左侧房室慢旁路的电生理特征和射频消融靶点的定位

目的 探讨左侧游离壁慢传导旁路的电生理特点和射频消融方法。方法 5例患诱发心动过速后用心室感知S2程序刺激中止心动过速确立心室为房室折返环的一部分。结果 4例中止心动过速时无心房逆行A波，1例有逆行A波，旁路1例有递减传导特点，均在心室侧消融成功。结论 心室感知S2心室程序刺激中止心动过速是鉴别房性心动过速的可靠方法，成功消融靶点A波较冠状窦标测导管最早A波提前8～22ms。     

特发性左心室室性心动过速合并房室旁路的诊断和射频导管消融术

目的 :报道特发性左心室室性心动过速 (ILVT)合并房室旁路的鉴别诊断和射频导管消融术 (RFCA)结果。方法 :15 6例ILVT患者 ,常规方法进行电生理检查和RFCA ,对诱发室性心动过速室房呈 1∶1传导的患者给予三磷酸腺苷2 0～ 3 0mg静脉注射 ,观察对三磷酸腺苷的反应。同时行RS2 刺激 ,观察有无A波提前 ,明确房室旁路逆传。结果 :5例对逆向传导无影响 ,逆传A波呈非向心性分布 ,同时心室RS2 刺激A波提前 ,证明存在房室旁路逆传 ,5条房室旁路全部消融成功。消融房室旁路后再次诱发ILVT时出现室房分离 ,于左后间隔记录到分支电位或心动过速时V波最早处消融ILVT成功。结论 :ILVT可以和房室旁路同时存在并导致室房 1∶1传导。     

左心室刺激在射频消融左侧房室旁路中的价值

目的室房传导的不完全阻断可能会导致房室折返性心动过速复发.鉴于心脏的解剖关系和电生理特点,推测左心室内刺激对于判定经左侧旁路的室房传导是否被彻底阻断要优于传统的右心室刺激.方法213例左侧旁路参与的顺向型房室折返性心动过速患者(男性125例),平均年龄(38±19)岁.在射频消融前、后均进行右心室心尖部S1S2程序刺激及S1S1分级递增刺激;射频消融后,在右心室刺激显示经旁路的室房逆传完全被阻断后,经大头消融电极在左心室游离壁进行S1S1和S1S2刺激.结果在常规右心室刺激显示经旁路的室房传导被阻断之后,共有6例患者在经大头电极以相同的条件在左心室刺激时显示经旁路的室房传导仍然存在.其中1例术前有心室预激,消融后预激已消失而室房传导仍存在,有2例仍能诱发出房室折返性心动过速.另l例既往接受消融后复发的病例在此次消融前即见到此现象.7例患者均接受射频消融,直至右心室心尖部和左心室刺激均无经旁路的室房传导.平均随访(18±9)个月,均无预激或房室折返性心动过速复发.结论在对左侧旁路参与的顺向型房室折返性心动过速进行射频消融治疗时,左心室刺激可以作为判定经左侧旁路的室房传导是否被完全阻断的电生理检查手段,这可能有助于减少左侧旁路射频消融之后房室折返性心动过速的复发机会.     

希氏束不应期左心室刺激鉴别窄QRS波心动过速1例

本文报道1例隐匿性左外侧游离壁旁路参与的顺向型房室折返性心动过速(O-AVRT), 在心室起搏下消融过程中, 冠状静脉窦A波激动顺序由冠状静脉窦远端最早突然变为近端最早, 并可诱发以心房激动顺序存在的心动过速。于右心室反复行希氏束不应期心室刺激(RS2)均未提前下一A波, 似乎不支持旁路参与, 左心室RS2证实为经第2条左侧房室旁路逆传的O-AVRT;消融成功。     

