房间隔缺损外科修补术后房性心律失常电解剖机制和射频消融

目的:探讨房间隔缺损(ASD)外科修补术后形成房性心动过速(房速)的心脏电生理机制。方法:回顾性分析因ASD术后房速于我院行导管射频消融治疗患者20例,在心动过速时电解剖标测右心房,根据激动标测及电压标测结果指导消融。结果:入选患者共诱发20种心动过速。8例患者为三尖瓣环峡部依赖房速,10例为同时围绕三尖瓣环及右房游离瘢痕的8字型折返,2例为围绕右房游离壁瘢痕顺钟向折返房速。对所有右房游离壁或前壁瘢痕至下腔静脉距离进行测量,双环折返及围绕三尖瓣环单环折返分别为(31±4)mm和(14±2)mm,前者明显高于后者。所有入选患者首次射频消融术成功率为100%,随访(25±14)个月,2例复发。结论:ASD术后患者间隔部位起源房速发生比例低。90%均为三尖瓣环相关房速。游离壁瘢痕至下腔静脉的不连续性为双环大折返房速提供了电解剖基础。     

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.     

先天性心脏病外科手术后切口性房性心动过速三维电磁导管标测及射频消融

目的；探讨天先性心脏病外科手术后切口性房性心动过速（房速）三维电磁导管（即Carto)标测特点及射频消融价值。方法：5例切口性房速患者，应用Carto系统标则右心房，实时重建心腔三维电解剖图，标识瘢痕区，观察电热图，传导图，于折返所经过的关键峡部位线性消融，结果：4例房速呈持续性，1例（三房心）术中不能诱发，电势图示低电压区主要分布于右房游离壁，在右房中侧壁下侧壁分别标测到瘢痕区1（S1）和瘢痕区2（S2）。4例持续性房速发生机理与折返有关，折返环位于低电压区，中心解剖障碍区均为中侧壁瘢痕区1，3例折返经过S1－S2，1例经过S1－三尖瓣环之间的关键峡部，于上述关键峡部消融，均获成功，三房心患者（未诱导心动过速）于S1－S及三尖瓣环－下腔静脉之间行线性消融，无并发症，随访2－24个月，其中1例（三房心）于术后1个月出现不典型心房扑动，结论：提示先天性心脏病术后房速的发生机理与折返有关，应用Carto系统标测可清楚地显示折返途径，消融折返所经过的关键峡部可望达到根治目的。     

先天性心脏病术后下腔静脉口-三尖瓣环峡部依赖性心房扑动的导管消融疗效分析

目的:报道先天性心脏病术后下腔静脉口-三尖瓣环峡部依赖性心房扑动的相对发生率及导管消融的疗效和安全性。方法:选择2002年1月-2006年4月在我院因先天性心脏病术后心房内折返性心动过速行射频消融的40例患者,应用常规电生理标测方法或三维标测方法(Carto和Ensite)指导导管消融,观察下腔静脉口-三尖瓣环峡部心房扑动相对发生率及其导管消融结果。结果:40例患者共诱发出50种房性心动过速,具有典型下腔静脉口-三尖瓣环峡部依赖性心房扑动心电图表现,且成功靶点在下腔静脉口和三尖瓣环峡部者31种(31／50,62．0％)。另外19种(19／50,38．0％)房性心动过速临床心电图表现与典型心房扑动不同,表现为P’波,其中11种(11／50,22．0％)成功靶点在右心房游离壁疤痕-下腔静脉峡部,瘢痕-上腔静脉峡部者2种,瘢痕与瘢痕之间峡部者2种;在瘢痕和三尖瓣环之间2种。房间隔补片和上腔静脉之间、房间隔补片和三尖瓣环之间各消融成功1种。40例患者射频消融成功,无并发症。随访1例患者心动过速复发,二次消融成功;1例患者出现持续性心房颤动伴RR长间歇,植入永久性起搏器。结论:先天性心脏病术后心房内折返性心动过速常常为下腔静脉口-三尖瓣环峡部心房扑动,导管消融具有较高的疗效和安全性。     

大折返房性心动过速的电解剖标测和导管射频消融

目的应用电解剖标测系统分析3例大折返房性心动过速(房速)的电生理机制并导航消融。方法3例房速患者(男1例,女2例),平均年龄51±12岁,心动过速病史19±11年。常规电生理检查初步确定房速所在心腔,使用电解剖标测系统构建心房三维模型,完成电压和激动标测,分析心动过速的机制并确定缓慢传导区(即关键峡部),使用冷生理盐水灌注导管消融。结果3例患者临床常规检查初步排除结构性心脏病,电压标测均显示被标测心房存在疤痕区。病例1为围绕三尖瓣环顺钟向的大折返房速,关键峡部位于三尖瓣环与后侧壁的疤痕之间。病例2为围绕上腔静脉逆钟向的大折返房速,关键峡部位于右房侧壁疤痕与上腔静脉之间。病例3为左房8字形折返,关键峡部位于左房顶部的两片疤痕之间。3例患者均在关键峡部消融成功,随访9～10个月未见复发。结论电解剖标测可以揭示大折返房速的基质,阐明折返机制,并有效指导消融。     

