左上间隔分支型室性心动过速的标测和消融一例

患者男性,34岁.反复发作性心悸10余年,曾于外院行2次射频消融未成功,心动过速时维拉帕米静脉注射有效.入院心电图示窄QRS波(103ms)心动过速,不完全右束支传导阻滞图形伴电轴右偏,可见房室分离,窦性夺获;电生理标测提示室性心动过速,在左后分支和左前分支区域行激动标测均未标测到理想靶点,遂逐步将标测导管移至左上间隔部,可记录到PP电位,室性心动过速时发生逆转,在此处消融成功,后在此处起搏所记录图形与室性心动过速图形完全一致,提示可能为局灶起源的微折返室性心动过速.     

阵发性室上性心动过速伴短HV间期导管消融一例

患者,女,16岁,反复心悸1年,再发8h。心电图提示室上性心动过速。术中心房程序刺激呈房室结双径路特征,并诱发典型房室结折返性心动过速且排除房性心动过速、房室旁道介导。消融前后及心动过速发作时,HV间期20~30ms,心室最早激动点位于右室中间隔。提示合并His束与心室异常连接,即束室纤维。且无逆传功能,不参与心动过速折返环路,属旁观通道,未进行消融治疗。     

特发性室性心动过速12例的电磁解剖标测系统标测和消融

目的评价电磁解剖标测系统(Carto)标测和指导射频消融在治疗特发性室性心动过速的临床应用价值。方法入选12例特发性室性心动过速患者,年龄(33±12)岁。心动过速周期(370±95)ms。室性心动过速持续发作时,7FNavi-Star在相关心室标测,实时重建心腔三维电解剖图,右心室室性心动过速在右心室流出道详细标测,根据激动图上最红色区域为较早激动部位,结合大头导管记录心室波最早、且起搏时体表12导联图形与心动过速一致处,作为消融靶点。左心室室性心动过速在间隔部细标,标识较体表QRS波及His束电位提前的P电位处,作为靶点。温控60℃放电消融。以基础态及静脉滴注异丙肾上腺素反复电生理检查.不可诱发室性心动过速作为成功消融终点。结果12例均成功消融,其中右心室室性心动过速7例,均位于右心室流出道前中间隔部,左心室室性心动过速5例,起源于左心室后中间隔4例、中下间隔近心尖部1例。1例左心室室性心动过速于心动过速在左心室后中间隔处标测时,室性心动过速终止,后标志此处作为靶点,放电消融成功。手术时间为(102±25)分钟,曝光时间为(11±7)分钟。随访6～18个月,无复发病例。结论Carto系统通过磁场标测定位,结合心内电图重建室性心动过速时心室电激动图,可有效快速寻找最早激动点或P电位处作为消融靶点,进行电解剖标测,并可在标测导管机械损伤终止室性心动过速处标志,结合起搏标测,作消融参考点指导消融,治疗特发性室性心动过速安全有效。     

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。     

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.     

隐匿性慢旁束心动过速的诊断和消融

２例隐匿性慢旁束折返性心动过速的诊断依据：１、心房和心室电刺激易诱发和终止心动过速；２、心动过速时体表心电图呈窄ＱＲＳ波，递行Ｐ波及ＰＲ〈ＰＲ；３、心动过速与右心室起搏均呈同样的偏心性心房激动顺序；４、心动过速时于希司速不应期刺激心室可提前夺获心房；５、经旁速室房传导呈递减性，未发现旁束有前传能力；６、射频消融心动过速的逆传支后表现为室房分离。射频消融需在心运过速或心起搏时仔细标测三尖瓣环，寻找最     

