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.     

动态基质标测在致心律失常右室心肌病患者室性心动过速射频消融中的应用

目的　探讨应用非接触球囊导管标测系统行动态基质标测,指导对致心律失常右室心肌病(ARVC)患者室性心动过速(室速)消融的价值。方法　应用非接触球囊导管标测系统在窦律下对 3例ARVC室速患者行动态基质标测,在确定室速的最早激动点、出口部位和传导顺序后,寻找与室速相关的峡部并行线性消融。结果　3例患者存在 3种不同形态的基质,分别位于右室流出道、右室前壁和右室前侧壁。共诱发 5种室速,平均心动周期为(348±65)ms,其中 3种室速起源于基质或基质边缘, 2种室速的起源远离基质; 1种室速经基质传导。5种室速全部消融成功。平均随访 20个月,无心动过速发作。结论　应用非接触球囊导管标测系统确定异常电生理基质有助于理解ARVC室速的发生机制和制定消融策略,行室速相关峡部的线性消融可有效治疗室速。     

经导管射频消融心律转复除颤器植入后电风暴

目的报道3例心律转复除颤器（ICD）植入后抗心律失常药物治疗无效的室性心律失常电风暴患者经导管射频消融的结果。方法2名男性与1名女性患者,年龄为75、55、37岁,分别患有陈旧性前壁心肌梗死、致心律失常性右心室心肌病、左心室心肌病。均在ICD植入后发生抗心律失常药物治疗无效的电风暴。应用Carto电解剖标测系统引导盐水灌注射频导管标测和消融室性心动过速（VT）。对可标测VT（持续性、血流动力学稳定）行激动和拖带标测;对不可标测VT,则在基质标测的基础上行起搏标测和／或短时间的拖带标测。结果3例患者中共诱发出5种形态的VT,4种血流动力学较稳定VT和1种血流动力学不稳定VT。成功消融了所有形态的VT,抑制了电风暴的急性发作。消融后随访的6、19和36个月中,仅1例患者出现1次ICD放电。结论在电解剖标测的基础上,应用盐水灌注射频导管消融ICD植入后抗心律失常药物治疗无效的电风暴有很好的疗效。     

经导管射频消融室性早搏或室性心动过速治疗心肌梗死后室性心律失常电风暴

目的报道射频消融治疗心肌梗死(MI)后抗心律失常药物治疗无效的室性心律失常电风暴4例,探讨其标测方法和消融效果。方法 4例病人均为男性,64岁、75岁、73岁和60岁。分别于前壁心肌梗死后19天、45天、3天和10天出现反复发作室性心动过速(室速)或室性颤动(室颤),经血运重建、抗心律失常药物治疗室速、室颤仍反复发作。病例1、3、4的单形或多形室速、室颤均有频发室性早搏诱发,病例2植入ICD后服用胺碘酮和β-受体阻滞剂使反复发作的室速暂时得到了控制,但ICD植入一月后室速再次频繁发作。室速均呈右束支阻滞(RBBB)图形伴心电轴左偏。标测和消融方法为在左心室内标测到室早或持续室速时最早激动处后进行射频消融。结果病例1、3、4均可记录到呈右束支阻滞(RBBB)伴电轴左偏和/或右偏形态的室早,在这3例患者中室早均可诱发室速。在频发室早下行标测和消融,激动标测显示3例患者的室早最早激动处在左心室中下部位,室早时浦肯野纤维电位提前体表心电图QRS波40-50ms,且窦性心律时在同一部位可记录到清晰的提前QRS波群的浦肯野纤维电位。3例分别于最早激动处且标测到浦肯野纤维处放电6次、8次和16次,均成功消融室早。病例3因为出现了另一形态的室早,于左室前内侧反复消融5次,另一形态室早亦消融成功。病例2中没有记录到室早,心室程序刺激诱发2种形态室速,呈右束支阻滞(RBBB)图形伴有电轴左偏。在左心室内标测到浦肯野纤维提前室速起始最早60ms处进行消融,成功消融室速。4例分别随访7年、6年、4年和6个月,病例1和病例3无室速和室颤复发,病例2有1次ICD放电,病例4复发室早诱发短阵室速,但无持续性室速、室颤和晕厥发生。结论 MI后频繁快速室性心律失常可能由起源于左室浦肯野纤维网的室早或室速所诱发,经导管射频消融室早或室速对?     

