUCTION: Acutely, when left atrial ablation is performed during atrial fibrillation (AF), the AF may persist and require cardioversion, or it may convert to sinus rhythm or to atrial tachycardia/flutter. The prevalence of these acute outcomes has not been described. METHODS AND RESULTS: Left atrial ablation, usually including encirclement of the pulmonary veins, was performed during AF in 144 patients with drug-refractory AF. Conversion to sinus rhythm occurred in 19 patients (13%), to left atrial tachycardia in 6 (4%), and to atrial flutter in 6 (4%). In the 6 patients with a focal atrial tachycardia, the mean cycle length was 294 +/- 45 ms. The tachycardia arose in the left atrial roof in 3 patients, the left atrial appendage in 2, and the anterior left atrium in 1. In 3 of 6 patients, the focal atrial tachycardia originated in an area that displayed a relatively short cycle length during AF. In 6 patients, AF converted to macroreentrant atrial flutter with a mean cycle length of 253 +/- 47 ms, involving the mitral isthmus in 5 patients and the septum in 1 patient. All atrial tachycardias and flutters were successfully ablated with 1 to 15 applications of radiofrequency energy. CONCLUSION: When left atrial ablation is performed during AF, the AF may convert to atrial tachycardia or flutter in approximately 10% of patients. Focal atrial tachycardias that occur during ablation of AF may be attributable to driving mechanisms that persist after AF has been eliminated, whereas atrial flutter results from incomplete ablation lines.     

Radiofrequency catheter ablation of atrial tachycardia

Background: Atrial tachycardia is a relatively uncommon arrhythmia which usually responds poorly to antiarrhythmic drug therapy. Transcatheter radiofrequency (RF) ablation is a new therapeutic modality for patients with atrial tachycardia. Aim: This study analyses our early experience with the treatment of atrial tachycardia by this technique. Methods: Thirteen consecutive patients (age 13–63 years) with 15 drug-refractory atrial tachycardia foci were treated with RF catheter ablation. Atrial tachycardia was mapped by seeking the earliest atrial activation in the right atrium in eight patients and in the left atrium in five. Results: Tachycardias were abolished in nine (69%) patients, including two sinoatrial re-entrant tachycardias and seven automatic atrial tachycardias, after 9±10 (range, one to 28) pulses of RF current. Six of these ablated atrial tachycardia foci were right sided and three were on the left. One patient had three separate right atrial tachycardia foci; one was eliminated. Tachycardia recurred after two weeks in one patient with apparently successful ablation of sinoatrial re-entrant tachycardia. One patient with successful ablation of a right atrial tachycardia developed cardiac tamponade requiring surgical intervention. Conclusion: This study demonstrates that atrial tachycardia arising from diverse sites can be eliminated by RF catheter ablation.     

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。     

三维标测指导下射频导管消融右心耳起源的局灶性房性心动过速

目的 报道应用三维标测指导射频导管消融起源于右心耳的局灶性房性心动过速(房速),并初步探讨其临床及心电学特征.方法 共6例患者(男性4例,女性2例,年龄(43±19)岁]临床诊断为窄QRS心动过速,其中3例曾行常规射频消融失败,4例左心房内径明显扩大.经电生理检查证实为房速.术中行EnSite-NavX激动标测或者Carto电解剖标测以明确局灶性房速并指出最早激动大致范围.在局部做精细标测找到心房最早激动处,于心动过速时应用盐水灌注导管放电消融,能量30～40 W,温度43℃.即刻成功指标为心动过速终止并不再被诱发.结果 6例心动过速平均心动周期为(343±53)ms.三维激动标测结果显示房速呈右心耳部位点状扩布,并且整个右心房激动时间占心动周期的27%±8%.成功消融靶点局部A波较体表心电图P波提前(52±13)ms.消融后行右心房心耳造影确认消融导管位置.6例右心耳房速均成功消融且未有并发症发生.随访3个月其中1例复发心动过速,经再次标测证实为三尖瓣前侧部局灶性房速并且成功消融.左心房扩大者心房内径较术前显著缩小[(41±6)mm对(36±6)mm,P＜0.05].结论 局灶性房速可起源于右心耳并可以成功消融.三维标测有助于靶点定位及消融成功.     