导管消融具有双向传导特性的Mahaim结室纤维

目的介绍具有双向传导特性Mahaim结室纤维的电生理机制及导管消融方法。方法患者女性,34岁,反复发作性心动过速病史7年。外院心电图示“阵发性室上性心动过速”。心动过速可被维拉帕米及普罗帕酮终止。入院各项检查排除器质性心脏病后行电生理检查及导管消融术。结果电牛理检查示窦性心律时AH=73ms、HV=42ms,QRS时限100ms。心动过速时QRS波形态与窦性心律时相似,伴有轻度电交替。心动过速在多数情况下室房呈分离状态,HV问期为42ms,与窦性节律时相同,有时室房呈1：1传导,最早心房激动位于希氏束记录处。右心室心尖部以400ms周长刺激时室房呈分离状态。心房增频刺激时QRS波逐渐增宽,直至充分预激。在QRS波增宽过程中,HV逐渐缩短直至H波融合于QRS波之中,刺激信号至QRS波的间期逐渐延长,反映了递减传导的过程。继续缩短心房刺激周长后突然旁路传导受阻,经房室结下传并出现传导跳跃现象,继传导跳跃后心动过速被诱发。心动过速可被三磷酸腺苷（ATP）终止,终止后房室经旁路前传,其QRS波形态与充分预激时相似。在心房刺激保持充分预激的前提下,沿三尖瓣环标测,于左前斜位45。三尖瓣环4点钟处标测到最早V波,此处较体表心电图QRS波提前25ms,单极记录呈Qs型,HA波与V波之间未见高频电位。于该点消融放电（60W×60℃）,2S后旁路传导消失。放电过程中未出现交界性心律。消融结束后心房程序电刺激仍有房室传导跳跃现象。随访18个月,未再有心动过速发作。结论本病例心动过速系Mahaim结室纤维所介导,该纤维具有双向传导功能,其上插入端位于房室结慢径区域,下插入端位于邻近房室沟的局部心室肌。心动过速时房室结-希氏-浦肯野系统为前传支,结室纤维作为逆传支。     

射频消融治疗起源于希氏束旁的局灶性房速3例

正1临床资料患者一,女,64岁。因阵发性心悸、胸闷3年收治。查体未见明显异常体征。心电图(ECG)见图1。心脏彩超未见异常,左室射血分数(LVEF) 56%。诊断:阵发性室上性心动过速。入院行心脏电生理检查,心室及冠状窦程序刺激未见旁道及房室结双径路证据,予异丙肾上腺素激发后冠状窦近端S1S2刺激诱发心动过速,腔内心电图(EGMs)示AA间期350 ms,AV 1∶1下传,心室起搏见室房分离,心室拖带后停止为V-A-A-V表现,支持房速。在三维电解剖标测系统(CARTO)指导下送入盐水大头行右房建模并激动标     

非接触心内膜激动标测系统指导房间隔缺损修补术后Ⅱ型心房扑动的射频消融(附一例报道)

评价非接触球囊导管标测系统 (EnSite 30 0 0 )在指导房间隔缺损 (ASD)修补术后心房扑动 (简称房扑 )的射频消融中的临床应用。 1例女性患者 ,41岁 ,ASD修补术后 2 2年开始频繁发作心动过速 ,体表心电图示Ⅱ型房扑。应用EnSite 30 0 0构建右房三维几何模型 ,标测心动过速的折返激动顺序 ,发现手术疤痕与三尖瓣环之间、下腔静脉与三尖瓣环之间为折返环路的关键峡部 ,应用导航系统指导峡部消融 ,成功阻断心动过速 ;消融后通过起搏标测判定峡部已达完全双向阻滞。随访 2 0个月 ,无心动过速复发。结论 :在ASD修补术后房扑的标测和消融中应用EnSite30 0 0系统是安全有效的 ,不仅能确定折返环路的关键峡部 ,而且能准确判断线性损伤的连续性。     

非接触心内膜激动标测系统指导房间隔缺损修补术后H型心房扑动的射频消融（附一例报道）

评价非接触球囊导管标测系统(EnSite 3000)在指导房间隔缺损(ASD)修补术后心房扑动(简称房扑)的射频消融中的临床应用。1例女性患者，41岁，ASD修补术后22年开始频繁发作心动过速，体表心电图示H型房扑。应用EnSite 3000构建右房三维几何模型，标测心动过速的折返激动顺序，发现手术疤痕与三尖瓣环之间、下腔静脉与三尖瓣环之间为折返环路的关键峡部，应用导航系统指导峡部消融，成功阻断心动过速；消融后通过起搏标测判定峡部已达完全双向阻滞。随访20个月，无心动过速复发。结论：在ASD修补术后房扑的标测和消融中应用EnSite 3000系统是安全有效的，不仅能确定折返环路的关键峡部，而且能准确判断线性损伤的连续性。     