逆行慢传导房室旁路的射频导管消融术

报道１１例在射频消融成功部位靶点不能标测到ＶＡ波融合的逆行慢传导隐匿性房室旁路电生理特点和射频消融。４例心动过速呈连续性，旁路位于间隔部位；７例心动过速呈阵发性，旁路均位于左侧游离壁。消融成功部位靶点图ＶＡ波不融合，ＶＡ间期１１５±１６ｍｓ，ＶＡ波之间等电位线间期１０～５０ｍｓ。     

伴连续性房室结功能曲线的房室结折返性心动过速的电生理分析

目的：探讨无房室结双径路特性的房室结折返性心动过速(AVNRT)的电生理特点。方法：所有心动过速患射频消融前常规行心内电生理检查。结果：845例射频病人中325例为AVNRT，其中有21例患房室结功能曲线呈连续性，其电生理特征：希氏束图上心房回波(A)先出现，A波落在室波升支或其前，希氏柬不应期内刺激心室，不能提前夺获心房，射频消融后心房刺激时AHmax明显缩短。结论：伴连续性房室结功能曲线的AVNRT患心房刺激不表现房室结双径路的电生理特性，其消融终点初步定为：心房心室S1S1、S1S2刺激不诱发AVNRT；无AHvH传导曲线跳跃；房室结前传不应期明显缩短。     

预激综合征患者出现房室折返性阵发性心动过速的决定因素

预激综合征患者可反复发生阵发性室上性心动过速。QRS综合波常狭窄,反映系通过正常房室通路顺行传导和异常结外旁路逆行传导的环行运动。引起这种心动过速的原因是心房冲动在异常旁路中阻滞而经过正常通路顺行传导,或由于心室冲动在正常通路中阻滞而经过异常旁路逆行传导。为何部分预激综合征患者有阵发性室上性心动过速而另部分则无,尚不清楚。本文测定正常和异常通路的顺行和逆行传导特性,比较能诱发和不能诱发房室折返性阵发性室上性心动过速的二组病人,以研究预激综合征患者出现房室折返性阵发性室上性心动过速的决定因素。方法:电生理研究包括用递增心房起搏和心房额外刺激方法以评价顺行传导以及用递增心室起搏     

旁路前传室端单向阻滞一例

1　临床资料　　患者女性 ,2 6岁。“频繁阵发性心动过速”史 10年 ,体表心电图无预激表现。入院后检查无器质性心脏病。患者继往接收 2次射频导管消融术 ,包括心室面标测和心房间隔穿刺心房面标测消融均失败。局部麻醉下行心内电生理检查 ,窦性心律时冠状静脉窦远端电极 (CS1- 2 )记录到 A波之后的旁路电位 ,旁路电位与 V波之间有一段时间距离 ,V波无提前 (附图 ) ,心房程序刺激 A波之后的旁路电位持续存在 ,而 V波无提前 ,体表心电图无预激表现。心室程序刺激旁路逆传时冠状静脉窦远端电极可以记录到V波和 A波之间的旁路电位 ,无逆传…     

Mahaim样纤维的电生理特点和射频消融治疗

目的　总结前传递减性右心房 -右心室旁路的电生理特点和射频消融结果。　方法　对 7例患者 ,其中男性 3例 ,女性 4例 ,平均年龄 (32± 16 )岁左束支阻滞图形的逆向型房室折返性心动过速患者进行电生理检查和射频消融治疗。　结果　 7例患者的旁路只有递减性前向传导功能 ,三磷酸腺苷能够阻断旁路的传导。心动过速时 ,行心房期前刺激和标测心室最早激动点 ,证实旁路起止于邻近三尖瓣环的右心房和右心室。于三尖瓣环上成功消融所有的旁路 ,消融部位的局部 V波明显提前 [平均 V-δ间期(2 5± 4) ms],但不伴有旁路电位。平均随访 (16± 5 )个月 ,无 1例心动过速复发。　结论　前传递减性右心房 -右心室旁路是“Mahaim样纤维”的一种类型 ,射频消融术为有效的治疗方法 ,成功消融部位可不伴有旁路电位。     

