Brugada波与特发性J波

一、Brugada波Brugada波的典型心电图表现是 ,右胸前V1～V3 导联的ST段抬高和右束支阻滞共同称为Bru gada波。因此 ,正确识别Brugada波对诊断Brugada综合征是十分重要的。1.Brugada波的典型心电图特点⑴右胸前导联的ST段抬高 :右心室肌的期前复极和 或传导延迟引起的右胸前导联V1～V3 的ST段抬高 ,呈穹隆型或马鞍型及下斜型两种表现 ,偶尔有电轴左偏 ,并伴有T波倒置 ,某些病例可在其他导联 (V4)上出现ST段的抬高 ,而且绝大多数Brugada波并无对应导联的ST段下移改变 ,QT间期并不延长。ST段抬高的诊断标准是 ,V1～V3 导联上J点至…     

Ⅱ型Brugada心电图改变与IRBBB的鉴别

目的Ⅱ型Brugada综合征和不完全性右束支传导阻滞(IRBBB)的心电图表现类似,V1导联均呈r Sr'型,但是它们的发病机制和治疗方法、预后完全不同,本研究试图发现二者在心电图指标的不同,以期减少Ⅱ型Brugada综合征早期就诊时的漏诊和误诊。方法选择心电图诊断为IRBBB的心电图146例,根据ST段形态将其分为:(1)ST段抬高组,分为两个亚组:①马鞍形ST段抬高组,也即Ⅱ型Brugada综合征样心电图改变(21例);②非马鞍形ST段抬高组,也即IRBBB伴ST段抬高,(28例);(2)非ST段抬高组,也即IRBBB不伴ST段抬高(97例),观察V1/V2S波上升肢与r'(或J波)下降肢之间的夹角(β角),经r'顶点(或J波顶点)的垂直线与r'下降肢(或J波下降肢)之间的夹角(α角)以及β角与基线形成的基底的长度,与β角顶点5mm垂直线相交的基底线的长度。结果①ST段抬高组α角以及β角显著大于无ST段抬高组(17.9±9.2 vs 15.5±7.1,p0.01,23.3±10.3 vs 20.8±9.0,p0.05);②Ⅱ型Brugada心电图样改变组α角以及β角显著大于IRBBB伴ST段抬高组,(20.7±10.1 vs 15.8±7.2,p0.05,25.6±11.3 vs 20.8±9.0,p0.05)。结论 ST段抬高的形态与α角以及β角有关,马鞍型的ST段抬高的α角以及β角明显增大,可以此作为诊断和鉴别诊断Ⅱ型Brugada样心电图改变与不完全性右束支阻滞的客观依据之一。     

典型Brugada综合征伴明显下壁导联心电图动态变化一例

患者男性,40岁.以"发作性意识丧失2年"入院,常规心电图示Brugada综合征Ⅱ型改变(V2导联呈"马鞍型"ST段抬高)并伴下壁导联S波增宽,升支与T波升支相连,ST段难以辨认.动态心电图显示心电图呈动态变化,尤其当心率减慢时,V2导联呈下斜型ST段抬高(Brugada综合征Ⅰ 型改变),下壁导联S波变得更宽,与T波...     

是Brugada综合征?还是Brugada波或者J波综合征?

贵刊 2 0 0 4年第 3期发表的一篇病例报告“胸前导联ST段广泛抬高的Brugada综合征一例”是一篇很有参考价值的少见病例 ,应以报道和深入探讨研究。但是其诊断结论的正确性和诊断思维的客观性值得提出讨论。正如世界著名心脏病学家WillisHurst所担心的那样 ,急需提高对J波或Brugada波和Brugada综合征的诊断认识和治疗水平 ,以利于正确处理患者[1] 。以J波或ST段抬高为特征的心电图现象已有 5 0年的历史 ,只能称为J波或ST段抬高 ,或称为Brugada波[2 ] ,可见于各种临床情况 ;而Brugada综合征是 1995年由世界著名心脏电生理学家、华人学…     

