食管心房调搏在室上速诊断中价值新探讨

目的：评价食管心房调搏对室上性心动过速诊断的准确性。方法：将111例室上速患者心内和食管电生理检查结果进行比较。结果：111例室上性心动过速患者中，经食管心房调搏检查，诊断为房室结内折返性心动过速（AVNRT）41例，准确率91％；诊断为房室折返性心动过速（AVRT）53例，准确率92％；诊断为房性心动过速（AT包括房内折返陛心动过速和房性自律性心动过速）6例，准确率100％；诊断为窦房结折返性心动过速（SART）1例，准确率100％。根据PE-PV1时距判定房速激动起源点以及左右房室旁道位置与心内电生理检查结果基本一致。结论：食管心房调搏在室上速诊断中具有很高的价值。     

食管电生理诊断阵发性室上性心动过速

目的探讨食管电生理诊断阵发性室上性心动过速(paroxysmal supraventricular tachycardia,PSVT)及分型的准确性。方法收集经食管电生理和心内电生理检查并行射频消融治疗的PSVT42例,将两种电生理对PSVT的诊断及分型进行比较,用X2检验,以P<0.05为差异有统计学意义。结果两种电生理检查诊断房室结双径路、慢快型房室结折返性心动过速、常见的顺向型房室折返性心动过速差异无显著性,食管电生理对房室旁路的粗略定位准确性较高,但对快慢型房室结折返性心动过速、慢房室旁路参予的房室折返性心动过速与房性心动过速不易辨别。结论食管电生理诊断常见类型的PSVT与心内电生理有相似的价值,且具有无创、简便、费用低等优点;但对不常见或复杂的PSVT不易辨别。     

食管心房调搏检查对窄QRS波群心动过速的诊断意义

目的 探讨食管电生理检查对窄QRS波群心动过速诊断的临床意义。方法 比较98例窄QRS波群心动过速食管和心内电生理检查的结果。结果 98例窄QRS波群心动过速97例分型诊断一致：房室折返性心动过速52例，房室结内折返性心动过速32例，心房内折返性心动过速和心房扑动各5例，房性自律性心动过速、窦房折返性心动过速和室性心动过速各1例。6例房性心动过速与54例房室折返性心动过速起源两种检查结果完全一致。结论 食管心房调搏对窄QRS波群心动过速的分型诊断和初步定位诊断具有很高的准确性，故可作为必要检查，有助筛选射频导管消融病例。     

食管电生理诊断室上性心动过速及其分型的意义

目的探讨食管电生理对室上性心动过速(SVT)诊断及分型的准确性。方法收集近两年经射频消融治疗的SVT病例,选择其中食管电生理和心内电生理资料完整的41例,将两种电生理检查对SVT诊断及分型比较,进行χ2检验,以P<0.05为差异有统计学意义。结果两种电生理检查诊断房室结双径路(DAVNP)、慢快型房室结折返性心动过速(AVNRT)、常见的顺向型房室折返性心动过速(AVRT)差异无统计学意义;食管电生理对房室旁路(AP)的粗略定位准确性较高,但对快慢型AVNRT、慢AP参于的AVRT与房性心动过速不易辨别。结论食管电生理虽不易辨别少见型SVT,但诊断常见型SVT及分型准确性方面与心内电生理有相似的价值,且具有无创、简便、费用低等优点。     

房室双旁道的食管心脏电生理特征

目的：探讨房室双旁道食管心脏电生理检查的特征性改变。方法：对14例经射频导管消融术证实的房室双旁道的食管心脏电生理检查作回顾性分析。结果：10例房室双旁道的电生理特征为：（1）心房起搏时显示两种不同的预激图形和／或特殊类型室性融合波群，经食管心房起搏有利于显现左侧旁道。（2）诱发出两种逆向型房室折返性心动过速，由两条旁道形成折返环路。（3）顺向型房室折返性心动过速时，出现两种不同的R－P^-间期和P^-波或房性融合波。（4）排除房室结双径路后，逆向型房室折返性心过速的频率快于顺向型房室折返性心动过速。（5）预激旁道的部位与顺向型房室折返性心动过速时P^-波提示的部位不同。（6）双旁道隐匿性传导是造成其中一条旁道丧失传导功能的重要因素之一。另4例未能表现出上述电生理特征，其中右侧隐性旁道合并左侧隐匿性旁道1例，右侧隐匿性双旁道1例，左侧隐匿性双旁道2例。结论：食管心脏电生理检查能够确诊大部分的房室双旁道，采用多导联同步记录及在房室折返性心动过速时仔细分析电生理表现有助于揭示房室双旁道。     