疑难性的房室及房室结折返性心动过速与房性心动过速快速简捷的鉴别方法

目的探讨简便、快捷鉴别疑难的房室及房室结折返性心动过速与房性心动过速的方法.方法分别对20例间隔旁路(包括4例慢旁路),20例房室结双径路(包括不典型房室结双经路1例)以及11例房速(6例房速,5例房室结双径路慢径路消融术后S1S1心房刺激模拟房速)患者,在心动过速过程中行心室RS2刺激,所有患者心室RS2刺激均能夺获心室并且逆传心房,而且不终止心动过速,观察心室刺激时心房的反应,反应方式分别为V＇-A＇-V-A(V＇S2刺激后心室波,A＇V＇波逆传心房波,V心动过速时室波,A心动过速时房波)或V＇-A＇-A-V.结果20例间隔区房室折返性心动过速的患者,心室RS2刺激的反应方式均为V＇A＇VA,其中16例V＇A＇间期＜A＇-V间期,4例慢旁道V＇A＇间期＞A＇V间期,V-A均较远(＞60ms),V＇A＇间期与VA间期相近.20例房室结折返性心动过速病人行心室RS2刺激的反应方式呈V＇A＇-V-A14例,呈V＇-A＇-A-V6例,1例不典型房室结折返性心动过速患者VA间期130ms,余13例呈V＇-A＇-V-A反应的患者VA均较近(VA＜60ms),6例呈V＇-A＇AV的患者AV较近或者融合(AV＜60ms).6例房速以及5例模拟房速患者心室RS2刺激均呈V＇-A＇-A-V反应,AV均较远(100ms).结论心动过速过程中行RS2心室刺激,是鉴别疑难的阵发性室上性心动过速的快速、简洁而有效的方法.     

房室多旁道的电生理特征及其射频消融治疗

目的 探讨房室多旁道的电生理特点及射频消融方法。方法 23例患者经电生理检查确定房室多旁道，应用心房和心室刺激诱发室上速，确定每条旁道的电生理特征及与心动过速的关系，按照标测部位对相关旁道逐步消融，以射频消融成功确定旁道位置。结果 23例中检出旁道49条，其中三条旁道3例；左侧多旁道12例，右侧多旁道2例，双侧多旁道9例；左侧多旁道以隐匿性为主；右侧多旁道多为显性；未见心动过速时右侧旁道前传而同侧旁道逆传现象。结论 多旁道患者应首先确定和消融与心动过速相关旁道；左侧多旁道应以诱发心动过速或快速心室起搏方法标测；右侧多旁道应同步描记12导联体表心电图，旁道消融成功可能仅见于QRS波的变化，双侧多旁道应首先消融左侧旁道。     

快慢型房室结折返性心动过速的电生理特点

目的分析快慢型房室结折返性心动过速（AVNRT）患者的临床特征、心电网和电生理检查特点、射频消融治疗特点,旨在为临床长RP。心动过速鉴别提供帮助。方法11例经心内电生理检查证实为慢快型房室结折返性心动过速的患者,回顾性分析其临床特征、心电图特点及电生理检查特点及射频消融治疗。结果心动过速表现为窄QRs波心动过速,RP’〉P’R,P。在Ⅱ、Ⅲ、aVF导联倒置,RP’间期为350±25ms,心率为1664-30bpm。11例患者中有3例出现室房逆传跳跃现象。心房程序刺激无明显跳跃现象,11例均可由心房StS：刺激诱发心动过速发作,且容易诱发,容易终止。心动过速发作时,5例CS9．10A波最早,6例HiS的A波最早,其中1例静推ATP心动过速终止。11例患者中9例经房室结改良消融传统慢径获得成功,2例在冠状静脉窦内消融成功,术后随访3个月以上均未再发作心动过速。结论长RP’心动过速的诊断和鉴别诊断有一定困难,如能排除慢旁道和房速,应考虑快慢型房室结折返性心动过速。     