心电图Brugada波新标准

BayésdeLunaA等2012年9月在JECG发表"Brugada波目前心电图诊断标准的专家共识"。现将心电图诊断新标准和鉴别诊断加以简单介绍。一.心电图新标准新标准将Brugada波心电图图形分为两型,图形1同之前共识中的经典1型,图形2包含了之前共识中的2型及3型(图1)。1.1型Brugada波的心电图特点V1～V2(或V3)导联呈下斜型图形,表现为右胸导联ST段抬高,T波对称倒置。一般不能看到清楚的r’。典型特征(图2A)所示:①V1导联QRS-ST起始部分抬高至少2mm,下斜型ST段呈凹型或直线型。     

高血钾伴低血钙致ST—T电交替1例

患者女,58岁。临床诊断:急性肾功能衰竭(少尿期)。血清钾6.8mmol/L,血清钙2.05mmol/L。心电图(附图)示,窦性P波消失,R-R不等,0.44—0.58s,Q-T间期0.42—0.44s,Ⅰ、V_1中似可见细小之f波,QRS波群显著增宽达0.14—0.16s,因V_5可见宽深S波,故可排除完全性左束支传导阻滞。ST段在Ⅰ呈水平与压低交替,在aVR、aVL呈水平与抬高交替,在Ⅱ、Ⅲ、aVF呈水平与上斜型抬高交替。T波在各导联均呈高、低(或深、浅)交替出现,在V_3、V_5仍然高尖。心电图诊断:心房颤动,心室内阻滞,ST-T电交替现象,Q-T间期延长,提示高血钾、低血钙表现。     

Brugada波心电图表现形式及与右束支传导阻滞的鉴别诊断

Brugada波是由QRS波群终末部出现的J波及伴有下斜型（穹窿型）的ST段抬高共同构成,此典型特征性表现主要出现在右心前的胸导联[V₁、V₂（或V₃）],并伴有这些导联的T波倒置^[1-2]。由于Brugada波的出现,使QRS波群呈类右束支传导阻滞（RBBB）型。Brugada波可以持续存在或间歇出现,若具有Brugada波且出现或曾经出现恶性心律失常发作导致晕厥或猝死等症状时则称为Brugada     

心脏性晕厥或猝死的若干高危心电表现

目的 探讨快速性心律失常所致心脏性晕厥或猝死的高危心电图表现。方法 分析入院时或入院后至少发生1次心脏性晕厥或猝死的33例患者发作时与发作前后的常规12导联心电图或持续心电监护心电图。结果 引起心脏性晕厥或猝死的若干高危心电图表现：①长Q—T间期综合征，②Brugada综合征，③异常J波，④复杂性室性期前收缩，⑤冠心病急性心肌梗死呈广泛前壁心肌梗死伴新出现的右束支传导阻滞及弓背抬高的ST段持续不降，或伴ST—T电交替；或广泛前壁心肌梗死伴墓碑样ST段抬高，⑥扩张型心肌病伴进展性QRS波群低电压。结论 心脏性晕厥或猝死存在多种高危心电图表现。     

Brugada波1例

患者男,44岁。心慌气短,胸前不适月余就诊。查体血压120/80 mmHg,彩色多普勒心脏B超结果正常,血脂血糖在正常范围,心电图示:窦性心律、心率85次/分,QRS间期0·09s,Q-T间期0·34s,平均心电轴+52°,ST-T在正常范围,V1、V2导联呈RS型,ST段呈下斜型抬高,T波倒置,QRS波终末与抬高的ST段融合,呈右束支阻滞图型,心电图诊断:①窦性心律;②Brugada波。随访心电图未见变化,无心律失常发生。讨论国内有关书中提出Brugada波后,有关文章相继刊出。右胸导联ST段抬高,右束支传导阻滞和T波倒置称为心电图右胸导联3联征,亦即Brugada波的典型表现…     