房内折返性心动过速并发房室结双径路的食管电生理分析

近年来 ,心脏电生理学研究证明 ,室上性心动过速(SVT)可以由折返激动及心肌异位自律性增强所引起。房内折返性心动过速 (IART)约占 5 %左右 ,而其并发房室结双径路 (DAVNP)或房室结内折返性心动过速 (AVNRT)者更少。现就我院在经食管电生理检查中 ,发现 IART并发 DAVNP者进行临床电生理分析。1　临床资料和方法1.1　临床资料　经食管电生理检查 ,查出 2 19例室上性心动过速 ,其中发现持续性 IART并发 DAVNP者 8例 (占SVT 3.7% )。 8例患者中 ,男 6例 ,女 2例 ,平均年龄 45 .3岁 ;病史 1年～ 2 5年 ,其中 2例有晕厥史 ;临床…     

无创性心电生理检查诊断室上性心动过速

近年通过临床电生理的研究,对阵发性室上性心动过速(简称室上速)的认识有了很大进展。目前知道室上速主要有下列5种类型,即房室结折返性心动过速(AVNRT),房室折返性心动过渡(AVRT),窦房折返性心动过速(SART),心房折返性心动过速(IART),心房自律性心动过速(AAT)。前4种其发病机制均为折返激动,而AAT则为异位节律点自律性增高所致。国外一般认为AVNRT是最常见的类型,其次为     

食道心房调搏对窄QRS波室上性心动过速机制研究

目的：了解食道心房调搏（TEAP）对窄QRS波室上性心动过速机制的鉴别。方法：采用无创性TEAP技术,对145例有心动过速史但无器质性心脏病的患者进行检查,诱发窄QRS汉心动过速。结果：检出的窄QES波折返阵性发性室上性心动过速中,房室折返性心;动过速及房室结内折返性心动过速占约大多数,房性折返性心动过速极少。结论：TEAP是鉴别窄QRS波PSVT机制的一种安全,有效的方法。     

差异性传导对房室及房室结折返性心动过速心内电图的影响

目的 分析差异性传导对室上性心动过速心内电图产生影响的机制,探讨解决问题的方法。方法 选择室上性心动过速病人357例,其中房室折返性心动过速出现差异性传导26/187例,房室结折返性心动过速出现差异性传导6/170例,观察出现差异性传导时心内电图的影响。结果 房室结折返性心动过速出现差异性传导时,心动过速的频率和心内电图无改变。右侧旁道介导的房室折返性心动过速出现右束支差传导心电图类似于慢一快型房室结折返性心动过速,同时伴心率下降。出现左束支差传时,心电图类似于慢一慢型房室结折返性心运过速或房速,心率不变,左侧旁道介导的房室折返性心动过速出现差传时,心内激动顺序不变,出现左束支差传时心率下降,右束支差传时心率不变。结果 差异性传导对房室结折返性心动过速及左侧旁道介导的房室折返性心动过速心内电图无影响。但对右侧旁道介导的房室折返性心动过速心内电图有较大的影响,旁道的电生理特性结合电生理检查有助于鉴别诊断。     

心动过速RR间期交替的发生机制及导管射频消融治疗

目的　分析QRS心动过速伴RR间期长短交替的发生机制及导管射频消融情况。方法　对 6例心动过速伴RR间期长短交替患者 ,常规行动态心电图及食管电生理检查。心内电生理检查提示存在房室旁路或房性心动过速伴房室结双径路 ,先进行旁路或房性心动过速的消融 ,消融成功后再进行心内电生理检查 (包括应用异丙肾上腺素进行心动过速诱发 ) ,如不能诱发心动过速则终止手术。若提示存在房室结多径路 ,则进行慢路径改良术。结果　食管电生理检查提示 :4例患者存在房室旁路伴房室结双径路 ;2例患者存在房室结三径路。心内电生理检查及消融结果显示 :3例患者为房室旁路伴房室折返性心动过速 ,成功消融后不能诱发房室结折返性心动过速 ;1例患者同时存在房室及房室结折返性心动过速 ,成功消融房室旁路后再改良慢路径 ;2例患者为房室结三径路 ,经慢径路改良后房室结传导曲线连续 ,未诱发心动过速。 6例患者无并发症发生 ,随访期间无心动过速发作。结论　室上性心动过速伴RR间期交替发生率较低 ,且均与房室结传导不连续有关。心动过速伴RR间期交替发生机制较为复杂 ,除了与房室结纵向传导的不连续有关外 ,还与其不应期密切相关。食管电生理检查与心内电生理检查相比对揭示RR间期交替的发生机制具有较高的诊断价值。     

