主动脉无冠窦内和二尖瓣环-主动脉连接处射频导管消融局灶性房性心动过速

目的报告18例主动脉无冠窦内和1例二尖瓣环-主动脉连接(MAAJ)处成功消融局灶性房性心动过速(房速),探讨该类房速的电生理特点及标测和消融方法。方法 18例患者,女性14例,平均年龄41-71岁,均有阵发性房速病史。心房刺激诱发房速后,分析体表心电图P波特点并于右房进行激动标测,如果最早心房激动邻近希氏束附近,少数患者在此处消融,其他患者和上述消融不成功患者,经主动脉逆行途径,在无冠窦内标测和消融。如果消融不能成功,则经房间隔穿刺途径至左房标测最早激动部位处消融。结果房速发作时体表心电图P波明显变窄(77.8±14.4)ms。右房激动标测均在希氏束附近标测到相对提前的心房激动,3例于此处消融失败。18例经主动脉逆行途径于无冠窦内标测到最早心房激动提前希氏束处心房激动0～20.0(平均10 ms),17例于无冠窦内消融成功,包括1例改用盐水灌注导管后消融成功。1例经无冠窦消融失败后,经穿刺房间隔于MAAJ处标测到最早心房激动处消融成功。随访3～38个月,均无复发。结论对于具有窄P波及标测右房最早激动位于希氏束附近的局灶性房速,经主动脉逆行途径在无冠窦内标测和消融具有很高的成功率,经穿刺房间隔在左侧MAAJ处消融或应用盐水灌注导管无冠窦内消融可能进一步提高消融成功率。     

三维标测下主动脉无冠窦起源局灶性房性心动过速的射频消融效果

目的:分析主动脉无冠窦起源房性心动过速(房速)的心内电生理标测特点及射频消融疗效。方法:对11例主动脉无冠窦起源房速在三维标测系统引导下行心内电生理标测及射频消融治疗。术中构建右心房、希氏束及主动脉根部电解剖模型,测量最早激动点与希氏束的距离,在房速最早激动部位行射频消融治疗。结果:心内电生理检查11例房速皆为局灶起源,右心房激动标测最早激动部位均在希氏束左侧或左后上方,领先冠状窦近端参照A波(21.0±7.9)ms,距希氏束(6.9±3.4)mm。主动脉根部标测房速最早激动部位皆位于无冠窦内,领先冠状窦近端参照A波(35.0±8.6)ms,距希氏束(7.3±4.6)mm;消融终止房速,巩固消融后重复术前诱发条件刺激不能诱发出房速。术中及术后无房室阻滞发生。术后随访6个月,房速无复发。结论:无冠窦起源房速消融安全性和成功率高,标测要点为右心房房速最早激动位于希氏束左侧或左后上方时应常规于主动脉根部标测明确是否无冠窦激动最为领先。     

经主动脉无冠窦内射频消融局灶性房性心动过速

目的探讨起源于主动脉无冠窦或其邻近组织的局灶性房性心动过速(简称房速)心脏电生理特点及经射频导管消融方法。方法 13例患者男3例,女10例,年龄52.7±9.8岁,阵发性房速病史4.2±4.5年。心房刺激诱发房速后,分析体表心电图P′波特点并于右房及主动脉无冠窦内进行激动标测。均于无冠窦内进行射频消融治疗。结果 13例心房刺激均能反复诱发或终止房速,平均周长340.9±46.0ms,房速时P′波时限77.8±14.4ms,明显短于窦性心律时P波时限111.2±10.3ms(P0.05)。常规激动标测,所有患者于His束处标测到相对提前的心房激动。经主动脉逆行方法 ,所有患者于无冠窦内标测到心房激动较His束处的心房激动提前9.3±6.1ms,放电1～2次于2～8s内终止房速。随访3～36个月,无复发病例及手术相关合并症。结论起源于主动脉无冠窦或其邻近组织的房速具有窄P′波及常规标测相对提前的心房激动位于His束处的特点。经主动脉无冠窦内标测消融是一种根治此类房速安全有效的方法 。     

