左房房性心动过速三维电磁导管标测系统(Carto)标测与射频消融

目的探讨左房房性心动过速(房速)三维电磁导管标测系统(Carto)系统标测特点及射频消融价值.方法 9例左房房速患者,应用Carto系统标测左心房,实时重建左房三维电解剖图;根据电解剖图,判断房速类型局灶性或大折返性房速;于心房最早激动点处或折返环的关键峡部消融.结果 9例患者中共有10个房速.在冠状静脉窦(CS) 电极中、远端或近端均记录到相对提早A波;9个房速为局灶性房速,激动图显示最早激动点位于肺静脉口部(5个)、左房后壁(2个)、左心耳口部(1个)、左心耳体部(1个);1个为大折返性房速,折返经过右上肺静脉口部与卵圆窝之间关键峡部.8个局灶性房速在上述最早激动点处消融,均成功终止房速,1个左心耳体部房速消融失败;大折返性房速于关键峡部行线性消融,获成功;随访6～30个月,其中1例局灶性房速术后次日复发,再次消融成功;无并发症;成功病例手术时间为90～140 min,X线照射时间为8～16 min.结论本组结果提示,应用Carto系统标测左房房速,判断房速类型准确、快速;指导消融安全、有效,可减少X线照射时间,进一步提高消融成功率,特别是对于常规方法消融失败病例尤有帮助.     

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.     

起源于左心耳局灶性房性心动过速的电生理特征和射频消融治疗

目的 报道一组起源于左心耳局灶性房性心动过速(房速)的电生理特征和射频消融治疗.方法 9例患者中男性5例,平均年龄(21±9)岁,经心内电生理检查和射频消融证实为起源于左心耳的房速,对其电生理特点及射频消融进行分析.结果 左心耳房速表现为无休止性或静脉滴注异丙肾上腺素诱发,程序刺激不能诱发或终止房速.左心耳房速有独特的体表心电图特征,所有患者P波Ⅰ、aVL导为负向,Ⅱ、Ⅲ、aVF导联P波高而直立.V_1导P波为直立或正负双向(以直立为主),V_2～V_6导P波为等电位线(5例)或<0.1 mV低幅直立(4例).常规心内标测,最早心房激动为CS远端.成功靶点处局部心房激动领先P波起始(36.7±7.9)ms.5例患者最终使用盐水灌注导管消融成功,随访(12 ±5)个月无房速复发.结论 左心耳房速有独特的心电图特征和房内激动顺序,对这类房速盐水灌注导管可能是更好的选择,左心耳内局灶消融长期随访安全有效.     

经射频导管消融起源于心耳的局灶性房速

目的起源于左、右心耳处的局灶性房性心动过速(房速)比较少见,本研究报告14例起源于左、右心耳的局灶性房速的电生理特性和射频导管消融结果。方法 14例患者年龄为12～55岁,均有反复发作心悸和心动过速的病史,11例心动过速呈无休止发作,抗心律失常药物难以控制,其中3例伴明显左心室增大。电生理检查明确局灶性房速机制,其它机制的室上性心动过速经详细的的电生理检查和心内标测排除。对14例患者均在房速时进行体表心电图分析和激动标测,在心动过速时双极和单极标测所示的最早心房激动部位处行射频导管消融。14例患者中,5例应用CARTO三维标测系统引导标测和消融;除3例患者外,其他11例患者均应用盐水灌注导管消融。结果 10例起源于右心耳的局灶性房速患者,房速时的P’波形态Ⅰ导联和Ⅱ、Ⅲ、aVF导联均为正向波,aVL导联P’波负向、正向、双向者分别是3例、3例和4例;V1导联负向波为主(7/10),V3～V6导联正向波为主(9/10),1例V1～V6导联P波全部为正向波。4例左心耳局灶性房速的P’波形态,Ⅰ和aVL导联均为负向波,Ⅱ、Ⅲ和aVF导联均为正向波,V1～V6导联均为正向波。10例右心耳起源房速均消融成功;4例左心耳起源房速2例消融成功,2例消融失败。14例均无围术期相关并发症发生。在随访期间,右心耳起源房速复发1例,经再次消融成功;其他成功消融患者在未服用抗心律失常药物下无房速复发,3例左心室增大患者随访中左心室基本恢复正常。结论起源于左、右心耳局灶性房速多呈无休止特点,可导致心动过速性心肌病。经射频导管消融心耳部(尤其是右心耳)起源局灶性房速有较高的成功率、较低的复发率和较好的安全性。     