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。     

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。     

致心律失常性右室心肌病的临床与电生理学特征

目的与方法 致心律失常性右室心肌病（ARVC）可引起严重心律失常，本文对6例ARVC患者进行了临床和电生理学特点观察和研究。结果 6例患者有室性心动过速（VT）的5例，多形性VT2例。所有患者均表现右心室（RV）扩大，可见到RV局部病变的2例，均没有见到左心室受累和明显的心功能受损。接受电生理学检查的4例患者中，有3例可以由电刺激诱发和终止，电生理标测2例源自RV心尖部，2例源自RV游离壁，与超声提示的RV病变部位有关。3例患者发生过阿斯综合征，其中有2例发生院外猝死，2例猝死病人均发作过多形性VT。结论 ARVC以RV进行性病变伴室性心律失常为特征。射频消融（RFCA）和ICD植入治疗、药物治疗是基本治疗手段，药物治疗以胺碘达隆加β－受体阻滞剂或索他洛尔(Sotalol)为多选，但是单纯的药物治疗并不能防止病人发生心脏性猝死。对于有条件的病人应该考虑进行RFCA或ICD治疗。     

射频消融治疗室性早搏触发特发性室性心动过速／心室颤动的病例分析

目的探讨射频消融治疗在室性早搏（室早）触发特发性室性心动过速／心室颤动（室速／室颤）中的作用。方法总结3例由室早触发室速／室颤的治疗经验,1例对室早进行射频消融（RF—CA）并植入心律转复除颤器（ICD）,另1例经射频消融未完全消除室早而选择植入ICD,第3例经射频消融成功消除室早,未再发室颤。结果随访2年,3例患者均存活,ICD未再记录到室速／室颤。结论在室早触发室速／室颤病例中,应分析室早与室速／室颤的相关性,给予个体化治疗,射频消融室早可以消除／减少晕厥和室颤的发作。     

致心律失常性右心室心肌病室性心动过速的导管射频消融

目的致心律失常性右心室心肌病（ARVC）所致的多形室性心动过速（室速）具有较高的死亡风险，心内非接触式标测可提供快速而准确的标测并指导消融。方法32例患者（男性26例，女性6例），年龄（37．2±13．8）岁，其中14例有晕厥／黑矇史，2例已植入心律转复除颤器（ICD）。所有患者均经左锁骨下静脉送入EnSite多电极矩阵导管进行非接触式标测。结果全部患者共诱发出67阵室速，其心电图形态不同，但均为左束支阻滞形室速。频率130～310（210．0±32．2）次／min，其中42阵室速的频率t〉200次／min。24例（75％）患者有〉t2种形态的室速。在非接触式标测指导下对室速的起源进行了片状消融。消融的即时成功率为84，4％（27／32），15．6％（5／32）的患者经消融后室速频率明显减慢。随访9～72（28．6±16．0）个月，无一例患者发生晕厥／黑矇。术中无并发症。随访期间81．3％的患者不服药亦无室速发生，其余均获得明显改善。结论ARVC所致的室速可在非接触式标测的指引下经片状射频消融而消除或获得明显改善。本组无一例发生心脏骤停或心脏性猝死。某些患者消融后可能出现迟发效应。     

非接触心内膜球囊标测系统指导瘢痕相关性室性心动过速标测和消融

目的 运用非接触心力膜球囊标测系统（EnSite3000系统）对瘢痕相关性室性心动过速（室速）进行心内膜标测，探讨瘢痕相关性室速电生理机制。标测和消融。方法 运用非开胸法建立心肌梗死后持续性单形性室速猎模型4只；同时选取致心律失常性右室心肌病（ARVC）合并室速患者2例，于左心室或左，右心室内各置入-EnSite3000球囊，分别构建左和（或）右心室的三维几何模型。确定心内膜瘢痕组织的部位，范围和边界，分析单形性室速的激动顺序，关键部位和折返环路及与瘢痕组织的关系，并制定消融策略指导消融。结果 （1）EnSite3000系统准确标测出4只猪左心室心梗后瘢痕组织，其部位，大小及边缘等均与病理一致。4只猪共诱发出8种形态的单形性室速，系统标测出2种室速为左心室典型的“8”字形折返途径，1种室速最早激动点位于左心室前侧壁瘢痕边缘。通过双心室球囊放置准确标测到2只猪5种形态室速在双心室内的激动路径，所有室速的关键位点均在瘢痕组织边缘或其中，6种室速位于左室，2种室速位于右室，可成功释放电流的3种室速消融有效，1种室速线性消融失败；4种室速因放电仅几秒钟即出现凡室颤动，且反复出现，使消融难以完成因而未获成功。（2）2例ARVC患者的右心室流出道处均可标测到类似瘢痕组织的低电压区，1例患者诱发出2种类型的折返性室速，均消融成功，随访4个月无室速发作；另1例患者2种室速，消融失败后置入心脏复律除颤器。结论 EnSite3000系统能准确标测到常规方法无法标测的室速相关性低电压区或瘢痕区域，确定瘢痕相关性室速的机制和关键位点，并精确导航，有助于提高瘢痕相关性室速的消融成功率，为此类室速的消融提供了较好的标测手段。如能结合消融方法和能源的改善，可望进一步提高这类室速的消融成功率。     