主动脉无冠状窦内射频导管消融前间隔局灶性房性心动过速

目的报告经主动脉无冠状窦内射频消融8例前间隔局灶性房性心动过速(房速)。方法8例患者男性3例,女性5例,平均年龄(50．6±12．3)岁。阵发性房速病史(7．5±5．5)年。术中心房和心室刺激诱发房速,分别在右心房、左心房和主动脉无冠状窦内标测最早心房激动,并进行消融。结果心房刺激能反复诱发和终止8例患者的房速,房速的平均周长(329±66)ms。右心房和左心房的前间隔部位标测相对提前的心房激动,但多次消融未成功。主动脉无冠状窦内的心房激动较希氏束处的心房波提前(11．6±7．2)ms,放电1～2次于8s内终止8例房速。随访(10．2±4．8)个月,无一例房速复发。结论主动脉无冠状窦内可作为消融前间隔局灶性房速的一种新途径,尤其适用于在希氏束部位消融失败的患者。     

经主动脉无冠状窦内射频消融治疗房性心动过速

目的:报告经主动脉无冠状窦内射频消融6例局灶性房性心动过速(房速)的消融结果。方法:6例患者中男女各3例。阵发性房速病史(6±3)年。常规心电图、心内电生理,术中心房和心室刺激诱发房速,分别在右心房、左心房和主动脉无冠状窦内标测最早心房激动,并进行射频消融。结果:心房刺激能反复诱发和终止6例患者的房速。心房内的前间隔部位标测相对提前的心房激动,但多次消融未成功。经主动脉无冠状窦内消融成功。平均随访3~17个月,无1例房速复发。结论:经主动脉无冠状窦消融前间隔房速是安全,有效的。     

射频消融术治疗主动脉无冠窦房性心动过速方法学特点

目的:探讨射频消融术治疗无冠窦房性心动过速(房速)的方法学特点.方法:分析14例无冠窦房速患者发作时体表心电图P波特点,展示发作时无冠窦、左房前间隔和希氏束最早激动的时间差异,5例患者采用三维(EnSite 3000 NavX)建模标测.结果:房速发作时P波时限(83±4)ms明显短于窦性心律时P波时限(106±9)ms,P＜0.05;右房最早激动点位于希氏束或其附近;无冠窦内最早心房激动较希氏束提前(10.8±7.2)ms,先于体表心电图P波提前(20.8±7.2)ms,5例患者通过房间隔穿刺术在左房前间隔测及的最早激动点较右房晚(4±2)ms.12例患者均在无冠窦内消融成功,2例患者在无冠窦内和希氏束后上方与无冠窦相对应处同时消融成功.随访4～30个月均无复发.结论:射频消融术是根治无冠窦房速的有效方法,对于房速消融不成功者,可选择在无冠窦内和希氏束后上方与无冠窦相对应处同时消融.     

主动脉无冠窦内射频消融前间隔房室旁路

目的 报道经主动脉无冠窦内射频消融前间隔房室旁路.方法 7例患者,男性4例,女性3例,平均年龄（38.4±14.7）岁.电生理检查证实存在房室旁路,并检查其前传逆传功能和诱发旁路参与的房室折返性心动过速.在心动过速时标测最早心房逆传激动点作为消融靶点.结果 7例心动过速时最早心房激动部位均位于前间隔区域,但经右心房途径反复消融均不能成功阻断旁路,而在无冠窦内可标测到最早逆传心房激动点并消融成功,无并发症出现.结论 主动脉无冠窦内消融可作为治疗前间隔房室旁路的一种新途径,特别适用于右心房前间隔区域消融失败的病例.     

