致心律失常右室心肌病室性心动过速的动态基质标测和射频消融

目的探讨应用非接触球囊导管标测系统行动态基质标测指导致心律失常右室心肌病室性心动过速(简称室速)消融的价值.     

非接触球囊标测指导血流动力学不稳定性或非持续性室性心动过速的射频消融

目的探讨非接触球囊标测在指导血流动力学不稳定性或非持续性室性心动过速(室速)射频消融中的作用。方法17例室速患者,年龄50岁±9岁,经心室刺激诱发血流动力学不稳定性或非持续性室速后,使用非接触标测系统ENSITE3000标测室速的出口和(或)慢传导区,然后使用温控大头导管在室速出口作环形消融或横跨慢传导区进行线性消融。结果17例患者共诱发18次室速,周长为336MS±58MS。15例患者可确定室速的出口,为QRS波前10MS±16MS;其中5例是心肌梗死后室速,9例为右室流出道室速。5例心肌梗死后室速均可确定舒张期慢传导区,最早的心内膜舒张期电活动在QRS波前60·1MS±42·6MS。3例非持续性室速均可确定最早的心室激动点。18次室速中15次消融成功,1例没有进行消融,2例消融失败。结论非接触球囊心内膜标测能成功指导血流动力学不稳定性或非持续性室速的射频消融。     

致心律失常右室发育不良心肌病的电生理基质和导管消融治疗(附二例报道)

目的报道2例致心律失常右室发育不良心肌病(ARVC)的电生理特征及导管消融结果。方法2例均以室性心动过速(简称室速)为首发症状。在窦性心律下,采用心脏电解剖标测系统构建右室并行起搏标测室速起源点。结果双极电压图上的低电压面积分别为36 cm2和48 cm2,室速起源于低电压的病变心肌与正常心肌的交界区,2例共有4种室速,采用线性消融后4种室速即刻均不能诱发,例2于术后第2天复发,但室率从188次/分降至160次/分,随访9个月和4个月未见室速复发。结论ARVC的电生理基质是病变心肌的低电压区,电解剖标测指导下的线性导管消融是一种有效的治疗方法。     

应用非接触球囊导管标测系统指导心动过速的心内膜标测与消融

目的观察非接触球囊导管标测系统指导难治性室性心动过速的标测与射频消融的有效性和优越性。方法5例患者均为男性，平均年龄33.2岁。经股静脉或股动脉置入64极球囊电极和射频消融导管至同一心室，计算机标测系统首先构建心腔的几何构型，然后建立心动过速的腔内等电势图，分析心动过速的最早起源点及折返激动的关键峡部，最终利用计算机导航系统指导消融导管至拟定靶点处进行环状或线形消融。结果5例患者共诱发出6种心动过速，心动过速平均周期为（336.6±42.7）ms。2例特发性左室室性心动过速及1例隐匿性束室纤维患者均消融成功。1例扩张型心肌病患者共有两种心动过速，一种起源于右室流出道，另一种起源于左室间隔部，前者消融成功，后者因导管操作致心动过速持续发作伴血流动力学不稳定而终止手术。1例致心律失常性右室心肌病患者于最早激动点处做环状消融，未获成功。5例患者术中和术后均无并发症发生。随访4个月，所有消融成功患者均未再有心动过速发作。结论非接触性球囊导管标测系统指导心律失常的心内膜标测与消融是安全、有效的，与常规的标测和消融方法比较，该系统有一定的优越性，尤其适用于复杂病例、血流动力学不稳定和非持续性室性心律失常的标测及指导射频消融。     