无器质性心脏病儿童房性心动过速的射频消融治疗

目的探讨无器质性心脏病儿童房性心动过速（房速）的电生理学机制、靶点标测和射频消融疗效。方法46例房速患儿行心内电生理检查和射频消融术,房速靶点标测采用激动标测方法,4例患儿采用三维电解剖学标测系统（CARTO系统）标测和指导消融。消融采用预设温度50～60℃。结果46例患儿均经电生理检查证实为局灶性房速,分别表现为短阵自限性、阵发持续性和持续无休止性心动过速,其中1例合并房室结折返性心动过速。射频消融成功41例,其中单一源性房速39例（右房27例,左房12例）,多源房速2例,成功率为89%。结论无器质性心脏病儿童房速的射频消融成功率较高,是一种安全有效的方法。     

Biatrial and three-dimensional mapping of spontaneous atrial arrhythmias in patients with refractory atrial fibrillation

INTRODUCTION: While atrial fibrillation (AF) initiation in the pulmonary veins has been well-studied, simultaneous biatrial and three-dimensional noncontact mapping (NCM) has not been performed. We hypothesized that these two techniques would provide novel information on triggers, initiation, and evolution of spontaneous AF and permit study of different AF populations. METHODS AND RESULTS: The origin of atrial premature beats (APBs), onset of spontaneous AF and its evolution were analyzed in 50 patients with AF in the presence or absence of structural heart disease (SHD) and in different AF presentations (group A: Persistent, group B: Paroxysmal). In 45 patients, spontaneous APBs in the right atrium (RA; n = 60) and left atrium (LA; n = 25) with similar regional distributions regardless of heart disease status were demonstrated. In total, 22 patients (44%) had > or =2 disparate regional origins. Biatrial regional foci were seen with equal frequency in patients with SHD (31%), without SHD (40%), in group A (32%), and in group B (36%). Biatrial mapping and NCM showed organized monomorphic atrial tachyarrhythmias arising in the RA (17), septum (17), or LA (21) and were classified as atrial flutter (RA = 34, LA = 8), macro-reentrant atrial tachycardia (RA = 1, LA = 3) or focal atrial tachycardia (RA = 2, LA = 7). Their regional distribution was more extensive in patients with SHD and persistent AF compared with patients without SHD or paroxysmal AF. Simultaneous biatrial tachycardias were observed only in group A patients and those with SHD. CONCLUSIONS: Simultaneous biatrial and NCM permits successful AF mapping in different AF populations and demonstrates a biatrial spectrum of spontaneous triggers and tachycardias. Organized monomorphic tachycardias with multiple unilateral or biatrial locations are commonly observed in human AF. Patients with heart disease or persistent AF have a more extensive distribution as well as simultaneous coexistence of multiple tachycardias during AF.     

Mechanisms of atrial tachyarrhythmias following surgical atrial fibrillation ablation