隐匿性束室纤维介导的心动过速(附一例报告)

目的 阐明隐匿性束室纤维介导的心动过速的电生理机制及其导管消融方法。方法 研究病例为男性、29岁,心动过速病史7年余。心动过速不能被腺苷三磷酸和维拉帕米终止,但可被普罗帕酮终止。曾在院外拟诊房室结折返性心动过速,两次行慢径改良术,但心动过速仍反复反作。在我院行电生理检查一次并在非接触球囊导管标测系统（即EnSite,3000）指导下标测和消融。结果 电生理检查示窦性心律时AH为75ms,HV 44ms,心房增频刺激及程序刺激未见心室预激现象。心室600ms起搏示室房分离,RS2程序刺激无逆传A波,提示室房逆传功能较弱。心房与心室均能诱发心动过速,但心室更易诱发。心动过速时室房分离。心动过速可呈窄QRS图形、左束支传导阻滞（LBBB）图形及右束支传导阻滞（RBBB）图形。LBBB和RBBB心动过速可自行转为窄QRS心动过速。窄QRS心动过速及RBBB图形时,心动周期为300ms;LBBB图形时,心动周期为316ms,明显长于前。三种心动过速时,希氏束激动均领先于右束支激动。维拉帕米和腺苷三磷酸不能终止心动过速。专房程序刺激及超速抑制不能终止心动过速,但可被心室程序刺激终止。EnSite 3000标测系统分析发现三种心动过速的最先激动点均位于心动过速的最先活动点均位于右室间隔上部,此处行环状消融后心动过速不再诱发。随访4个月,临床无心动过速发作。结论 该患的心动过速由隐匿性束室纤维介导,其折返环路包括正常的希－浦传导系统、心室和束室纤维,其消融方法与室性心动过速相似;EnSite3000标测系统指导此类心动过速的消融有极大的优越性。     

Electrophysiologic characteristics and radiofrequency ablation of concealed nodofascicular and left anterograde atriofascicular pathways

INTRODUCTION: True nodoventricular or nodofascicular pathways and left-sided anterograde decremental accessory pathways (APs) are considered rare findings. METHODS AND RESULTS: Two unusual patients with paroxysmal supraventricular tachycardia were referred for radiofrequency (RF) ablation. Both patients had evidence of dual AV nodal conduction. In case 1, programmed atrial and ventricular stimulation induced regular tachycardia with a narrow QRS complex or episodes of right and left bundle branch block not altering the tachycardia cycle length and long concentric ventriculoatrial (VA) conduction. Ventricular extrastimuli elicited during His-bundle refractoriness resulted in tachycardia termination. During the tachycardia, both the ventricles and the distal right bundle were not part of the reentrant circuit. These findings were consistent with a concealed nodofascicular pathway. RF ablation in the right atrial mid-septal region with the earliest atrial activation preceded by a possible AP potential resulted in tachycardia termination and elimination of VA conduction. In case 2, antidromic reciprocating tachycardia of a right bundle branch block pattern was considered to involve an anterograde left posteroseptal atriofascicular pathway. For this pathway, decremental conduction properties as typically observed for right atriofascicular pathways could be demonstrated. During atrial stimulation and tachycardia, a discrete AP potential was recorded at the atrial and ventricular insertion sites and along the AP. Mechanical conduction block of the AP was reproducibly induced at the annular level and at the distal insertion site. Successful RF ablation was performed at the mitral annulus. CONCLUSION: This report describes two unusual cases consistent with concealed nodofascicular and left anterograde atriofascicular pathways, which were ablated successfully without impairing normal AV conduction system.     

