经导管射频消融治疗右室流出道室性期前收缩的临床研究

目的探讨导管射频消融治疗右室流出道室性期前收缩的方法及有效性。方法对38例右室流出道频发室性期前收缩患者采用激动标测结合起搏标测的方法进行射频消融治疗。术前根据体表心电图初步判断起源部位。结果 38例患者中37例消融成功,成功率为97.4%,随访(15.9±14.8)个月,无1例复发,亦无手术相关并发症发生。结论采用激动标测结合起搏标测消融右室流出道室性期前收缩安全有效且成功率高。     

左室Summit起源的室性心律失常的标测与消融

目的:探讨左室顶部(Summit区)起源的室性心律失常的电生理特征及消融策略的有效性。方法:52例起源于左室Summit区室性心律失常患者,术中依据体表心电图形态进行序贯标测,常规于右室流出道、主动脉窦、主动脉窦瓣下与主动脉瓣环二尖瓣环连接处、心大静脉,标测部位未能领先体表25 ms,放弃消融,于相应部位继续标测。标测部位领先体表大于25 ms,试消融,依据消融部位靶电位及消融疗效,采取对应解剖部位补充消融策略。结果:主动脉窦消融成功22例,左冠窦瓣下及AMC消融成功8例,心大静脉消融成功3例,右室流出道与主动脉窦联合消融4例,主动脉窦瓣上瓣下联合消融成功10例。心大静脉、主动脉窦及主动脉窦瓣下联合消融成功2例。手术未成功3例。结论:左室Summit区起源室性心律失常须行右室流出道、主动脉窦、主动脉瓣环二尖瓣环连接处、心大静脉多部位序贯标测,于最早领先激动点消融。依据最早激动点局部电位及消融疗效,联合对应解剖部位消融。该消融策略是有效及安全的。     

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。     

射频消融治疗右室流出道起源室性心律失常的临床分析

目的:总结射频消融治疗右室流出道起源的室性心律失常的疗效、安全性;分析其ECG特征及心脏转位对其初步定位的影响。方法:入选右室流出道起源的室性心律失常射频消融患者246例,其中顺钟向转位30例,逆钟向转位99例,通过同步12导联ECG,分析ECG特征及进行初步定位,在Ensite velocity 3.0Nav标测系统指导下,结合激动标测、起搏标测进行靶点定位消融。结果:本组手术成功率为96.3%,复发率3.7%,并发症发生率0.4%,右室流出道起源室性心律失常的ECG有一定的特征性。结论:射频消融治疗右室流出道起源的室性心律失常是有效及安全的;体表发作图分析对其初步定位有一定帮助;心脏转位对于ECG初步定位鉴别右室流出道起源部位(间隔部/游离壁)没有影响。     

以右室流出道尖峰电位指导射频消融治疗室性心律失常

目的探讨以右室流出道尖峰电位指导消融右室流出道室性心律失常的可行性与效果。方法39例特发性室性心律失常患者,心电图初步定位心律失常起源于右室流出道。将患者分为尖峰电位标测组(n=20)和起搏标测组(n=19)。尖峰电位法的消融靶点为激动最提前的尖峰电位。结果尖峰电位组20例患者中有3例因未能标测到尖峰电位,故转为单纯起搏标测组,成功率为94.1%(16/17)。单纯起搏标测组中1例未能诱发心律失常,1例因并发症终止手术,1例消融失败,成功率为95.0%(19/20)。两组的成功率差别无显著性(P>0.05),但尖峰电位组操作时间(55±20.1 mins)和X线透照时间(27±12.5 mins)均低于起搏标测组(分别是72±27.8 mins;36±14.1mins。P均<0.05)。结论尖峰电位指导右室流出道室性心律失常消融是一种安全有效的标测方法。     

先天性心脏病合并右室流出道来源的室性心律失常的处理

<正>随着三维标测系统的应用,来源于右心室流出道的室性心律失常的射频导管消融,成功率可达95%以上[1~3];先天性心脏病并发室性心动过速的导管消融多见于先天性心脏病外科修补术后[4~9],而先天性心脏病合并来源于右室流出道的室性心律失常的导管消融少见报道[9,10]。本文报道房间隔缺损(简称房缺)、室间隔缺损(简称室缺)和动脉导管未闭各1例合并右室流出道起源的室性心律失常的     