心脏外科手术后房性心律失常的三维电解剖标测和射频消融

目的应用Carto系统对心脏外科手术后房性心律失常患者进行三维电解剖标测和射频消融。方法入选心脏外科手术后房性心律失常患者29例,平均年龄（47±13）岁,男性15例,女性14例。在心动过速时,电解剖标测三维重建右心房和／或左心房。根据双极电图电压确定瘢痕区。对于折返性房性心动过速（房速）,线性消融关键峡部或瘢痕区与正常解剖障碍区之间或两瘢痕区间,对于局灶性房速,点消融局部最早激动区域。结果29例患者中,共标测39种心动过速,右心房切口性房速13例（45％）,右心房峡部心房扑动（房扑）19例（66％）,其中单一出现患者11例（38％）,伴发出现患者8例（28％）,即时消融成功率93％（27／29）,无消融术相关并发症发生。随访（26±20）个月,2例复发,1例再次消融成功。结论心脏外科手术后房性心律失常常见为右心房切口性房速和右心房峡部房扑,Carto电解剖标测系统可有效指导射频消融治疗。     

Carto标测指导导管消融心脏病术后心房内折返性心动过速

目的：心脏外科术后的心房折返性心动过速（IART）折返环涉及无传导的或各向异性的传导障碍区，本研究的目的是利用三维电解剖标测系统（Carto）标测这些障碍区并确定与折返环的关系，指导导管消融。方法：22例患者共26种IART进行了Carto标测，首先确定形成IART的基质以及与折返环的关系，并在其峡部消融。结果：22例患者诱发出27种心动过速，对其中26种进行标测，12种IART中心障碍区为三尖瓣环，其消融靶点在下腔静脉一三尖瓣环峡部；12种IART中心障碍区在右心房游离壁，其消融靶点在其周围；2种IART中心障碍区在房间隔，并在此障碍区下方消融成功。即刻成功21例，其中峡部消融成功者12例、游离壁消融成功者7例、间隔部消融成功者2例。平均随访（22±7）个月，20例无心律失常发生而不需用药。结论：可以利用三维电解剖标测方法标测IART基质，这些基质构成IART的中心传导障碍区，消融靶点常常位于其周围。     

射频导管消融典型心房扑动和手术疤痕折返性房性心动过速共存一例

典型心房扑动(房扑)的成功消融部位是右心房的先天性峡部(三尖瓣环-下腔静脉峡部)，而对于手术疤痕折返性房性心动过速(疤痕折返性房速)，消融部位则是与手术疤痕相关的后天性峡部。本文报道1例共存有上述两种心动过速患者的成功消融过程。     

Carto系统电解剖标测和射频消融治疗致心律失常性右心室心肌病的室性心动过速

目的 评价在致心律失常性右心室心肌病(ARVC)患者,应用Carto系统进行电解剖标测并指导射频消融治疗室性心动过速(室速)的有效性.同时探讨其室速发生机制.方法 伴有室速反复发作的19例ARVC患者入选,平均年龄(35±13)岁,男性15例,女性4例.消融术前1例植入植入型心律转复除颤器(ICD),因放电频繁行消融治疗.1例为无休止型室速,发作持续2 d.在窦性心律和/或心动过速时,电解剖标测三维重建右心室,根据双极电压高低确定疤痕区、正常心肌和临界边缘区.对于折返性室速,在关键峡部或在疤痕区与三尖瓣环之间或两疤痕区间行线性消融,对于局灶性室速,在局部最早激动区域点消融.结果 每个患者有1～5种室速,共在19例患者记录到36种室速.16种血流动力学稳定的室速于心动过速发作时行电解剖标测.可确定为折返性12种(75%),其中8种室速围绕三尖瓣环,另4例患者4种室速为局灶性.即时消融成功率为74%(14/19).随访1～46个月,原成功消融的4例室速复发.无消融术相关并发症发生.结论 应用Carto系统电解剖标测可安全有效指导射频消融治疗.ARVC患者的室速,有相对较高的失败和复发率.折返性和局灶性室速均可发生该类器质性心脏病患者,折返性多见.     

