食管心房调搏诱发室性心动过速5例分析

１４２０例病人经食管心房调搏检查诱发室速９例（６．３４‰）。其中５例经心房起搏或程控早搏刺激诱发持续性室速，且均符合分支型室速。食管心房调搏检查均发现有房室分离及室性融合波，２例经心房电刺激终止，３例不能终止，经静推维拉帕料而终止，剂量３－２０ｍｇ。食管心房调搏检查对分支型室速有一定的临床意义。     

食管心房调搏对阵发性室上性心动过速发病机制研究

使用无创伤性食管心房调搏（TEAP）心电生理检查法，对58例原因不明的阵发性室上性心动过速（PSVT）在非发作期进行程控或非程控心脏刺激，旨在探讨PSVT的发病机制，电生理特征以及TEAP对其临床研究的价值。结果：诱发示PSVT的共47例（折返机制），占81．0％，不能诱发11例（非折返机制），占19．0％。说明折返机制系PSVT的主要发病机制。又根据程控刺激中所表现的不同心电生理特征，47例折返性PSVT又可分为不同机制的折返。其中房室结内折返性23例，房室折返性17例，心房内或窦房折返性7例，说明前两种折返系折返性PSVT的主要折返机制，与国内外报道相似。     

心得安防止室上性心动过速的电生理效应

心得安作为一种β体阻滞剂,已被国内外广泛应用于防止阵发性室上性心动过速(PSVT),但国内尚缺乏有关的详尽的电生理资料。本文采用无创性食管心房起搏方法,观察心得安防止PSVT的电生理效应,以弥补这方面的不足。1 对象与方法1.1 对象 患者30例,男13例,女17例,年龄33±12岁,均有反复PVST史且经心房起搏诱发PSVT。房室结折返性心动过速(AVNRT)12例,房室反复性     

房室顺序起搏的A-V间期

病态窦房结综合征双结病变型等是植入DDD起搏器的最佳适应证。人体植入DDD起搏器后，就如植入一个窦房结和房室结，心房的电活动可经DDD起搏器设置的A-V间期下传至心室。由于心房激动经体内自身房室结下传更有利于保护心脏的功能，故一般情况下，DDD起搏器将起搏A-V问期程控得比自身P-R间期长，以保证激动尽量经自身房室结下传。研究发现，当P-R间期在120-180ms时心功能较好，故选择合适的AV延迟以及与自主神经（心率）相适应的A-V间期对双腔起搏至关重要。而且，与频率相适应的房室顺序传导，可以产生较好的血流动力学影响。     

心房起搏脉冲传导延迟患者AV问期的优化

目的探讨心房起搏至心房除极波时间延迟患者设置起搏的房室间期（PAV）的方法及远期心房起搏的有效性。方法分析2005年1月至2012年12月我院起搏器植入后发生心房起搏至心房除极波时间延迟≥lOOms的患者10例,病窦综合征（SSS）患者的房室间期设置为最大值,并最大限度开启房室问期滞后功能;对房室传导阻滞（AVB）患者设置PAV的值为：140～180ms＋心房起搏至心房除极波延迟时间,不开启AV滞后。结果经1个月至7年随访,5例SSS患者心室起搏比例〈10％,3例SSS患者心室起搏比例30％。50％,Holter显示心室起搏时为假性融合波,l例SSS患者及1例AVB患者为心室起搏心律,起搏比例〉99％,保证了房室问期的生理性。10例患者心房起搏阈值均〈1．5／0．4ms,未发生心房起搏阈值增高及失夺获。结论心房起搏至心房除极波时间延迟患者远期的心房起搏夺获是安全的;设置起搏器PAV间期要将心房起搏至心房除极波延迟时间计算其中,程控随访中应注意观察程控仪中监护图的心房波,房室传导阻滞患者可延长房室间期后观察心房波,部分患者因监护导联显示不清,需要通过12导联心电图进行观察,避免心房起搏至心房除极波延迟病例被遗漏．导致增加心室起搏及非生理性的房室间期。     

