快频率依赖性室房逆传左侧隐匿性房室旁道参与的心动过速及射频导管消融

目的探讨快频率依赖性室房逆传特性左侧隐匿性房室旁道的电生理特点及射频消融。方法对8例心电图显示窄QRS波群心动过速的患者行电生理检查,分析房室、室房传导情况、心动过速特点、旁道定位,并行射频消融。结果8例患者均证实存在快频率依赖性室房逆传特性左侧隐匿性旁道,在较慢频率起搏右心室时旁道逆传发生阻滞,而以中等频率起搏时表现为间断旁道逆传,较快频率起搏时才表现为旁道1：1传导且均诱发了房室折返性心动过速,于快频率心室刺激下标测消融靶点,消融均获成功。结论左侧隐匿性房室旁道有时可发生快频率依赖性室房逆传现象,并伴发房室折返性心动过速,在射频消融中需注意分辨,以免漏诊。     

射频消融治疗具有快频率依赖性室房逆传特性的旁道

目的报道具有快频率依赖性室房逆传特性的房室旁道电生理检查及射频消融结果。方法4例患者,均有阵发性心悸史,且发作时心电图均显示为窄QRS波心动过速,按常规方法接受心脏电生理检查及射频消融治疗。结果4例均证实存在旁道的快频率依赖性室房逆传,且均诱发了房室折返性心动过速,室房逆传最早激动部位均为左房。于快频率心室刺激下标测消融靶点,消融均获成功。结论旁道的快频率依赖性传导为一种少见电生理现象,可伴发房室折返性心动过速。     

右心室双旁道预激综合征的心电图表现

患者男性,27岁,有阵发性室上性心动过速史15年。体表心电图显示 B 型预激综合征(图1),呈间歇性,非预激时与旁道消融成功后的心电图一致(图2),临床初步判断为右后间隔旁道,1993年3月22日行射频消融术,以心室起搏时消融导管局部电图最短 VA 为靶点,先在右心室中部间隔区找到靶点,消融后局部VA 延长,说明该处有一旁道被消去。但仍能诱发房室折返性心动过速,又找到右后间隔区另一靶点,消融后无室房逆传,不能诱发心动过速,说明另一条旁道被消去,证实本例具有右中间隔及右后间隔两条旁道。     

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。     

左心室起搏下标测并消融左侧隐匿性旁路一例

本文报道１例左侧隐匿性旁路患者,右心室起搏的冲动只经房室结逆传。为此,在消融电极导管的第３、４极起搏左心室的同时,采用消融电极导管的１、２极标测靶点,并消融成功。现报道如下：１　　临床资料　　　　患者男性,５４岁。因反复阵发性室上性心动过速而于２００１年３月５日入院行射频导管消融术。局部麻醉下经静脉放置冠状静脉窦、高位右心房、希氏束、右心室电极。室上速发作时冠状静脉窦远端Ａ波明显提前,诊断为左侧游离壁隐匿性旁路参与逆传的房室折返性心动过速。用不同频率行右心室起搏,均为希氏束处Ａ波领先,提示冲动不…     

加速的右房下部逸搏心律 射频消融术并发左侧气胸

患者男,26岁。反复发作阵发性心动过速8年于1999年1月18日入院。临床诊断:预激综合征(WPW)、阵发性前传型房室反复性心动过速。20日行旁道射频导管消融术。术中标测旁道位于右侧间隔部,以25～30W放电,持续120s,预激波消失。分别行心房和心室旁道端起搏,均未能诱发出旁道的前传与逆传及其参与折返的心动过速,手术操作穿刺     

