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。     

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.     

CARTO系统指导射频消融的应用评价

目的对比研究CARTO标测系统在指导消融术中的弊与利.方法 6例病人同时接受CARTO及普通心内电信号标测双系统指导下的射频消融.其中左房局灶性房速3例、右房房速1例、左室非典型部位特发性室速1例、先心矫形及修补术后室速1例.除1例房速外,均为接受第二或第三次手术的病人,普通心内电信号标测同常规,CARTO电解剖标测系统利用电磁原理首先建立感兴趣区的三维空间,然后诱发心动过速,心动过速时标测折返环,窦性心律下或心动过速时进行消融.结果 6例病人成功4例.未成功的两例病人为因心包填塞中止手术的患者,其中1例为左房局灶性房速、1例左室非典型部位特发性室速,心包穿刺后缓解,无1例死亡.结论 CARTO电解剖标测系统的优点在于可以术中描绘出心动过速的折返环路、无须太多的X线曝光量、提高复杂心律失常射频消融的成功率,节省手术时间.但对于简单心律失常来讲,建立感兴趣区的三维结构,要耗用不必要的标测时间,使简单问题复杂化,此外费用较高.由于CARTO系统无法观察到整个导管的走性情况,导管在心腔内的张力无法判断,因此容易出现心包填塞等并发症.因此CARTO电解剖标测系统的主要优势在于器质性心脏病引起的复杂心律失常的射频消融.     

CARTO标测指导心肌梗死后室性心动过速的射频消融

心肌梗死 (MI)后室性心动过速 (VT)的基质存在解剖上的复杂性并且血液动力学常常是不稳定的 ,因此射频导管消融的成功率是有限的。本研究的目的是运用电解剖标测 (CARTO)指导VT的射频消融 ,以便弄清折返环和梗死区的关键峡部 ,此可能增加临床消融的效率。 19例MI的病人 (年龄 6 6± 7岁 ,其中男性 17例 )因VT拟作 2 0次消融 [17例在服用抗心律失常药 ,7例已安装埋藏式心脏转复除颤器 (ICD) ]。所有病例均反复发作临床型VT(周期为 42 3± 87ms)。在VT时或窦律 /右室起搏 (SR/RVP)行左室CARTO标测。对 13例 14次血液动力学稳定的VT实施标测 ,包括 2例无休止性慢VT。仅 8例临床性VT ,在心动过速时完成了整个左室的重建 ,另 6例因反复机械损伤MI区内关键性峡部 ,使临床型VT不再诱发。 12例在SR/RVP时完成左室标测 ,包括 6例关键性峡部损伤及 6例血液动力学不稳定者。在 8例CARTO标测的VT中 ,有 3例呈现典型的“8字”型折返环 ,2例沿二尖瓣 (MA)激动心室。在 8例VT中 ,于关键性峡部放电消融 ,其中 6例VT终止 ,平均放电 2次 ;然后行线性消融连接两个疤痕区域或连接疤痕与MA环 ,平均放电 16次。在SR/RVP时标测 ,可见 1个或多个疤痕区域 ,4例在诱发VT时放电 ,均终止了VT ;另 8例因极不稳定的血液动力学或机械损?     

右心室造影结合CARTO标测指引射频导管消融法洛四联症术后室性心动过速

目的:应用右心室造影结合电解剖标测（CARTO标测）指引经盐水灌注射频导管消融法洛四联症术后室性心动过速（VT）5例。方法: 5例患者中4例为男性,6～38岁,法洛四联症术后2～16年反复出现阵发性心悸,发病时体表心电图均表现为持续性VT且药物治疗无效,2例有晕厥史。均不同意放置埋藏式心脏复律除颤器（ICD）。应用右心室造影结合CARTO标测指引消融VT的方法如下:首先进行右心室造影明确右心室解剖及肺动脉瓣环位置,并作为解剖路标,在窦律时行右心室电压标测,标记低电压手术疤痕和室间隔补片区域,明确VT发生基质。而后心室程序电刺激诱发VT,如血流动力学稳定,则在VT时行拖带标测,确定并消融VT关键峡部;如血流动力学不稳定或不能诱发持续性VT,则在窦律时行起搏标测,在局部起搏时和VT有相同或相近的体表心电图并伴较长的刺激到QRS波时间的部位消融,并消融有晚电位或碎裂电位的电屏障区。结果: 5例患者可诱发出6种形态VT,VT周长230～310 ms,5种为持续性VT,其中1种血流动力学不稳定;另1种为非持续性VT。3例患者在VT时标测和消融,2例患者在窦律下标测后消融。6种形态VT均为疤痕折返机制,6种VT均消融成功。随访12～30月,无VT复发。结论: 右心室造影能明确法洛四联症术后右心室及肺动脉瓣环解剖结构,CARTO标测可以定位室间隔补片和外科手术疤痕,在明确这些VT发生基质基础上指引射频导管消融法洛四联症术后VT可取得较高的成功率。     

