Brugada综合征三例

Brugada综合征心电图主要表现为:V1～V3导联的ST段抬高、T波倒置,伴有或不伴有右束支传导阻滞.临床特征:患者可突然发生晕厥、室速、室颤或猝死,其特点是:无明显诱因,常发生在10Pm～8Am之间,既夜间睡眠期间.尸检无明显异常.应将Brugada综合征现象作为恶性心律失常高危因素的标志,予以高度重视,密切跟踪观察,并进行必要的检查和治疗.Brugada综合征与早期复极综合征有着相似之处,需要与之鉴别.     

Brugada综合征2例临床分析

目的了解Brugada综合征的心电图特点，从而识别此类病人。方法分析2例Brugada综合征的心电图特点。结果Brugada综合征的心电图都表现为不完全性RBBB，V1～V3导联ST段抬高。结论对于有反复晕厥或心悸、胸闷等症状的青壮年男性，若心电图表现为不完全性RBBB，V1～V3导联ST段抬高，要高度警惕Brugada综合征的可能性。     

高位右侧胸前导联对揭示Brugada综合征心电图的有效性

目的:探究高位右侧胸前导联在揭示Brugada综合征心电图征中的应用意义。方法:选取本院2012年6月-2014年9月收治的伴有猝死家族史(心电图胸前导联呈ST段抬高)的3个家系(9个成员)为试验组,另择取同期来本院体查的32例健康体检者为对照组,均行常规与高位右侧胸前导联心电图检查,探究高位右侧胸前导联对Brugada综合征心电图征诊断的应用价值。结果:试验组9个成员均行体格、超声心动图检查,家系1常规与高位右侧胸前导联未显现Brugada综合征心电图特征;家系2先证者常规心电图J波呈现增高,V1’~V3’导联J波呈增高趋势,维持0.15~0.5 m V;家系3中的例1、例3心电图提示为Brugada综合征,V1"~V3"导联J波明显增高,维持0.2~0.7 m V。32例健康体检者中,20例常规心电图呈早期复极,1例V1’~V3’导联J波明显增高,11例V1"~V3"导联J波显著增高,所有健康体检者均不吻合Brugada综合征心电图诊断标准。结论:相较于常规心电图而言,高位右侧胸前导联心电图能有效提升Brugada综合征心电图诊断阳性率,临床上应引起足够重视。     

Brugada综合征

Brugada综合征符合亦称右束支传导阻滞、ST段抬高、猝死综合征,是指在无器质性心脏病的情况下发生的"特发性"心室颤动(IVF),心电图呈右束支传导阻滞、V1～V3导联ST段抬高和猝死的一组病征.     

Brugada综合征研究现状

<正>Brugada综合征是由于编码心脏Na离子通道的基因突变引起的离子通道功能异常而导致的一组综合征。其临床特征为:1心脏无器质性改变,结构功能正常;2特征性右胸导联(V1^V3)ST段呈下斜型或马鞍型抬高,伴有或不伴有右束支阻滞;3致命性室性快速性心律失常:室性心动过速或心室颤动发作引起反复晕厥和猝死。多数发生于青年男性,常有晕厥或猝死家族史,目前唯一被证明能有效预防Brugada综合     

Brugada综合征26例临床分析

①目的探讨Brugada综合征的主要临床特征。②方法对26例Brugada综合征患者的临床资料和心电图特征进行回顾性分析。③结果患者主要见于青壮年男性,猝死发生时记录到可救治的心室颤动和多形性室性心动过速;心电图呈右束支传导阻滞型,V1、V2导联以ST段下斜型抬高、T波倒置为主。④结论Brugada综合征以青壮年男性为主,心电图表现与文献资料相似。有家族史者比无家族史者病情更凶险。     

Brugada综合征的心电图特性

Brugada P．Brugada J于1992年报告8例发生多形性心动过速或心室颤动事件的病人，经临床检查、超声心动图、心血管造影以及心肌活检均未发现器质性心脏病的证据，平时心电图Q—T间期正常，但有右束支阻滞和右胸导联（V1-V3）ST段抬高等改变。现有学者又发现室性期前收缩时V1～V3导联呈马鞍型，ST段抬高的程度与心源性晕厥发作，亦是支持Brugada综合征诊断的一种有力佐证，ST段抬高越明显可能预示更濒临晕厥发作，后来世界各大洲相继均有报道，但分布以亚洲特别是东南亚多见。此病发病相对较轻。平时心绞痛、胸闷、呼吸困难等症状，发病时主要表现为晕厥或猝死。多在夜间睡眠中发生，故有意外夜间猝死综合征之称。     