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。     

特发性室性心动过速靶点标测与射频消融方法研究

目的探讨特发性室性心动过速（ＩＶＴ）有效靶点标测与射频导管消融（ＲＦＣＡ）放电方法。方法６７例ＩＶＴ病人行ＲＦＣＡ治疗。右室ＩＶＴ（ＩＲＶＴ）和左室ＩＶＴ（ＩＬＶＴ）采用激动标测和起搏标测相结合方法寻找靶点,右室流出道（ＲＯＴ）ＩＲＶＴ用双大头导管交替标测或放置１根４极或１０极电极导管于ＲＯＴ作为参考电极。采用预设６０～７０℃渐增功率温控放电进行消融。结果６７例ＩＶＴ消融成功６２例,成功率９２．５％,其中２３例ＩＲＶＴ成功２１例,１例靶点位于右室流入道,消融成功,２２例位于ＲＯＴ,２０例消融成功;４４例ＩＶＴ成功４１例,１例靶点位于左室游离壁,消融成功,４３例位于左室室间隔部,４０例成功。４例术后出现少量心包积液。结论激动标测和起搏标测相结合是提高ＩＶＴ消融成功率的有效方法。渐增功率温控放电安全可靠。     

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。     

以心室高频电位和以激动标测法消融室性心律失常的比较

目的探讨窦性心律下射频消融延迟的高频电位(HFP)防治室性心律失常的可行性、安全性及有效性。方法 36例住院的室性心律失常患者,17例在窦性心律下以延迟的HFP为指导实施消融(HFP组),其中遗传性心脏病5例,冠心病1例;19例在激动标测指导下实施消融(激动标测组),其中冠心病1例,心肌炎1例。比较两组手术效果、X线曝光时间、手术总时间及安全性。结果 HFP组消融靶点10例位于左室间隔面、2例左室乳头肌周围、2例右室流出道、1例左室后间隔及右室流出道偏间隔部、2例位于右室流出道肺动脉瓣上;激动标测组消融靶点6例位于左室间隔面、10例位于右室流出道、2例位于左冠窦及右室流出道、1例位于右室游离壁。HFP组的即刻成功率为94.1%(16/17),激动标测组为84.2%(16/19)。两组即刻成功率、X线曝光时间、手术总时间均无明显差异(P0.05),均无并发症。随访14.6±5.8个月,6例复发,其中HFP组3例,复发率17.6%(3/17),一直服药治疗;激动标测组3例,复发率15.8%(3/19)。结论在窦性心律下射频消融延迟的HFP,在较长的随访期内可有效防止室性心动过速/心室颤动的复发。     

Variation of QRS morphology of premature ventricular contractions originate from the left‐ventricular outflow tract during ablation

Idiopathic ventricular arrhythmias originating from the aortic sinus of Valsalva often show preferential conduction to the right‐ventricular outflow tract, which may render radiofrequency ablation more difficult. We describe a patient with symptomatic premature ventricular contractions of left‐ventricular outflow tract origin presenting with a variation of QRS morphology during ablation. The correlation between the characteristics of local voltage potentials and the real origin site of the ventricular arrhythmia is discussed.     

Dynamic Changes of QRS Morphology of Premature Ventricular Contractions During Ablation in the Right Ventricular Outflow Tract: A Case Report

Electrocardiographic characteristics can be useful in differentiating between right ventricular outflow tract (RVOT) and aortic sinus cusp (ASC) ventricular arrhythmias. Ventricular arrhythmias originating from ASC, however, show preferential conduction to RVOT that may render the algorithms of electrocardiographic characteristics less reliable. Even though there are few reports describing ventricular arrhythmias with ASC origins and endocardial breakout sites of RVOT, progressive dynamic changes in QRS morphology of the ventricular arrhythmias during ablation obtained were rare.This case report describes a patient with symptomatic premature ventricular contractions of left ASC origin presenting an electrocardiogram (ECG) characteristic of right ventricular outflow tract before ablation. Pacing at right ventricular outflow tract reproduced an excellent pace map. When radiofrequency catheter ablation was applied to the right ventricular outflow tract, the QRS morphology of premature ventricular contractions progressively changed from ECG characteristics of right ventricular outflow tract origin to ECG characteristics of left ASC origin.Successful radiofrequency catheter ablation was achieved at the site of the earliest ventricular activation in the left ASC. The distance between the successful ablation site of the left ASC and the site with an excellent pace map of the RVOT was 20 mm.The findings could be strong evidence for a preferential conduction via the myocardial fibers from the ASC origin to the breakout site in the right ventricular outflow tract. This case demonstrates that ventricular arrhythmias with a single origin and exit shift may exhibit QRS morphology changes.     