Catheter Ablation for the Treatment of Paroxysmal Supraventricular Tachycardia

Catheter Ablation for PSVT. Radiofrequency catheter ablation has evolved into a front-line curative therapy for patients who have paroxysmal supraventricular tachycardia secondary to Wolff-Parkinson-White syndrome, AV nodal reentrant tachycardia, and atrial tachycardia. In patients with accessory pathways, cure rates exceed 90% in almost all anatomic locations. Equally high success rates are noted in patients with atriofascicular pathways and the permanent form of junctional reciprocating tachycardia. Complications secondary to catheter ablation of accessory pathways occur in 1% to 3% of patients and include cardiac perforation, tamponade, AV block, and stroke. In patients with AV nodal reentrant tachycardia, selective slow pathway ablation is curative in over 95% of patients with a very low risk of AV block. Atrial tachycardias originating in both the left and right atria can he successfully ablated in over 80% of patients. Given the overall effectiveness of this procedure, radiofrequency catheter ablation should be considered as front-line therapy in patients with recurrent or drug-refractory paroxysmal supraventricular tachycardia. Although an effective therapy, the risks and benefits of this procedure need to be assessed in all patients who are candidates for this procedure.     

Usefulness of predischarge electrophysiologic study in predicting late outcome after surgical ablation of the accessory pathway in the Wolff-Parkinson-White syndrome.

A predischarge electrophysiologic study was performed in 113 patients with the Wolff-Parkinson-White (WPW) syndrome who had undergone surgical ablation of the accessory pathway. The study was performed 5 to 20 (mean 10 +/- 3) days after surgery. There were 82 male and 31 female patients (aged 4 to 58 years, mean 36 +/- 13). Sixty-one patients (54%) had manifest, 52 (46%) had concealed and 12 (11%) had multiple accessory pathways. All but 1 patient had atrioventricular reentrant tachycardia incorporating single or multiple accessory pathways during the control electrophysiologic study. The accessory pathways were located in the left ventricular free wall in 60% of cases, right ventricular free wall in 22%, posteroseptum in 13%, and anteroseptum in 5%. The predischarge electrophysiologic study showed that the accessory pathway was capable of anterograde and retrograde conductions in 4 patients (all with manifest WPW syndrome). Four patients showed induction of supraventricular tachycardia, including 2 with atrioventricular reentrant tachycardia, and 2 with atrioventricular nodal reentrant tachycardia. Recurrence of supraventricular tachycardia was noted in 5 patients during a follow-up of 28 +/- 26 months. Of these 5 patients, 2 had inducible and 3 had no inducible supraventricular tachycardia during the predischarge electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)     

Atrial tachycardia with slow pathway conduction mimicking typical atrioventricular nodal reentrant tachycardia.

A 68-year-old woman with palpitations underwent electrophysiologic testing. During burst atrial pacing the PR interval exceeded the RR interval and induced a supraventricular tachycardia consistent with a typical AV nodal reentrant tachycardia (AVNRT). Radiofrequency ablation of the slow pathway during the tachycardia immediately produced 2 : 1 AV conduction. After slow AV nodal pathway ablation an atrial tachycardia (AT) remained inducible with the earliest atrial activation around the HB region. Radiofrequency ablation at the site of earliest atrial activation interrupted the AT without AV block. AT originating from the HB region with slow pathway conduction may mimic typical AVNRT.     