起源于主动脉窦内的房性心动过速、频发室性早搏的射频消融治疗

目的报道4例局灶性房性心动过速（房速）,3例频发室性早搏（室早）经主动脉途径在左冠窦和无冠窦内标测和射频消融的结果。方法对4例房速、3例频发室早进行常规心电图、心内电生理检查和射频消融治疗。结果4例阵发性房速患者的标测靶点位于主动脉窦内,在无冠窦成功消融;3例频发室早在左冠窦内标测及消融成功。术中无并发症,随访3～31个月,无1例复发。结论在主动脉无冠窦、左冠窦内射频消融是可行的且能达到安全、有效的治疗目的。尤其适用于在常规、经典部位消融失败的患者。     

无冠窦起源房速的电生理特征与射频消融

目的进一步分析起源于主动脉无冠窦房性心律失常的心电生理特征及射频消融治疗。方法11例患者经心内电生理检查和射频消融证实的起源于主动脉无冠窦局灶性房速,对其临床特征,心电生理特点及射频消融进行分析。结果无冠窦房速大多为女性,表现为阵发性,为心房或心室程序刺激诱发和终止。所有患者房速心电图P波窄而低幅,Ⅱ,Ⅲ,aVF和v,导联P波负正双向,Ⅰ,aVL导联直立,V2～V6导联P波负向。心内最早激动位于希氏束远端,并领先于体表P波起始（15±3）ms。无冠窦内标测最早激动等于或早于希氏束远端,局部电位特征为大A小V（或大V）,无希氏束电位,11例患者无冠窦内放电均在8秒内终止心动过速,均无并发症,无抗心律失常药物随访12±5月所有患者均无心动过速复发。结论主动脉无冠窦房速有独特的临床特征,心电图特征及心房内激动顺序,长期随访这类房速射频消融有良好的治疗效果。     

二尖瓣环间隔起源局灶性房性心动过速电生理特征与射频消融

目的探讨二尖瓣环间隔起源局灶性房性心动过速(房速)心电图(ECG)特性,电生理特性和射频消融治疗(RFA)。方法 13例患者经心内电生理检查证实起源于二尖瓣环间隔侧房速(简称二尖瓣间隔房速),其中男性6例,女性7例,年龄23~47(35±12)岁,心动过速病史1~6年。结果 12例患者经穿房间隔途径标测消融成功,1例经主动脉逆行途径标测消融成功。根据局部电位特征,X线影像和三维标测系统确定成功消融位点分别为:二尖瓣环前间隔旁8例,二尖瓣环中间隔到前间隔之间3例,二尖瓣环后间隔2例。所有房速心电图V1导P波均表现出负正双向,右房激动标测显示最早右房激动点位于间隔侧(希氏束区域或冠状窦近端)。13例患者成功靶点局部电位均为小A大V,9例局部电位A波为复杂或碎裂的。所有患者均无明显并发症,12例长期随访无心动过速复发。结论二尖瓣环间隔区域是重要的房速起源点,常见于前间隔旁,其有独特P波形态和心内激活顺序。经穿间隔或逆行主动脉途径消融二尖瓣环间隔房速,安全有效。     

心房后间隔局灶性房性心动过速的电生理特征及射频消融

目的 探讨起源于心房后间隔及邻近区域局灶性房性心动过速（房速）心脏电生理特点及射频导管消融特点.方法 入选23例患者,男12例,女11例,平均年龄（48.3±19.3）岁,自发或心房程序刺激诱发房速后,分析体表心电图P＆#39;波特点并于后间隔各个部位进行激动标测和射频消融治疗.结果 23例心房刺激均能反复诱发或终止房速,平均周长（346.7±61.8） ms,房速时P＆#39;波时限明显短于窦性心律时P波时限[（86.2±14.0）ms对（115.4±19.9） ms,P＜0.05].体表P＆#39;波表现为Ⅰ导联多呈等电位线,下壁导联呈深倒负向波,aVR和aVL导联呈正向波,V3～W5导联呈负向波.常规激动标测,所有患者于冠状静脉窦口（CSO）附近标测到相对提前的心房激动,其中12例起源于右后间隔,6例起源于CSO及近端,2例起源于心中静脉,3例起源于左后间隔.靶点提前体表P＆#39;波平均（34.4±18.0） ms,放电开始至心动过速终止时间为（6.2±4.2）s,11例患者放电过程中出现交界区心律.所有患者均消融成功,其中3例需应用盐水灌注导管.随访4个月～ 10年,无复发病例及手术相关并发症.结论 后间隔局灶性房速P＆#39;波形态具有特异性,对导管消融定位意义较大.由于解剖的复杂性,部分病例标测和消融困难,需结合右心房后间隔、冠状静脉窦（CS）内和/或其分支、左心房后间隔等多部位标测和/或消融方能获得成功.     

