持续快速心房起搏对犬肺静脉及心房组织连接蛋白43和Ⅲ型胶原的影响

目的　探讨持续快速心房起搏对犬肺静脉和心房组织连接蛋白 43(Cx43)和Ⅲ型胶原的影响。方法　16只杂种犬,随机分为持续快速心房起搏组(8只)和正常对照组 (8只 ),前者以 400次 /min的频率持续起搏 10周,建立心房颤动(房颤)动物模型。分别取两组犬的左上肺静脉、左房游离壁和右心耳等部位的心肌组织进行Cx43的免疫荧光半定量分析和Ⅲ型胶原纤维定量分析。结果10周后快速心房起搏组所有犬均可诱发出持续性房颤。快速心房起搏组犬肺静脉、左房游离壁和右心耳部位的Cx43水平显著高于正常对照组犬各相应的部位 (肺静脉: 3370 .91±275. 11与1405 .82±90. 38, P<0. 05;左房游离壁: 2448. 68±272 .10与 1467. 12±147 .93,P<0. 05;右心耳: 2331 .96±199 .61与 1288. 27±216 .22, P<0 .05)。快速心房起搏组犬肺静脉Cx43的水平显著高于左心房游离壁和右心耳(P<0. 05),而左心房和右心耳部位的Cx43水平差异无统计学意义 (P>0. 05)。持续快速心房起搏组犬肺静脉、左房游离壁和右心耳等部位的Ⅲ型胶原含量显著高于正常对照组犬各相应部位(肺静脉: 3301 97±309 70与 1404 56±178 02, P<0 05;左房游离壁: 2477 86±190. 43与1479. 20±187 .17, P<0 .05;右心耳: 2045 .92±139 .43与 1417. 07±139. 43,P<0 .05 )     

坎地沙坦对家兔快速心房刺激所致缝隙连接蛋白40重构的影响

观察血管紧张素Ⅱ受体1拮抗剂坎地沙坦(Candesartan)对快速心房起搏刺激时家兔心房肌连接蛋白40(Cx40)重构和组织钙(Ca2+)含量的影响,探讨其防治心房颤动的可能机制。32只家兔随机分为3组:对照组(n=8)、快速刺激组(Ⅰ组,n=12)、Candesartan+快速刺激组(Ⅱ组,n=12)。经颈内静脉将电极置入右房,对照组不给予心房刺激,后两组以600次/分行快速心房刺激,并且Ⅱ组于快速刺激前30min开始按0.5mg·kg-1·min-1分持续静脉给予Candesartan8h,另外两组则给予等量的生理盐水。用免疫荧光标记激光共聚焦显微镜检测Cx40的含量和分布,用生化方法检测右心耳组织Ca2+含量。结果:与对照组相比,Ⅰ组和Ⅱ组心房组织Cx40含量降低(0.83±0.14μm2/μm3,2.05±0.36μm2/μm3vs2.35±0.26μm2/μm3,P<0.01或0.05)、分布不均一,Ⅰ组Ca2+含量升高(5.5±1.6μmol/gvs2.9±0.8μmol/g,P<0.01);与Ⅰ组相比,Ⅱ组心房Cx40含量增加(P<0.01)、分布不均一的程度减轻,Ca2+含量降低(3.2±1.1μmol/gvs5.5±1.6μmol/g,P<0.01)。结论:坎地沙坦能有效减轻心房快速刺激所致Cx40重构,其机制之一可能与降低心房Ca2+含量的异常升高有关。     

心肌肥大时间隙连接分布的改变及其对传导特性的影响

目的 探讨压力超负荷所致左室心肌肥大时间隙连接(GJ)分布的改变及其对兴奋冲动传导特性的影响。方法 12只犬随机分为正常对照组(n=4)和主动脉缩窄组(n=8);主动脉缩窄组通过缩窄腹主动脉4周而形成左室心肌肥大,对照组则仅行假手术;应用心外膜标测法测定左室心肌传导速度;应用激光共聚焦显微镜技术和荧光免疫组织化学方法对肥大心肌间隙连接的主要成分连接蛋白43(connexin43,Cx43)进行定量研究。结果(1)主动脉缩窄组和对照组左室心肌细胞总的Cx43表达量无明显差异;(2)对照组心肌细胞端对端连接处Cx43的表达量与侧对侧连接处的Cx43表达量的比值为(1.43±0.18),主动脉缩窄组的比值为(0.72±0.08),两组之间存在显著性差异(P<0.01);(3)对照组左室心肌纵向传导速度与横向传导速度比为(3.20±0.28),主动脉缩窄组的比为(2.48±0.25),两组之间存在显著性差异(P<0.01)。结论 压力超负荷所致的左室心肌肥大可出现间隙连接分布模式的改变和兴奋冲动在心室肌传导的各向异性增大,这种改变可能是心肌肥大时常伴发心律失常的重要原因之一。     