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.     

Mechanical interruption of postinfarction ventricular tachycardia as a guide for catheter ablation

BACKGROUND: Mechanical trauma has been described as a helpful guide for ablation of atrial tachycardias and accessory pathways. In postinfarction ventricular tachycardia (VT), the reentrant circuit is partly endocardial and therefore may be susceptible to catheter trauma. OBJECTIVES: The purpose of this study was to determine the prevalence and significance of VT termination resulting from catheter trauma. METHODS: A consecutive series of 39 patients (mean age 68 +/- 7 years, ejection fraction 0.25 +/- 0.02) underwent left ventricular mapping for postinfarction VT. Mapping was performed during 62 hemodynamically tolerated VTs (mean cycle length 451 +/- 88 ms). Only hemodynamically tolerated VTs that did not terminate spontaneously and VTs that were reproducibly inducible were included in the study. VT termination was considered mechanical only if it was not caused by a premature depolarization. RESULTS: In 13 of 62 VTs (21%) in 8 of 39 patients (21%), either VT terminated during catheter placement at a particular site (n = 7) or a previously reproducibly inducible VT became no longer inducible with the mapping catheter located at a particular site (n = 6). The stimulus-QRS interval was significantly shorter at sites where mechanical trauma affected the reentrant circuit compared with sites having concealed entrainment (102 +/- 56 ms vs 253 +/- 134 ms, P = .003). At the site that was susceptible to mechanical trauma, the pace map was identical or highly similar in 13 of 13 VTs. After radiofrequency ablation at these sites, the targeted VTs were no longer inducible. No patient had recurrence of the targeted VT during a mean follow-up of 15 +/- 11 months. CONCLUSIONS: Catheter contact at a critical endocardial site can interrupt postinfarction VT or prevent its induction. Radiofrequency ablation at sites of mechanical termination of VT has a high probability of success.     

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.     

Long-term results after ablation of infarct-related ventricular tachycardia.

OBJECTIVES: The purpose of this study was to assess the long-term effects of ablation of infarct-related ventricular tachycardia (VT) and the subsequent requirement for implantable cardioverter-defibrillator (ICD) therapy. BACKGROUND: The long-term consequences after initially successful catheter ablation of infarct-related VT remain unclear. METHODS: Forty patients who presented with infarct-related VT were studied using noncontact mapping to guide ablation. RESULTS: One hundred forty VTs were mapped using the noncontact mapping system, including 36 (25.7%) clinical VTs. An endocardial exit site was determined in 100% of VT circuits, diastolic endocardial activity in 77 VTs (55%), and complete circuits in 24 VTs (17.1%). Eighty-one VTs (57.9%) were targeted for ablation, of which 67 (82.7% of targeted) were successfully ablated, including 27 clinical VTs (75% of clinical). Documented recurrence of an ablated VT occurred in 7.5% of patients over 36.3 +/- 21.0 months of follow-up. Episodes of new or recurrent, nontargeted VT or ventricular fibrillation (VF) occurred in 37.5% and VT recurrence without documentation of cycle length in 5%. In patients with ICDs, mean shock frequency was reduced from 6.8 +/- 7.3 per month in the year prior to ablation to 0.05 +/- 0.12 per month after ablation, over 24.7 +/- 18.9 months of follow-up (P < .0001). CONCLUSIONS: In patients with infarct-related VT, noncontact mapping-guided VT ablation is associated with a high procedural success rate, and VT recurrence necessitating ICD therapy delivery is significantly reduced. However, only 42.5% of patients remain free from VT/VF 3 years after ablation. Catheter ablation for infarct-related VT is indicated as an adjunctive therapy in patients with symptomatic VT but cannot substitute for ICDs and antiarrhythmic drugs.     