经射频导管消融起源于心耳的局灶性房速

目的起源于左、右心耳处的局灶性房性心动过速(房速)比较少见,本研究报告14例起源于左、右心耳的局灶性房速的电生理特性和射频导管消融结果。方法 14例患者年龄为12～55岁,均有反复发作心悸和心动过速的病史,11例心动过速呈无休止发作,抗心律失常药物难以控制,其中3例伴明显左心室增大。电生理检查明确局灶性房速机制,其它机制的室上性心动过速经详细的的电生理检查和心内标测排除。对14例患者均在房速时进行体表心电图分析和激动标测,在心动过速时双极和单极标测所示的最早心房激动部位处行射频导管消融。14例患者中,5例应用CARTO三维标测系统引导标测和消融;除3例患者外,其他11例患者均应用盐水灌注导管消融。结果 10例起源于右心耳的局灶性房速患者,房速时的P’波形态Ⅰ导联和Ⅱ、Ⅲ、aVF导联均为正向波,aVL导联P’波负向、正向、双向者分别是3例、3例和4例;V1导联负向波为主(7/10),V3～V6导联正向波为主(9/10),1例V1～V6导联P波全部为正向波。4例左心耳局灶性房速的P’波形态,Ⅰ和aVL导联均为负向波,Ⅱ、Ⅲ和aVF导联均为正向波,V1～V6导联均为正向波。10例右心耳起源房速均消融成功;4例左心耳起源房速2例消融成功,2例消融失败。14例均无围术期相关并发症发生。在随访期间,右心耳起源房速复发1例,经再次消融成功;其他成功消融患者在未服用抗心律失常药物下无房速复发,3例左心室增大患者随访中左心室基本恢复正常。结论起源于左、右心耳局灶性房速多呈无休止特点,可导致心动过速性心肌病。经射频导管消融心耳部(尤其是右心耳)起源局灶性房速有较高的成功率、较低的复发率和较好的安全性。     

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。     

射频消融治疗起源于心房下部局灶房性心动过速

对6例起源于右房下部及3例起源于冠状静脉窦口局灶性房性心动过速(简称房速),行常规心内电生理检查,明确房速时心房激动顺序,寻找心房激动最早起源点标测与消融,临床随访评价疗效。结果:6例右房下部房速心电图Ⅱ、Ⅲ、aVF、V1导联P′为负,Ⅰ、aVL为正,3例冠状窦口部房速心电图Ⅱ、Ⅲ、aVF及V1导联P′波为负\正双向,Ⅰ、aVL P′低平,不易区别。成功消融靶点双极电图A-P间期40±15 m s。结论:体表心电图可大致区分房速起源部位。     

心房耳尖部持续性房性心动过速的临床特点和射频消融

目的：报道心房耳尖部房性心动过速（房速）的临床特点和射频消融结果。方法：对7例[男性2例，女性5例，平均年龄（24．8±7．9）岁]房速患者进行体表心电图和动态心电图检查。采用三维电解剖（Carto）标测系统，确定房速病灶的起源部位和指导经导管射频消融。结果：7例房速均为持续性发作（5～432个月，中位数96个月），未发现器质性心脏病。房速起源于右心房耳尖部（1例）和左心房耳尖部（6例），呈局灶性和异常自律性增高机制。7例房速均消融成功，无并发症。随访7～28个月（中位数15个月），无一例房速复发。结论：心房耳尖部房速表现为持续性发作和异常自律性增高机制。采用三维电解剖标测系统和盐水灌注消融导管，可提高病灶定位的准确性和消融的成功率。     