“特发性”瘢痕相关性左心房房性心动过速—电解剖标测和消融结果

目的 报道1组无明显器质性心脏病,无外科手术或导管消融史的左心房折返性房性心动过速(房速)的电解剖标测特点及消融结果.方法 共10例[男3例,女7例,年龄37 ～72(57.4±14.6)岁]符合上述特征的左心房房速患者接受电解剖标测和导管消融.结果 所有房速的折返环均位于大面积低电压(双极电压≤0.5 mV)区域内,低电压区域内可标测到1～5(2.6±1.2)个双电位线和/或电静止瘢痕区,这些传导障碍区和左心房固定的解剖屏障(如二尖瓣环)构成各个折返环必经的关键峡部.8例在折返环峡部内可记录到低幅,长时限碎裂电位,平均振幅(0.21±0.05)mV,平均时限(123±14) ms,占心动过速周长43％±5％.选择折返环峡部特别是长时限碎裂电位为消融靶点,10例均通过1～3(平均2次)次局部放电即终止房速,首次消融后2例复发房速,再次消融成功,随访共(14±10)个月,所有患者无房速复发.结论“自发”的左心房广泛瘢痕形成构成本组房速的“致心律失常基质”,折返环内存在的狭窄且传导缓慢的峡部对维持房速非常重要,并易于消融成功.     

Mechanisms of right atrial tachycardia occurring late after surgical closure of atrial septal defects

Postatriotomy atrial tachycardia ablation. INTRODUCTION: In patients without structural heart disease, the most frequently occurring AT is the common atrial flutter. In patients with repaired congenital heart disease other mechanisms of AT may occur, due to the presence of an atriotomy that can provide a substrate for reentry. The aim of the present study was to identify the mechanisms of atrial tachycardia (AT) occurring late after atrial septum defect (ASD) repair, with the help of a three-dimensional electroanatomical mapping system. METHODS AND RESULTS: Twenty-two consecutive patients presenting with AT underwent complete electroanatomic mapping (CARTO, Biosense Webster, Diamond Bar, CA) of spontaneously occurring and inducible right ATs. Complete maps of 26 ATs were obtained. Three tachycardia mechanisms were identified: single-loop macroreentrant atrial tachycardia (MAT) (n=7), double-loop MAT (n=18), and focal AT (n=1). In all MATs, protected isthmuses were identified as the electrophysiological substrate of the arrhythmia, most frequently the cavotricuspid isthmus (CTI) (n=24), and a gap between the inferior vena cava and a line of double potentials (n=11). A mean number of 13.5+/-2.1 radiofrequency applications were delivered to transect these critical parts of the circuit. During a follow-up of 25+/-16 months the RF ablation was acutely successful in all patients. Thirteen patients (59%) had an early recurrence of MAT and needed an additional ablation procedure. One of those patients needed two additional ablation procedures. CONCLUSIONS: Three-dimensional electroanatomic mapping is useful to identify postsurgical AT mechanisms; the CTI isthmus is involved in 92% MAT, and if the right atrial free wall (RAFW) abnormal tissue related to surgical scar is present this substrate contributes to the MAT circuit.     

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.     

Electroanatomic characterization of conduction barriers in sinus/atrially paced rhythm and association with intra-atrial reentrant tachycardia circuits following congenital heart disease surgery

INTRODUCTION: The electrophysiologic mechanism of intra-atrial reentrant tachycardia (IART) is generally thought to be a macroreentrant circuit revolving around a nonconductive or highly anisotropic barrier. However, the electrical and anatomic substrate that supports these circuits has been incompletely defined. Our objectives were to characterize the atria of patients with IART using electroanatomic mapping in sinus or atrially paced rhythm and to determine whether electrical barriers identified in sinus/atrially paced rhythm are associated with IART circuits. METHODS AND RESULTS: Eighteen patients with IART and a remote history of repaired or palliated congenital heart disease were studied [8 biventricular repair, 8 single ventricle palliation (7 Fontan), and 2 Mustard repair]. Thirteen patients had a right AV valve. In sinus/atrially paced rhythm, electrical evidence of a crista terminalis was identified in 11 patients, an atriotomy in 12, and > or = 1 right atrial free-wall scar in 11. In 26 IART circuits characterized, 12 used the right AV valve as a central obstacle, 6 used a right atrial free-wall scar, 3 used an atriotomy, 3 used the crista terminalis, and 2 circuits used an atrial septal scar. All central obstacles used by IART circuits were identified in sinus/atrially paced rhythm. CONCLUSION: The crista terminalis, atriotomy, and right atrial scars can be identified in patients with repaired congenital heart disease by electroanatomic mapping in sinus/atrially paced rhythm. These conduction barriers frequently function as the central obstacle for IART. Demonstration of such features may help focus investigational mapping without reliance on spontaneous initiation of the tachycardia.     