Bmgada综合征26例临床分析

①目的 探讨Brugada综合征的主要临床特征.②方法 对26例Brugada综合征患者的临床资料和心电图特征进行回顾性分析.③结果 患者主要见于青壮年男性,猝死发生时记录到可救治的心室颤动和多形性室性心动过速;心电图呈右束支传导阻滞型,V1、V2导联以ST段下斜型抬高、T波倒置为主.④结论 Brugada综合征以青壮年男性为主,心电图表现与文献资料相似.有家族史者比无家族史者病情更凶险.     

Brugada综合征1例

Brugada综合征是西班牙学者Brugada 1992年首先报道的[1] 。是没有心脏结构改变而具有特异性的心电图表现 ,能反复发生室颤而引起的心脏猝死的一种新的心脏综合征。我院于 2 0 0 2年 6月遇到 1例Brugada综合征患者现报告如下。1　临床资料患者 ,男性 ,4 3岁 ,因凌晨 4时睡眠中突然出现胸闷 ,全身乏力 ,神志清醒 ,持续约 4 0min ,症状未完全消失。急查心电图示 :窦性心律 ,V1～V3导联ST段抬高0 .3～ 0 .6mv ,并呈完全性右束支传导阻滞图形 ,P -R间期 0 .2 0s ,Q -T间期 0 .34s。既往无心脏病史 ,心电图正常 ,门诊可疑以急性前间壁心肌梗…     

新疆哈萨克族Brugada综合征患者的调查分析

目的:Brugada综合征是一种可引起室颤和猝死高危风险的心脏离子通道异常疾病,心电图表现为右束支传导阻滞伴V1～V3导联阵发性或持续性ST段抬高(≥0.1mV).目前尚未见中国哈萨克族人群Brugada综合征发病率的资料.文中通过对新疆地区哈萨克族住院患者心电图的回顾性分析,初步了解哈萨克族人群Brugada综合征的流行病学情况. 方法:按照Brugada综合征的心电图诊断标准,对新疆哈密市巴里坤县1995年1月至2006年8月9046例心电图资料进行筛选. 结果:9046例中,年龄16～74岁,平均(37.7±14.6)岁.23例心电图呈Brugada样心电图征,发生率为2.54‰,其中男性11例,女性12例,男、女发生率分别为4.16‰(11/2643)和1.87‰(12/6403),差异有显著性意义(P＜0.05).年龄16～45岁和＞45岁人群中发生率分别为3.42‰及1.34‰,两年龄组间有显著性差异(P＜0.05).其中典型(Ⅰ型)和不典型(Ⅱ、Ⅲ型)Brugada心电图改变分别为2例及21例,发生率分别为0.22‰及2.32‰. 结论:Brugada样心电图征在新疆哈族住院患者总发生率为2.54‰,以青壮年男性多见.     

Electrocardiographical case. Asymptomatic patient with ST-segment elevation

A 46-year-old man complained of recurrent episodes of giddiness which was not associated with chest pain or breathlessness. There was no family history of sudden death. Clinical examination was unremarkable.12-lead electrocardiogram (ECG) showed ST segment elevation in the right precordial leads, with coved ST segment elevation at its J point followed by a negative T wave with no isoelectric separation, specifically in V2. These ECG features are characteristic of the Brugada syndrome. He underwent a flecanide challenge which produced further elevation of ST segment at its J point and spontaneous ventricular ectopy. Electrophysiological studies induced ventricular fibrillation with 3 extra stimuli. An implantable cardioverter-defibrillator was implanted for prevention of sudden cardiac death. The Brugada syndrome is discussed.     

J波综合征的研究进展

Brugada综合征、原发性心室颤动都是心源性猝死的主要原因。与上述综合征相似,过早复极综合征不仅在心电图中有J波形态、时限和幅度的显著改变,其电生理机制也可能相同。现通过探讨J波定义及其细胞电生理和离子流机制,并分别描述Brugada综合征、过早复极综合征、原发性心室颤动的心电图特征,为临床发现这类高危猝死信号和预防提供参考。     

发热与Brugada综合征(21例报告)