右室流出道间隔部与心尖部起搏贴心功能的影响

目的了解右室流出道间隔部起搏和右室心尖部起搏参数的差异及对心功能的影响。方法65例安装DDD起搏器的患者随机分为右室心尖部（RVA）与右室流出道间隔部（RVS）起搏进行置入时及术后3个月起搏参数、左室射血分数的分析。结果两组基线资料无显著差异，术后15min及3个月两组的起搏阂值、感知、阻抗均无差异，术后3个月右室流出道间隔部组左室射血分数显著高于右室心尖部组（0．57&#177;0．04vs0．50&#177;0．03，p〈0．05）。结论右室流出道间隔部起搏安全可行，且对心功能的影响优于右室心尖部起搏。     

组织多普勒成像评价右室心尖部起搏与右室流出道起搏对心功能的影响

目的研究比较右室心尖部起搏（RVAP）与右室流出道起搏（RVOTP）两种不同起搏方式对室壁运动的同步性、心功能的影响。方法病窦综合征,Ⅲ度房室传导阻滞患者实施右室心尖部起搏15（男9,女6）例;实施右室流出道起搏10（男6,女4）例。所选患者均植入双腔起搏器,时间为术后3个月。利用组织多普勒速度-时间曲线分别测量室间隔及左室各壁的基底段、中间段、心尖段的收缩达峰时间,在常规二维超声切面上测量心排出量（CO）、心脏指数（CI）、每搏量（SV）、心搏出量指数（SVI）、左室射血分数（LVEF）。结果右室流出道起搏比右室心尖部起搏时CO[（4.7±1.1）vs（5.6±1.0）L/min,P<0.05]、CI[（3.1±0.7）vs（3.7±0.5）L/（min.m2）,P<0.05]、SV[（70±14）vs（82±11）ml/次,P<0.05]、SVI[（42±9）vs（49±9）ml/（次.m2）,P<0.05]、LVEF[（46±7）vs（57±15）%,P<0.05]均显著增加,收缩达峰时间显著缩短且一致性好（P<0.05）。结论右室流出道起搏与右室心尖部起搏相比,接近正常的房室和心室激动顺序,使心室的收缩和舒张过程更协调,心室同步化更好,心功能得到更好的改善。组织多普勒技术能定量和半定量心室的同步性,具有广阔的临床应用前景。     

超声检查对肥厚型梗阻性心肌病起搏治疗血液动力学变化的探讨

用超声技术探讨起搏器对肥厚型梗阻性心肌病 (HCM)的作用机理。观察 4例HCM(左心导管和造影检查确诊 )患者的如下指标 :①起搏器置入前、后左室梗阻部位形态及运动变化情况 ;②不同起搏间期对左室心肌各部位收缩期运动顺序的影响 ;③观察自主心律与起搏心律对心功能的影响。结果 :①起搏后左室流出道动力性梗阻减轻 (76 .3± 5 2 .8vs 16 1.5± 47.4mmHg ,P <0 .0 5 )。但起搏后 ,肥厚的心肌收缩期梗阻左室流出道现象依然存在。②双腔起搏时 ,左室心肌激动顺序未见变化 ,但传导时限延长 (6 2 .5± 7.4vs 45 .5± 7.7ms,P <0 .0 5 )。③起搏后左室收缩、舒张诸项指标下降。结论 :起搏干扰心肌传导、激动和收缩的正常过程 ,使得其同步性劣于窦性心律时 ,由此可导致左室收缩压力以及狭窄处压力梯度的下降     