多极导管粗标消融导管经Swartz鞘细标的方法消融右心房房性心动过速

目的　探讨右心房房性心动过速的导管标测和消融方法。方法　常规电生理检查确诊 12例右心房房性心动过速后 ,2 0极标测导管在右心房内弯曲、旋转粗标右心房的不同面 ,寻找较体表心电图 P波提前的相对较早的心房内心电图 ,以此心电图的电极对作为参考点 ,消融导管通过 Swartz鞘在该点附近仔细标测 ,寻找最早心房激动点消融。射频消融的能量从 15 W开始逐渐递增至 2 5 W。结果　 12例右心房房性心动过速均消融成功 ,无并发症 ,随访 (2 6± 14 )月未见复发。成功消融部位在冠状窦口附近 5例 ,希氏束附近 2例 ,房间隔中部 3例 ,右心房高侧壁 2例。消融成功部位的心房内心电图较 P波提前 (42± 12 ) m s。终止房性心动过速初始放电能量均为 15 W,时间均在5 s内。放电次数 2～ 6次。X线曝光时间 (38± 16 ) min。结论　多极标测导管粗标 ,消融导管经 Swartz鞘细标寻找最早心房激动消融右心房房性心动过速的方法简单有效     

Atrial components contributing to pseudo r' deflection in lead V1 in slow/fast atrioventricular nodal reentrant tachycardia: analysis of the atrial activation sequence by basket catheter isochronal mapping.

Electrocardiographic recognition of the P' wave during tachycardia is very useful in the diagnosis of supraventricular tachycardias. In slow/fast (S/F) atrioventricular nodal reentrant tachycardia (AVNRT), no discrete P' waves are observed on ECG and pseudo r' deflection in lead V1 (pseudo r') is commonly recognized. However, the atrial components that contribute to the genesis of pseudo r' in lead V1 have not been described and this study aimed to clarify them by analysis of the whole activation sequence of the right atrium using Basket catheter isochronal mapping. The study group comprised 48 patients with AVNRT. Pseudo r' was defined as an upward deflection in the terminal portion of the QRS complex during tachycardia that was not recognized during sinus rhythm and it occurred in 45 patients (94%). During S/F AVNRT, the retrograde atrial activation was earliest on His bundle electrogram, followed by the coronary sinus ostium, distal coronary sinus and high right atrium. Only the high lateral aspect of the right atrium was activated after the end of the QRS complex. The interval between the onset of QRS in multiple surface ECG leads and the atrial activities on high right atrium was similar to the V-r' interval in lead V1 (111+/-20ms, 117+/-11 ms) and correlated with the V-r' interval (r=0.56). Pseudo r' deflection in lead V1 is a highly sensitive indicator of S/F AVNRT, and appears to result from the activation of the superolateral aspect of the right atrium.     