目的 对1997~2004年入住我们医院的21例Brugada综合征的病例进行回顾性分析。方法 观察Bruga患者的诱发因素、临床表现、实验室检查、心电图、24h动态心电图及超声心动图,探讨发热与Brugada综合征系。结果 21例(男20例,女1例)确诊为Brugada综合征的患者中有4例(均为男性)为发热性疾病诱发室性起病。结论 发热作为Brugada综合征的常见诱发因素,在临床诊疗过程当中应该引起临床医生的特别注意。     

发热与Brugada综合征（21例报告）

目的 对1997～2004年入住我们医院的21例Brugada综合征的病例进行回顾性分析。方法 观察Brugada综合征患者的诱发因素、临床表现、实验室检查、心电图、24h动态心电图及超声心动图，探讨发热与Brugada综合征之间的关系。结果 21例(男20例，女l例)确诊为Brugada综合征的患者中有4例(均为男性)为发热性疾病诱发室性心律失常起病。结论 发热作为Brugada综合征的常见诱发因素，在临床诊疗过程当中应该引起临床医生的特别注意。     

Brugada syndrome--an update

A diagnostic triad characterizes Brugada syndrome. It consists of a right bundle branch block, ST-segment elevation in leads V1-V3 and sudden cardiac death (SCD). Approximately 50% of patients with Brugada syndrome noted to have familial occurrence, this suggests a genetic component of the disease. Mutations in gene SCN5A, an encoder for human cardiac sodium channel on chromosome 3p21, causes Brugada syndrome. Before considering the diagnosis of Brugada syndrome, exclude precordial ST-segment elevation secondary to acute coronary syndrome, electrolyte imbalance, myocarditis, drug over dosage (cocaine, tricyclic antidepressants), and arrhythmogenic right ventricular cardiomyopathy/dysplasia. Intravenous administration of ajmaline, flecainide, and procainamide may exaggerate the ST-segment elevation, or unmask it when it is initially absent in patients with suspected Brugada syndrome. Programmed electrical stimulation (PES) may help in risk stratification, and in some cases, establish the diagnosis. However, the accuracy of PES in predicting outcome is debatable, especially in patients showing an asymptomatic Brugada ECG, and reporting no family history of SCD. Treatment with an implantable cardioverter-defibrillator (ICD) is the only established effective therapy for the disease. With ICD therapy, the mortality rate at a 10 year follow-up was 0%. Supporting data for long-term pharmacological therapy with quinidine, or isoproterenol for prevention of SCD, in these patients, is uncomplete. Future advances in understanding the molecular mechanisms of Brugada syndrome may provide answers to many of the controversial issues in the management of this disease.     

Electrical heterogeneity of canine right ventricular transient outward potassium currents

Background Some studies have confirmed that the right ventricular walls of most rodents, such as canines and humans, have evident transient outward potassium current (Ito1) heterogeneity, and this heterogeneity is closely related to J point elevation, J wave formation, and some ventricular tachycardias such as ventricular fibrillations caused by Brugada syndrome. This study is designed to investigate transmural electrical heterogeneity of the canine right ventricle during repolarization (phase 1) from the viewpoint of 4-aminopyridine sensitive and calcium-independent Ito1. Methods Adult canine single right ventricular epicardial (Epi) cells, mid-myocardial (M) cells, and endocardial (Endo) cells were enzymatically dissociated. Whole cell voltage-clamp recordings were made to compare the Ito1 values of the three cell types. Results At 37℃ and using 0.2 Hz and +70 mV depolarizing test potentials, the average peak Ito1 values of Epi cells and M cells averaged (4070±1720) pA and (3540±1840) pA, respectively. The activated and inactivated Epi and M cells kinetic processes were in accordance with the Boltzmann distribution. Compared with Ito1 in Epi cells and M cells, the average peak Ito1 in Endo cells was very low, averaged (470±130) pA. Conclusions These results suggest that there are evident differences and potent gradients in Ito1 between the three cardiac cell types, especially between Epi and Endo cells. These differences are among the prominent manifestations of right ventricular electrical heterogeneity, and may form an important ionic basis and prerequisite for some malignant arrhythmias in the right ventricle, including those arising from Brugada syndrome and other diseases.     

