Carto标测指导下射频导管消融特发性右心室流出道室性心动过速

目的探讨Carto标测特发性右心室流出道室性心动过速(RVOT-VT)的方法和对射频导管消融(RFCA)的指导作用;分析RVOT-VT起源点与12导联心电图的关系,探讨12导联心电图对RVOT-VT起源点定位的辅助作用.方法14例特发性RVOT-VT患者,男性6例、女性8例,平均年龄(39.0±8.0)岁.所有病人均行常规电生理检查,对诱发室性心动过速(VT)或有频发室性早搏(PVCs)的病人,采用Carto标测VT或PVCs的最早激动点作为RFCA的靶点.如不能诱发VT或无频发PVCs患者,在窦性心律下标测RVOT的解剖结构,然后进行起搏标测,寻找起搏心电图与临床上VT或PVCs的心电图相同或相似的最佳起搏点作为RFCA的靶点.通过成功的RFCA确定每例VT起源点在RVOT的部位,然后分析每例VT起源点对应的12导联心电图特征.结果14例病人中,有8例病人手术时在基础状态下或静脉滴注异丙肾上腺素后有频发的PVCs,通过捕捉和标测PVCs重构RVOT的解剖结构和PVCs的电激动顺序,顺利地标出PVCs的最早激动点作为RFCA的靶点.另6例临床上有持续性VT的病人,有2例术中诱发出持续性VT.在VT状态下用Carto标测VT的最早激动点作为RFCA的靶点.2例只诱发短阵持续性VT和另2例只有在静脉滴注异丙肾上腺素后诱发出非持续性VT的患者,用起搏标测找出最佳消融靶点.所有14例RVOT-VT均成功地进行了RFCA,成功率为100%.VT起源于间隔部8例(57%),后壁4例(29%),外侧壁2例(14%).I、aVR和aVL导联上的QRS波形态有助于确定VT起源点在间隔部或游离壁;V3导联上的R/S比值有助于确定VT起源点在RVOT的上部或下部.结论Carto标测通过在VT或PVCs时行激动顺序标测或无VT和PVCs时行起搏标测可以准确地确定VT或PVCs的起源点,并有效地指导RFCA.VT或PVCs的12导联心电图有助于在术前定位VT或PVCs在RVOT的起源点.     

室性心动过速起源点标测与电消融及手术治疗

作者对８例室性心动过速（ＶＴ）患者进行９次ＶＴ起源点标测与电消融及手术治疗，其中１例直流电导管消融手术（ＤＣＣＡ）后１５个月复发，再次行消融术。８例中，１例为开胸术中心外膜标测，１例由体表ＥＣＧ定位，其余均为导管电极心内膜标测。８例共标出９个ＶＴ起源点，左室４个，右室５个。１例在开胸术中施行心外膜ＤＣＣＡ，２例手术切除ＶＴ起源点，其余５例６个起源点施行ＤＣＣＡ，其中３例次先行导管射频消融术（ＲＦＣＡ），不成功者而改用ＤＣＣＡ。结果显示，１例心内膜ＤＣＣＡ后１５个月ＶＴ复发，进行第２次心内膜ＤＣＣＡ后控制（术中先施行ＲＦＣＡ无效），２例分别施行心外膜与心内膜ＤＣＣＡ后仍发ＶＴ，分别服美西律与维拉帕米即可控制。前者随访１９个月、后者１２个月未再发作，其余５例随访１４～３４个月（２１．６±７．６）均未服药而无ＶＴ发作。这提示，对于顽固性ＶＴ患者，只要准确定位ＶＴ起源点，电消融或外科手术可望获得满意疗效。     

特发性室性心动过速射频导管消融标测方法探讨

目的探讨特发性室性心动过速（IVT）的标测方法.方法对52例行射频消融的IVT患者进行标测.39例源于右心室的IVT采用消融导管右心室起搏标测法,以起搏时与室性心动过速（室速）发作时的12导联心电图QRS波形态与振幅完全相同的起搏部位为消融靶点.12例起源于左心室的IVT以发作时消融电极导管在左心室内标测到较体表心电图QRS波提前≥20 ms的最早高频低振幅电位为消融靶点（激动顺序标测法）,1例左心室室速采用起搏标测法.结果左心室IVT消融成功率100%（13/13）,右心室IVT消融成功率94.87%（37/39）.结论起源于左心室的IVT宜采用激动顺序标测法,起源于右心室的IVT宜采用起搏标测法.     