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。     

50例室性心律失常导管射频消融治疗临床分析

目的:报道不同类型室性心律失常的射频导管消融(RFCA)体会。方法:50例室性心律失常患者中男20例、女30例,年龄14～70(43.21±13.31)岁。除1例为陈旧性心肌梗死冠状动脉旁路移植术(CABG)后持续性室性心动过速(VT)、5例为致心律失常性右室心肌病(ARVC)外,其余44例均为非器质性心脏病室性心律失常。43例非器质性心脏病室性心律失常采用传统的起搏与激动标测。6例器质性心脏病VT及1例多源室性期前收缩(PVC)在非接触标测系统EnSite3000指导下进行消融治疗。结果:①48例消融成功,2例失败,成功率96%,4例复发。②右室流出道(RVOT)起源的VT和PVC具有典型的心电图特征,表现为典型的左束支传导阻滞型伴电轴右偏。RVOT的起源点不同,其12导联心电图特征不同,Ⅰ、Ⅱ、Ⅲ和aVF导联呈RR'型,V1～3具有深S波是游离壁起源的特征。ARVC表现为典型的左束支传导阻滞型伴电轴右偏,窦性心律时V1～3T波浅倒置,心脏核磁或心脏超声心动图见右室心肌运动减弱。③1例ARVC和1例陈旧性心肌梗死CABG术后病例在消融过程中出现心室颤动,经电除颤后继续消融成功。结论:RFCA是一种安全、有效...     

采用心内非接触式标测的右心室流出道室性心动过速的射频消融

目的 右心室流出道(right ventricular outflow tract,RVOT)的解剖结构使得对该部位的室性心动过速(ventricular tachyeardia,VT,室速)标测定位的难度较大,远期成功率也较低,为此,采用心内非接触式标测指导导管消融。方法 20例患者(男性12例,女性8例),年龄14～59(35.1±12.3)岁。其中6例有晕厥或黑矇史,7例既往曾接受射频消融未获成功。全部患者均在RVOT内放置EnSite3000标测导管,在窦性心律下进行疤痕标测和心动过速时进行最早激动标测,并根据标测结果使用EnSite 3000导管的导航功能指导消融定位。消融前并进行起搏标测。结果 20例患者共诱发出22种RVOT室速,其中3例还伴其它起源的室性早搏(室早)。疤痕标测提示,13例患者有电学意义上的疤痕区域,且有11例室速起源于该疤痕区域。25个室速或室早起源点中1例起源于近肺动脉瓣口部,10个位于间隔侧,其余均偏游离壁,其中7个偏RVOT后壁中、下部,4个偏前壁中、下部,3个位于游离壁侧;病变基质的直径为6～42 mm,平均(16.8±9.2)mm。非接触式标测所确定的最早激动处电位平均领先体表20～62(41.0±13.8)ms;与自发的室性心动过速相比,起搏标测下14例的12个导联QRS形态完全一致,11/12个导联一致的为10例,1例有10/12导联一致。全部室速和室早均消融成功。在标测确定的     

Hoffmayer积分(109)

起源于右室流出道的室早、室速临床常见,90%的特发性右室流出道室早、室速经射频消融可获根治。但该部位又是致心律失常性右室心肌病(ARVC)的患者心脏发育不良三角的顶端部位,故其伴发的室早、室速也能位于该部位。当室早或室速符合右室流出道室早、室速的心电图特征时,究竟属特发性还是伴发于ARVC者,Hoffmayer最近提出鉴别两者的心电图积分法。     