INTRODUCTION: Typical and atypical atrial flutters (AFLs) and atrial tachycardias (ATs) have been reported in patients with prior surgical atrial fibrillation ablation. The underlying mechanisms for this group of atrial tachyarrhythmias have not been well characterized and the efficacy of catheter ablation in their treatment is unknown. METHODS AND RESULTS: Twenty patients (6 females) with a surface ECG diagnosis of AFL or AT following surgical atrial fibrillation ablation underwent 26 electrophysiology studies. Patients manifesting sustained, organized, and beat-by-beat reproducible atrial electrical activity underwent complete right and left atrial catheter mapping and catheter ablation. One patient had no inducible tachyarrhythmia, while 5 patients had nonmappable arrhythmias. Nineteen of the 31 potentially mappable atrial tachyarrhythmias were completely characterized in 14 patients. The underlying mechanisms were macro-reentrant left AFL (n = 9), focal left AT (n = 3), typical right AFL (n = 6), and atypical right AFL (n = 1). Of the 19 completely characterized atrial arrhythmias, catheter ablation was performed for 18, and the procedure was successful for 13 of these. After a mean follow-up of 15 +/- 10 months, 15 of 20 patients (75%) were in sinus rhythm including 10 of 13 patients (77%) with AT/flutter ablation. Ten patients, including 6 following ablation, were maintaining sinus rhythm without antiarrhythmic medications. CONCLUSIONS: Patients with an ECG diagnosis of AFL or AT following surgical atrial fibrillation ablation may have multiple tachycardia mechanisms with the right or left atrium as the site of origin. Many of these rhythms may resolve with further maturation of surgical atrial fibrillation ablation (SAFA) lesions or be treatable with antiarrhythmic medication. However, persistent tachyarrhythmias can often be treated successfully with catheter mapping and ablation.     

Atrial Tachycardia Confined Within the Left Atrial Appendage

AT Confined Within the LAA. Left atrial tachycardias are often seen following catheter ablation of persistent atrial fibrillation (AF). We report here an unusual case where AF was converted to sinus rhythm following catheter ablation, but ongoing atrial tachycardia confined within the left atrial appendage (LAA) was observed. Although the LAA tachycardia was dissociated from the atrium in sinus rhythm, bidirectional conduction between the left atrium and the LAA was, however, demonstrated after tachycardia termination. (J Cardiovasc Electrophysiol, Vol. 21, pp. 933‐935, August 2010)     

Factors determining clockwise and counterclockwise conduction patterns in atrial reentrant tachycardias: a rabbit model of atrial flutter

INTRODUCTION: In the development of atrial flutter due to reentry, the crista terminalis is supposed to pose a conduction barrier, but the role of its longitudinal conduction in determining the propagation pattern of the reentrant impulse is not known. In rabbit right atrial preparations, we induced reentrant atrial tachycardias and examined the effects of transverse section of the crista terminalis on the development and conduction patterns of arrhythmias. METHODS AND RESULTS: Right atrial preparations from 12 albino rabbits were placed endocardial surface down in a chamber with an array of 48 bipolar electrodes to draw activation maps. A single premature stimulus was delivered to induce tachycardias at the free wall. In the control, five instances of tachycardia per preparation were induced and another five were induced after cutting the crista terminalis. In the control, the mean duration of tachycardia was 127.1+/-25.2 seconds. The tachycardia was counterclockwise in 39 of 60 instances, clockwise in 12, and undetermined in 4 defined as "atypical." After transverse section of the crista terminalis, the duration was prolonged to 372.6+/-30.4 seconds, but the conduction patterns were not changed. In the free wall, counterclockwise reentry had a broader wavefront and faster conduction than clockwise reentry. CONCLUSION: Longitudinal conduction block at the crista terminalis contributed to maintenance of reentrant atrial tachycardias, but had no influence on their propagation patterns. Clockwise and counterclockwise rotation of impulses in reentrant tachycardias had different paths and velocities of the wavefront in the free wall of the right atrium.     

Bi-focal atrial tachycardia mimicking atrial fibrillation: fusion and interference between two distinct tachycardias

Irregular tachycardias mimicking atrial fibrillation (AF) have previously been described. We report a case of a 60-year-old man with an antiarrhythmic drug-resistant atrial tachycardia (AT) mimicking AF. The tachycardia consisted of two distinct ATs with interference of one repetitive AT with another sustained AT. Radiofrequency (RF) ablation of two distinct right atrial foci eliminated the irregular tachycardia. Although catheter-based pulmonary vein isolation has become a popular therapeutic approach for patients with symptomatic AF, careful evaluation of the intracardiac recordings in the patients undergoing RF ablation for AF is important.     