左侧旁道消融伴发二尖瓣峡部阻滞的临床观察

目的:探讨经房间隔途径行左侧旁道射频消融过程中,不经意二尖瓣峡部阻滞发生的解剖机制及电生理特征。方法:回顾性分析2016年1月至2018年1月贵州省人民医院单中心收治的左侧旁道并房室折返性心动过速患者,研究纳入经房间隔途径行左侧旁道射频消融患者共59例,经股静脉途径送入二极电极至右心室,经左锁骨下静脉或右股静脉送入十级电极至冠状窦。行心房及心室期前刺激,递减刺激及快速刺激诱发心动过速,必要时静滴异丙肾上腺素辅助诱发。经房间隔顺行性途径送入消融电极至左心房室环标测房室旁道,行射频消融治疗。并对消融过程中发生二尖瓣峡部阻滞的患者进行电生理研究并探讨可能发生机制。结果:59例经房间隔途径消融的左侧旁道患者中,4例患者消融过程中发生二尖瓣峡部阻滞,发生率约6.8%。其中3例患者二尖瓣峡部阻滞后心动过速周长不变,体表心电图节律整齐;1例患者二尖瓣峡部阻滞后心动过速周长长短不等,体表心电图心动过速发作频率减慢,节律完全不整齐。4例患者消融过程中二尖瓣峡部阻滞均表现为冠状窦电极室房逆传间期延长,心动过速未能终止,激动顺序由离心性传导转为向心性传导,经调整消融电极至原消融部位更远端消融成功。结论:左侧旁道消融过程中可能不经意导致二尖瓣峡部阻滞,其发生率低。掌握其心内电生理特征及心内电图的变化有助于缩短手术时间,避免无效消融。     

异丙肾上腺素依赖性左侧旁路诊断及射频消融一例

在隐匿性旁路引起的房室折返性心动过速的消融中,心内电生理检测,行心室S1S1刺激时,根据VA激动顺序可判断隐匿性旁路且诱发房室折返性心动过速.近来,我们发现1例患者只有在异丙肾上腺素诱发下才出现旁路逆传并诱发房室折返性心动过速.此种现象极罕见,现报导如下:     

左右房室旁道交替性逆传参与房室折返性心动过速射频消融成功一例

患者男性,28岁,因发作性心悸5~6年入院。心内电生理检查发现右侧His束旁道及左侧游离壁隐匿性旁道交替性逆传参与顺向型房室折返性心动过速,其VV(RR)间期330~350ms,并且QRS波形态一致。导管消融成功阻断旁道传导,随访9个月心动过速无复发。结论:左右旁道交替性逆传参与同次房室折返性心动过速发作,临床相对少见,应注意识别。     

逆向型房室折返性心动过速的临床特点

探讨逆向型房室折返性心动过速 (ADRT)的临床特点。 397例预激综合征患者进行常规电生理检查和导管射频消融术 ,2 2 (5 .5 % )例 (包括Mahaim纤维旁道 12例 )诱发出ADRT ,心动过速的周长为 30 2± 5 6 (2 30～ 4 10 )ms,2例心动过速时出现低血压伴有头晕 ,4例在心动过速时演化为心房颤动。通过与患者既往临床心电图比较 ,证实 17例有ADRT临床发作 ,常见于多旁道和年轻的患者 (15 / 2 2例 ) ,12例同时伴有顺向型房室折返性心动过速。 19例多旁道患者中 15例逆传经旁道 ,4例逆传经旁道和 /或房室结。 3例单旁道患者在静脉点滴异丙肾上腺素后诱发ADRT ,逆传经房室结。参与构成ADRT的 4 1条旁道 19条位于右侧游离壁 ,9条位于右后间隔 ,3条位于左后间隔 ,7条位于左侧游离壁。 12例前传经Mahaim纤维的ADRT ,其逆传旁道均位于后间隔。 7例普通旁道参与的心动过速其前传支和逆传分别位于右侧、左侧游离壁。 3例单旁道均位于右侧游离壁。结论 :ADRT最常见于多旁道患者并有多种形成机制。     

Electrophysiologic mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline,pilsicainide, disopyramide,procainamide) in induction of atrioventricular re-entrant tachycardia

