律平对房室旁道的电生理作用

应用经食道心房调搏方法观察心律平对房室旁道的电生理作用。结果显示：（１）心律平可明显延长房室旁道前向传导的有效不应期（ＥＲＰ）。（２）对心房和房室传导系统ＥＲＰ亦有延长作用。（３）可降低经旁道１：１下传心室率,并可延长经旁道逆传时间和心动过速周期长度。（４）４／１２例病人持续性房室折返惺 心动过速终止发作,并且证实均止于旁道的逆传途径。以上资料表明心律平延长房室旁道ＥＲＰ的作用,是其治疗预激登工快     

心脏电生理检查在心律失常诊断和治疗中的应用(下)

旁道电生理检查 1.旁道前向传导性质,心房调搏基本不延长旁道前向传导时间。最大前向传导能力取决于旁道有效不应期。通常200次心房起搏(300ms)保持1∶1房室传导能力,房室传导时间0.08～0.16秒。知心房肌不应期短于旁道不应     

预激症候群伴房扑、房颤者为何不宜用异搏定?

<正> 异搏定的主要作用是阻止窦房结、房室结等慢反应细胞的Ca~(2+)内流.降低自律性.延长房室结不应期,有利于消除经房室结折返导致的室上性心动过速.但在预激症候群伴房扑、房颤患者,异搏定可引起心室率加快.其机理为:①异搏定可直接缩短预激旁道(心房与心室间的异常传导途径)的不应期.加速冲动经旁道由心房至心室的前向传导.②抑制房室结的逆向传导.使经由旁道逆向通过房室结的冲动次数减少,间接增加旁道的前向传导.③异     

快频率依赖性旁道所致室上速的射频消融技巧初探

目的：总结具有快频率依赖性房室旁道心动过速电生理检查及射频消融方法技巧。方法：12例患者中,男7例,女5例,年龄23～78岁,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,采用右室心尖部S1S1和S1S2起搏,分析室房传导情况、心动过速特点、旁道位置确定及射频消融治疗。结果：所有患者均证实存在快频率依赖性旁道的室房逆传,并诱发了房室折返性心动过速。旁道位于左前游离壁4例（33.3%）,左侧壁2例（16.7%）,左后壁旁道1例（8.3%）,右侧10点左右3例（25%）,7点左右2例（16.7%）。7例（58.3%）患者旁道当S1S1（250～360ms）刺激周长逐渐缩短至一定周期时具有1∶1室房传导功能,5（41.7%）患者有间隙性旁道逆传阻滞,均呈2∶1室房逆传阻滞,左侧旁道患者在S1S2刺激递减到一定程度时可见偏心传导现象。在右室快频率S1S1或在偏心传导的S1S2起搏下标测靶点,所有患者均消融成功。结论：旁道的快频率依赖性传导为一种少见电生理现象,电生理检查过程中应该特别注意室房逆传阻滞以及S1S2刺激递减到一定程度时的偏心传导现象。于快频率或偏心传导时的S1S2心室刺激下标测消融靶点,消融均可获得成功。     

静脉注射慢心律治疗室上性心动过速的电生理效应

对26例经食道调搏诱发出的阵发性室上性心动过速（PSVT）患者予静脉注射慢心律转复，并在用药前后测定心脏传导的电生理参数，以了解慢心律治疗PSVT的电生理效应。结果乃冽PSVT患者静注慢心律200mg之后，其中23例在4．5±3分钟之内转为窦性心律，转复率达88．4％。用药前后，窦房结恢复时间（SNRT），校正窦房结恢复时间（CSNBT），房室顺传文氏点，房室结有效不应期（ERPAVN），房室结双径路快径路功能不应期（FRPFP）及有效不应期（ERPFP），慢径路功能不应期（FRPSP）及有效不应期（ERPSP）均无明显改变（P＞0．05）。但用药后，窦房结传导时间（SNCT延长（P＜0．05），慢径路传导时间（TSP）缩短（P＜0．05）。提示慢心律静注治疗PSVT安全有效，用药后缩短TSP为其终止房室结内折返性心动过速（AVNR）的主要机制。由于静注慢心律对窦房结功能的抑制作用，老年人、窦房结功能低下者需慎用。     

射频消融中的旁道特殊逆传阻滞

在对预激综合征(WPW)旁道的射频消融术中,大部分WPW旁道电生理特征符合一定规律,使旁道的定位及消融术得以顺利进行,但旁道存在的一些特殊的传导现象会影响到电生理检查的诊断及消融治疗。我们在对102例房室旁道患者行射频消融术时,腔内电生理检查发现4例旁道患者存在着与正常电生理检查时不同的其它形式的旁道逆传阻滞。本文就其发生机制及临床意义作初步探讨。     