Clinical and electrophysiological spectrum of idiopathic ventricular outflow tract arrhythmias.

OBJECTIVES: This study sought to compare and contrast the clinical and electrophysiological characteristics of outflow tract arrhythmias. BACKGROUND: Idiopathic ventricular outflow tract arrhythmias manifest clinically in 3 forms: 1) paroxysmal sustained monomorphic ventricular tachycardia (SMVT), 2) repetitive nonsustained ventricular tachycardia (NSVT), or 3) premature ventricular contractions (PVCs). Although these arrhythmias have a similar site of origin, it is unknown whether they share a common mechanism or similar clinical features. METHODS: A total of 127 patients (63 female [50%], mean age 51 +/- 15 years) were evaluated for outflow tract arrhythmias. RESULTS: A total of 36 (28%) presented with the index clinical arrhythmia of SMVT, 46 (36%) with NSVT, and 45 (35%) with PVCs. The sites of origin of the arrhythmias were similar among the 3 groups, occurring in the right ventricular outflow tract in 82%. Sustained ventricular tachycardia was more likely to be induced during exercise in the SMVT (10 of 15 patients [67%]) than NSVT or PVCs groups (p < 0.01). Sustained outflow tract ventricular tachycardia was induced at electrophysiology study in 78% of SMVT patients, 48% of NSVT patients, and 4% of PVCs patients. Adenosine was similarly effective in all 3 groups (p = NS). CONCLUSIONS: Patients with outflow tract arrhythmias can be differentiated based on the subtype of arrhythmia. However, the observation that approximately 50% of patients with NSVT and approximately 5% of patients with PVCs have inducible sustained ventricular tachycardia that behaves in an identically unique manner to those who present with sustained ventricular tachycardia (e.g., adenosine-sensitive) suggests that rather than representing distinct entities, outflow arrhythmias may be considered a continuum of a single mechanism.     

特发性室性心律失常的射频消融

目的特发性室性心律失常（IVA）是指不伴有明显器质性心脏病的室性心动过速（室速）或室性早搏（室早）,约占所有室性心律失常的10％左右。本文系统分析925例IVA病例,探讨IVA的临床、电生理和射频消融的特点。方法本文回顾性分析了从1994年3月至2009年2月,925例IVA患者的临床特点,射频消融治疗的过程和结果。925例病人,男性500例,女性425例,平均年龄（36．65±14．81）岁。临床证实为IVA患者,并且排除了器质性心脏病。在停用抗心律失常药物5个半衰期后,进行电生理检查和射频消融治疗。结果特发性右心室室性心律失常（IRVA）516例,特发性左心室室性心律失常（ILVA）409例,IRVA多发生于女性,发病的平均年龄40岁,大多数表现为频发室早伴有反复单形室性心动过速,出现黑喙症状为14．3％;ILVA多发生于男性,发病的平均年龄33岁,多表现为持续性室速,出现黑矇症状为5．9％。IRVA有486例（94．2％）起源于右心室流出道,而在右心室流出道起源的室速／室早里,又以起源于间隔面的多见,占78％左右,起源于游离壁的占10％左右,其余的12％起源于二者之间的部位。射频消融多采用寻找心内膜最早激动点结合起搏标测来寻找合适的靶点。ILVA最多见的类型是左心室特发室速（ILVT）,有272例（66．5％）,ILVT主要起源于左后分支区域,也可以起源于左前分支区域和临近希氏束部位。主要用激动顺序标测结合浦肯野电位的方法确定消融靶点。IRVA的516例患者射频消融即刻成功率为89．3％。ILVA射频消融即刻成功率为93．7％。结论IVA患者虽然没有器质性心脏病,但是伴有多种临床症状,少部分病人甚至出现黑矇、晕厥,应积极行射频消融治疗,预防出现心室颤动危及生命。     

