预激综合征的外科治疗

报告1986年3月至1988年4月间经心电图、心电向量图、心电生理等检查确诊的预激综合征8例,其中 B 型5例,A+B 型1例,右前间隔型1例,隐匿型1例。经心外膜标测、定位后,行手术切割和心肌内酒精注射。随访平均16个月,效果满意。     

预激综合征外科治疗的手术配合

预激综合征是由于心房与心室之间的传导径路除正常传导系统外尚并存有异常传导通道(也可称异常传导束Kent束)所致。心电图特征为在室性心律的基础上,R波的升支有顿挫或切迹,称为delta波即预激波。临床表现可有心律失常,严重可引起猝死。外科手术治疗的目的是破坏异常传导束,从而达到根治目的。     

预激综合征的外科治疗

在心脏发育、房室环成熟过程中,除正常心脏传导系统外,其余的通路均由房室纤维环隔断。如残留某个通路未被隔断,即成为异常通路,亦称附加旁路。常见的异常房室间通路有Kent氏束通路,其常位于左室游离壁及房室环内或右室游离壁内,极少位于前、后间隔;由心房到房室束的James束及起于房室结、房室束或束支而终于心室肌部的Mahaim纤维也是异常通路。存在异常通路的患者有的无症状,有的偶然发生过心动过速,有的只在心电图上发现预激δ波及QRS异常增宽。在某些条件下,心房冲动经此异常通路激动心室,可发生预激综合征(WPW)而出现阵发性频繁心动过速,影响血流动力学,甚至危及生命,必须治疗。1 诊断 对WPW术前须行电生理心内膜、心外膜标测,以确定预激点位,类型,旁路的径路等。1.1 右心导管心内膜标测①A型预激:导管电极在冠状静脉窦内标测。当窦性心律时示AV最短,V波领先。另一导管在右心室行起搏时,冠状窦内标测示VA最短、逆行A波领先,则异常通路在     

经心内膜Kent束切断术治疗预激综合征

经心内膜行Kent束切断治疗预激综合征5例,共切断Kent束9支,皆获成功。其中3例合并Ebstein畸形,均一次手术矫正,疗效满意。手术指征为药物不能控制的心功过速反复发作者、心源性昏厥和先天性心脏畸形需手术治疗者。     

预激综合征的内科治疗

预激综合征的内科治疗主要是针对由于心室预激的存在而引起的快速性心律失常,尤其     

预激综合征并发房颤的急诊治疗

预激综合征并发房颤是一种较为严重的心律失常 ,个别患者可并发低血压和心功能不全 ,导致严重的循环障碍 ,而诱发室颤甚至猝死。因此门诊及时准确的诊断和有效治疗 ,对患者预后有很大影响。我院近年来门诊共治疗预激并发房颤患者 13例 ,现就门诊急救方面的体会总结如下。一、临床资料 1 一般资料 :13例患者中男性 9例 ,女性 4例 ,年龄 30岁～ 6 6岁 ,平均 41岁。合并高血压 1例 ,冠心病 2例 ,血压偏低 2例 ,心功能不全 1例。 2 临床特点 :预激综合征多无症状 ,并发房颤的则常有心悸、胸闷、气短 ,亦可伴有心功能不全征象 ,甚至可诱发心力衰…     

射频消融术治疗预激综合征6例

射频导管消融术(RFCA)治疗阵发性室上性心动过速是近几年来应用于临床的新技术,也是根治难治性室上性快速心律失常的方法。我们医院自从1995年初开始进行射频消融术治疗预激综合征伴阵发性室上性心动过速6例,取得了满意的疗效,现报告如下。     

Mahaim型预激综合征的诊断和治疗

近年来，随着心脏电生理研究的进展和射频消融术（RFCA）在心律失常治疗中的广泛应用，对Mahaim纤维及其引起的心律失常，提出了新的观点。本文对传统的Ma－haim纤维和近年的新进展作一综述。IMabalm综合征概念的形成及治艾1973年Mahaim和Benatt“‘在尸体解剖中首次发现从房室结到心室肌的异常连接纤维，称为结室旁道（nodoven－tricularbypasstract）。解剖发现除了有结室分道外，还有从房室束水平至心室肌的旁道纤维，称为束室旁道（fasciculo－ventrlcularbypasstract）。两者店来都被称为Mahaim纤维D，‘］。此后，许多作者相继报…     

预激综合征的快速室上性心律失常的诊断和治疗

预激综合征的快速室上性心律失常的诊断和治疗预激综合征的临床表现决定于旁束的电生理性能，临床上最重要的问题是旁束引起的阵发性室上性心动过速（室上速）及／或心房颤动（房颤）。本节将介绍导致预激最常见的房室旁束（ｋｅｎｔ束）所参与的室上性快速心律失常。预激...     