Tpeak-Tend interval as a new risk factor for arrhythmic event in patient with Brugada syndrome

Objective:To evaluate Tpeak-Tend (Tp-e) interval in surface standard ECG as a new risk factor for arrhythmic event in patient with Brugada syndrome. Methods: 23 male patients with Brugada syndrome and 20 male patients with paroxysmal supraventricular tachycardia (PSVT) as the control group were investigated in this study. Tp-e interval in surface standard ECG was compared between BrS and PSVT patients. Results: Tp-e interval in BrS patients was significantly longer than that in PSVT patients (109.57±22.86 ms vs. 88.50±13.08ms, P＜0.05). There was significant difference in Tp-e interval between 16 BrS patients with arrhythmic events (including syncope, clinical ventricular fibrillation [VF] and programmed electrical stimulation [PES]-induced VF) and 7 BrS patients without arrhythmic events and PSVT patients (118.12±20.40ms vs.90.00±15.27ms, P＜0.05; 118.12±20.40ms vs. 88.50±13.08ms, P＜0.05). However, Tp-e interval was similar in BrS patients without arrhythmic events and PSVT patients (90.00±15.27ms vs 88.50±13.08ms, P＞0.05). Conclusion: The prolongation of Tp-e interval could serve as a new noninvasive event predictor for arrhythmic events in patients with Brugada syndrome.     

Cost-Effectiveness of Implantable Cardioverter-Defibrillators in Brugada Syndrome Treatment

Brugada syndrome is characterized by an ST-segment elevation in the right precordial ECG leads and a high incidence of sudden death in patients with structurally normal hearts. Some trials have demonstrated that the cost-effectiveness of ICD implantation treatment in patients with structurally abnormal hearts is more favorable than that of control treatment. We used Treeage pro 2005 to estimate costs and survival among the Brugada syndrome patients who received either an ICD or were treated by control therapy of I_to-blocking properties (quinidine) or β-blockers (propranolol). In conclusion, our analysis suggests that prophylactic implantation of an ICD has good cost-effectiveness in patients with Brugada syndrome who are at high risk of sudden death. ICD treatment has shown a cost-effectiveness ratio below $9,591 per QALY gained from trials of defibrillator vs β-blockers for Unexplained Death in Thailand (DEBUT). The control therapy of quinidine may be a good choice for patients who are infants or living in developing countries.     

Brugada综合征心电图检出情况的初步分析

目的 初步分析52 461份心电图Brugada综合征的检出情况。方法 2009年3月—2011年12月,从我院门诊心电图室收集常规心电图52 461份,严格按照筛选标准检出具有Brugada综合征特征的心电图,并对检出的病人进行随访。结果 共检出Brugada心电图征病人39例（0.74‰）,均为男性,其中Ⅰ型10例,Ⅱ型26例,Ⅲ型3例。39例中确诊Brugada综合征6例,疑似诊断1例。确诊的6例病人,4例安装了埋藏式心律转复除颤器（ICD）,现生存良好;2例拒绝安装ICD者死亡。结论 Brugada综合征在本组人群中检出率为0.11‰,占已检出Brugada心电图征的15％;建议对于确诊的Brugada综合征病人给予ICD治疗,否则发生猝死的可能性较大。     

Brugada综合征临床教学难点的探讨

目的 探讨进一步提高Brugada综合征(brugada syndrome,BrS)临床教学效果的相关方法。 方法 Brugada综合征是现代临床医学中重要的疾病范畴,是心脏病学中重要的疾病之一,其病死率和病残率均极高,虽然Brugada综合征常以极其严重的临床危害而令人恐惧,但在临床教学中,学员却对该病危害性与严重性的认识存在严重不足,警惕性也明显不高,因此在诊疗过程中对该病的医疗风险防范意识相对不足,再加上多数教学人员对该病的相关基础知识也比较薄弱,所以在临床教学过程中对Brugada综合征相应临床内容的讲解变得十分困难,导致学生也难以深入理解,以至于学习的积极性与兴趣较低。 结果 针对上述临床教学上存在的一系列问题和现实情况及相关难点,在重视理论的基础上,密切结合临床实际,制定详细的教学计划,根据Brugada综合征的临床特点,将其发病机制、病因等列为教学的主要内容,将临床心电图作为教学重点和难点,教学时间上予以侧重。采用理论讲解与案例教学相结合、针对不同层次的学员采用逐一分层化的教学和管理模式、重视基础理论及充分调动学生参与的积极性。在传统临床教学模式的基础上,充分利用现代网络等多媒体教学工具的强大图形处理能力,动静互变能力和强大的模拟能力,直观形象地再现了Brugada综合征发病过程,大大地提高了Brugada综合征的临床教学效率与效果。 结论 通过以上措施的实施,我们发现在对不同来源的学员教学工作中取得了较好的实际效果,提高了BrS的临床教学效率,同时也提高了BrS的临床诊断准确率。