不同心电图特征对特发性室性期前收缩右室流出道起源部位诊断价值比较

目的 比较体表心电图鉴别右室流出道室性期前收缩具体起源点的诊断价值。 方法 分析经射频导管消融治疗室性期前收缩靶点明确为右室流出道的139例患者（其中右室流出道间隔部起源的111例,游离壁起源的28例）的体表心电图特点,以室性期前收缩时Ⅰ导联主波形态、QRS波时限、胸前导联移行及下壁三肢体导联有无顿挫进行分析,评估其对鉴别右室流出道室性期前收缩具体起源点的准确性。 结果 以室性期前收缩的QRS波宽度≥140 ms判断为右室流出道游离壁起源的灵敏度为86%,特异度为58%;以下壁三肢体导联均有顿挫或切迹判断为游离壁起源的灵敏度为64%,特异度为91%;以Ⅰ导联主波向上判断游离壁起源的灵敏度为86%,特异度为73%。 结论 I导联主波方向及下壁三肢体导联有无顿挫能对鉴别游离壁还是间隔起源有较大实用价值。     

Idiopathic left ventricular tachycardia: assessment and treatment

Idiopathic left ventricular tachycardia (VT) has been classified into three subgroups according to mechanism: verapamil-sensitive, adenosine-sensitive, and propranolol-sensitive types. VT can be categorized also into left fascicular VT and left outflow tract VT. Although the mechanism of fascicular VT is verapamil-sensitive reentry, the mechanism of left outflow tract VT is not homogeneous. Fascicular VT can be classified into three subtypes: (1) left posterior fascicular VT with a right bundle branch block (RBBB) and superior axis configuration (common form); (2) left anterior fascicular VT with RBBB and right-axis deviation configuration (uncommon form); and (3) upper septal fascicular VT with a narrow QRS and normal axis configuration (rare form). Posterior and anterior fascicular VT can be successfully ablated at the mid-septum guided by a diastolic Purkinje potential or at the VT exit site guided by a fused presystolic Purkinjepotential. Upper septal fascicular VT also can be ablated at the site indicated by a diastolic Purkinje potential. The mechanism of left ventricular outflow tract VT is most likely adenosine-sensitive triggered activity. This VT can be classified into three subtypes according to the location where catheter ablation is successful, i.e., (1) endocardial origin; (2) coronary cusp origin; and (3) epicardial origin. The R-wave duration and R/S-wave amplitude in V1/V2 can be used to differentiate coronary cusp VT from other types of outflow tract VT. Recognition of the characteristics of the various forms of this group of arrhythmias should facilitate appropriate diagnosis and therapy.     

Electrophysiologic characteristics of sustained ventricular tachycardia occurring after repair of tetralogy of fallot

The electrophysiologic characteristics of sustained ventricular tachycardia occurring after total repair of tetralogy of Fallot are reported. Four patients, 8 to 31 years of age, who had spontaneous episodes of sustained ventricular tachycardia underwent electrophysiologic study to determine the mechanism and site of origin of the tachycardia. In each patient, the tachycardia could be reproducibly initiated and terminated by programmed electrical stimulation. In two patients, initiation and maintenance of the tachycardia depended on the development and perpetuation of continuous electrical activity in the right ventricular outflow tract. These observations suggested a reentrant mechanism. In each patient, catheter endocardial mapping demonstrated the site of origin to be the right ventricular outflow tract. In two patients intraoperative mapping showed the reentrant circuit originating at the site of healed right ventriculotomy site. We conclude that sustained ventricular tachycardia after repair of tetralogy of Fallot in our patients was caused by reentry at the site of the previous operation in the right ventricular outflow tract.     

Left ventricular outflow tract tachycardia originating from the right coronary cusp: identification of location of origin by endocardial noncontact activation mapping from the right ventricular outflow tract

Idiopathic left ventricular outflow tract (LVOT) tachycardia has been shown to originate from a supravalvular site in some patients. Considerable attention recently has focused on identifying this variant of LVOT tachycardia on 12-lead ECG. We report the case of 15-year-old boy in whom a noncontact three-dimensional mapping electrode deployed in the right ventricular outflow tract (RVOT) assisted in identifying a supravalvular LVOT tachycardia. Observation of two early breakthrough sites in the RVOT and right ventricular septum suggested a right aortic cusp origin of the tachycardia. Pace mapping in the right aortic cusp identified a successful ablation site.     