Narrow QRS Tachycardia with Ventriculoatrial Dissociation Mediated by a Left Fasciculoventricular Fiber

A 30-year-old man presented with narrow QRS tachycardia. The intracardiac electrocardiogram showed an atrial-HIS (AH) interval of 75 msec and a HIS-ventricular (HV) interval of 44 msec during baseline. Atrial incremental pacing revealed HV shortening, with apparent incomplete right bundle branch block (RBBB) morphology without QRS complex axis deviation. The induced tachycardia exhibited several QRS morphologies: a narrow QRS, complete RBBB and complete left bundle branch block (LBBB) morphology. Spontaneous conversion of the QRS pattern from wide to narrow was observed. The cycle length of the tachycardia was significantly shortened (from 316 to 272 ms) from LBBB morphology to narrow QRS complex. The atrial activation was dissociated from the ventricular activation during all tachycardias. Each QRS complex during tachycardia was preceded by a HIS deflection and HV interval was 35 ms, which was shorter than that of sinus rhythm. HIS deflection was earlier than right bundle potential during all kinds of tachycardia. This tachycardia is most likely mediated by a left fasciculoventricular fiber which connects the HIS bundle below the atrioventricular node to the myocardial tissue of the left ventricle. The HIS-Purkinje system is used as an antegrade conduction limb and the fasciculoventricular fiber as a retrograde limb in the tachycardia circuit.     

Electrophysiologic characteristics of ventricular extrastimulation-induced dissipation of functional bundle branch block associated with supraventricular tachycardia

INTRODUCTION: Linking-related anterograde functional bundle branch block during supraventricular tachycardia (SVT) is due to repetitive concealed retrograde conduction of impulses from the contralateral bundle branch and can be eliminated by a critically timed premature ventricular beat (PVB). We assessed the electrophysiologic characteristics of PVB-induced dissipation of functional bundle branch block during SVT. METHODS AND RESULTS: During SVT with functional bundle branch block, PVB was delivered from the right ventricular apex, scanning the tachycardia cycle length (CL) with 10-msec decrements in the coupling interval in 14 patients (3 AV nodal reentrant tachycardia and 11 orthodromic AV reciprocating tachycardia). Dissipation was achieved in group 1: functional right bundle branch block (RBBB) in 4, functional left bundle branch block (LBBB) in 4, and both functional RBBB and LBBB in 1 with a dissipation zone occupying 4% to 13% (mean 8.5%) of the tachycardia CL. The outer limits were 22+/-16 msec and 68+/-14 msec < tachycardia CL; the inner limits were 56+/-18 msec and 90+/-24 msec < tachycardia CL for RBBB and LBBB, respectively (both P < 0.05). Dissipation could not be achieved in group 2 (4 RBBB and 1 LBBB) due to CL-dependent bundle branch block and/or local ventricular refractoriness. CONCLUSION: During SVT, functional bundle branch block due to "linking" often can be dissipated by timely PVB delivered from the right ventricular apex within a narrow zone of the tachycardia CL. Our findings suggest that the dissipation zone is affected by the pattern of functional bundle branch block relative to the site of PVB delivery.     

左束支区域起搏可改善右束支阻滞的心电图表现

目的:旨在观察左束支区域起搏(LBBAP)纠正右束支阻滞(RBBB)的临床效果及心电图特点.方法:本研究为单中心、前瞻性观察性研究,纳入2018年4月至2019年12月间入院有心室起搏指征,存在基线RBBB图形且QRS波群时限≥120 ms、左心室射血分数>50％并接受LBBAP的患者,分析LBBAP纠正RBBB的临床...     