三维标测指导致心律失常性右心室心肌病室性心动过速的射频消融

目的介绍致心律失常性右心室心肌病（ARVC）室性心动过速（室速）的三维标测方法及其消融策略。方法21例ARVC室速患者,因1—4种抗心律失常药物治疗无效,临床上呈反复发作、无休止发作或植入型心律转复除颤器（ICD）植入后频繁放电治疗,接受导管消融治疗。其中,男性19例,女性2例,平均年龄（32±12）岁。9例患者接受电解剖（Carto）标测,12例患者接受非接触标测（EnSite—Array）。在首先明确病变基质的基础上,通过激动标测、拖带标测及起搏标测,分析心动过速的起源、可能的传导径路及其出口以及它们与病变基质的关系。通常于心动过速的出口处及其周边行局灶消融,术中病变基质周边的延迟激动电位应一并消融。结果21例患者,2例呈无休止发作,1例患者表现为频繁室性早搏及加速性室性自主心律,余18例患者消融中共诱发出34种心动过速。所有心动过速均呈左束支阻滞形,平均心动过速周长为（289±68）ms。16例患者（28种室速）消融治疗即刻成功,3例患者（7种室速）部分成功,2例患者（2种室速）消融失败,即刻消融成功率76．2％。所有患者消融术后继续服用抗心律失常药物。平均随访6～30（1d±7）个月,成功患者中2例复发,其中1例再次消融成功;未达即刻成功的5例患者,经抗心律失常药物治疗后,均无室性心律失常事件发生,其中包括1例消融后植入ICD者。结论三维标测系统可首先明确ARVC患者的病变基质,在此基础上结合激动标测和心内各种电刺激技术,可直观显示心动过速的起源、缓慢传导区出口及折返环路,以此制定消融策略可成功治疗ARVC室速。心动过速起源于心肌深部或ARVC病变进展,是消融失败和复发的常见原因。     

非接触球囊导管标测系统指导心房扑动消融的初步经验

目的　评价非接触球囊导管标测系统在心房扑动 (房扑 )标测和射频消融中的临床应用。方法　 7例房扑患者 ,年龄 (6 0± 10 )岁 ,男 4例 ,女 3例。其中 1例为房间隔缺损修补术后 ,2例为采用常规方法消融典型房扑后复发患者。应用非接触球囊导管标测系统构建右房三维几何模型 ,标测心动过速的折返激动顺序和关键峡部 ,并利用其导航系统指导峡部的线性消融。消融后分别于峡部两侧起搏判断峡部阻滞情况。结果　 6例患者诱发出房扑 ,心动过速周长 (2 16± 2 2 )ms。6例房扑均为峡部依赖型 ,2例呈逆钟向传导 ,4例呈顺钟向传导 ;4例房扑呈双环折返激动 ;7例消融均成功 ,房扑不再诱发 ,峡部呈完全双向传导阻滞 ;手术时间 (30 0± 12 9)min ,X线曝光时间 (2 5 0± 6 5 )min ,放电次数 (2 5 7± 12 1)次。无手术并发症。随访 3～ 14个月无复发病例。结论　在房扑标测和消融中应用非接触球囊导管标测系统是安全有效的 ,不仅能确定折返环路 (特别是双环折返激动 )的顺序和关键峡部 ,而且能准确判断线性损伤的连续性 ,同时可减少X线曝光时间。     

非接触球囊标测系统指导下右室流出道室性期前收缩导管消融疗效及体表心电图应用价值

目的:探讨非接触球囊标测系统指导下右室流出道室性期前收缩（室早）导管消融疗效及体表心电图应用价值。方法:术前根据同步12导联体表心电图室早的形态特征初步判断室早起源部位,对58例药物治疗无效的顽固性室早患者进行导管射频消融治疗,其中26例采用传统标测法,32例采用非接触球囊标测法（Ensite三维标测法）。结果:①非接触球囊标测法与传统标测法相比较,成功率高（100% vs. 81%）、复发率低（3% vs. 19%）,X线曝光时间短［(3.6±1.4)min vs.(32±12)min］;②标测和消融结果显示30例患者室早起源于右室流出道间隔部,其中7例起源于前间隔,9例起源于中间隔,14例起源于后间隔。22例患者室早起源于右室流出道游离壁,其中7例起源于前游离壁,4例起源于中游离壁,11例起源于后游离壁。体表心电图特征对判断室早起源部位具有较高的灵敏度、特异度和准确度。结论:非接触球囊标测系统指导右室流出道室性心律失常射频消融安全有效,仔细分析心电图室早QRS波形态特征有助于判定室早起源部位,并缩短手术时间。     