Right ventricular outflow tract tachycardias in patients without apparent structural heart disease

We have investigated 13 patients with monomorphic ventricular tachycardia which originated from the right ventricular outflow tract. No patient had evidence of organic heart disease. There were 3 males and 10 females, aged 13-53 years. All had non-invasive investigations including an exercise electrocardiogram, chest radiography, echocardiograms and gated blood pool scintigraphy. Ten patients underwent cardiac catheterisation. Five patients had a prolonged QTc on their resting electrocardiogram. The remaining investigations showed no evidence of organic heart disease. Ten patients had ventricular arrhythmias which were completely suppressed during maximal exercise but which recurred in the immediate post-exercise period. A further 2 patients with no arrhythmias before exercise had ventricular tachycardia in the post-exercise period. Electrophysiology studies were performed in 5 patients with syncopal episodes, suggesting an automatic focus in 4. Four patients required specific antiarrhythmic surgery for symptoms refractory to medical therapy. Pace-mapping at operation confirmed the origin to be within the right ventricular outflow tract in all. Thus, we have identified a group of patients who have ventricular tachycardia originating from the right ventricular outflow tract in whom there is no apparent structural heart disease. Their arrhythmias are influenced by exercise and are probably due to an automatic focus. Four patients required surgery for ventricular tachycardias and recurrent syncopal episodes refractory to medical therapy.     

Spatial resolution of pace mapping of idiopathic ventricular tachycardia/ectopy originating in the right ventricular outflow tract

BACKGROUND: Pace mapping has been used to identify the site of origin of focal ventricular arrhythmias. The spatial resolution of pace mapping has not been adequately quantified using currently available three-dimensional mapping systems. OBJECTIVE: The purpose of this study was to determine the spatial resolution of pace mapping in patients with idiopathic ventricular tachycardia or premature ventricular contractions originating in the right ventricular outflow tract. METHODS: In 16 patients with idiopathic ventricular tachycardia/ectopy from the right ventricular outflow tract, comparisons and classifications of pace maps were performed by two observers (good pace map: match >10/12 leads; inadequate pace map: match < or =10/12 leads) and a customized MATLAB 6.0 program (assessing correlation coefficient and normalized root mean square of the difference (nRMSd) between test and template signals). With an electroanatomic mapping system, the correlation coefficient of each pace map was correlated with the distance between the pacing site and the effective ablation site. The endocardial area within the 10-ms activation isochrone was measured. RESULTS: The ablation procedure was effective in all patients. Sites with good pace maps had a higher correlation coefficient and lower nRMSd than sites with inadequate pace maps (correlation coefficient: 0.96 +/- 0.03 vs 0.76 +/- 0.18, P <.0001; nRMSd: 0.41 +/- 0.16 vs 0.89 +/- 0.39, P <.0001). Using receiver operating characteristic curves, appropriate cutoff values were >0.94 for correlation coefficient (sensitivity 81%, specificity 89%) and < or =0.54 for nRMSd (sensitivity 76%, specificity 80%). Good pace maps were located a mean of 7.3 +/- 5.0 mm from the effective ablation site and had a mean activation time of -24 +/- 7 ms. However, in 3 (18%) of 16 patients, the best pace map was inadequate at the effective ablation site, with an endocardial activation time at these sites of -25 +/- 12 ms. Pace maps with correlation coefficient > or =0.94 were confined to an area of 1.8 +/- 0.6 cm2. The 10-ms isochrone measured 1.2 +/- 0.7 cm2. CONCLUSION: The spatial resolution of a good pace map for targeting ventricular tachycardia/ectopy is 1.8 cm2 in the right ventricular outflow tract and therefore is inferior to the spatial resolution of activation mapping as assessed by isochronal activation. In approximately 20% of patients, pace mapping is unreliable in identifying the site of origin, possibly due a deeper site of origin and preferential conduction via fibers connecting the focus to the endocardial surface.