Paroxysmal supraventricular tachycardia with complete atrio-ventricular block or dissociation]

Recent studies have shown the high incidence of concealed Bundles of Kent in the reentry circuits of paroxysmal supraventricular tachycardia. Arguments in favour of the nodal or junctional level of reentry were observed in supraventricular tachycardia with complete atrioventricular dissociation. Two such cases under went electrophysiological investigation. In the first case, tachycardia was terminated by a complete infrahisian block. However, during atrioventricular dissociation, tachycardia could be initiated by a single atrial stimulus after an increased nodal conduction time and terminated by a single atrial stimulus or cardiac message. In the second case the supraventricular tachycardia presented with complete atrioventricular dissociation due to a retrograde ventriculo-atrial block. Atrial stimulation at progressively higher rates and premature atrial extra stimuli initiated the tachycardia but could not terminate it, so confirming the non-participation of the atrium in the reentry circuit. These two cases suggest that the ventricle (case I) and the atrium (case II) are not indispensable links in junctional or nodal reentry circuits. Case II was suggestive of a common initial pathway developing retrograde unidirectional block during tachycardia.     

抗心动过速起搏器诱发的心动过速

抗心动过速起搏器采用AAI-T工作方式时如发生感知不足能诱发心动过速,提高感知灵敏度或改用OAO-T工作方式可有效纠正之。     

Anti-tachycardia radiofrequency pacemakers. Experience with 44 cases

Programmed cardiac stimulation may be performed externally using implanted radiofrequency receiving capsules. Between 1979 and 1984, 44 patients underwent implantation of these devices, 12 with atrial leads for supraventricular tachycardias (8 orthodromic reciprocating tachycardias, 1 intranodal junctional tachycardia and 3 atrial tachycardias), and 32 with ventricular leads for ventricular tachycardias. In the first case the transmitter was given to the patients so that they could terminate the tachycardias themselves. In the second case, the transmitter was kept in the cardiology department. All patients were also prescribed prophylactic antiarrhythmic drugs. The radiofrequency method was effective in 11 out of 12 cases of supraventricular tachycardia with a follow-up period ranging from 24 to 65 months (average 45 +/- 11 months). In the ventricular tachycardia group, the device was used in 11 patients to terminate ventricular tachycardia and in all patients to evaluate the efficacy of the antiarrhythmic therapy by provocative programmed stimulation with a follow-up ranging from 2 to 81 month (average 24 +/- 20 months). This palliative therapeutic method has reduced the number of hospital admissions in these patients. The indications are relatively few because of the efficacy of currently available antiarrhythmic agents and the possibility of radical treatment of tachyarrhythmias by surgery or catheter ablation.     

慢传导旁道的临床特征及射频消融治疗

目的 探讨慢传导旁道的临床、电生理检查特点及消融方法.方法 对5例心动过速时RP’>P’R的患者行电生理检查及射频消融治疗.结果5例患者电生理检查显示心室逆传文氏现象及递减传导,且消融靶点处VA不融合.取A波最早处做为消融靶点均获成功,随访2～13个月无复发.结论 慢传导旁道具有特殊的电生理特性,射频消融是有效的根治方法.     

Transcoronary chemical ablation of ventricular tachycardia in chronic chagasic myocarditis.

OBJECTIVE. A case of incessant ventricular tachycardia in a patient with Chagas' disease that was successfully terminated by chemical ablation is reported. BACKGROUND. Chagas' disease is a common medical problem in South America. Ventricular tachyarrhythmias, atrioventricular conduction disturbances, congestive heart failure and sudden cardiac death are important manifestations of this disease. METHODS. Selective catheterization of the coronary artery supplying the arrhythmogenic area was performed by using a conventional angioplasty system and the arrhythmogenic area was ablated by injection of 96% sterile ethanol. RESULTS. Ethanol (96%) injection initially in a lateral branch of the left circumflex artery and 2 days later in the proximal segment of the artery resulted in termination of ventricular tachycardia. Two weeks after ablation, programmed ventricular stimulation failed to induce ventricular tachycardia. CONCLUSION. Transcoronary chemical ablation should be considered in selected cases of Chagas' disease with incessant ventricular tachycardia.