右室心尖部起搏对心脏功能正常患者左室收缩同步性及功能的影响

目的应用超声心动图组织多普勒技术评价右室心尖部起搏对左室收缩同步性及心脏功能的影响,探讨起搏诱发的心室不同步收缩对于心脏功能的影响机制。方法65例置入双腔起搏器的病窦综合征患者分别在心室节律全部为起搏节律或室上性节律状态下行常规及组织多普勒超声心动图检查,测量左室收缩功能及收缩同步性指标。结果右室完全起搏模式下左室收缩功能下降(射血分数:0.58±0.07 vs 0.61±0.01,P<0.001),左室6节段收缩期平均速度下降(4.0±1.5cm/s vs 4.7±1.6cm/s,P<0.001),心室收缩同步性下降(12节段达峰时间标准差:37.5±12.5ms vs 23.7±10.2ms,P<0.001),心室同步性恶化程度与收缩功能恶化中度相关(r=0.37,P<0.05)。结论右室心尖部起搏可致左室收缩不同步及左室功能降低。     

环孢霉素A干预钙调神经磷酸酶信号通路对持续心房起搏犬心房Cx40/Cx43表达的影响

目的: 观察钙调神经磷酸酶抑制剂环孢霉素A（CsA）对持续心房起搏（atrial tachypacing,ATP）模型犬心房中Cx40/Cx43表达分布的影响,探讨CsA抑制钙调神经磷酸酶信号通路（CaN）激活是否具有一定的抗心房重构的作用。方法: 健康杂种犬18只,随机分为对照组（sham组）、心房快速起搏组（ATP组,植入固律型单腔起搏器,以400次/min持续起搏8周）及CsA干预组(在快速心房起搏组处理因素的基础上,喂食CsA 8周),每组6只。8周后,处死所有实验犬,采用免疫荧光染色法及蛋白印迹法,检测各组实验犬心房组织中Cx40/Cx43表达及分布的情况。结果: 持续快速心房起搏8周,可导致犬左右心房中Cx40的表达明显增加（P<0.01）,但CsA干预组Cx40表达增加的程度明显小于ATP组（P<0.05）。Cx40的分布方式,ATP组和CsA干预组均呈现出明显的异质性,均有端端连接减少,侧侧连接增加的现象。Cx43蛋白表达的趋势与Cx40不同:快速起搏8周后,犬左右心房组织中Cx43的表达均明显减少（P<0.01）,但减少的程度CsA干预组小于ATP组（P<0.05）。Cx43的分布方式,ATP组及CsA干预组均表现为异质性增加,端端连接减少,侧侧连接增加。结论: CsA可减少ATP导致的Cx40/43表达的重构性变化,提示CsA可能具有一定的抑制心房重构的作用。     

超声检查对肥厚型梗阻性心肌病起博治疗血液动力学变化的探讨

用超声技术探讨起搏器对肥厚型梗阻性心肌病(HCM)的作用机理.观察4例HCM(左心导管和造影检查确诊)患者的如下指标①起搏器置入前、后左室梗阻部位形态及运动变化情况;②不同起搏间期对左室心肌各部位收缩期运动顺序的影响;③观察自主心律与起搏心律对心功能的影响.结果①起搏后左室流出道动力性梗阻减轻 (76.3±52.8 vs 161.5±47.4 mmHg,P<0.05).但起搏后,肥厚的心肌收缩期梗阻左室流出道现象依然存在.②双腔起搏时,左室心肌激动顺序未见变化,但传导时限延长(62.5±7.4 vs 45.5±7.7 ms,P<0.05).③起搏后左室收缩、舒张诸项指标下降.结论起搏干扰心肌传导、激动和收缩的正常过程,使得其同步性劣于窦性心律时,由此可导致左室收缩压力以及狭窄处压力梯度的下降.     

充血性心力衰竭对犬肺静脉肌袖结构的影响

目的探讨充血性心力衰竭（CHF）对犬肺静脉（PV）肌袖结构的影响。方法将16只杂种犬,随机等分为CHF组和对照组,CHF组以240次/min的频率在右室持续起搏4周,建立CHF模型;对照组埋置起搏器但不起搏;Burst刺激诱发心房颤动（AF）。分别取两组犬的PV肌袖组织,用天狼星红染色进行纤维化定量分析和胶原组成分析。用免疫组化染色法对缝隙连接蛋白43（Cx43）进行半定量分析。结果4周后,进行快速右室起搏的CHF组的所有犬均可诱发出稳定CHF。终止起搏后,CHF犬的持续AF（>15min）的诱发率为87.5%（7/8）,显著高于对照犬（P<0.01）。CHF组PV肌袖纤维化的程度明显增加,总胶原的含量显著高于对照组的相应部位[（5.3±1.0）%vs（2.1±0.7）%,P<0.01]。CHF组Ⅲ型胶原的含量及Ⅲ型胶原与I型胶原含量的比值均显著高于对照组[（4.6±1.0）%vs（1.6±0.7）%和（7.9±3.2）vs（3.0±1.9）,P<0.01];但I型胶原的含量与对照组无显著差异[（0.6±0.2）%vs（0.6±0.3）%]。CHF组PV肌袖内Cx43的水平显著高于对照组[（3.3±0.6）%vs（2.8±0.7）%,P<0.05];其PV肌袖内细胞侧侧连接处Cx43的分布较对照组增加。结论CHF对PV肌袖结构具有显著影响。     