Electrophysiologic study in 42 cases of unexplained syncope

Forty two patients with unexplained syncope underwent intracardiac electrophysiologic study to identify the cause of syncope and to select appropriate therapy. Electrophysiologic abnormalities were demonstrated in 26 patients (62%): sustained ventricular tachycardia in 7 patients (27%) of the abnormal group. His-Purkinje system dysfunction in 4 (15.4%), atrioventricular nodal dysfunction in 4 (15.4%), atrioventricular nodal reentrant supraventricular tachycardia in 2 (7.7%), atrial flutter in 1 (3.8%), sinoatrial nodal dysfunction in 2 (7.7%), carotid sinus hypersensitivity in 3 (11.5%) and hypervagotonia in 3 (11.5%). The results of this study suggest that electrophysiologic study should be considered in patients with unexplained syncope. Electrophysiologic study in an effective method for approaching the diagnosis and improving management of unexplained syncope.     

快慢型房室结双径路心电图特征

目的 观察和总结快慢型房室结双径路患者临床心电图的表现及特征。方法 8例快慢型房室结双径路的诊断均经心内电生理检查证实。根据心电图、动态心电图、食管心房调搏及心内电生理检查等资料进行心电图特点的观察和总结,8例患者均进行了射频消融术的治疗。结果 8例患者心电图显示隐匿性房室结双径路的特点,同时还有以下几个特点：（1）100％伴有单次快慢型房室结折返性房早：（2）心动过速频率100－150bpm,相对较慢;（3）8例患者房室结前传曲线圆滑而无中断现象。射频消融术均获成功。结论 本文首次提出快慢型房室结双径路是一种隐匿性房室结双径路的概念,其具有较多特征性的心电图表现,注意这些特征对心电图及临床诊断有较大的助益,射频消融术是其安全有效的治疗方法。     

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。     

The mechanisms of exercise provocation of supraventricular tachycardia

Treadmill exercise tests, electrophysiologic studies, and isoproterenol infusions were performed in 14 patients with exercise provocable supraventricular tachycardia to delineate the mechanisms of exercise provocation of paroxysmal supraventricular tachycardia. Treadmill exercise tests reproducibly provoked supraventricular tachycardia in all patients. Supraventricular tachycardia similar to that provoked by exercise occurred spontaneously during isoproterenol infusions in 9 of 11 patients tested. The specific supraventricular tachycardia diagnoses of all patients were atrial reentrant tachycardia (two patients), automatic atrial tachycardia (three), atrial flutter-fibrillation (one), atypical junctional tachycardia (two), and orthodromic atrioventricular (AV) reentrant tachycardia (six) as defined by electrophysiologic studies. Various mechanisms of exercise or isoproterenol induction of supraventricular tachycardia were identified. A critical heart rate and/or appropriate sympathetic state was found to provoke all instances of reentrant or automatic atrial tachycardia and atypical junctional tachycardia. A properly timed atrial premature beat provoked five of six cases of AV reentrant tachycardia and the only case of atrial flutter-fibrillation. The remaining case of AV reentrant tachycardia was induced by a ventricular premature beat. In conclusion, the mechanisms of exercise provocation of reentrant or automatic supraventricular tachycardia are multiple and include a critical sinus rate, increased sympathetic tone, and properly timed atrial or ventricular premature beats.     

Adenosine-Sensitive Atrial Reentrant Tachycardia Originating from the Atrioventricular Nodal Transitional Area

Adenosine-Sensitive AT from AVN Area. Introduction : Atrial tachycardia shows wide variations in its electrophysiologic properties and sites of origin. We report an atrial tachycardia with ECG manifestations and electrophysiologic characteristics similar to an atypical form of AV nodal reentrant tachycardia (AVNRT).
Methods and Results : This supraventricular tachycardia was observed in 11 patients. It was initiated by atrial extrastimulation with an inverse relationship between the coupling interval of an extrastimulus and the postextrastimulus interval. Its induction was not related to a jump in the AH interval, and its perpetuation was independent of conduction block in the AV node. Ventricular pacing during tachycardia demonstrated AV dissociation without affecting the atrial cycle length. A very small dose of adenosine triphosphate (mean 3.9 ± 1.2 mg) could terminate the tachycardia. The earliest atrial activation during tachycardia was recorded at the low anteroseptal right atrium with a different intra-atrial activation sequence from that recorded during ventricular pacing, where the tachycardia was successfully ablated in 9 of 10 attempted patients. Bidirectional AV nodal conduction remained unatttched after successful ablation.
Conclusion : There may he an entity of adenosine-sensitive atrial tachycardia probably due to focal reentry within the AV node or its transitional tissues without involvement of the AV nodal pathways. This tachycardia can he ablated without disturbing AV nodal conduction from the right atrial septum.     