变异性心绞痛诱发ST段抬高型电交替的动态心电图分析

目的对变异性心绞痛(VAP)诱发ST段抬高型电交替的动态心电图(DCG)分析。方法选择16例VAP在DCG中发生ST段损伤性抬高的患者,对伴有ST段电交替、室性心律失常的进行比较。结果16例ST段抬高中有4例出现ST段电交替,占25%。ST段抬高型电交替室性心律失常发生率100%;不伴有ST段抬高型电交替室性心律失常发生率46%。结论VAP诱发ST段抬高型电交替在DCG诊断中具有重要的临床价值。     

T Wave Alternans Does not Assess Arrhythmic Risk in Patients with Brugada Syndrome

Background: Brugada syndrome is associated with a risk for sudden death, but the arrhythmic risk in an individual Brugada syndrome patient is difficult to predict. Pathologic changes in the early repolarization phase of the ventricular action potential probably constitute part of the arrhythmogenic substrate in Brugada syndrome. Microvolt T wave alternans (TWA) assesses dynamic beat‐to‐beat changes in repolarization and has been suggested as a marker for repolarization‐related sudden death. We therefore tested whether TWA is an indicator for arrhythmias in Brugada syndrome with a focus on right precordial ECG leads. Methods: We assessed TWA in nine symptomatic, inducible patients with established Brugada syndrome and in seven healthy controls. TWA was assessed at rest and during exercise using both standard methods and an algorithm that assesses TWA in the early ST segment and the right precordial leads. Results : None of the Brugada patients developed TWA in this study irrespective of analysis at rest or during exercise, neither using standard methods nor when the early ST segment was included in the analysis. When the early ST segment was included in the analysis, nonsustained TWA was found in three out of seven, and sustained TWA in one control. Conclusion: T wave alternans is not an appropriate test to detect arrhythmic risk in patients with Brugada syndrome.     

Intravenous administration of class I antiarrhythmic drugs induced T wave alternans in a patient with Brugada syndrome

A 71-year-old man who experienced aborted sudden death was referred to our hospital. Coronary artery disease and cerebral accident were ruled out by conventional tests. The 12-lead ECG obtained at rest showed a right bundle branch block pattern and ST segment elevation in leads V1 to V3. Double ventricular extrastimuli at coupling intervals >180 msec induced ventricular fibrillation (VF) twice during electrophysiologic study. Intravenous administration of procainamide accentuated ST segment elevation in leads V1 to V3, and visible T wave alternans was induced in leads V2 and V3 at a dose of 450 mg. Initiation of T wave alternans was not associated with changes of the cardiac cycle or development of premature beats. When procainamide infusion was discontinued, T wave alternans disappeared before the elevated ST segment returned to the control level. Pilsicainide also accentuated ST segment elevation and induced similar T wave alternans in leads V2 and V3. Class I antiarrhythmic drug-related T wave alternans has been reported rarely in Brugada syndrome, but it may represent enhanced arrhythmogenicity of VF. We need to monitor closely and study the clinical implications of T wave alternans in Brugada syndrome.     

急性心脏事件体表心电图预警

心脏性猝死(SCD)严重威胁人类的健康,体表心电图的某些改变可对SCD危险因素进行分层和预测。这些改变包括室性早搏、室性心动过速、心室颤动或心室扑动、电风暴(ES)、极速心房颤动(AF)、病态窦房结综合征(SSS)、急性ST段偏移、急性缺血性J波、ST-T动态演变、坏死性Q波突然消退、特征性T波、恶性早期复极综合征及Brugada波。Epsilon波提示致心律失常性右心室发育不良。窄而深的Q波警示年轻人肥厚型梗阻性心肌病。     

Class I antiarrhythmic drug and coronary vasospasm-induced T wave alternans and ventricular tachyarrhythmia in a patient with Brugada syndrome and vasospastic angina