肺静脉异常电活动引起持续性心房颤动的电生理特点和消融治疗

目的　报道 4例肺静脉异常电活动引起持续性心房颤动 (房颤 )的电生理特点和消融治疗。方法　 4例患者的临床表现和心电图记录提示为持续性房颤。经股静脉和锁骨下静脉穿刺置入高位右房 (HRA)和冠状静脉窦 (CS)电极 ,并行房间隔穿刺和肺静脉造影 ,置入 10极环状电极 (Lasso电极 )进行各肺静脉标测。观察自发和诱发房颤时的心腔各部位局部电活动的周期及规则性 ,以局部异常电活动出现最早、持续异常电活动最紊乱的肺静脉作为靶肺静脉。在房颤持续时消融电隔离靶肺静脉至左房连接处 ,以房颤终止和异常电活动消失为消融终点。结果　 4例患者异常电活动起源于右上肺静脉 (3例 )和左上肺静脉 (1例 )。靶肺静脉局部电活动频率快且不规则 ,间断出现短阵性周期缩短。靶肺静脉口部消融分别于放电 1～ 18次时房颤终止 ,3例伴有异常电活动终止 ,1例肺静脉内仍显示快速异常电活动 ,经肺静脉内局灶消融后电活动终止。随访 4～ 17个月 ,无房颤复发。结论　肺静脉内异常电活动是部分持续性房颤的发生机制 ,射频消融肺静脉口部可隔离和消除异常电活动而终止房颤     

Focal para-hisian atrial tachycardia with dual exits

Focal atrial tachycardias (AT) in the right atrium (RA) tend to cluster around the crista terminalis, coronary sinus (CS) region, tricuspid annulus, and para-hisian region. In most cases, the AT focus can be identified by careful activation mapping, and completely eliminated by radiofrequency (RF) catheter ablation. However, RF ablation near the His bundle (HB) carries a risk of inadvertent damage to the atrioventricular (AV) conduction system. Here we describe a patient with an AT originating in the vicinity of the AV node, which was successfully ablated earlier from non-coronary aortic cusp (NCC), and recurred with an exit from para-hisian location. Respiratory excursions of the catheter were associated with migration to the area of HIs. This was successfully ablated during controlled apnoea, using 3D electroanatomic mapping.     

Predicting the arrhythmogenic foci of atrial fibrillation before atrial transseptal procedure: implication for catheter ablation

INTRODUCTION: Use of endocardial atrial activation sequences from recording catheters in the right atrium, His bundle, and coronary sinus to predict the location of initiating foci of atrial fibrillation (AF) before an atrial transseptal procedure has not been reported. The purpose of the present study was to develop an algorithm using endocardial atrial activation sequences to predict the location of initiating foci of AF before transseptal procedure. METHODS AND RESULTS: Seventy-five patients (60 men and 15 women, age 68 +/- 12 years) with frequent episodes of paroxysmal AF were referred for radiofrequency ablation. By retrospective analysis, characteristics of the endocardial atrial activation sequences of right atrial, His-bundle, and coronary sinus catheters from the initial 37 patients were correlated with the location of initiating foci of AF, which were confirmed by successful ablation. The endocardial atrial activation sequences of the other 38 patients were evaluated prospectively to predict the location of initiating foci of AF before transseptal procedure using the algorithm derived from the retrospective analysis. Accuracy of the value <0 msec (obtained by subtracting the time interval between high right atrium and His-bundle atrial activation during atrial premature beats from that obtained during sinus rhythm) for discriminating the superior vena cava or upper portion of the crista terminalis from the pulmonary vein (PV) foci was 100%. When the interval between atrial activation of ostial and distal pairs of the coronary sinus catheter of the atrial premature beats was <0 msec, the accuracy for discriminating left PV foci from right PV foci was 92% in the 24 foci from the left PVs and 100% in the 19 foci from the right PVs. CONCLUSION: Endocardial atrial activation sequences from right atrial, His-bundle, and coronary sinus catheters can accurately predict the location of initiating foci of AF before transseptal procedure. This may facilitate mapping and radiofrequency ablation of paroxysmal AF.     

Focal atrial tachycardia originating from the non-coronary aortic sinus: electrophysiological characteristics and catheter ablation.