如何分析起搏器对室性早搏的反应

起搏器对室性早搏(简称室早)的定义为:被感知的心室事件与其前面的心室事件之间没有起搏或感知的心房事件。若起搏器感知到室早后心室后心房不应期(PVARP)不变,当房室结存在逆传功能时,逆传的P波有可能被起搏器感知而诱发起搏器介导的心动过速(PMT);若起搏器感知室早后起搏器自动延长PVARP,则有可能避免逆传P波被起搏器感知而诱发PMT。当室早的联律间期较长时,根据起搏器对室早的定义可知如室早位于起搏或感知的心房事件后将不会被起搏器定义为室早,而是被定义为经房室结下传的室上性激动,因此室早后的PVARP不会延长,这可使室早后经房室结逆传的P波被起搏器感知并触发心室起搏,甚至诱发PMT。起搏器生产厂家不同、型号不同、程控参数不同,对室早的反应可能也不同,分析起搏器对室早的反应需结合起搏器生产厂家、型号、程控参数、室早的联律间期等。     

经食道心房调搏诊断阵发性室上性心动过速的临床价值

目的探讨经食管心房调搏（TEAP）检查诊断阵发性室上性心动过速（PSVT）的临床价值。方法纳入临床诊断为PSVT患者74例,通过TEAP检查予以诱发以及终止PSVT,记录并分析PSVT心电图参数,包括诱发窗口、诱发频率、房室结不应期等,并与心腔内电生理（IEPS）检查结果进行比较。结果 TEAP检查的诱发窗口、诱发频率、房室结不应期与IEPS检查结果相关性良好（P＜0.05）, TEAP检查诊断PSVT的符合率达83.8%（62/74）,诱发的PSVT均能通过TEAP予以终止。结论 TEAP检查可有效评估PSVT的电生理特性,准确率高,值得临床广泛应用。     

左侧隐匿性房室旁道频率依赖性室房传导及心动过速特点

报道4例经导管射频消融证实的左侧隐匿性房室旁道（LCAP）空房（VA）传导及心动过速特点。4例室上性心动过速患者均接受了心内电生理检查（EPS）：①4例均于右空心尖（RVA），其中1例于多个部位（右室流出道、左室及旁道在室端)行分级递增起搏（S1S1），观察VA传导情况；②于高位右房行S1S1及程控期前（S1S2）刺激诱发心动过速，观察有无房室给双径路。结果显示,RVA起搏经LCAP1：1VA传导窗口为40～120m，上限为400～350ms，下限为360～270ms；若RVA起搏周长在窗口之外，VA完全分离或偶经LCAP逆传。其中1例多部位起搏结果与RVA起搏结果相似。4例均对诱发心动过速，周长为330～360ms，但不能持续，A波逆传受阻于旁道而自动终止。提示LCAP若受到3相、4相阻滞或旁道之外如其他旁道竞争传导、房室结逆传干扰等因素的影响，可发生频率依赖性VA传导，EPS诱发的心动过速可能不持续。因此，认识这些特点，有助于LCAP的诊断，避免误诊、漏诊。     

经食管心房调搏对阵发性室上速诱发与终止的临床价值

目的：研究经食管心房调搏对阵发性室上性心动过速（PSVT）诱发与终止的价值。方法：选择237例有心动过速发作史的患者进行食管心房调搏检查,如果诱发出阵发性室上速,进行12导联心电图记录后,予以短阵快速刺激或程序期前刺激终止之。另外对54例急诊PSVT患者直接予以短阵快速刺激或程序期前刺激终止之。结果：在被检的237例患者中诱发出PSVT148例,占62．4％（其中房室结双径87例,房室折返为61例）。对其202例PSVT患者均采用短阵快速刺激或程序期前刺激。PSVT即刻终止的有196例,转复成功率97％。结论：经食管心房调搏可作为PSVT筛选检查及终止的首选方法。     

名词解释

起搏器介入性心动过速起搏器介入性心动过速(pacemaker mediatedtachycardia ,PMT)为由起搏器诱发和维持的心动过速,多发生于双心腔起搏器患者。最常见的是折返性或循环性心动过速,折返环的一部分是由起搏器组成的。常由室性早搏逆传入心房所诱发,亦可由房早所致,或由心房过度感知引起。发生该形式的PMT尚需存在室房逆传,同时室房逆传时间超过心室起搏后心房不应期。心电图特点是起搏的QRS波后有逆行P波,P R间期等于所程控的房室延迟,心动过速频率等于或接近起搏器最大跟随频率(曹静　杨俊娟)折返　　折返(reentry)指心脏的一次激动经…     