Electrocardiographic Diagnosis of Atrial Tachycardia: Classification,P‐Wave Morphology,and Differential Diagnosis with Other Supraventricular Tachycardias

Atrial tachycardia is defined as a regular atrial activation from atrial areas with centrifugal spread, caused by enhanced automaticity, triggered activity or microreentry. New ECG classification differentiates between focal and macroreentrant atrial tachycardia. Macroreentrant atrial tachycardias include typical atrial flutter and other well characterized macroreentrant circuits in right and left atrium. Typical atrial flutter has been described as counterclockwise reentry within right atrial and it presents a characteristic ECG “sawtooth” pattern on the inferior leads. The foci responsible for focal atrial tachycardia do not occur randomly throughout the atria but tend to cluster at characteristic anatomical locations. The surface ECG is a very helpful tool in directing mapping to particular areas of interest. Atrial tachycardia should be differentiated from other supraventricular tachycardias. We propose a diagnostic algorithm in order to help the physician to discriminate among those. Holter analysis could offer further details to differentiate between atrial tachycardia and another supraventricular tachycardia. However, if the diagnosis is uncertain, it is possible to utilize vagal maneuvers or adenosine administration. In conclusion, in spite of well–known limits, a good interpretation of ECG is very important and it could help the physician to manage and to treat correctly patients with atrial tachycardia.     

Nonpharmacological treatment of atrial tachycardia.

The authors analyse the efficacy and safety of catheter ablation and atrial pacing for the treatment of atrial tachycardia. Radiofrequency catheter ablation was selected whenever the arrhythmogenic focus was located on the free-wall or in the meso-septal area of the right atrium. In opposition, overdrive atrial pacing was chosen for tachycardias originating near the sinus complex or in the left atrium. Both therapies were safe, but had a low efficacy in converting the tachycardia into sinus rhythm. However, catheter ablation allows an irreversible destruction of small septally located foci. Thus, both the anatomical and the electrophysiological characteristics of the foci can be important factors in the selection of the most appropriate nonpharmacologic therapy.     

房性心动过速的射频消融治疗

探讨房性心动过速 (简称房速 )的电生理机制、标测方法及射频消融结果。 2 3例房速 :右房房速 15例 ;左房房速 8例 ,其中左上肺静脉口房速 3例、右上肺静脉口房速 2例、左下肺静脉口下方房速 1例、右下肺静脉口下方房速 2例。结果 :15例右房房速成功 13例 ,成功率为 87% ;左房房速 8例全部成功 ,成功率为 10 0 % ,总成功率为91.3%。成功消融靶点的A波较体表心电图P′波提前 44± 6ms。随访 2～ 36个月 ,无复发。结论 :射频消融治疗房速 (包括左房非经典部位房速 )是一种安全有效的方法     

Catheter ablation of regular atrial arrhythmia following surgical treatment of permanent atrial fibrillation

Ablation of Atrial Tachycardia after Antiatrial Fibrillation Surgery. INTRODUCTION: Surgical treatment of atrial fibrillation (AF) is gaining widespread acceptance. However, therapeutic modalities for secondary regular atrial tachycardia are still empiric. METHODS AND RESULTS: After linear atrial cooled-tip radiofrequency ablation (SICTRA) during cardio-surgical procedures to cure permanent AF, patients with regular atrial tachycardia were identified. Invasive electrophysiology including electroanatomic mapping was performed. Catheter ablation was directed to suppress atrial arrhythmia depending on activation mapping findings. Follow-up was performed after 3 months and then after every 6 months. Of 238 patients, 12 (5.0%) were identified with regular secondary arrhythmias (12 +/- 7 months after surgery) including 9 (3.8%) with persistent forms originating from the right atrium (RA) in six (66%) (isthmus-dependent macroreentry in 4, incisional macroreentry in 1, and RA ectopy in 1). All patients with RA origin of the tachycardia were successfully ablated. Two patients had left atrial (LA)-macroreentry circling around the mitral valve indicating insufficiency of the intraoperative ablation procedure: one patient was successfully ablated within the LA isthmus, in the other patient no complete conduction block could be induced. One patient had LA-macroreentry degenerating into AF, and ablation was not performed. During follow-up (9 +/- 4 months), no recurrences of atrial tachycardias were documented after successful ablation. CONCLUSIONS: Persistent regular "secondary" arrhythmia occurred in 3.8% (9/238) of patients after SICTRA to treat permanent AF. Predominantly (67%; 6/9), the arrhythmia was located in the RA mostly incorporating the RA-isthmus. Catheter ablation was highly effective for RA tachycardia (100%). In three cases (33%), LA-macroreentry was documented and catheter ablation was successful in only one patient (overall success 78%).     