射频消融治疗风湿性心脏病二尖瓣置换术后房性心动过速

目的报道一组风湿性心脏病二尖瓣置换术后房性心动过速（房速）的机制及射频消融效果。方法共入选22例（男8例）二尖瓣置换术后持续性房速患者,在心动过速状态下采用三维电解剖系统建立右心房或左心房激动标测图和电压图,标出瘢痕区、低电压区及双电位区,并揭示心动过速的机制。根据标测结果选择心动过速的关键峡部或起源点进行消融。结果22例患者共标测33种心动过速,17例次房速起源于右心房（51．5％）,16例次房速起源于左心房（48．5％）。符合大折返机制的31例次（93．9％）,符合局灶起源机制的2例次（6．1％）。消融术中即时成功率90．9％（20／22）。随访过程中5例患者仍有房速发作,3例再次消融成功。结论二尖瓣置换术后房速机制复杂且个体化,在三维电解剖标测指导下射频消融治疗效果满意。     

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.     

Three-Dimensional Electromagnetic Catheter Technology:

Electroanatomical Mapping. Introduction : The difficult catheter orientation and navigation associated with conventional technology and mono-/multiplane fluoroscopy may complicate ablation procedures of atrial tachycardias. A new three-dimensional catheter technology for electroanatomical mapping of the right atrium and ablation of ectopic atrial tachycardia is described.
Methods and Results : A novel electromagnetic catheter-based mapping system was investigated for electroanatomical mapping of the entire right atrium in 12 patients. The system reconstructed three-dimensional maps from the multitude of endocardial sites that were sequentially mapped and color coded the individual activation times. The electrophysiologic information was superimposed on the geometry of the mapped area. The anatomical landmarks of the right atrium, i.e., the tricuspid annulus. mouth of the coronary sinus, ostia of the superior and inferior venae cavae, and right atrial appendage, could he depicted in all cases. The sinus node area and the preferential conduction along the crista terminalis could be delineated. In four patients with ectopic atrial tachycardia, the earliest endocardial activation could be identified with high spatial resolution as a "hot spot." After completion of the mapping procedure, the ablation catheter could be reliably renavigated to the site of origin, and ablation was successful with one or two impulses. In one patient with previous atrial septal repair, the activation map allowed the reconstruction of a long line of conduction block induced by the atriotoniy.
Conclusion : Three-dimensional electroanatomical mapping of the right atrium allowed detailed reconstruction of the chamber geometry and activation sequence. The sites of origin of ectopic atrial tachycardias could be identified precisely. The system allowed accurate renavigation to the site of earliest activation, thereby guiding successful ablation of the foci.     

Non-fluoroscopic electroanatomical mapping (CARTO system) in the ablation of atrial tachycardias

INTRODUCTION AND OBJECTIVES: The recent introduction of navigation systems has made substantial improvements in cardiac electrophysiological mapping. We present our experience with non-fluoroscopic electroanatomical mapping in patients with atrial tachycardias. PATIENTS AND METHOD: We studied 24 consecutive patients with atrial tachycardias (10 of whom had undergone previous radiofrequency ablation which failed). In all patients we performed electroanatomical mapping of the atria with the CARTO system, which combines electrophysiological and spatial information and allows visualization of atrial activation in a three-dimensional anatomical reconstruction of the atrial cavity. Mapping was performed during tachycardia (22 patients) or in sinus rhythm (2 patients), using a left atrial approach in 12 patients. Cooled-tip ablation was performed in 3 patients. RESULTS: Three-dimensional mapping distinguished clearly and rapidly between reentrant (9 patients) and focal mechanisms (15 patients). Radiofrequency catheter ablation was aimed at the critical isthmus of conduction (voltage maps) in patients with macroreentrant tachycardias. For focal tachycardias the catheter was re-navigated within the target area (activation maps) to the earliest focus of ectopic impulses. Acute success was obtained in 19 patients (79.2%), with early recurrence in 2 of them. Fluoroscopy time was 60 (21 min). CONCLUSIONS: Visualization of atrial activation in a three-dimensional reconstruction of the atria with the CARTO electroanatomical mapping system facilitated the integration of electrophysiological and anatomical information in patients with atrial tachycardias. This technique is potentially helpful in ensuring successful treatment of the substrate of tachycardia in this selected group of patients.     