左侧慢旁道参与的房室折返性心动过速的导管射频消融治疗

目的探讨左侧慢旁道参与的心动过速的电生理特点及射频消融治疗的安全性有效性。方法对3例左侧慢旁道参与的房室折返性心动过速的导管射频消融（RFCA）治疗。结果 3例患者的室上速均为窄QRS波群,RP间期〉PR间期。电生理特点为：心动过速的最短RP间期〉140ms;旁道的逆传具有递减性传导的性质。结论 RFCA治疗慢旁道参与的心动过速有与快纤维房室旁道不同的电生理特点,射频消融治疗是安全、有效的。     

预激征合并快速心律失常的临床研究进展

<正> 预激征易合并两种类型快速心律失常。常见的一种是房室反复性心动过速(AVRT),另一种是房颤。近年来对预激征合并快速心律失常的临床研究有了明显的进展。现将有关资料综述如下。一、预激征合并AVRT的分类及诊断预激征存在有房室结通道以外的旁道。两者具有不同的电生理特性。旁道的特点是:传导速度快而不应期长;其传导为“全或无”,即随着心率的加快冲动或下传或受阻;其不应期和心房、心室肌相似,随着心率加快而缩短。房室结通道的特点为:传导速度慢而不应期短;随着心率加快而不应期延长。这就意味着旁道与房室结通道不同,     

心房纤颤的心内射频治疗

报道１２例快速心房纤颤患者经起源消融术阻断旁道，希氏束或改良室结，使房颤得到纠治或房颤的心室率得到控制，提示某些房颤的发生与旁道有关，阻断旁道可消除房颤，而改良房室结可使房室结前传文氏和２：１阻滞点前移，有效不应期延长，而达到控制心室率的目的。     

预激综合征患者发生阵发性心房颤动机制的探讨

目的分析预激综合征（WPW）患者旁道的电生理特性以及消融旁道后计算P波离散度,探讨阵发性房颤（PAF）发生机制。方法WPW合并旁道介导的阵发性心动过速患者127例。消融前超声心动图测量左心房内径,左心室射血分数;电生理检查测定旁道的前传和逆传不应期。消融成功术后24h描记12导联心电图测量P波最大时限、P波最小时限,计算P波离散度。根据既往有无PAF发作分为2组分析。结果有PAF发作组23例,无PAF发作组104例。2组在年龄、左心房内径、左心室射血分数均无显著差异,具有可比性。射频消融术中旁道存在逆传者在两组间无显著差别。消融前有PAF发作组旁道前传和逆传不应期较无发作组短。消融术后心电图P波最大时限和P波离散度有PAF发作组显著长于无发作组。P波离散度的增加提示窦性激动在心房传导的非均质和不连续性。结论旁道有效不应期缩短和窦性激动在心房内的非均质传导在WPW患者房颤发生中起重要作用。     

Electrophysiologic effects and efficacy of cibenzoline in patients with supraventricular tachycardia.

Electrophysiologic effects of intravenous (i.v.) cibenzoline were evaluated in 18 patients with accessory pathways or dual atrioventricular (AV) nodal pathways (12 men and 6 women with a mean age of 44 +/- 18 years). Twelve patients had accessory AV pathways, including 6 patients with a manifest accessory pathway. Six patients had AV nodal reentrant tachycardia (AVNRT). Electrophysiologic studies were performed before and after cibenzoline (1.4 mg/kg i.v.) infusion for 5 min. Sinus cycle length did not change significantly after cibenzoline administration. Cibenzoline increased both the AH (85 +/- 20 vs. 91 +/- 21 ms, p less than 0.05) and HV intervals (41 +/- 10 ms vs. 53 +/- 11 ms, p less than 0.001). Neither the atrial nor ventricular effective refractory period (ERP) was altered by cibenzoline. Complete block in the accessory pathway occurred antegradely in 4 patients and retrogradely in 1 patient. Cibenzoline prevented induction of AV reentrant tachycardia (AVRT) in 3 of 8 patients with sustained orthodromic AVRT by abolishing retrograde accessory pathway conduction or prolonging the retrograde accessory pathway ERP. Of 5 patients who continued to have inducible AVRT before and after cibenzoline administration, the tachycardia cycle length was increased in 3, mainly due to the increase in retrograde accessory pathway conduction time. Cibenzoline prevented induction of sustained AVNRT in 4 of 5 patients by prolonging the minimum pacing cycle length, maintaining 1:1 ventriculoatrial (VA) conduction through the retrograde fast AVN pathway or shortening the antegrade fast AVN pathway ERP equal to the slow AVN pathway. In one patient who had an uncommon type of AVNRT, sustained tachycardia was induced by cibenzoline.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of a novel class III antiarrhythmic agent, E-4031, on reentrant tachycardias in rabbit right atrium.