非接触标测在室性心动过速消融中的应用

非接触球囊标测系统以其独有的优势展现了全新的电生理标测方法,在多种心律失常的消融过程中,扮演着重要角色,尤其是室性心律失常的消融,现对非接触球囊标测系统的特点及在室性心动过速消融中的作用分别总结和叙述。     

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。     

非接触式标测指导特发性左心室室性心动过速的射频消融

目的　虽然采用传统标测技术指导特发性左心室室性心动过速 (idiopathicleftventriculartachycardia ,ILVT)射频消融的效果较满意 ,但临床上仍存在一些疑难或复发病例。为此 ,我们使用非接触式标测技术指导ILVT的射频消融。方法　共 13例患者 ,均为男性 ,平均年龄 (31 0± 14 3)岁 ,其中8例既往共接受 15次射频消融术。将EnSite电极导管置于左心室心尖部以获取心内膜等电位图 ,并使用其导航功能指导消融。结果　 13例患者均诱发并标测到ILVT ,其中 5例起源于室间隔中下部 ;3例起源于心尖部 ;3例起源于室间隔中上部 ,2例起源于主动脉根部。全部ILVT均在EnSite标测到的最早激动处消融成功 ,其中 ,有 9例ILVT在EnSite滤波设置为 8Hz时 ,在心内膜等电位图上最早激动部位可见峡部状狭窄区 ,此处消融均一次成功。仅 3例VT于消融靶点处有浦肯野电位。平均X线暴露时间 (2 6± 12 )min。随访 (13 0± 6 2 )个月 ,1例患者有VT复发 ,但心电图和EnSite标测显示为另一起源 ,再次消融成功。结论　心内非接触式标测技术有望提高ILVT尤其是复杂和疑难病例导管消融治疗的成功率。建议使用 8Hz做为目前版本下ILVT标测的标准滤波参数。     

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.     

窦性心律下非接触式标测指导线性消融治疗特发性左心室室性心动过速

目的 大多数特发性左心室室性心动过速(ILVT)是起源于左后分支(LPF)浦肯野纤维网的折返性心动过速,因而利用非接触式标测系统在窦性心律下标测LPF并经其导航系统指导线性消融治疗ILVT是可行的,现介绍此方法的安全性和有效性。方法 6例患者,1例既往接受3次射频导管消融术,临床呈无休止发作;1例为常规消融术后1个月复发;4例为常规首次接受射频导管消融术患者。其中男性5例,女性1例,平均年龄15～58(34.00±16.26)岁。常规电生理检查明确ILVT诊断后,将球囊电极导管经股动脉逆行送入至左心室心尖部,构建几何构形后建立窦性心律的等电位图。结果 窦性冲动沿希氏束向下传导,在间隔中部不到心尖处激动局部间隔心肌并很快激动整个左心室。局部虚拟电图显示,在间隔部激动的每个QRS波前均有高频、低幅的电位,该电位与QRS波之间的距离随激动的推移而逐渐缩短;心室激动爆发点处的局部电图呈QS型。在心室激动爆发点上方1 cm处于LPF区域作垂直于LPF激动方向的线性消融,消融后所有患者均出现不同程度的左后分支阻滞图形,线性消融的平均放电次数为4～8(5.66±1.50)次,消融完毕后心动过速均不能诱发。平均随访7～13(10.00±2.76)个月,所有患者均无心动过速复发。结论 窦性心律下标测LPF并指导线性消融治疗ILVT不仅安全有效     