Phase 3 and phase 4 block in the accessory pathway

Pacemaker activity at a site proximal to the area of a conduction disturbance has been postulated as depressing conduction in late diastole (phase 4 block). To elucidate the correlation between the site of phase 4 depolarization and that of a conduction disturbance, we examined seven patients with intermittent Wolff-Parkinson-White syndrome who had tachycardia (phase 3) and bradycardia (phase 4) dependent on block in the accessory pathway. In each patient, antegrade conduction over the accessory pathway was absent at the sinus rate. During premature atrial stimulation a "window" of accessory pathway conduction was identified in each patient. The outer limit of the window ranged from 420 to 670 ms; the inner limit, from 330 to 620 ms. The duration of the window ranged from 20 to 160 ms. Four patients with orthodromic atrioventricular reentrant tachycardia exhibited preserved retrograde accessory pathway conduction. In one patient with unsustained orthodromic atrioventricular reentrant tachycardia, retrograde accessory pathway conduction also exhibited phase 3 and phase 4 blocks. The remaining two patients had no retrograde accessory pathway conduction. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation eliminated a phase 4 block in antegrade accessory pathway conduction. These results suggest that 1) an antegrade phase 4 block may have phase 4 depolarization in the accessory pathway and block at the ventricular insertion of the accessory pathway; 2) a retrograde phase 4 block may have a conduction disturbance at the atrial insertion of the accessory pathway; and 3) a complete retrograde block may occur at the atrial insertion of the accessory pathway.     

Rate-dependent accessory pathway conduction due to phase 3 and phase 4 block. Antegrade and retrograde conduction properties.

Six patients who had antegrade phase 3 and phase 4 block in the accessory pathway were examined. In each patient, antegrade conduction over the accessory pathway was absent both at the sinus rate and at slower heart rates. During premature atrial stimulation a "window" of accessory pathway conduction was identified in all patients. The outer limits of the window ranged from 480 ms to 670 ms. The inner limits ranged from 410 ms to 620 ms. The durations of the window ranged from 20 ms to 160 ms. Three patients with orthodromic atrioventricular reentrant tachycardia showed preserved retrograde accessory pathway conduction. The remaining three patients had impaired retrograde accessory pathway conduction. One of the patients showed retrograde phase 4 block in the accessory pathway. In two patients, retrograde concealed conduction in the accessory pathway induced by ventricular stimulation prolonged the outer limit of the window in the antegrade accessory pathway conduction. These findings suggest that the mechanism of antegrade phase 3 and phase 4 block in the accessory pathway may be spontaneous diastolic depolarization in the accessory pathway and conduction disturbance at the ventricular and/or atrial insertion of the accessory pathway.     

房室结双径路合并房室旁路的折返性心动过速及射频消融治疗

目的本研究旨在探讨房室结双径路（ＤＡＶＮＰ）合并房室旁路（ＡＰ）的电生理特征和射频消融要求。方法对２１８例阵发性室上性心动过速（ＰＳＶＴ）进行电生理检查，观察ＰＳＶＴ的前传和逆传途径，然后对ＡＰ或房室结慢径（ＳＰ）进行消融治疗。结果２１８例ＰＳＶＴ中检出ＤＡＶＮＰ＋ＡＰ１０例，检出率为４．６％。其中ＳＰ前传、ＡＰ逆传（ＳＰ－ＡＰ折返）４例，快径（ＦＰ）前传、ＡＰ逆传（ＦＰ－ＡＰ折返）１例，ＳＰ－ＡＰ折返并ＦＰ－ＡＰ折返或ＳＰ／ＦＰ交替前传折返４例，ＳＰ前传、ＦＰ逆传（ＡＰ旁观）１例。１０例患者均作ＡＰ消融，诱发房室结折返性心动过速（ＡＶＮＲＴ）的３例加作ＳＰ消融，术后随访均无复发。结论ＤＡＶＮＰ合并ＡＰ者ＡＰ均作为逆传途径，阻断ＡＰ是消融关键；ＡＰ旁观者也应作ＡＰ消融；仅有ＡＨ跳跃延长者不必接受房室结改良；ＡＰ消融者应作ＤＡＶＮＰ电生理检查。     