Sustained symptomatic sinus node reentrant tachycardia: incidence, clinical significance, electrophysiologic observations and the effects of antiarrhythmic agents

The clinical, electrocardiographic and electrophysiologic determinants and effects of antiarrhythmic agents on sustained sinus node reentrant tachycardia remain poorly defined. Of 65 consecutive men undergoing electrophysiologic studies for symptomatic paroxysmal supraventricular tachycardia over a 4 year period, 11 (16.9%), who ranged in age from 39 to 76 years, demonstrated sustained sinus node reentrant tachycardia. On the surface electrocardiogram, before electrophysiologic studies, the following diagnoses were considered in the 11 patients: sinus node reentrant tachycardia on the basis of an RP'/P'R ratio of greater than 1 and P wave configuration similar to that of sinus P waves (7 patients); atrioventricular (AV) nodal reentrant tachycardia on the basis of an RP'/P'R ratio of less than 1 (3 patients); and paroxysmal atrial tachycardia with AV block (1 patient). All 11 patients had a history of recurrent palpitation, 4 had syncope, 2 had dizzy spells and 9 had organic heart disease. Sustained sinus node reentrant tachycardia could be reproducibly induced in all 11 patients during atrial pacing or premature atrial stimulation, or both, over a wide echo zone. The tachycardia could be terminated by carotid sinus massage, atrial pacing and premature atrial stimulation. Characteristics of tachycardia included: high-low activation sequence; cycle lengths of 250 to 590 ms with wide fluctuations of 20 to 180 ms in individual patients; RP'/P'R ratio of greater than 1 in 8 (73%) of the 11 patients and a ratio of less than 1 in 3 (27%). Induction of sustained sinus node reentrant tachycardia was prevented by intravenous ouabain (0.01 mg/kg body weight) in two of two patients, by intravenous verapamil (10 mg) in two of two patients and by intravenous amiodarone (5 mg/kg body weight) in four of four patients. In contrast, intravenous propranolol (0.1 mg/kg body weight) did not affect induction of sustained sinus node reentrant tachycardia in two of two patients. It is concluded that sustained sinus node reentrant tachycardia, seen in 16.9% of the study patients with paroxysmal supraventricular tachycardia, is not as benign as previously believed; it is frequently associated with organic heart disease; it demonstrates wide variations in cycle length, unlike other forms of paroxysmal supraventricular tachycardia; it can masquerade as AV nodal reentrant tachycardia and paroxysmal atrial tachycardia with AV block on the surface electrocardiogram in 36% of patients; and it is responsive to intravenous administration of ouabain, verapamil or amiodarone.     

Mechanisms of cardiac arrhythmias after the Mustard operation for transposition of the great arteries

To determine the mechanisms of the cardiac arrhythmias frequently seen after the Mustard operation for transposition of the great arteries, intracardiac electrophysiologic studies were performed in 52 children 1 to 8 years after the Mustard operation. Sinus nodal automaticity as judged from the response to rapid atrial pacing was abnormal in 28 of the 52 children. Sinoatrial conduction (conduction of the sinus impulse to the atrium) was found to be abnormal in three of nine patients studied with the atrial extrastimulus method. Conduction of the sinus impulse from the high right atrium to the atrioventricular (A-V) node was abnormally delayed in only 2 of 41 subjects. The low lateral wall of the right atrium was depolarlzed late in 3 of 11 subjects (including the preceding 2). Two subjects showed delayed A-V nodal conduction and one delayed His-Purkinje conduction. The mechanism of supraventricular tachycardia induced in the laboratory was determined to be sinoatrial nodal reentry in four subjects and atrial muscle reentry in four. Two of the four with atrial muscle reentry had prolonged high right atrium to low lateral right atrium intervals during sinus rhythm.

Thus, damage to the sinus node remains the most common cause of arrhythmias after the Mustard operation. In addition, delayed atrial conduction may predispose to atrial muscle reentrant tachycardia.