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。     

标测浦肯野电位和舒张期电位在特发性左心室室性心动过速消融中的作用

目的探讨特发性左心室室性心动过速(ILVT)射频导管消融中标测浦肯野电位(Pur P)和舒张期电位(DP)的作用。方法44例患者,男性30例,女性14例,年龄9~74岁,无明显器质性心脏病证据,均有阵发性心悸史,ILVT时心电图表现为右束支阻滞伴心电轴左偏41例、右束支阻滞伴心电轴右偏3例。在ILVT时标测到最早Pur P或DP的部位进行消融。结果44例患者的ILVT均在左心室间隔左后分支(41例)或左前分支(3例)分布的范围内消融成功。25例和19例分别在标测到PurP(Pur P组)和DP(DP组)的部位消融成功,成功消融部位Pur P或DP分别提前体表心电图QRS波19~40(27±6)ms和26~60(41±10)ms(P<0.01)。在DP组的19例中,13例在标测到DP时可同时标测到Pur P,6例局部仅能标测到DP;12例首先在标测ILVT时较早的Pur P部位消融不能成功,后通过标测DP消融成功。成功消融ILVT的平均放电次数在Pur P组和DP组分别为4次和2次。DP组较Pur P组消融ILVT的成功部位在间隔部上移约0.5~2.0cm。成功消融ILVT后,窦性心律下体表心电图心电轴明显改变的发生率在Pur P组和DP组分别为44%和84%(P<0.05)。平均随访(23±12)个月,41例起源于左后分支的ILVT复发3例,均为Pur P组。结论ILVT通过标测室速时的Pur P和DP均可能消融成功,DP通常较Pur P有更早的激动时间,在标测到DP处消融有非常高的成功率和通常需要较少的消融次数。成功消融ILVT后,窦性心律下发生心电轴明显改变的发生率在DP组增高。     

Idiopathic epicardial ventricular tachycardia with origin remote from vascular structures

We report a case of a patient with idiopathic left ventricular tachycardia (VT) successfully ablated from the epicardial aspect of the left ventricle, after a previous failed endocardial ablation. The VT appeared to be catecholamine sensitive. An excellent epicardial pacemap was found in the midlateral region of the left ventricle, remote from vascular structures. Following ablation, the patient discontinued antiarrhythmic drug use and has not experienced any recurrence of VT for more than 2 1/2 years.     

Verapamil-sensitive left posterior fascicular ventricular tachycardia after myocardial infarction

Verapamil-sensitive fascicular ventricular tachycardia (VT) of right bundle branch block (RBBB) and superior axis pattern is typically seen in young patients with structurally normal hearts and considered “idiopathic”. Recently, involvement of the Purkinje system in post-infarction monomorphic VT that mimics such idiopathic fascicular VT has been described. In this report we describe a case of a patient who following myocardial infarction developed left posterior fascicular Purkinje reentrant VT that was sensitive to verapamil. The VT was successfully treated by radiofrequency ablation guided by three dimensional electroanatomical CARTO™ mapping. Our case highlights that involvement of Purkinje fibers should be considered in post infarction patients with VT of narrow QRS duration, RBBB morphology and superior axis. Recognition of such VT is clinically important, as this arrhythmia is amenable to curative catheter ablation.     

特发性左心室流出道心外膜侧室性心动过速

目的报道9例经电生理检查证实的特发性左心室流出道心外膜侧室性心动过速(室速)的体表心电图及电生理检查特点.方法男性5例,女性4例,年龄15～58岁,6例为运动诱发的持续性室速,3例为运动诱发的非持续性室速.结果室速时,9例体表心电图QRS波全部呈现右束支阻滞图形(8例胸前导联V1-V6呈现高R波),Ⅱ、Ⅲ、aVF导联为高R波,Ⅰ、aVL导联为QS波.电生理检查,右心室和左心室心内膜标测未发现最早心室激动点,在较早心室心内膜激动处的心内电图多呈现起始部低幅电位,提示远场电位.心室内起搏标测未发现与室速体表心电图12导联QRS波形态相同的起搏点.8例通过心脏静脉系统标测发现最早的心室激动点[体表心电图最早QRS波前15～50ms,平均(32±12)ms]和完全或近乎完全的起搏标测位于心大静脉的远端1例、心前间隔静脉的近端7例.1例患者在左心室流出道消融成功,1例患者在心大静脉远端血管内消融成功.其他患者在右心室和/或左心室内消融失败.结论心脏静脉标测可以鉴别出特发性左心室流出道心外膜侧室速.     