Summary We evaluated the electrophysiological mechanisms of adverse effects of class I antiarrhythmic drugs (cibenzoline in seven patients, pilsicainide in two, and disopyramide in two, and procainamide in three) in the induction of orthodromic atrioventricular re-entrant tachycardia (AVRT). In 14 patients (10 males, 4 females; mean age 37±18 years) who had inducible AVRT despite the administration of class I drugs, electrophysiological effects of class I antiarrhythmic drugs were evaluated using programmed electrical stimulation techniques. In 4 out of 6 patients with a manifest accessory pathway, class I drugs induced unidirectional conduction block of the accessory pathway (antegrade conduction block associated with preserved retrograde conduction) and enhanced the induction of AVRT with atrial extrastimulation. In eight patients with a concealed accessory pathway, the outward or inward expansion of the tachycardia induction zone was observed in patients who had greater prolongation of the conduction time than the refractory period of the retrograde accessory pathway after class I drugs. During ventricular extrastimulation, the induction of bundle branch reentry after class I drugs initiated the AVRT in patients with either manifest or concealed accessory pathways. We conclude that the adverse effects of class I drugs are mainly due to induction of unidirectional retrograde conduction of the manifest accessory pathway and the greater prolongation of the retrograde conduction time of the concealed accessory pathway than the refractory period, regardless of the subclassification of class I drugs.     

左室起搏对判断左侧旁道射频消融终点的意义

探讨左室起搏对判断左侧旁道射频消融终点的价值。 6 4例左侧旁道患者进行了常规电生理检查和射频消融。按消融终点不同分二组 :A组消融后显性预激以delta波消失、右室心尖部 (RVA)起搏无旁道逆传 ;隐匿性旁道以RVA起搏旁道无逆传作为成功标准。B组除了A组标准外 ,再加上左室消融电极 (ABL)直接起搏 ,如旁道也无逆传 ,则终止消融。所有患者术后随访 1个月～ 1年。结果A组 5 0例 :显性预激 17例、隐匿性旁道 33例。显性预激即刻成功消融 16例 ,因反复发作心房扑动、心房颤动而未消融 1例 ;隐匿性旁道即刻成功 31例 ,因未诱发出心动过速及导管无法到位而未消融各 1例 ,术后 1～ 35天复发 5例 ,再次消融成功。B组 14例 :9例显性预激、5例隐匿性旁道。 9例显性预激消融后ABL起搏发现 4例残存隐匿性旁道 ,巩固消融后消失。 1例隐匿性旁道RVA起搏偶尔经左侧旁道逆传 ,而ABL起搏则旁道显示逆传 ,消融成功。B组术后无复发。结果提示 :左室起搏可揭示右心室起搏不显示的左侧隐匿性旁道、对判断旁道消融是否彻底以及减少旁道消融术后复发具有重要意义     

希氏束旁起搏鉴别间隔部隐匿性AVRT与AVNRT的临床价值

目的：探讨希氏束旁起搏鉴别间隔部隐匿性房室旁道与慢一快型房室结折返性心动过速（AVNRT）的临床价值。方法：采用希氏束逆传不应期心室早搏刺激法将61例患者分别诊断为37例慢一快AVNRT和24例间隔部房室折返性心动过速（AVRT）；再对61例患者采用希氏束旁起搏方法进一步检测。结果：采用希氏束旁起搏法检测37例AVNRT患者中有6例未检测成功，其余31例均为逆传房室结图形；24例AVRT患者中4例未检测成功，15例呈逆传旁道／旁道图形，5例呈非逆传旁道／旁道图形。如以逆传旁道／旁道图形为标准，鉴别间隔快旁路引起的AVRT与慢一快型房室结折返性心动过速，敏感性75％，特异性可达1009／6。结论：希氏束旁刺激法对鉴别诊断AVRT与AVNRT有较高的特异性。     

Electrophysiologic effect of a new Ca(2+)-antagonist, TA-3090 on supraventricular tachycardia and conduction system]