OBJECTIVES: We sought to investigate electrophysiological characteristics and catheter ablation in patients with focal atrial tachycardia (AT) originating from the non-coronary aortic sinus (AS). BACKGROUND: In patients with failed ablation of focal AT near the His bundle (HB) region, an origin from the non-coronary AS should be considered because of the close anatomical relationship. METHODS: This study included 9 patients with focal AT, in 6 of whom attempted radiofrequency (RF) ablation had previously failed. Activation mapping was performed during tachycardia to identify an earliest activation in the atria and the AS. The aortic root angiography was performed to identify the origin in the AS before RF ablation. RESULTS: Focal AT was reproducibly induced by atrial pacing. Mapping in atria demonstrated that the earliest atrial activation was located at the HB region, whereas mapping in the non-coronary AS demonstrated that an earliest atrial activation preceded the atrial activation at the HB by 12.2 +/- 6.9 ms and was anatomically located superoposterior to the HB in all 9 patients. Also, His potentials were not found at the successful site in the non-coronary AS in all 9 patients. The focal AT was terminated in <8 s in all 9 patients. Junctional beats and PR prolongation did not occur during RF application in all 9 patients. No complications occurred in any of the nine patients. All 9 patients were free of arrhythmias without antiarrhythmic drugs during a follow-up of 9 +/- 3 months. CONCLUSIONS: In patients with focal AT near the HB region, mapping in the non-coronary AS can improve clinical outcome.     

Successful catheter ablation of focal atrial tachycardia from the non-coronary aortic cusp.

We describe a patient with frequent episodes of unusual paroxysmal supraventricular tachycardia. During the electrophysiological examination, the tachycardia was easily induced and terminated by atrial pacing. The earliest activation during right atrial activation mapping was located near the atrioventricular node and the His bundle. However, detailed mapping of the aortic root demonstrated that the local activation in the non-coronary aortic cusp preceded the activation at the His bundle region. Radiofrequency catheter ablation at this site terminated the tachycardia with no complications.     

Limiting left-sided catheter dwelling time using 3-D NavX to mark and reaccess the left atrium via prior transseptal puncture site

Introduction

Ablations requiring transseptal access to the left heart place patients at increased risk for stroke, bleeding, and post-procedural cognitive dysfunction and other complications. Diminishing left atrial catheter dwelling time may decrease these risks. 3-D NavX can be used to facilitate reaccess of transseptal puncture sites to allow catheter removal from the left atrium immediately after ablation, with reaccess through the prior transseptal site if required. Here, we describe the techniques employed and our experience using 3-D NavX to limit left atrial catheter dwelling time by marking and reaccess of the left atrium via the previously marked transseptal puncture site, a potentially radiation-free technique.

Methods

With the use of 3-D NavX, a right atrial geometry is created. The patent foramen ovale is marked by using a standard EP catheter, or the transseptal puncture site is marked using 3-D NavX by creating a unipolar electrode on the transseptal needle at the time of puncture and at the time of catheter withdrawal of the ablation catheter from the left atrium. Marking the access site allows the catheter to be removed from the left side of the heart immediately after the ablation. If reaccess to the left atrium is required, the previously marked transseptal site is used to navigate the ablation catheter to reaccess the left atrium. All patients <30 years who had undergone this technique were evaluated. Data gathered included patient demographics, need for and success of transseptal reaccess, left atrial catheter dwelling time, and complications.

Results

The transseptal site was marked by 3-D NavX in 54 patients. We were able to successfully reaccess the transseptal puncture site using 3-D guidance in all 10 patients where it was desired. In these 54 patients, the complication rate was low with one small post-procedural pulmonary embolism and one right bundle branch block. No other complications were noted. The median procedure time was 105 min (range 58–446 min), the median total fluoroscopic time for the entire procedure was 1.3 min (range 0.0–30.8 min), and the median left-sided catheter dwelling time was 21 min (range 6–112 min).

Conclusions

In our retrospective review, reaccess of transseptal puncture site was reproducible, and early removal of the catheter from the left side was without the need for repeat transseptal punctures. This technique decreases the time the catheter dwells in the left atrium, which could decrease risks such as clotting, bleeding, and cognitive dysfunction.