Atrial tachycardia originating at the tricuspid annulus

We report a patient with re-entrant atrial tachycardia that originated at the inferolateral tricuspid annulus. Single atrial extra-stimulation reproducibly induced the atrial tachycardia with an inverse relationship between the coupling interval of extra-stimulation and the return cycle of the first tachycardia beat. A real-time three-dimensional electroanatomical mapping showed focal atrial activation spreading semi-radially from the tricuspid annulus. The tachycardia was successfully eliminated by radiofrequency ablation at the earliest atrial activation site, preceding by 27 ms the arbitrary determined onset of surface P wave. An accelerated atrial rhythm with similar P-wave morphology to that of the tachycardia was observed at the successful ablation site during radiofrequency application. The mechanism of this tachycardia seems to be due to re-entry originating in or around the possible accessory atrioventricular node without ventricular connection.     

Electroanatomical mapping for visualization of atrial activation in patients with incisional atrial tachycardias.

AIMS: Incisional atrial tachycardias in patients following surgery for congenital heart disease are based on complex structural abnormalities in these hearts. The aim of this study was to evaluate the use of the electroanatomical mapping system, CARTO, in consecutive patients with different forms of incisional atrial tachycardia. METHODS AND RESULTS: The electroanatomical mapping system combines electrophysiological and spatial information and allows visualization of atrial activation in a three-dimensional anatomical reconstruction of the atria. Electroanatomical mapping of right atrial activation was performed in 10 patients after surgery for congenital heart disease, surgery for Wolff-Parkinson-White syndrome, or heart transplantation presenting with 13 incisional atrial tachycardias. The three-dimensional mapping allowed a rapid distinction between focal (n=3) and reentrant mechanisms (n=10) and visualization of the activation wavefronts along anatomical and surgically created barriers. Electroanatomical activation maps (mean right atrial activation time 213+/-107 ms) were constructed with 89+/-60 catheter positions during an average mapping time of 48+/-33 min. Reentrant tachycardias propagating through the tricuspid annulus-vena cava inferior isthmus (n=6) or along periatriotomy loops (n=4) were identified in eight patients. Ectopic atrial foci near surgical scars could be localized in three patients. Catheter ablation by creation of a lesion in a critical isthmus of conduction or by targeting the arrhythmogenic focus eliminated 11 of 13 incisional atrial tachycardias. CONCLUSION: Visualization of atrial activation in a three-dimensional reconstruction of the right atrium using the electroanatomical mapping system CARTO facilitates understanding of the mechanism and defines the reentrant circuits of incisional atrial tachycardias. This new method may improve the success rate of electrophysiologically guided and anatomically guided catheter ablation of incisional atrial tachycardias.     

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     

Pace mapping for the localization of focal atrial tachycardia arising near the mitral annulus

Of the various therapeutic modalities available to treat ectopic atrial tachycardia, radiofrequency catheter ablation has shown excellent results. It is usually possible to localize the earliest site of endocardial activation by conventional or newer three-dimensional mapping techniques. We report a case of ectopic atrial tachycardia, wherein the tachycardia was being repeatedly interrupted by mechanical trauma. Finally, with the help of P wave pace mapping, the tachycardia was localized near the posterolateral part of the mitral annulus, and successfully ablated. This report demonstrates the utility of P wave pace mapping in ectopic atrial tachycardia.     

Localized reentrant tachycardia in the aorta contiguity region mimicking perimitral atrial flutter in the context of atrial fibrillation ablation

We describe a case with a focal atrial tachycardia (AT) masquerading as perimitral atrial flutter revealed after circumferential pulmonary vein antral isolation for atrial fibrillation. It was successfully terminated and became noninducible by a point ablation on the left atrial anterior wall (LAAW) near the mitral annulus in contact with the aortic root and on the left superior pulmonary vein–left atrial appendage ridge, without any linear ablation, using electroanatomical mapping and conventional precise mapping with a maximum amplified gain within the low-voltage area. The AT revealed in our case was an LAAW–aorta contiguity area-related AT.     

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

目的报道13例主动脉无冠窦内和1例二尖瓣环一主动脉连接（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14例患者,男性3例女性11例,平均年龄（54．4±10．4）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’波特点并于右心房进行激动标测,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心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。右心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。14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柬处心房激动0～20．0（10．1±6．3）ms,13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’波及标测右心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。