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.     

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。     

Ablation of ventricular tachycardia in the setting of coronary artery disease

Ablation of reentrant ventricular tachycardia (VT) is an accepted therapy for certain patients with VT caused by coronary artery disease (CAD). Its use is currently limited to patients with sustained, monomorphic, hemodynamically tolerated VT. The use of entrainment in mapping reentrant VT has made possible increasingly accurate localization of critical sites on the reentrant pathway that are amenable to ablation. Recent work has examined the accuracy with which various mapping criteria are able to predict successful ablation of reentrant VT in patients with CAD. Other recent studies have investigated attempted ablation of all inducible VTs in patients with multiple VT morphologies. In the future, substrate mapping may make possible ablation of VT in patients with nonsustained or fast, hemodynamically unstable VTs, thus allowing VT ablation to become a first-line therapy for many patients with VT in the setting of CAD.     

Long-term results of catheter ablation for ventricular tachycardia in arrhythmogenic right ventricular cardiomyopathy/dysplasia

AimsThis study analyzed the arrhythmogenic substrates and mechanisms of ventricular tachycardia (VT), and long-term outcomes of catheter ablation in patients with arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D).MethodsNine patients (1 female, 40±17 years) with ARVC/D and sustained monomorphic VT (SMVT) exhibiting left bundle branch block morphology of the QRS complex were studied. The diagnosis of ARVC/D was confirmed by means of echocardiography, magnetic resonance imaging, and electroanatomic mapping in all patients.ResultsThe patients underwent 10 ablation procedures. At the initial ablation, the mean VT rate was 196±21 (170–240) bpm. In total, 17 VT types were observed. One VT type with left axis (+I, aVL), or right axis (+II,III,aVF) of the QRS complex was present in 3 and 1 patient, respectively. Two VT types of left and intermediate (+I, II, aVL) axis or of left and right axis of the QRS complex were observed in 3 and 2 patients, respectively. Multiple VT types with left axis QRS complex recurred in 1 patient. One VT displayed characteristics of focal arrhythmia, the mechanism of remaining VTs was clearly macroreentrant. The critical slow-conducting isthmus of the reentry circuit was located at the infero-lateral aspect of tricuspid annulus and was bounded by the annulus and baso-lateral wall scar in 7 VTs; the isthmus was located within the scars in the remaining VTs. During 52±31 (12–93) month follow-up since the last ablation, 8 (89%) patients remained free from any VT recurrence without antiarhythmic drug.ConclusionsPatients with ARVC/D frequently presented ≥1 SMVT type. The critical isthmus of reentry circuit was dominantly located close to the tricuspid annulus. Long-term outcome of extensive endocardial ablation was favorable with isolated VT recurrences in one patient.     

Entrainment mapping and radiofrequency catheter ablation of ventricular tachycardia in right ventricular dysplasia

Objectives. The purpose of this study was to determine if entrainment mapping techniques and predictors of successful ablation sites previously tested in coronary artery disease can be applied to ventricular tachycardia (VT) in arrhythmogenic right ventricular dysplasia (ARVD).Background. VT in ARVD has not been well characterized. Reentry circuits in areas of abnormal myocardium are the likely cause, but these circuits have not been well defined.Methods. Mapping of 19 VTs in 5 patients with ARVD was performed. At 58 sites pacing entrained VT and radiofrequency current (RF) was applied to assess acute termination of VT.Results. Sites classified as exits, central/proximal, inner loop, outer loop, remote bystander and adjacent bystander were identified by entrainment criteria. The reentrant circuit sites were clustered predominantly around the tricuspid annulus and in the right ventricular outflow tract (RVOT). RF ablation acutely terminated VT at 13 sites or 22% of the applications. Of the 19 VTs, eight were rendered noninducible and three were modified to a longer cycle length. In 2 patients ablation at a single site abolished two VTs.Conclusion. VT in ARVD shows many of the characteristics of VT due to myocardial infarction. Entrainment mapping techniques can be used to characterize reentry circuits in ARVD. The use of entrainment mapping to guide ablation is feasible.