伴右心室出口的左心室起源缺血性室性心动过速的标测和消融

目的折返性的缺血性室性心动过速（VT）绝大多数发生于左心室并表现为右束支阻滞（RBBB）图形。本文报道1组VT折返环位于左心室但出口在右心室且表现为左束支阻滞（LBBB）的病例。方法32例因陈旧性心肌梗死伴VT而接受电生理检查和射频消融的患者,其中4例临床有LBBB形态的VT。使用非接触等电位和虚拟单极标测判断VT起源,结合舒张中期电位（MDP）和拖带标测确定折返关键通路和消融靶点。用盐水冲洗电极导管在折返环的关键峡部行线性消融。结果全部32例患者中,4例临床有LBBB型VT者均成功被诱发,其中1例有两种LBBB型VT,1例同时有RBBB型VT但周长与LBBB型相同;另有1例共有6种形态的VT,包括RBBB和LBBB型。在右心室内的非接触式等电位标测可迅速确定VT在右心室的传出部位,该处的虚拟单极标测显示rS型提示左心室起源。3例在左心室成功拖带并消融成功,靶点均紧邻左心室间隔,其中1例位于下壁,1例在前壁,1例两种LBBB型VT分别在前壁和下壁间隔旁消融成功。随访1～4．2年,未服抗心律失常药无VT发作。而1例诱发出6种单形（包括RBBB和LBBB型）VT患者因巨大室壁瘤及心功能障碍不能耐受而中途放弃消融。结论紧邻室间隔的前壁和下壁心肌梗死后的左心室起源VT可能因在右心室有出口而表现为LBBB型,需要在标测和消融时予以注意。     

Concealed entrainment as a guide for catheter ablation of ventricular tachycardia in patients with prior myocardial infarction

Fifteen consecutive patients with drug-refractory, recurrent, sustained, monomorphic ventricular tachycardia and a history of remote myocardial infarction underwent catheter ablation of ventricular tachycardia. Shocks of 100 to 300 J were delivered to sites at which pacing during ventricular tachycardia resulted in concealed entrainment, in which the ventricular tachycardia accelerated to the pacing rate, there was a long stimulus to QRS interval and there was no change in the configuration of the QRS complex during pacing at several rates compared with the configuration during ventricular tachycardia, thus identifying a zone of slow conduction in the reentrant circuit. Concealed entrainment was demonstrated in nine (60%) of 15 patients, and the stimulus to QRS intervals were 90 to 400 ms. At sites of concealed entrainment, the endocardial activation time relative to the QRS complex during ventricular tachycardia ranged from -125 to +50 ms, the timing of the local electrogram relative to the QRS complex was the same during entrainment as during ventricular tachycardia and the pace map during sinus rhythm was discordant with that of the ventricular tachycardia in seven patients. In the six patients in whom a site of concealed entrainment could not be identified, the target site for ablation was selected on the basis of identification of an isolated mid-diastolic potential, activation mapping and pace mapping. The mean (+/- SD) cumulative number of joules delivered to the target site was 306 +/- 140. A successful long-term clinical outcome was achieved in 9 of the 15 patients (mean follow-up 20 +/- 7 months). The clinical success rate was the same whether the target site was selected on the basis of concealed entrainment (five of nine, 56%) or on the basis of the other mapping techniques (four of six, 67%). In conclusion, the responses to pacing suggest that sites at which there is concealed entrainment may be located within a zone of slow conduction in the ventricular tachycardia reentry circuit, although not necessarily in an area critical for the maintenance of reentry. The long-term clinical efficacy of catheter ablation targeted to sites of concealed entrainment is about 60%, similar to the results achieved when conventional mapping techniques are used.     

Functional bundle branch block and orthodromic reciprocating tachycardia cycle length: do not bet on accessory pathway location.

AIMS: To show 2 examples in which the analysis of the effect of bundle branch block on orthodromic reciprocating tachycardia cycle length was misleading. METHODS AND RESULTS: We performed an electrophysiological study in two patients with orthodromic reciprocating tachycardia showing a transition from wide to narrow QRS during tachycardia. Our two cases of left bundle branch block during reciprocating tachycardia using infero-septal pathways show that ventricular to atrial conduction time prolongation may be larger than 30 ms and may be concealed by a shortening of atrial to ventricular conduction time. In the 2 cases, the atrial insertion of the accessory pathway could be successfully ablated from the right atria at the ostium of the coronary sinus. CONCLUSIONS: The observation of the association between left bundle branch block and cycle length prolongation during reciprocating tachycardia may be associated with a successful ablation at the ostium of the coronary sinus.     