Effects of a new antiarrhythmic agent, E-4031, on reentrant types of tachycardias in rabbit right atrial preparations were studied using the microelectrode technique. E-4031 at concentrations of 0.1 and 1.0 microM prolonged the refractory period (RP) of the atrium and atrioventricular node (AVN) without affecting the intraatrial conduction time. In 13 of 17 preparations, premature stimulation repeatedly induced tachycardias lasting more than 10 beats. Twelve of 13 preparations exhibited a smooth AV conduction curve and showed activation patterns compatible with intraatrial reentry (IAR) during tachycardias, whereas the remaining preparation started tachycardia with a jump on the AV conduction curve, indicating dual AVN reentrant tachycardia (AVNRT). Application of 0.1 and 1.0 microM E-4031 completely prevented the initiation of both types of tachycardias by producing intraatrial conduction block due to prolonged effective refractory period (ERP) of the atrium. The results indicated that E-4031 exhibiting pure class III antiarrhythmic properties is effective for prevention of reentrant type of supraventricular tachycardias (SVTs).     

婴儿阵发性室上性心动过速38例药物治疗及临床分析

目的:探讨婴儿阵发性室上性心动过速(PSVT)的心电图分型和药物治疗情况,总结药物治疗经验。方法:分析38例婴儿PSVT入院后的临床资料和药物治疗情况。结果:房室折返性心动过速(AVRT)17例(44.7%),房室结折返性心动过速(AVNRT)12例(31.6%),自律性房性心动过速2例(5.2%),未分型7例(18.4%),合并器质性心脏病11例(28.9%)。AVRT患儿用普罗帕酮转复率为100%,ATP为75.0%,地高辛为37.5%;AVNRT用普罗帕酮转复率为90.0%,ATP为83.3%,地高辛为40.0%,胺碘酮为66.7%。结论:正确的心电图分型对婴儿PSVT治疗药物的选择有指导意义,不同药物对不同类型的PSVT的治疗效果不同。     

Effects of verapamil on accessory pathway properties and induction of circus movement tachycardia in patients with the Wolf-Parkinson-White syndrome

The electrophysiological effects of 0.2 mg/kg of intravenously administered verapamil (mean plasma level, 51.3 ng/ml) were evaluated using intracardiac recordings and electrical stimulation in 10 patients with the concealed or manifest Wolff-Parkinson-White syndrome. Verapamil produced a minimal effect on both the antegrade and retrograde effective refractory periods of the accessory pathway and the retrograde conduction time over the accessory pathway, but significantly lengthened the intranodal conduction time as well as the effective and functional refractory periods of the atrioventricular (AV) node. Reproducible sustained circus movement tachycardia was initiated in 8 patients before administration of verapamil and in 2 after verapamil. The sustained tachycardia could no longer be initiated in 6 patients because of an increase in AV nodal refractoriness. In 4 patients, atrial echoes were induced at longer premature beat intervals due to a greater AV conduction delay of the atrial impulse. The cycle length of the tachycardia was lengthened in 2 patients, reflecting an increase in the A-H interval after verapamil administration. In conclusion, these results show that verapamil has no apparent effect on either antegrade or retrograde accessory pathway properties and suggest that verapamil does indeed prevent sustained circus movement tachycardia by increasing the AV nodal refractoriness in some patients with the Wolff-Parkinson-White syndrome.     

索他洛尔在房室旁道射频消融术中的应用

目的探讨索他洛尔在房室旁道射频消融(RFCA)术中的应用。方法18例旁道患者在常规电生理检查后顿服索他洛尔160mg,分别于服药后30、60、90、120和150min重复测量各项电生理参数。结果服药前后心房(A)、心室(V)、房室结(AVN)、旁道前传(APa)、旁道逆传(APr)有效不应期(ERP)分别为(211±24)msvs(243±36)ms、(205±11)msvs(242±28)ms、(269±48)msvs(343±97)ms、(263±45)msvs(400±160)ms、(232±37)msvs(298±50)ms(P<0.05)。无1例旁道阻断。窦房结恢复时间(SNRT)、窦性周长(SCL)分别为(1165±209)msvs(1456±371)ms、(724±116)msvs(996±178)ms(P<0.05)。3例房颤服药后不再诱发,2例心内电刺激难以终止的房室折返性心动过速(AVRT)服药后自行终止于房室结前传。18例患者均消融成功,随访7～18个月,无1例复发。结论索他洛尔显著延长心脏ERP,但不影响旁道的RFCA,能够预防或抑制RFCA术中导管和电刺激诱发的房颤,方便了手术操作。     

Electrophysiologic effects and antiarrhythmic efficacy of recainam in patients with supraventricular tachycardia.