动脉硬化疾病患者右室流出道起搏的探讨

目的探讨动脉硬化疾病患者适宜的起搏部位。方法7例(冠心病3例、高血压4例)置入翼状电极至右室心尖部后起搏及感知功能障碍的患者,重置螺旋电极至右室流出道,观察其前后的起搏及感知功能。结果7例右室流出道起搏的起搏阈值较右室心尖部起搏显著降低,感知阈值较右室心尖部显著升高(0.5±0.2Vvs8.7±1.6V,10.6±3.6mVvs2.7±0.8mV,P<0.01),阻抗无明显差异。随访16±6个月,无电极脱位,起搏感知功能良好。结论右室流出道可作为有动脉硬化病史患者的起搏部位。     

A New Approach for the Comparison of Conduction Abnormality between Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia and Brugada Syndrome

Background: Right ventricular outflow tract ventricular tachycardia (RVOT‐VT), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/ARVD), and Brugada syndrome (BrS) were characterized by arrhythmias originating in the right ventricle, and the pathophysiologic mechanism underlying these arrhythmias has not been fully understood. Methods: This study consisted of 40 subjects, including 20 patients with RVOT‐VT, 10 patients with BrS, and 10 ARVD patients. The parameters on the signal‐averaged electrocardiography (ECG) and the frequency components recorded from the wavelet‐transformed ECG were compared between the three groups. Late potentials were positive in none of the patients with RVOT‐VT, seven of the patients with BrS, and all of ARVD patients. Results: In Brugada and ARVD patients, the power of high‐frequency components (80–150 Hz) was developed to a greater extent than in RVOT‐VT patients. In the power analysis of the high‐frequency components between BrS and ARVD, the frequency showing the greatest power was significantly higher in ARVD patients than that in BrS patients (145.4 ± 27.9 Hz vs 81.7 ± 19.9 Hz, P < 0.01). Conclusions: High‐frequency components were developed in ARVD and BrS, but not in RVOT‐VT. The frequency levels showing high power by wavelet analysis obviously differ between ARVD and BrS. Wavelet analysis may provide new insight into unsolved mechanisms in arrhythmogenic right heart disease. Ann Noninvasive Electrocardiol 2011;16(3):263–269     

Idiopathic Reentrant Right Ventricular Outflow Tract Tachycardia With Presystolic Potential of Central Pathway

Idiopathic Reentrant RVOT VT With Presystolic Potential . A 12‐year‐old girl with recurrent palpitation due to idiopathic ventricular tachycardia (VT) with a left bundle branch block configuration and inferior axis was referred to our hospital. During the VT, a spiky presystolic potential (SP) was recorded at the septum of right ventricular outflow tract (RVOT) just below pulmonary valve. The SP was entrained with a decremental property by pacing from right ventricular apex. Concealed entrainment was observed by pacing where the SP was recorded. Delivery of radiofrequency current targeting the SP abolished the VT. The SP with the decremental property could represent the central pathway of this idiopathic RVOT reentrant VT. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1174‐1177)     

Reentrant ventricular tachycardia originating in the right ventricular outflow tract: slow conduction identified by right coronary artery ostium pacing.