Radiofrequency catheter ablation of ventricular tachycardia originating in the left posterior and left anterior fascicles in a patient with prior myocardial infarction

A 61-year-old man with prior anteroseptal myocardial infarction (ejection fraction: 40%) presented with recurrent episodes of palpitations. Twelve-lead ECG during palpitations showed an incessant ventricular tachycardia (VT1) with right bundle branch block (RBBB) morphology and inferior axis. Electrophysiologic study revealed that the clinical VT originated from the anterolateral left ventricle. A Purkinje potential preceded onset of the QRS complex by 34 ms. Radiofrequency ablation guided by the Purkinje potential terminated the VT1. Another ventricular tachycardia (VT2) showing RBBB morphology with superior axis and originating from the posteroseptal left ventricle, was induced by programmed ventricular stimulation. A Purkinje potential preceded onset of the local ventricular potential by 120-130 ms in this VT. Radiofrequency ablation guided by the Purkinje potential terminated the VT2.     

Diminished left ventricular dyssynchrony and impact of resynchronization in failing hearts with right versus left bundle branch block.

OBJECTIVES: We compared mechanical dyssynchrony and the impact of cardiac resynchronization therapy (CRT) in failing hearts with a pure right (RBBB) versus left bundle branch block (LBBB). BACKGROUND: Cardiac resynchronization therapy is effective for treating failing hearts with conduction delay and discoordinate contraction. Most data pertain to LBBB delays. With RBBB, the lateral wall contracts early so that biventricular (BiV) pre-excitation may not be needed. Furthermore, the magnitude of dyssynchrony and impact of CRT in pure RBBB versus LBBB remains largely unknown. METHODS: Dogs with tachypacing-induced heart failure combined with right or left bundle branch radiofrequency ablation were studied. Basal dyssynchrony and effects of single and BiV CRT on left ventricular (LV) function were assessed by pressure-volume catheter and tagged magnetic resonance imaging, respectively. RESULTS: Left bundle branch block and RBBB induced similar QRS widening, and LV function (ejection fraction, maximum time derivative of LV pressure [dP/dt(max)]) was similarly depressed in failing hearts with both conduction delays. Despite this, mechanical dyssynchrony was less in RBBB (circumferential uniformity ratio estimate [CURE] index: 0.80 +/- 0.03 vs. 0.58 +/- 0.09 for LBBB, p < 0.04; CURE 0-->1 is dyssynchronous-->synchronous). Cardiac resynchronization therapy had correspondingly less effect on hearts with RBBB than those with LBBB (i.e., 5.5 +/- 1.1% vs. 29.5 +/- 5.0% increase in dP/dt(max), p < 0.005), despite similar baselines. Furthermore, right ventricular-only pacing enhanced function and synchrony in RBBB as well or better than did BiV, whereas LV-only pacing worsened function. CONCLUSIONS: Less mechanical dyssynchrony is induced by RBBB than LBBB in failing hearts, and the corresponding impact of CRT on the former is reduced. Right ventricular-only pacing may be equally efficacious as BiV CRT in hearts with pure right bundle branch conduction delay.     

Electrophysiological and clinical observations in patients with alternating bundle branch block.

Electrophysiological studies (His bundle recordings and atrial stimulation) were performed in nine patients who manifested periods of both right and left bundle branch block (RBBB and LBBB). In seven of the patients, alternating bundle branch block appeared to reflect intermittent or chronic bundle branch block superimposed on incomplete (but electrocardiographically complete) block of the contralateral bundle branch. In three of these seven, shift from one bundle branch block pattern to the other was associated with reproducible change in H-V (mean change 30 msec), and could be induced by alteration of cardiac rate with carotid massage, coupled atrial stimulation, and rapid atrial pacing. In one of the seven, RBBB with a P-R of 0.20 seconds preceded chronic LBBB with a P-R of 0.24 seconds, implying that RBBB had been incomplete. In three of the seven, although a definite mechanism of alternation could not be demonstrated, transient contralateral bundle branch block occurred superimposed on chronic ipsilateral bundle branch block, implying that the ipsilateral block was incomplete. Two patients manifested periods of narrow QRS, LBBB, RBBB, and paroxysmal A-V block. Based upon pathological data (one case), this pattern appeared to reflect a lesion involving the distal His bundle and proximal bundle branches. In the total group of patients, clinical course was primarily determined by the severity of heart disease and not by occurrence of A-V block. The conduction defect in the majority of patients was surprisingly benign.