致心律失常性右室心肌病的临床研究和家系调查

目的 对7例致心律失常性右室心肌病(ARVC)及其中的3个家系中的34个成员进行调查。方法病史、临床检查、标准12导联心电图、超声心动图和心室晚电位测定。5例进行电生理检查。结果 超声心动图发现5例右室扩大伴搏动减弱，8例右室前壁局限性运动减弱或收缩期膨出，1例下壁局限性变薄和收缩期膨出。心电图显示完全性和不完全右束支阻滞样改变各5例，肢体导联低电压2例，23例右胸(V1-V4)和／或下壁(Ⅱ、Ⅲ、aVF)导联T波倒置，25例V1导联QRS时间明显延长(P<0．01)．13例心室晚电位阳性。电生理检查，5例患者可诱发≥2种的呈左束支阻滞图形室性心动过速(室速)，2例诱发心室颤动(室颤)；右室一处或多处起搏阈值增高或不能有效起搏。1家系2例猝死。1例ARVC合并侏儒症。5例患者反复发作呈左束支阻滞图形的室性心动过速，1例伴有配对间期极短的多形性室速和反复晕厥发作，12例有呈左束支阻滞图形室性早搏。结论 本研究结果提示ARVC是一遗传性疾病．右室结构与功能异常、心电图复极异常和起源于右室室性心律失常是其最常见的表现。     

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。     

Human histopathology of electroanatomic mapping after cooled-tip radiofrequency ablation to treat ventricular tachycardia in remote myocardial infarction

INTRODUCTION: Catheter ablation of ventricular tachycardia (VT) in remote myocardial infarction (MI) often requires excessive mapping procedures. Documentation of the electrical substrate via electrogram amplitude may help to identify regions of altered myocardium resembling exit areas of reentrant VTs. METHODS AND RESULTS: A patient with multiple symptomatic monomorphic VTs (biventricular ICD, remote MI) underwent electroanatomic substrate mapping (CARTOtrade mark) for VT ablation. Regions of scar (bipolar electrogram amplitudes or=1.5 mV), and "altered" myocardium (0.5-1.5 mV) were identified. Ablation was directed to regions with "altered" myocardium based on pace map correlation. After ablation the clinical VT did not reoccur. The patient died due to worsening of heart failure 7 days afterward. During postmortal evaluation specified sites of electroanatomic mapping were correlated to histopathological findings. Annotated scar areas were documented to consist of areas with massive fibrosis (>or=80% of mural composition). Ablations were found to span through regions with intermediate fibrosis (21-79%) mapped as "altered" myocardium. Ablation produced transmural coagulation necrosis of mesh-like fibrotic tissue with interspersed remnants of myocardial cells up to a maximum depth of 7.0 mm. Subendocardial intramural bleedings were universal findings 7 days after ablation. CONCLUSIONS: Electroanatomic substrate mapping for VT ablation sufficiently identified regions of scar and normal myocardium. Regions with bipolar electrogram amplitudes between 0.5 and 1.5 mV were found to correlate to areas of "intermediate" fibrosis (21-79%) with only remnant strands of myocardial cells and were identified as target region for ablation. Cooled-tip endocardial radiofrequency ablation lead to transmural coagulation necrosis up to a depth of 7.0 mm.     

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.     

Endocardial and epicardial radiofrequency ablation of ventricular tachycardia associated with dilated cardiomyopathy: the importance of low-voltage scars

OBJECTIVES: The purpose of this study was to evaluate the occurrence, locations, and relationship of ventricular tachycardia (VT) to low-voltage areas in dilated cardiomyopathy (DCM). BACKGROUND: The substrate causing monomorphic VT after infarction is characterized by regions of low-voltage (<1.5 mV) scar on electroanatomic maps. The substrate causing VT associated with DCM is less well defined. METHODS: A total of 28 patients were studied with endocardial (26 patients) and epicardial (8 patients) electroanatomic mapping. The VT circuits were defined by entrainment or pace mapping. RESULTS: Ventricular tachycardia was due to focal VT in 5, bundle-branch re-entry in 2, and myocardial re-entry in 22 patients (both focal and re-entry VTs in 1 patient). All patients with myocardial re-entry had endocardial (20 of 20 patients) and/or epicardial (7 of 7 patients mapped) scar. Most (63%) endocardial scars were adjacent to a valve annulus. Of the 19 VT circuit isthmuses identified, 12 were associated with an endocardial scar and 7 with an epicardial scar. All myocardial re-entrant VTs were abolished in 12 of 22 patients, and inducible VT was modified in 4 patients. During follow-up of 334 +/- 280 days, 54% of patients with myocardial re-entry were free of VT despite frequent episodes before ablation. CONCLUSIONS: The VTs in DCM are most commonly the result of myocardial re-entry associated with scar. Scars are often adjacent to a valve annulus, deep in the endocardium, and can be greater in extent on the epicardium than on the endocardium. The use of epicardial mapping and radiofrequency is likely to improve success.     