非接触式球囊标测系统指导右室心肌病并多种室性心动过速射频消融的有效性观察

目的:观察非接触式球囊标测系统(EnSite 3000系统)指导右室心肌病并复杂性室性心动过速(室速)射频消融的有效性.方法:右室心肌病并室速2例患者经心室刺激诱发出室速后,使用EnSite 3000系统标测室速的起源点、出口和(或)慢传导区,然后使用温控大头导管在室速起源点和出口作环形消融或横跨慢传导区进行线性消融.术后反复刺激并异丙肾卜腺素诱发.结果:2例患者术中均分别诱发出3种不同形态、不同频率的室速,其中2种起源于右室流出道中间隔,2种来源于下后壁,2种起源于侧后壁,均消融成功.静滴异丙肾七腺素均未诱发室速,术中、术后无任何并发症发生.随访7～8个月,服用胺碘酮0.2 qd,美托洛尔12.5 mg/qd或bid,未发作心动过速.结论:EnSite 3000系统能成功指导右室心肌病并复杂性室速的射频消融.     

非接触标测在伴有晕厥的右室流出道室性心动过速消融中的应用

目的比较非接触标测与传统导管方法对伴有晕厥的右室流出道室性心动过速消融的疗效和安全性。方法入选经心电图或24 h动态心电图证实为右室流出道室性心动过速且伴晕厥的住院患者共29例,应用非接触式球囊标测系统进行消融组10例,采用传统标测方法进行导管射频消融的对照组19例。结果两组手术消融的即刻成功率均为100%,但非接触标测组消融的部位减少[(3.3±2.1)个比(5.6±3.1)个,P0.05],手术时间[(73.4±34.6)min比(129.6±56.9)min,P0.05]、X线曝光时间[(13.2±7.8)min比(24.4±19.7)min,P0.05]缩短,且并发症发生率及6个月随访的复发率有降低趋势。结论应用非接触标测系统指导消融伴晕厥的右室流出道室性心动过速比常规消融更可靠、省时和安全。     

特发性左室室性心动过速非接触球囊导管系统的标测与消融

介绍非接触球囊导管标测系统 (EnSite 30 0 0系统 )指导难治性特发性左室室性心动过速的标测与射频消融的初步经验。 5例男性病人 ,年龄 33± 17(17～ 6 2 )岁 ,常规方法标测和导管消融失败 2 .4± 1.1(1～ 4)次。常规放置高位右房和右室电生理导管 ,运用置入左室的 6 4极球囊导管和大头电极 ,系统重建三维心内膜几何模型和等电势 ,经右室导管诱发VT ,心动过速周期为 32 3.8± 48.1ms。EnSite 30 0 0系统标测到VT的最早激动点分别位于左后间隔中下部、左侧间隔后下部左束支下方、后下间隔近心尖部、左室后壁近基底部和左后间隔中部。在最早激动点和关键峡部分别行点状、环状和线性消融。 2例患者在心动过速时放电、3例患者在窦性心律时消融 ,均获成功。成功消融靶点处的单极电图均为QS型。X线曝光时间为 2 5± 12min。随访 7.8± 4.6 (1～ 11)个月所有患者均未发作心动过速。结果表明 ,与常规方法比较 ,EnSite 30 0 0系统所建立的心腔三维模拟等电势图可直观地显示心动过速的起源点、传导途径和关键峡部 ,系统模拟的单极腔内电图的形态也有助于判断病灶起源部位及提高消融成功率 ,尤其适用于常规方法消融失败的室性心律失常的标测 ,其独特的导航系统可引导消融导管到达靶点部位指导射频消融 ,并可减少X?     

Electroanatomic mapping characteristics of ventricular tachycardia in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia.