体表电位标测判定预激综合征旁路的评价

目的 评价体电位标测在房室旁路定位中的准确性和可行性。方法 ５２例常规行身频导管消融（ＲＦＣＡ）的显性激综合征（Ｗｏｌｆｆ－Ｐａｒｋｉｎｎｏｎ－Ｗｈｉｔｅ ｓｙｎｄｒｏｍｅ,ＷＰＷ）病人,订前后体表电位标测（Ｂｏｄｙ Ｓｕｒｆａｃｅ Ｐｏｔｅｎｉｔａｌ Ｍａｐｐｉｎｇ,ＢＳＰＭ）。旁路定位采用：（１）等电位图：除极４０ｍｓ后,稳定持续１０ｍｓ以上的极上值位置。（２）等积分图,等积分图中极小值的位置     

后间隔房室旁路体表心电图的定位诊断

目的 探讨预激综合征在左、右及后间隔旁路的位置与体表心电图特征性改变的相关关系。方法 以80例预激综合征射频消融前后作对照,寻找体表心电图的特征性改变与左、右及后间隔旁路位置关系,确定体表心电图定位左、右及后间隔旁路的鉴别诊断标准,并计算其鉴别诊断的敏感性、特异性和准确率。结果 体表心电图的8大特征变化与预激左右后间隔旁路定位鉴别诊断有关,即V1导联QRS波形态、Δ波方向;Δ波及QRS波的额面电轴及二者差值;Ⅲ导联R／S波比值;胸前导联R／S＞1的转折点;PV1-PE间距。根据以上8大特点对术前80例预激重新定位,其鉴别诊断敏感性、特异度及准确率在右后间隔旁路分别是88．2％、83．3％和77．5％,而左后间隔是83．3％、88．2％、87．5％。结论 B型预激旁路绝大部分位于右后间隔旁路,但也不排除左后间隔旁路,尤其是左后旁路预激不安全时可出现B型预激改变,上述体表心电图的8大特征有助于二者鉴别诊断。     

心电图对预激综合征房室旁道定位的评价

选择五种文献报告的心电图房室旁道定位的标准,对30例正常人和45例经手术治愈的预激综合征患者术前心电图进行定位诊断.以心脏标测和手术证实的旁道部位和正常人无房室旁道为金标准,依据五种标准对本组资料的判定结果进行定位准确性评价.各标准特异度均为100%,其敏感度依次为:Rosenbaum标准93.3%,Gallagher标准71.1%.WHO标准64.4%,Lindsay标准60%,Reddy标准53.3%.笔者综合以上标准优点及本组资料,初步提出常见房室旁道部位定位特征.     

预激综合征的房室旁道定位

根据国外旁道定位标准结合自己经验绘出心电图导联与房室环平面关系示意图对48例预激综合征房室旁道进行定位:左侧游离壁25例(52.1％),左后游离壁7例(14.6％),后间隔7例(14.6％),前间隔6例(12.5％),右游离壁0例,双旁道3例(6.3％)。手术治疗19例,其中单旁道17例,双旁道2例,共计21条旁道;除1条靠近希氏束的前间隔旁道未切断外,20条旁道均被切断,手术总成功率为95.2％,其中左游离壁旁道(15条)均被切断,成功率为100％。手术结果说明本方法定位简单、精确度较高。     

Accessory pathway associated with an anomalous coronary vein in a patient with Wolff-Parkinson-White syndrome

We report a case of Wolff-Parkinson-White syndrome coexistent with atresia of the coronary sinus (CS) ostium and persistence of the left superior vena cava. The accessory pathway was located at the blind end of the CS, which was bumped with mechanical loss of preexcitation during mapping by a catheter from within the CS. The accessory pathway was successfully ablated with radiofrequency energy applied to this site from the right atrium. This unique combination of anatomically matched anomalies may be important in suggesting a potential embryologic link between the accessory pathway and the coronary vein.     

Diprafenone for treatment of Wolff-Parkinson-White syndrome

Summary The effect of intravenous (1.5 to 2.0 mg/kg body weight) and oral (300 to 375 mg/d) diprafenone was studied in 15 patients with the Wolff-Parkinson-White syndrome and symptomatic supraventricular tachycardia. Intravenous application of diprafenone significantly increased atrioventricular nodal conduction time as well as the effective refractory periods of the right ventricle and the accessory pathway in both the antegrade and retrograde directions. Antegrade conduction block in the accessory pathway occurred in two patients after the dose was increased to 2.0 mg/kg body weight. Intravenous diprafenone suppressed the inducibility of supraventricular tachycardia in two patients, but the tachycardia cycle length was significantly increased in all other patients. Fourteen patients were treated with oral diprafenone, and 11 were asymptomatic during a 17-month follow-up, two of these after the dose had been increased to 375 mg/d. Oral therapy had to be withdrawn in two patients because of adverse gastrointestinal side effects and in one because of recurring bronchospasm.     