We investigated the effect of a new Ca-antagonist, TA-3090 on supraventricular tachycardia (SVT) and conduction system, comparing it with the effect of Diltiazem Hydrochloride, in 11 patients who had paroxysmal SVT attacks. Seven of the 11 patients presented atrioventricular reentrant tachycardia (AVRT) via retrograde concealed conduction through an accessory pathway, and the others presented AV nodal reentrant tachycardia (AVNRT). After SVT was induced by means of programmed electrical stimulation at high right atrium, TA-3090 (0.1 mg/kg body weight) or Diltiazem (0.2 mg/kg) was administered intravenously for 3 minutes. TA-3090 terminated nine of 11 SVTs, while Diltiazem terminated four of 4 SVTs. On termination of SVT, both drugs interrupted A-H conduction during AVRT and the slow pathway during AVNRT. After TA injection, five of 11 SVTs could not be induced by programmed electrical stimulation, while two of 4 SVTs could not be induced after Diltiazem. In AVRT, three patients in which TA-3090 prevented SVT induction had a longer AV node effective refractory period than that of the others in which TA-3090 could not prevent SVT (330 +/- 46 vs 210 +/- 24 msec, p less than 0.01). However, SVT was induced more easily than before in three of the 11 patients treated with TA-3090 administration, and in one of the 4 patients treated with Diltiazem administration.(ABSTRACT TRUNCATED AT 250 WORDS)     

Successful elimination of concealed accessory pathway-mediated tachycardia by ablation of AV nodal slow pathway

We report a case of atrioventricular reentrant tachycardia (AVRT) using a concealed para-Hisian accessory pathway for retrograde conduction, which also required anterograde conduction over the AV nodal slow pathway to maintain the tachycardia. The shortest VA interval during AVRT (70 ms) was noted at a site with His bundle electrogram amplitude of 0.25 mV. The AVRT was cured by radiofrequency ablation of the AV nodal slow pathway without affecting accessory pathway conduction. The patient has not reported any sustained palpitations at 2 years after ablation while receiving no medications. The case presented in this report illustrates a para-Hisian AVRT that was successfully eliminated by an unconventional approach of ablation of the atrial inputs to the AV nodal slow pathway.     

下位法射频消融慢径路改良房室结治疗室上性心动过速23例

用下位法射频消融慢径路改良房室结治疗房室结折返性心动过速(AVNRT)18例,房室折返性心动过速(AVRT)5例.AVNRT中16例为慢—快型,1例快—慢型,1例慢—快型与快—慢型并存,18例慢径路全部阻断成功.AVRT中1例显性预激,4例隐性预激,有5例慢径路和3例房室旁路消融成功.射频放电时21例出现结性心律.无严重并发症出现.AVNRT病人中随仿1—15个月有1例复发,第二次射频成功.认为下位法射频消融阻断慢径路成功率高,并发症少.     

Encainide for treatment of atrioventricular reciprocating tachycardia in the Wolff-Parkinson-White syndrome

Oral encainide, varying from 75 to 300 mg/day (mean 174 mg/day), was administered to 52 patients with drug-resistant atrioventricular reciprocating tachycardia (AVRT) associated with the Wolff-Parkinson-White syndrome. Electrophysiologic studies were performed before and during drug treatment. Encainide resulted in anterograde accessory pathway block in 15 of 37 (41%) and retrograde accessory pathway block in 11 of 46 (24%) patients. In patients With residual accessory pathway conduction, encainide significantly prolonged the shortest pacing cycle length maintaining anterograde (261 ± 26 to 404 ± 85 ms) and retrograde (279 ± 46 to 436 ± 87 ms) accessory pathway conduction, as well as the anterograde accessory pathway effective refractory period (271 ± 32 to 329 ± 73 ms). AVRT could not be induced during encainide therapy in 20 of 49 patients (41%). In the remaining patients, AVRT cycle length increased (319 ± 44 to 426 ± 90 ms, p <0.001) due to prolongation of HV and ventriculoatrial intervals. During follow-up (mean 38.5 months), 30 patients continued to take the drug and 7 patients with favorable drug response subsequently elected to undergo surgical accessory pathway ablation (71% overall favorable response). Encainide was ineffective in 11 patients, was discontinued because of drug intolerance in 2 patients and exacerbated ventricular tachycardia in 2 patients. Lack of AVRT inducibility at encainide electrophysiologic study did not always predict recurrence-free follow-up. Encainide is an effective and well-tolerated drug to prevent recurrence of AVRT in patients with Wolff-Parkinson-White syndrome.     