BACKGROUND: Ventricular tachycardia (VT) in arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVD) has been previously explored using entrainment mapping techniques but little is know about VT mechanisms and the characteristics of their circuits using an electroanatomical mapping system. METHODS AND RESULTS: Three-dimensional electroanatomical mapping was performed in 11 patients with well tolerated sustained VT and ARVD. Sinus rhythm mapping of the right ventricle was performed in eight patients showing areas of low bipolar electrogram voltage (<1.2 mV). In total 12 tachycardias (mean cycle length 382+/-62 ms) were induced and mapped. Complete maps demonstrated a reentry mechanism in eight VTs and a focal activation pattern in four VTs. The reentrant circuits were localized around the tricuspid annulus (five VTs), around the right ventricular outflow tract (one VT) and on the RV free lateral wall (two VTs). The critical isthmus of each peritricuspid circuit was bounded by the tricuspid annulus with a low voltage area close to it. The isthmus of tachycardia originating from the right ventricular outflow tract (RVOT) was delineated by the tricuspid annulus with a low voltage area localized on the posterior wall of the RVOT. Each right ventricular free wall circuit showed an isthmus delineated by two parallel lines of block. Focal tachycardias originated on the right ventricular free wall. Linear radiofrequency ablation performed across the critical isthmus was successful in seven of eight reentrant tachycardias. The focal VTs were successfully ablated in 50% of cases. During a follow-up of 9-50 months VT recurred in four of eight initially successfully ablated VTs. CONCLUSIONS: Peritricuspid ventricular reentry is a frequent mechanism of VT in patients with ARVD which can be identified by detailed 3D electroanatomical mapping. This novel form of mapping is valuable in identifying VT mechanisms and in guiding RF ablation in patients with ARVD.     

Catheter ablation of stable and unstable ventricular tachycardias in patients with arrhythmogenic right ventricular dysplasia

INTRODUCTION: A reentrant circuit within an area of abnormal myocardium is suspected as the origin of ventricular tachycardia (VT) in patients with arrhythmogenic right ventricular dysplasia (ARVD). OBJECTIVES: To examine the relationship between the reentrant circuits of VT and the abnormal electrograms in ARVD, and to assess the feasibility of a block line formation in the reentrant circuit isthmus utilizing electroanatomical mapping system (CARTO) guidance. METHODS AND RESULTS: An electrophysiological study and catheter ablation (CA) were performed in 17 ARVD patients (13 men, 47 +/- 17 year) using CARTO. Endocardial mapping during sinus rhythm demonstrated electrogram abnormalities extended from the tricuspid annulus (TA) or the right ventricular outflow tract in 16 of 17 patients. In 13 hemodynamically stable VTs, the reentrant circuits and critical slow conduction sites for the CA were investigated during VTs. The entire macro-reentrant pathway was identified in 6/13 stable VTs (figure-of-8 in 4, single loop in 2). In the remaining seven VTs, a focal activation pattern was found in four and an unidentifiable pattern in three. CA successfully abolished all the macro-reentrant and focal tachycardias, however, not effective in three unidentifiable VTs. In the 13 cases with unstable VT, the linear conduction block zone was produced between the sites with abnormal electrograms and the TA. Ultimately, 23/26 VTs (88%) became noninducible after the CA. During follow-up (26 +/- 15 months), 13/17 patients remained free from any VT episodes. CONCLUSIONS: CARTO is useful for characterizing the anatomical and electrophysiological substrates, and for identifying the optimal ablation sites for VT associated with ARVD.     

致心律失常性右室心肌病的CARTO系统电生理基质标测和射频导管消融

目的应用CARTO系统对致心律失常性右室心肌病(ARVC)患者进行电解剖标测并指导射频消融治疗其室性心动过速(简称室速)。方法入选伴有室速反复发作的25例ARVC患者,年龄36±12岁,男性17例,有家族成员35岁以下早发猝死史3例。术前行常规心电图、心室晚电位、心脏B超检查。在窦性心律或/和心动过速时,电解剖标测三维重建右室。术中6例同时行右室造影检查。根据双极电图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,线性消融关键峡部或疤痕区与三尖瓣环之间或两疤痕区间;对于局灶性室速,点消融局部最早激动区域。结果 20%(5/25)体表心电图发现前壁或下壁导联Epsilon波,心室晚电位阳性占88%(21/25),心脏B超发现右室不同程度的局部或整体扩张,56%(14/25)可见局部囊袋状向外膨出。所有患者均出现1～5(2±1)种左束支阻滞型室速,其中5例合并频发室性早搏,1例伴心房扑动,1例伴左后间隔旁道。即时消融成功率为72%(18/25)。随访14±10(4～36)个月,原消融成功的5例室速复发。1例消融失败伴晕厥史的患者植入ICD治疗。无手术相关并发症和死亡发生。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。CARTO系统标测的电压图,参考术前心电图、心脏B超及右室造影可了解病变心肌的分布范围,对初步确定室速的病理基质有帮助。     