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.     

Value of high-density endocardial and epicardial mapping for catheter ablation of hemodynamically unstable ventricular tachycardia

BACKGROUND: Percutaneous epicardial mapping has been used for ablation of recurrent ventricular tachycardia (VT). OBJECTIVES: The purpose of this study was to use a combined epicardial and endocardial mapping strategy to delineate the myocardial substrate for recurrent VT in both ischemic (n = 12) and nonischemic cardiomyopathy (n = 8), and to define the role of epicardial ablation. METHODS: Electroanatomic mapping was performed in 20 patients. High-density voltage maps were obtained by acquiring both endocardial and epicardial electrograms. Electrograms derived from six patients with structurally normal hearts were used as controls. A total of 26 VTs were targeted in the 20 patients. RESULTS: Most VTs (23/26 [88.5%]) were hemodynamically unstable. In patients with ischemic cardiomyopathy, the extent of endocardial scar was greater than epicardial scar. A definable pattern of scar could not be demonstrated in nonischemic cardiomyopathy. Pathologic examination of explanted hearts in two patients with nonischemic cardiomyopathy demonstrated that low-voltage areas were not always predictive of scarred myocardium. A substrate-based approach was used for catheter ablation. Catheter ablation was performed on the endocardium in all patients; additional epicardial delivery of radiofrequency energy was required in 8 (40%) of 20 patients for successful ablation. During follow-up (12 +/- 4 months), 15 (75%) of 20 patients have been arrhythmia-free. CONCLUSION: Patients with ischemic cardiomyopathy tend to have a larger endocardial than epicardial scar. Use of epicardial and endocardial electroanatomic mapping to define the full extent of myocardial scars allows successful catheter ablation in patients with hemodynamically unstable VTs.     

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.     

Radiofrequency catheter ablation of ventricular tachycardias

Management of patients with ventricular tachycardia (VT) is often difficult. Drug therapy is often ineffective. Implantable cardioverter defibrillators (ICDs) can terminate VT episodes but do not prevent them. Radiofrequency (RF) catheter ablation can suppress arrhythmias in selected patients. However, the procedure is often challenging and success rates lower than for ablation of supraventricular tachycardias. The mapping and ablation approach depends on the VT mechanism. Monomorphic VT in patients without structural heart disease is referred to as idiopathic and has a focal origin. These VTs can be abolished by ablation in most of the patients. In VT due to reentry within an area of scar from an old myocardial infarction or cardiomyopathic process, critical parts of the circuit may be difficult to localize, rendering RF ablation challenging. In patients with monomorphic VT, prevention of VT recurrence can be achieved in 55% to 80% of patients. Multiple morphologies of VTs and circuits that are located deep in the endocardium are common problems that reduce efficacy. Furthermore, mapping to identify target regions for ablation can be more difficult if VT is rapid and not tolerated, or not inducible. Recently, multisite mapping of the arrhythmia substrate during sinus rhythm or multisite activation mapping of a few VT beats were shown to be effective for ablation of these "unmappable VTs". Bundle branch reentry tachycardia occur in patients with nonischemic cardiomyopathies, mostly valvular heart disease and can be successfully abolished with RF ablation of the right bundle. However, some of these patients may develop recurrences due to other types of VT. Recent technical developments have increased efficacy and simplified the approach of RF ablation of VT in patients with structural heart disease. However, long-term efficacy is not accurately predictable and implantation of an ICD is mandatory in most of the patients with severely depressed left ventricular function.     

Catheter ablation of mitral isthmus ventricular tachycardia using electroanatomically guided linear lesions

Mitral isthmus ventricular tachycardia uses a reentrant circuit with a critical isthmus of conduction bounded by the mitral valve proximally and a remote inferior infarction scar distally. Successful catheter ablation requires placement of a lesion to transect the isthmus so as to prevent wavefront propagation. We report a case with previously unsuccessful ablation in which focal isthmus ablation failed to eliminate arrhythmia. Electroanatomic mapping demonstrated a wide tachycardia isthmus, and a linear lesion placed from the edge of the inferior infarct (as demonstrated on the three-dimensional voltage electroanatomic map) to the base of the mitral valve successfully eliminated tachycardia. In some patients with mitral isthmus VT, a wide isthmus requires linear lesion placement to fully transect the isthmus and eliminate tachycardia. Electroanatomic mapping can be used to define isthmus boundaries and thus guide successful ablation.