A case of reentrant ventricular tachycardia (VT) originating from the right ventricular outflow tract (RVOT) is described. An electrophysiological study revealed that programmed stimulation from the right ventricle apex induced 2 types of VT with similar left bundle branch block configuration and inferior axis. Yet, VT cycle length (CL) was different; one was stable, sustained VT with a CL of 360 ms and the other was hemodynamically intolerable VT with a CL of 330 ms. Similarly for both VTs, perfect pace mapping was obtained at the anterior septum beneath the pulmonary valve in the RVOT, and exits of both VTs were very close. Entrainment mapping during stable VT was performed and the anterior septum RVOT was designated as the exit for the stable VT. Intriguingly, entrainment pacing from the ostium of the right coronary artery showed that the post-pacing interval was identical to VTCL. The stimulus to QRS interval was very long (340 ms) during entrainment with concealed fusion, and the right coronary artery ostium was therefore consistent with the VT reentry circuit inner loop or the upper portion of the VT reentry circuit exit. These findings suggest that the stable VT reentry circuit had a slow conduction zone from the ostium of the right coronary artery to the exit in the anterior septum RVOT. When radiofrequency catheter ablation was performed at the 2 exits of the anterior septum RVOT, both VTs then could not be induced.     

Electrocardiographic characteristics of repetitive monomorphic right ventricular tachycardia originating near the His-bundle

INTRODUCTION: Most idiopathic nonreentrant ventricular tachycardia (VT) and ventricular premature contractions (VPCs) arise from the right or left ventricular outflow tract (OT). However, some right ventricular (RV) VT/VPCs originate near the His-bundle region. The aim of this study was to investigate ECG characteristics of VT/VPCs originating near the His-bundle in comparison with right ventricular outflow tract (RVOT)-VT/VPCs. METHODS AND RESULTS: Ninety RV-VT/VPC patients underwent catheter mapping and radiofrequency ablation. ECG variables were compared between VT/VPCs originating from the RVOT and near the His-bundle. Ten patients had foci near the His-bundle (HIS group), with the His-bundle local ventricular electrogram preceding the QRS onset by 15-35 msec (mean: 22 msec) and His-bundle pacing produced a nearly identical ECG to clinical VT/VPCs. The HIS group R wave amplitude in the inferior leads (lead III: 1.0 +/- 0.6 mV) was significantly lower than that of the RVOT group (1.7 +/- 0.4 mV, P < 0.05). An R wave in aVL was present in 6 of 10 HIS group patients, while almost all RVOT group patients had a QS pattern in aVL. Lead I in HIS group exhibited significantly taller R wave amplitudes than RVOT group. HIS group QRS duration in the inferior leads was shorter than that of the RVOT group. Eight of 10 HIS group patients exhibited a QS pattern in lead V1 compared to 14 of 81 RVOT group patients. HIS group had larger R wave amplitudes in leads V5 and V6 than RVOT group. CONCLUSION: VT/VPCs originating near the His-bundle have distinctive ECG characteristics. Knowledge of the characteristic QRS morphology may facilitate catheter mapping and successful ablation.     

A quantitative and qualitative analysis of the virtual unipolar electrograms from non-contact mapping of right or left-sided outflow tract premature ventricular contractions/ventricular tachycardia origins

Objective

This study was conducted to examine the virtual unipolar electrogram configuration of right/left outflow tract (OT) premature ventricular contraction (PVC)/ventricular tachycardia (VT) origins obtained from a non-contact mapping system (NCMS).

Methods

The subjects consisted of 30 patients with OT-PVCs/VT who underwent NCMS-guided ablation. We evaluated the virtual unipolar electrograms of the origin on 3D right ventricular (RV)-OT isochronal maps.

Results

Successful ablation was achieved from the RV in 20 patients (RVOT group), and it failed in 10 (non-RVOT group: including left-sided/pulmonary artery/deep RVOT foci). On the virtual unipolar electrograms, the earliest activation (EA) preceded the QRS onset by 11.2?±?2.6 ms in the RVOT group and by 7.4?±?10.5 ms in the non-RVOT group (P?=?0.138). The negative slope of the electrogram at the EA site (EA slope₅), quantified by the virtual unipolar voltage amplitude 5 ms after the EA onset, was significantly steeper in the RVOT group than in the non-RVOT group (0.66?±?0.52 mV vs. 0.14?±?0.17 mV, P?=?0.005). Cutoff values for the EA-to-QRS onset time and EA slope₅ of ??8 ms and >0.3 mV, respectively, completely differentiated the RVOT group from the non-RVOT group. A lesser EA slope₅ was associated with a greater radiofrequency energy delivery required to terminate RVOT-PVCs/VT.

Conclusions

These demonstrate the importance of the virtual unipolar electrograms from OT-PVC/VT origins obtained with the NCMS. The virtual EA predicts both successful and potentially difficult ablation sites from the RV side.     