Catheter ablation of haemodynamically unstable or non-sustained ventricular tachycardia

BACKGROUND: Ventricular tachycardia (VT) may be haemodynamically unstable or non-sustained, interfering with detailed activation mapping. Non-contact mapping permits beat-by-beat analysis of VT, projected upon a 3-dimensional reconstructed geometry of the cardiac chamber. Objective - The aim of the present study is to determine the utility of non-contact endocardial mapping to guide ablation of haemodynamically unstable VT or non-sustained VT. METHODS AND RESULTS: Eighteen VTs in 17 patients were induced (cycle length 336 +/- 58 ms) and mapped. Three patients were mapped during premature ventricular complexes (PVCs) because sustained VT could not be induced. Analysis of the archived non-contact activation maps was performed to identify the exit point and/or the diastolic pathway of theVT reentry circuit.The endocardial exit points (10 +/- 16 ms before QRS) were defined in 17/18 VTs (94%). A diastolic pathway was identified in 5/6 ischaemic VTs.The earliest activation sites were identified in all 3 patients with PVCs. Radiofrequency current was applied around the exit point or to create a line of block across the diastolic pathway. Catheter ablation was performed in 17/18 VTs, including 3 patients mapped using only PVCs. Ablation was successful in 16/18 VTs (89%) and in 1 5/17 patients (82%). Catheter ablation was not performed in one patient (peri-hisian VT) and was unsuccessful in one patient (mapped during PVCs). CONCLUSIONS: Non-contact endocardial mapping is useful to guide radiofrequency catheter ablation of untolerated or non-sustained VTs.     

Relationship between successful ablation sites and the scar border zone defined by substrate mapping for ventricular tachycardia post-myocardial infarction

INTRODUCTION: It is unknown if identification of scar border zones by electroanatomical mapping correlates with successful ablation sites determined from mapping during ventricular tachycardia (VT) post-myocardial infarction (MI). We sought to assess the relationship between successful ablation sites of hemodynamically stable post-MI VTs determined by mapping during VT with the scar border zone defined in sinus rhythm. METHODS AND RESULTS: Forty-six patients presenting with hemodynamically stable, mappable monomorphic VT post-MI and who had at least one such VT successfully ablated were prospectively included in the study. In each patient, VT was ablated by targeting regions during VT that exhibited early activation, +/- isolated mid-diastolic potentials, and concealed entrainment suggesting a critical isthmus site. Prior to ablation, a detailed sinus-rhythm CARTO voltage map of the left ventricle was obtained. A voltage <0.5 mV defined dense scar. Successful VT ablation sites were registered on the sinus voltage map to assess their relationship to the scar border zone. Of the 86 VTs, 68% were successfully ablated at sites in the endocardial border zone. The remaining VTs had ablation sites within the scar in (18%), in normal myocardium (4%), and on the epicardial surface (10%). There were no significant differences in VT recurrence amongst the different groups. CONCLUSION: Successful ablation sites of hemodynamically stable, monomorphic VTs post-MI are often located in the scar border zone as defined by substrate voltage mapping. However, in a sizable minority, ablation sites are located within endocardial scar, epicardially, and even in normal myocardium.     