Recainam is a new antiarrhythmic agent with class Ic properties. To evaluate its electrophysiologic effects and antiarrhythmic efficacy in patients with recurrent supraventricular tachycardia (SVT), programmed electrical stimulation was performed in 10 patients before and after intravenous recainam (loading dose 0.8 mg/kg, infusion 1 mg/kg/h), and in four patients on oral recainam 1,200 mg/day. Five patients had atrioventricular (AV) node reentrant tachycardia; five had AV-reciprocating tachycardia. There were no significant changes in electrocardiographic and intracardiac intervals after either intravenous or oral recainam. After intravenous recainam, the ventricular effective refractory period (ERP) shortened (231 +/- 14-219 +/- 9 ms, p less than 0.05). The antegrade ERP of all three bidirectional accessory pathway markedly prolonged, but the effect on retrograde accessory pathway and AV node ERPs was unremarkable. SVT induction was prevented in three of 10 patients and SVT cycle length increased modestly in seven (357 +/- 44-374 +/- 42 ms, p = 0.07). On oral recainam, an increase in the frequency of spontaneous SVT occurred in two patients. At the doses given, recainam caused less electrophysiologic change than expected, had modest antiarrhythmic efficacy, and might have significant arrhythmogenic potential.     

Effect of tiapamil in the Wolff-Parkinson-White syndrome

The effect of tiapamil was studied in 9 patients with the Wolff-Parkinson-White syndrome using programmed stimulation of the heart. Before the drug, sustained orthodromic tachycardias could be initiated in 7 patients and antidromic tachycardia in 2 by premature atrial and/or ventricular stimulation. An intravenous bolus of tiapamil, 2 mg/kg, terminated the tachycardia in 7 out of 8 cases by a block in the atrioventricular (AV) node. Tiapamil lengthened the effective refractory period of the AV node in the only patient in whom it could be measured and the atrial effective refractory period in 1 out of 9 cases, but the drug had no influence on antegrade or retrograde refractory periods of the accessory pathway or on that of the ventricle. The AV nodal conduction time (A-H interval) was prolonged. Following tiapamil, it was not possible to initiate the tachycardia in 4 cases, in 2 patients the tachycardia zone widened, and in 3 it was unaltered. In the latter cases, the cycle length of the tachycardia was increased. Tiapamil appears to be useful for the termination of tachycardia and also for its prevention in some cases. In others, it may facilitate the inhibition of tachycardia. The delayed AV nodal conduction during sinus rhythm augments the area of ventricular preexcitation, which may facilitate the electrocardiographic localization of the accessory pathway.     

Electrophysiological effects of a new antiarrhythmic agent, nicainoprol, in humans

The electrophysiological effects of nicainoprol, a new antiarrhythmic drug, were evaluated in a heterogeneous group of 23 patients aged 59 +/- 15 (mean +/- standard deviation) years. Nicainoprol was administered intravenously as a bolus of 1-2 mg/kg followed by continuous infusion at two dose levels. Electrophysiologic study was performed before and during the infusion at a steady-state drug level on each dose. The sinus node recovery time was unaltered in patients with normal sinus node function and was markedly prolonged in three of six patients with sinus node dysfunction. The intranodal conduction time (p less than 0.01) and the infranodal conduction time (p less than 0.001) increased, and the QRS duration (p less than 0.05) lengthened significantly even during 1 mg/kg/h. During 2 mg/kg/h, these times were further prolonged and, in addition, the intra-atrial conduction time (p less than 0.05), atrioventricular nodal effective and functional refractory periods (p less than 0.01), as well as the Wenckebach cycle length (p less than 0.001) also increased significantly. Similar depressant effects on the retrograde ventriculoatrial conduction system were also produced by nicainoprol. Retrograde His-atrioventricular nodal conduction was blocked in six of eight patients with this condition and was prolonged in the remaining two. Sustained supraventricular tachycardia was induced in seven patients, five of whom received nicainoprol during the tachycardia. The termination of supraventricular tachycardia was exclusively due to ventriculoatrial block in all five subjects, three with orthodromic circus movement tachycardia and two with atrioventricular nodal reentrant tachycardia of the slow-fast type. The reinducibility of supraventricular tachycardia could be prevented in five of seven patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

普罗帕酮致严重心血管不良反应8例

本文报道普罗帕酮(propafenone)致严重心血管不良反应8例。静脉注射普罗帕酮7例中,显著血压下降者6例;窦房结功能抑制3例;急性左心衰竭2例;心房扑动患者静脉给药后,心房扑动变为1:1传导,心室率显著加快1例;另1例心房扑动患者,口服普罗帕酮600mg/d,9d后发生完全性房室传导阻滞,呈缓慢室性自搏性心律伴显著血压下降。作者推荐先用最低有效量,逐渐加量,特别对左室功能受损,窦房结功能不全和有传导障碍者,尤须谨慎。