Verapamil-sensitive left anterior fascicular ventricular tachycardia associated with a healed myocardial infarction: changes in the delayed Purkinje potential during sinus rhythm

Uncommon association of left anterior fascicular ventricular tachycardia (VT) with a healed myocardial infarction (MI) is described. A 55-year-old man with a history of anteroseptal MI had verapamil-sensitive VT. The VT exhibited a right bundle branch block configuration and right-axis deviation. The VT exit was located at the left ventricular anterolateral wall. At the mid-anterior left ventricular septum, delayed Purkinje potentials were seen during sinus rhythm, and the optimal pace map was obtained with pace delay. During the VT, diastolic and systolic Purkinje potentials were simultaneously recorded at the same site. Ablation targeting the delayed potentials during sinus rhythm prolonged the time between QRS onset and the delayed potentials, and the VT no longer became inducible when the delayed potentials were completely eliminated. Left anterior fascicular VT develops in post-MI patients; ischemia-injured His-Purkinje system may be involved in the mechanism of the VT.     

Ventricular tachycardia in ischemic heart disease substrates

Advances in the treatment of myocardial infarction (MI) have improved survival after ischemic cardiac injury. Post-infarct structural and functional remodeling results in electrophysiologic substrates at risk for monomorphic ventricular tachycardia (MMVT). Characterization of this substrate using a variety of clinical and investigative tools has improved our understanding of MMVT circuits, and has accelerated the development of device and catheter-based therapies aimed at identification and elimination of this arrhythmia.This review will discuss the central role of the ischemic heart disease substrate in the development MMVT. Electrophysiologic characterization of the post-infarct myocardium using bipolar electrogram amplitudes to delineate scar border zones will be reviewed. Functional electrogram determinants of reentrant circuits such as isolated late potentials will be discussed. Strategies for catheter ablation of reentrant ventricular tachycardia, including structural and functional targets will also be examined, as will the role of the epicardial mapping and ablation in the management of recurrent MMVT.     

Characterization of the right ventricular substrate participating in postinfarction ventricular tachycardia

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Pacemaker-induced ventricular tachycardia in patients with acute inferior myocardial infarction

We analysed a group of 35 consecutive patients with acute myocardial infarction—23 of the inferior, 12 of the anterior wall—who needed temporary pacing for bradycardiac arrhythmias. We observed in three patients ventricular tachycardias induced by pacemaker stimuli falling onto the vulnerable part of the cardiac cycle due to improper sensing. All three had an inferior myocardial infarction involving the right ventricle. Because the pacemaker electrode in this condition lies in the vicinity of the infarcted myocardium sensing problems occur more frequently and re-entry tachy-cardias can be triggered more easily. It represents a possible risk of pacemaker treatment in this group of patients who, on the other hand, often need cardiac pacing in the acute phase following the development of transient AV-block.     

Non-contact mapping in the treatment of ventricular tachycardia after myocardial infarction

The treatment of ventricular tachycardia (VT) in patients with underlying ischaemic heart disease (IHD) remains a challenge. Ablation of these arrhythmias may have a significant impact on quality of life for patients. For those patients with haemodynamically unstable VT, ablation success rates have been improved by the use of non-contact mapping. Care has to be taken in the analysis and interpretation of non-contact mapping studies, as chamber size and filter settings have a large effect on the appearance of the activation maps produced. Despite this limitation the majority of VT exit sites and part of the diastolic pathway can be identified with non-contact mapping techniques.