Preferential Locations for Critical Reentry Circuit Sites Causing Ventricular Tachycardia After Inferior Wall Myocardial Infarction

Reentrant VT Post MI. Introduction : For relatively slow monomorphic ventricular tachycardia (VT) after myocardial infarction, entrainment can be used to identify reentry circuit "isthmus sites" (exit sites and sites proximal to the exit) where radioifrequency (RF) catheter ablation has the greatest likelihood of interrupting reentry. Similarities in coronary and ventricular anatomy may cause such sites to form in preferential locations. The objective of this study is to determine if there are preferential locations for reentry circuit isthmus regions in chronic inferior wall infarctions causing VT.
Methods and Results : Catheter mapping and RF catheter ablation was performed in 21 patients with an old inferior wall myocardial infarction and VT. The inferior wall was divided into 9 anatomic regions: 3 apical, 3 mid, and 3 basal segments. Of 46 different VTs, an endocardial isthmus site was identified in one or more zones in 28 (61%), with 10 VTs having isthmus sites in two or more adjacent regions. Isthmus zones were found in a basal region of the left ventricle in 24 (86%) of 28 VTs, in a mid segment in 9 (32%) VTs, and in an apical segment in 1 (4%) (P = 0.002). Of 30 RF current applications that terminated VT, 21 (70%) were at basal isthmus sites.
Conclusion : The high prevalence of endocardial isthmus zones near the base of the left ventricle suggests that the mitral annulus often plays a role in defining the margins of reentry circuits that cau.se relatively slow VTs after inferior wall myocardial infarction.     

Impact of different activation wavefronts on ischemic myocardial scar electrophysiological properties during high-density ventricular tachycardia mapping and ablation

Introduction

Scar-related ventricular tachycardia (VT) usually results from an underlying reentrant circuit facilitated by anatomical and functional barriers. The later are sensitive to the direction of ventricular activation wavefronts. We aim to evaluate the impact of different ventricular activation wavefronts on the functional electrophysiological properties of myocardial tissue.

Methods

Patients with ischemic heart disease referred for VT ablation underwent high-density mapping using Carto®3 (Biosense Webster). Maps were generated during sinus rhythm, right and left ventricular pacing, and analyzed using a new late potential map software, which allows to assess local conduction velocities and facilitates the delineation of intra-scar conduction corridors (ISCC); and for all stable VTs.

Results

In 16 patients, 31 high-resolution substrate maps from different ventricular activation wavefronts and 7 VT activation maps were obtained. Local abnormal ventricular activities (LAVAs) were found in VT isthmus, but also in noncritical areas. The VT isthmus was localized in areas of LAVAs overlapping surface between the different activation wavefronts. The deceleration zone location differed depending on activation wavefronts. Sixty-six percent of ISCCs were similarly identified in all activating wavefronts, but the one acting as VT isthmus was simultaneously identified in all activation wavefronts in all cases.

Conclusion

Functional based substrate mapping may improve the specificity to localize the most arrhythmogenic regions within the scar, making the use of different activation wavefronts unnecessary in most cases.     

室性心动过速的基质标测与消融

目的 探讨使用Carto三维系统标测致心律失常性右心室心肌病(ARVD/C)室性心律失常的基质来指导导管消融的安全性和有效性.方法 自2007年7月至2008年4月,北京大学第一医院心内科连续收治4例ARVD/C患者,年龄28～53岁,男性3例,女性1例,其中1例患者有直系亲属猝死家族史,发作性室性早搏/室性心动过速(VT)病史3个月至24年.使用Carto三维系统进行电解剖电压标测,局部电压低于1.5 mV的区域判断为病变心肌,低于0.5 mV的区域为瘢痕区,结合传统的激动顺序标测、起搏标测、拖带标测和心室内碎裂电位,识别病变心肌范围和心动过速折返路径以指导消融.结果 4例患者电生理检查共诱发出7种形态的左束支阻滞形、VT,电解剖电压标测的低电压区主要位于右心室流人道的基底部和偏间隔部,在病变心肌与正常心肌交界区和/或环绕病变心肌的最早激动处做线性消融,4例患者均获消融即刻成功,无并发症.4例患者消融术后随访3个月至1年,有1例出现复发,口服胺碘酮控制,至今无晕厥和猝死.结论 ARVD/C的VT标测与消融安全可靠,应用三维系统进行电解剖电压标测与传统的心电标测方式相结合,可更精确判断ARVD/C的室性心律失常基质和有效提高消融成功率.