Concealed anterograde accessory pathway conduction during the induction of orthodromic reciprocating tachycardia

The purpose of this study was to determine whether concealed anterograde accessory pathway conduction occurs during the induction of orthodromic tachycardia by an atrial extrastimulus (S2). Sixteen patients with an overt (n = 9) or concealed (n = 7) accessory pathway had inducible orthodromic tachycardia by S2 during an atrial drive (S1) cycle length of 500 to 650 ms. A ventricular extrastimulus (S3) was introduced coincident with the His depolarization resulting from S2 during the longest S1S2 interval that reproducibly induced orthodromic tachycardia. The S1S3 interval was decreased in 10 ms steps until S3 reached ventricular refractoriness. Retrograde accessory pathway conduction of S3 in the presence and absence of S2 was compared at the same S1S3 intervals. In the absence of S2 there was retrograde accessory pathway conduction after S3 in each patient. In the presence of S2, in patients with overt pre-excitation, retrograde accessory pathway conduction after S3 was absent in one patient, prolonged in four patients and present only after long S1S3 intervals in three patients. Only one patient had unchanged retrograde conduction regardless of the presence or absence of S2. In patients with a concealed accessory pathway, retrograde accessory pathway conduction after S3 was absent in five patients and was prolonged in two. Thus, concealed anterograde accessory pathway conduction was present in 15 of 16 patients at the time of orthodromic tachycardia induction. In conclusion, concealed anterograde accessory pathway conduction occurs in a majority of patients with an overt or a concealed accessory pathway during induction of orthodromic tachycardia by an atrial extrastimulus.(ABSTRACT TRUNCATED AT 250 WORDS)     

Clinical and electrophysiologic observations in patients with concealed accessory atrioventricular bypass tracts

In 12 of 46 consecutive patients with paroxysmal supraventricular tachycardia or atrial flutter-fibrillation, without electrocardiographic evidence of ventricular preexcitation, electrophysiologic studies suggested the presence of accessory atrioventricular (A-V) pathways capable only of retrograde conduction (concealed Wolff-Parkinson-White syndrome). The ages of these patients ranged from 29 days to 71 years (mean 39.2 years). Most patients were clinically symptomatic with palpitations, dizziness, weakness or congestive heart failure. One patient had “cardiac dysrhythmia” described by an obstetrician during intrauterine life. Eleven patients manifested A-V reciprocating tachycardia involving the normal pathway for anterograde conduction and the accessory pathway for retrograde conduction. The remaining patient manifested recurrent paroxysms of atrial flutter-fibrillation as a result of rapid ventriculoatrial activation through the accessory pathway during the atrial vulnerable phase.

The electrophysiologic observations were analyzed with regard to clinical and electrocardiographic characteristics in these patients. The presence of concealed accessory pathways should be suspected in patients presenting with (1) an “incessant” form of tachycardia, (2) spontaneous onset of A-V reciprocal rhythms or reciprocating tachycardias after acceleration of the sinus rate without antecedent atrial extrasystoles or P-R interval prolongation, (3) slowing of the tachycardia rate consequent to the development of functional bundle branch block, (4) retrograde P waves (negative in leads II, III and aVF) discernible after the QRS complexes, with the R-P interval being shorter than the P-R interval during both A-V reciprocal rhythm and reciprocating tachycardia, and (5) oc-currence of atrial flutter-fibrillation in association with A-V reciprocal rhythms.

It is suggested that medical treatment in patients having concealed accessory pathways should be aimed at increasing the refractoriness of either the A-V node or the accessory pathway for reciprocating tachycardia, while increasing the refractoriness of the atrium and the accessory pathway in cases with atrial flutter-fibrillation. Pacemaker therapy and surgical intervention may be indicated in selected patients refractory to antiarrhythmic agents.