三维电解剖指导右心室流出道特发性室性心动过速的导管消融

目的探讨三维电解剖指导右心室流出道特发性室性心动过速导管消融临床效果和安全性。方法经心脏超声,心脏X线检查,运动负荷试验/冠状动脉造影未见器质性心脏病表现的30例右心室流出道室性心动过速患者,分别在自身室性心动过速或心室起搏标测时进行三维电解剖重建,根据三维电解剖标测激动结果进行消融。结果 30例室性心动过速患者27例即刻消融成功,消融失败3例。术后随访6个月,1例心动过速复发。未发生任何手术相关并发症。结论三维电解剖指导右心室流出道特发性室性心动过速导管消融是一种安全、有效的方法。     

右室永久起搏可行的后备电极放置部位——右室流出道

为探讨冠心病心肌纤维化、合并糖尿病或恶性肿瘤放射治疗后出现房室阻滞的患者右室永久起搏可行的后备电极放置部位，对３例电极脱位至右室流出道、９例因上述疾病主动将电极置入右室流出道的患者进行了起搏阈值测定及随访。结果：１２例患者右室流出道起搏阈值（电压：０．８６±０．１０Ｖ，脉宽：０．３±０．０４ｍｓ）较右室心尖部起搏阈值（电压：５．０±６．０６Ｖ，脉宽：１．５２±０．７７ｍｓ）显著降低，Ｐ＜０．０１。随访６８．５±３４．６５个月无电极脱位，起搏功能良好。结果提示右室流出道是永久起搏可行的后备电极放置部位。     

Preferential conduction across the ventricular outflow septum in ventricular arrhythmias originating from the aortic sinus cusp.

OBJECTIVES: The purpose of this study was to examine the relationship between the origin and breakout site of idiopathic ventricular tachycardia (VT) or premature ventricular contractions (PVCs) originating from the myocardium around the ventricular outflow tract. BACKGROUND: The myocardial network around the ventricular outflow tract is not well known. METHODS: We studied 70 patients with idiopathic VT (n = 23) or PVCs (n = 47) with a left bundle branch block and inferior QRS axis morphology. Electroanatomical mapping was performed in both the right ventricular outflow tract (RVOT) and aortic sinus cusp (ASC) during VT or PVCs. RESULTS: The earliest ventricular activation (EVA) was recorded in the RVOT in 55 patients (group R) and in the ASC in 15 (group A). In all group R patients, the closest pace map and successful ablation were achieved at the EVA site. Although a successful ablation was achieved at the EVA site in all group A patients, the closest pace map was obtained at the EVA site in 8 and RVOT in 7 (with an excellent pace map in 4). The stimulus to QRS interval was 0 ms during pacing from the RVOT and 36 +/- 8 ms from the ASC. The distance between the EVA and perfect pace map sites in those 4 patients was 11.9 +/- 3.0 mm. CONCLUSIONS: Ventricular arrhythmias originating from the ASC often show preferential conduction to the RVOT, which may render pace mapping or some algorithms using the electrocardiographic characteristics less reliable. In some of those cases, an insulated myocardial fiber across the ventricular outflow septum may exist.     

右室流出道间隔部起搏电极定位方法的临床研究

目的探讨右室流出道(RVOT)间隔部位起搏的电极定位操作方法。方法具备心脏永久起搏指征的患者(n=40),随机分为A、B两组,每组20例。根据右室解剖学特征,设计了双弯曲导线指引导丝塑型,比较应用该塑型指引导丝(B组)与常规单个弯曲塑型指引导丝(A组)在RVOT间隔部起搏术中操控主动固定电极中应用效果。结果起搏阈值、导线电极阻抗无显著差异,感知R波振幅B组较A组低(12.32±3.80mVvs9.28±3.34mV,P=0.037);电极定位操作X线曝光时间A组大于B组(23.29±9.23minvs12.85±5.82min,P=0.002),电极固定次数A组大于B组(2.64±1.22次vs1.62±0.77次,P=0.015)。两组RVOT间隔部定位成功率:A组14/20(70%),B组18/20(90%),但未显示统计学差异;RVOT间隔部失败者均固定于低位间隔部。术后3个月内仅A组1例导线脱位。结论RVOT间隔部电极定位双弯曲指引导丝支撑下操作,减少X线曝光时间和电极固定次数,比单弯曲指引导丝方法更加简单化。两种方法均安全、稳定。