预激性心肌病

预激综合征可诱发扩张型心肌病,以往常报道预激综合征伴反复发生或持续性的快速性心律失常可发展为扩张型心肌病,即心动过速性心肌病。另外,预激综合征可合并肥厚型心肌病。而预激综合征还可诱发另一类扩张型心肌病,即预激性心肌病,也称为预激介导性心肌病,是由于心室同步兴奋和收缩的电机械特性受到影响,进而影响心脏的机械功能,造成心室重构而引起的。它除了具备扩张型心肌病的诊断条件外,尚具备下述两个特点:1无症状的预激综合征,即临床上没有反复或持续性快速性心律失常发作史;2体表12导联心电图提示显性预激,并且为右侧旁道。对于预激性心肌病,射频消融术是安全有效的治疗方法。     

Molecular genetic analysis of PRKAG2 in sporadic Wolff-Parkinson-White syndrome

INTRODUCTION: Mutations in the PRKAG2 gene that encodes the gamma2 regulatory subunit of AMP-activated protein kinase have been shown to cause autosomal dominant Wolff-Parkinson-White (WPW) syndrome associated with hypertrophic cardiomyopathy. Prior studies focused on familial WPW syndrome associated with other heart disease such as hypertrophic cardiomyopathy. However, such disease accounts for only a small fraction of WPW cases, and the contribution of PRKAG2 mutations to sporadic isolated WPW syndrome is unknown. METHODS AND RESULTS: Subjects presented for clinical electrophysiologic evaluation of suspected WPW syndrome. WPW syndrome was diagnosed by ECG findings and/or by clinically indicated electrophysiologic study prior to enrollment. Echocardiography excluded hypertrophic cardiomyopathy. Denaturing high-performance liquid chromatography and automated sequencing were used to search for PRKAG2 mutations. Twenty-six patients without a family history of WPW syndrome were studied. No subject had cardiac hypertrophy, and only one patient had associated congenital heart disease. Accessory pathways were detected at diverse locations within the heart. Two polymorphisms in PRKAG2 were detected. [inv6+36insA] occurred in intron 6 in 4 WPW patients and [inv10+10delT] in intron 10 in 1 WPW patient. Both occurred in normal unrelated chromosomes. No PRKAG2 mutations were detected. CONCLUSION: This study shows that, unlike familial WPW syndrome, constitutional mutation of PRKAG2 is not commonly associated with sporadic WPW syndrome. Although polymorphisms within the PRKAG2 introns were identified, there is no evidence that these polymorphisms predispose to accessory pathway formation because their frequency is similarly high in both WPW patients and normal individuals. Further studies are warranted to identify the molecular basis of common sporadic WPW syndrome.     

Mechanisms for atrial fibrillation in patients with Wolff-Parkinson-White syndrome

INTRODUCTION: Paroxysmal atrial fibrillation (PAF) frequently occurs in patients with Wolff-Parkinson-White (WPW) syndrome. To elucidate the mechanisms for PAF, we performed electrophysiologic studies (EPS) before and after ablation of accessory pathways (APs). METHODS AND RESULTS: We investigated 24 patients with WPW syndrome who had AV reciprocating tachycardia and prior PAF and had undergone successful ablation of APs. Patients in whom atrial fibrillation (AF) was induced by EPS at day 7 after ablation were considered the inducible AF group (n = 14), and patients in whom AF was not induced by EPS at day 7 after ablation were considered the noninducible AF group (n = 10). Fifteen patients with AV nodal reentrant tachycardia (AVNRT) but without PAF who underwent ablation of the slow AV nodal pathways served as the control group (AVNRT group). Maximal atrial conduction delay and conduction delay zone, which are indices of atrial vulnerability, were measured before and after ablation. Before ablation, maximal atrial conduction delay and conduction delay zone were significantly greater (P < 0.0001 and P < 0.0001, respectively) in the two WPW syndrome groups than in the AVNRT group, indicating increased atrial vulnerability in WPW syndrome with PAF. After ablation, these parameters did not change in the inducible AF group, whereas they were significantly (P < 0.0001) decreased in the noninducible AF group and were not different from those in the AVNRT group, indicating normalized atrial vulnerability in the noninducible AF group after ablation. The prospective study demonstrated that PAF recurred only in the inducible AF group during long-term follow-up (17+/-7 months). CONCLUSION: The findings of this study suggest that there are two mechanisms of PAF in patients with WPW syndrome: one mechanism is reversible and AP-dependent atrial vulnerability, and the other is intrinsic and AP-independent atrial vulnerability.     

经导管射频消蚀治疗预激综合征及房室结双径路16例报告

以射频消蚀14例预激综合征(15例次)及2例房室结双径路患者.14例预激综合征患者共16条旁道,其中左游离壁11条,左后间隔、左中间隔、左后侧壁、右前间隔及右游离壁各1条.全部首次消蚀成功(100%).1例12小时后复发者再次消蚀成功.2例房室结双径路患者成功地阻断慢通道.无严重并发症.随访3～16周均未复发.