AV nodal reentrant tachycardia using three different AV nodal pathways

In a patient with frequent paroxysmal supraventricular tachycardia, an electrophysiologic study was performed. Although by programmed atrial stimulation only double AV nodal pathways could be documented, three distinct forms of AV nodal reentrant tachycardia could be induced. By programmed atrial stimulation a typical AV nodal reentrant tachycardia was initiated, by programmed ventricular stimulation, an AV nodal reentrant tachycardia was induced with an antegrade conduction time of 215 ms and a retrograde conduction time of 160 ms. Furthermore, a third form of tachycardia was induced with alternating cycle length due to two different antegrade conduction times, whereas retrograde conduction time was almost identical, irrespective of the antegrade conduction time. The patient received betaxolol (20 mg day-1); during a second electrophysiologic study, the tachycardia could not be induced, and it did not occur spontaneously during a follow-up period of 14 months.     

The paradoxical adverse effect of verapamil for treating clinical paroxysmal supraventricular tachycardia

The intravenous administration of verapamil to 2 patients with paroxysmal supraventricular tachycardia (PSVT) resulted in an induction of PSVT during a programmed electrophysiological stimulation study. Each patient had a documented episode of PSVT. Baseline programmed stimulation studies revealed neither induction of PSVT nor an atrial echo; however, PSVT was induced immediately after injecting verapamil (0.15 mg/kg) intravenously in both patients. In 1 patient, the study was repeated 2 days later and similar results were obtained. The serum concentration of verapamil when PSVT was induced was about 80 ng/ml in both cases. Clinicians using verapamil should note that this antiarrhythmic drug may aggravate PSVT, depending on critical changes in AV nodal conduction and refractoriness.     

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.     

Atrial fibrillation in patients with an accessory pathway: importance of the conduction properties of the accessory pathway

To investigate how the electrophysiologic properties of the accessory pathway affect the occurrence of atrial fibrillation in the Wolff-Parkinson-White syndrome, programmed stimulation data of 57 patients with overt pre-excitation and 33 patients with a concealed accessory pathway with documented circus movement tachycardia were reviewed. Atrial fibrillation had occurred spontaneously in 31 (54%) of the 57 patients with the Wolff-Parkinson-White syndrome and in 1 (3%) of the 33 with a concealed accessory pathway (p less than 0.001). Sustained atrial fibrillation was induced in 23 of 31 patients with the Wolff-Parkinson-White syndrome and spontaneous atrial fibrillation (Group A), in 7 of 26 patients with the Wolff-Parkinson-White syndrome without spontaneous atrial fibrillation (Group B) and in 5 of 33 patients with a concealed accessory pathway (Group C). The anterograde effective refractory period of the accessory pathway was shorter in Group A than in Group B (252 versus 297 ms, p less than 0.001). There were no differences among groups in PA interval, right to left atrium conduction time, cycle length of tachycardia and atrial and retrograde accessory pathway effective refractory period. Atrial fibrillation is more frequent in patients with the Wolff-Parkinson-White syndrome than in those with a concealed accessory pathway. Patients with overt pre-excitation and atrial fibrillation have a shorter anterograde accessory pathway refractory period. It seems therefore that the anterograde rather than the retrograde conduction properties of the accessory pathway are the critical determinants of atrial fibrillation in the Wolff-Parkinson-White syndrome.     

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.     

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)     

Effects of intravenous flecainide acetate in patients with concealed atrioventricular pathway with supraventricular tachycardia]

The acute efficacy and electrophysiologic effects of intravenous flecainide acetate (1.5 mg/kg) on 10 patients with concealed AV pathway with supraventricular tachycardia (SVT) by esophageal programmed electrical stimulation were evaluated. The results showed that: (1) the drug has marked depressing effects on the retrograde accessory pathway conduction and minimal effects on the antegrade AV nodal conduction; (2) there were no effects on the patients with normal sinus node function; (3) the drug has little side effects during the studies; (4) flecainide terminated induced SVT in 9 of 10 cases (90%), and prevented induced SVT in 7 of 9 cases (78%).