Comparison of Atrial-His Intervals During Tachycardia and Atrial Pacing in Patients with Long RP Tachycardia

Long RP Tachycardia. Introduction : The purpose of this study is to describe a simple and reliable diagnostic maneuver that allows for the rapid differentiation of atypical AV nodal reentrant tachycardia (AVNRT) from other causes of long KP tachycardia. Long RP tachycardias may he caused by atypical AVNRT, orthodromic reciprocating tachycardia (ORT) involving a slowly conducting retrograde accessory pathway, or atrial tachycardia. The differentiation of atypical AVNRT from ORT or atrial tachycardia may be difficult, especially when the differential diagnosis includes a posteroseptal accessory pathway or an atrial tachycardia arising in the posteroseptal right atrium.
Methods and Results : Twelve patients with atypical AVNRT, 21 with ORT, and 12 with an atrial tachycardia diagnosed using conventional criteria were enrolled In this study. The atrial-His (AH) interval was measured at the His-bundle position during the tachycardia and during atrial pacing from the high right atrium at the tachycardia cycle length in the setting of sinus rhythm. In patients with atypical AVNRT, the mean AH interval was 69 msec ± 50 msec (± SD) longer during high right atrial pacing than during the tachycardia (P < 0.001). In 10 of 12 patients with atypical AVNRT, the AH interval during atrial pacing was more than 40 msec longer than the AH interval measured during the tachycardia. In contrast, in patients with ORT or atrial tachycardia, the differences in AH interval between atrial pacing and tachycardia were never more than 20 and 10 msec, respectively.
Conclusion : The difference in the AH interval between atrial pacing and the tachycardia allows a simple and rapid means of differentiating atypical AVNRT from other types of long RP tachycardias.     

A novel pacing maneuver to localize focal atrial tachycardia

Background: Although focal atrial tachycardias cannot be entrained, we hypothesized that atrial overdrive pacing (AOP) can be an effective adjunct to localize the focus of these tachycardias at the site where the post-pacing interval (PPI) is closest to the tachycardia cycle length (TCL).
Methods: Overdrive pacing was performed in nine patients during atrial tachycardia, and in a comparison group of 15 patients during sinus rhythm. Pacing at a rate slightly faster than atrial tachycardia in group 1 and sinus rhythm in group 2 was performed from five standardized sites in the right atrium and coronary sinus. The difference between the PPI and tachycardia or sinus cycle length (SCL) was recorded at each site. The tachycardia focus was then located and ablated in group 1, and the atrial site with earliest activation was mapped in group 2.
Results: In both groups the PPI-TCL at the five pacing sites reflected the distance from the AT focus or sinus node. In group 1, PPI-TCL at the successful ablation site was 11 ± 8 msec. In group 2, PPI-SCL at the site of earliest atrial activation was 131 ± 37 msec (P < 0.001 for comparison). In groups 1 and 2, calculated values at the five pacing sites were proportional to the distance from the AT focus or sinus node, respectively.
Conclusions: The PPI-TCL after-AOP of focal atrial tachycardia has a direct relationship to proximity of the pacing site to the focus, and may be clinically useful in finding a successful ablation site.