Use of a 3-dimensional electroanatomical mapping system for catheter ablation of macroreentrant right atrial tachycardia following atriotomy

The purpose of this study was to utilize a 3-dimensional (3D) electroanatomical mapping system (CARTO) to characterize the reentrant circuit in macroreentrant right atrial tachycardia (AT) following right atriotomy. Right atrial mapping was performed during incessant AT in a patient who had a right atriotomy for closure of an atrial septal defect. During AT, the right atrial free wall exhibited a large contiguous area of low bipolar voltage (≤0.5 mV, 7.3 cm in length, and 6.3 cm in width). Two discrete scars, showing no electrical potential, were identified within the large low-voltage area. A larger vertical scar (thought to be from the atriotomy) and a smaller second scar (possible inferior vena cava cannulation scar) formed a narrow channel (1.5 cm in width) between these 2 scars. Right atrial activation propagated around the large upper scar, and then propagated through the channel between the 2 scars. A single application of radiofrequency current within the channel eliminated the macroreentrant AT. In conclusion, macroreentrant AT following right atriotomy was associated with 2 discrete scars and utilized the isolated channel between the 2 scars. Ablation within the channel effectively eliminated macroreentrant AT after atriotomy and eliminated the requirement for linear ablation between one or more of the scars and the tricuspid annulus.     

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。     

Layered activation of epicardial scar in arrhythmogenic right ventricular dysplasia: possible substrate for confined epicardial circuits

Background- Ventricular tachycardia ablation in arrhythmogenic right ventricular dysplasia (ARVD) is more successful when including epicardial ablation. Scarring may cause independent, layered epicardial activation and promote epicardially confined ventricular tachycardia circuits. We aimed to characterize transmural right ventricular activation in ARVD patients and to compare this with reference patients without structural heart disease. Methods and Results- Eighteen ARVD patients underwent detailed endocardial and epicardial sinus rhythm electroanatomic mapping. Bipolar activation was annotated at the sharpest intrinsic deflection including late potentials and compared with 6 patients with normal hearts. Total scar area was larger on the epicardium (97±78 cm(2)) than the endocardium (57±44 cm(2); P=0.04), with significantly more isolated potentials. Total epicardial activation time was longer than endocardial (172±54 versus 99±27 ms; P<0.01), and both were longer than in reference patients. Earliest endocardial site was the right ventricular anteroseptum in 17 of 18 ARVD patients versus 5 of 6 controls (P=0.446), and latest endocardial site was in the outflow tract in 13 of 18 ARVD patients versus 4 of 6 controls and tricuspid annulus in 5 of 18 ARVD patients versus 2 of 6 controls (P=1.00). In reference patients, epicardial activation directly opposite endocardial sites occurred in 5.2±1.9 ms, suggesting direct transmural activation. In contrast, ARVD patients had major activation delay to the epicardium with laminar central scar activation from the scar border, not by direct transmural spread from the endocardium. Conclusions- Transmural right ventricular activation is modified by ARVD scarring with a delayed epicardial activation sequence suggestive of independent rather than direct transmural activation. This may predispose ventricular tachycardia circuits contained entirely within the epicardium in ARVD and explains observations on the need for direct epicardial ablation to eliminate ventricular tachycardia.     

经皮穿刺心外膜电-解剖标测及射频消融心肌梗死后室性心动过速的实验研究

目的探讨经心外膜途径在电-解剖标测系统指导下行射频消融治疗心肌梗死后室性心动过速的可行性和安全性。方法成年中华小型猪共7只,采用经皮穿刺的方法将球囊置于左前降支中下部,封堵150 min建立心肌梗死模型。3～5周后将心肌梗死模型猪,行电生理检查诱发室性心动过速。经胸穿刺进入心包腔,采用电-解剖标测系统在窦性心律下进行心外膜电压标测和线性消融。射频消融后再次行电生理检查,不能再诱发室性心动过速为消融成功。结果存活的心肌梗死模型的猪7只,3～5周后行电生理检查,共诱发出单形性室性心动过速共8种,7种表现为右束支阻滞图形,1种表现为左束支阻滞图形,室性心动过速(VT)周长平均在(338±66)ms。1只猪同时诱发心室颤动,电除颤转复窦性心律。7只猪心包穿刺均成功,完成心外膜电压标测,沿瘢痕区到二尖瓣环或正常心肌区逐点进行线性消融。射频消融后再次行电生理检查,6只猪不能再诱发室性心动过速。结论经胸穿刺进入心包腔行心外膜标测和消融治疗心肌梗死后室速的方法是安全可行的,心外膜标测消融心肌梗死后室速的方法可以作为心内膜消融的一种有效补充方法。