A 50-year-old man presented with a history of transient chest pain and palpitations. The 12-lead ECG at rest showed normal sinus rhythm. A slight ST segment elevation was observed in leads V1 to V3. During hospitalization, atrial fibrillation developed, and oral pilsicainide was administered. Thirty minutes after the drug was given, the ECG showed marked ST segment elevation in leads V1 to V3, and T wave alternans became visible in leads V2 and V3. Self-terminating ventricular tachycardia was initiated following frequent ventricular premature complexes, which showed a left bundle branch block pattern. The coronary angiogram was normal, but in the provocation test of vasospastic angina, acetylcholine administration into the left coronary artery resulted in complete occlusion of the left anterior descending and circumflex arteries. Marked ST segment elevation developed in leads I, aVL, and V3 to V6 concomitant with visible QT/T alternans in leads V4 and V5, and ventricular tachyarrhythmia was initiated. Brugada syndrome and vasospastic angina coexisted in this patient, and T wave alternans can be used as a predictor of ventricular tachyarrhythmias in such patients.     

ST-T alternans and myocardial ischemia

Previous studies using intracoronary electrocardiography have demonstrated that ST-T alternans can develop during standard balloon coronary angioplasty. Total occlusion with a large amount of myocardium in jeopardy is the postulated prerequisite. In this study, the authors used perfusion balloons instead of standard balloons, so coronary perfusion was maintained and ischemia was minimized. Fourteen patients with standard balloon technique and 11 patients with perfusion balloon technique were studied. The ST segment was less elevated during perfusion angioplasty (0.15 +/- 0.05 mV vs 1.04 +/- 0.19 mV, p<0.001). There were six (43%) patients with ST-T alternans with standard balloon technique compared with none in the perfusion balloon group (p<0.001). In this study, the authors found that there was less ischemia, less ST segment elevation, and lack of ST-T alternans on the intracoronary electrocardiogram during perfusion balloon angioplasty. These findings support the postulate that a large amount of ischemic myocardium is a prerequisite for ST-T alternans.     

冠状动脉造影为三支或双支病变的心电图临床研究

目的探讨冠脉病变患者心电图ST-T的改变与冠脉病变的关系。方法随机选取2000年-2003年收治并行冠状动脉造影的60例冠心病患者,造影前常规描记12导联心电图,观察ST-T改变。结果46例三支病变患者中心电图ST段压低者仅6例,T波倒置者17例。14例双支病变患者中,ST段压低者仅1例,T波倒置者5例。结论冠状动脉病变严重程度与心电图表现缺乏一致性。     

Atypical behavior of QTc and ST-T intervals in a patient with the Brugada syndrome

We present a 56-year-old man who was admitted to an emergency service after receiving an electric shock. The ECG showed a J point and ST segment elevation of up to 5 mm in leads V1 to V3, which normalized in 24 hours. The ajmaline test caused elevation of the J point and of the ST segment up to 12 mm in leads V1 to V3, QTc lengthening, and QTc and T wave alternans. These results denoted alterations in the duration of myocardial action potentials, a common finding in patients with Brugada syndrome and long QT syndrome.     

Noninvasive Risk Stratification of Subjects with a Brugada‐Type Electrocardiogram and No History of Cardiac Arrest

Background: Recent studies suggest that the Brugada‐type electrocardiogram (ECG) is much more prevalent than the manifest Brugada syndrome. Although invasive electrophysiologic investigations have been proposed as a risk stratifier, their value is controversial, and alternative noninvasive techniques may be preferred. We sought a noninvasive strategy to detect a high‐risk group in a long‐term follow‐up study of subjects with a Brugada‐type ECG, and no history of cardiac arrest. Methods: This study enrolled 124 consecutive subjects with a Brugada‐type ECG. Prognostic indices included: age, sex, a family history of sudden death, syncopal episodes, a spontaneous coved‐type ST‐segment elevation, maximal magnitude of ST‐segment elevation, a spontaneous change in ST segment, a mean QRS duration, maximal QT interval, QT dispersion, late potentials (LP) by signal‐averaged ECG, and microvolt T‐wave alternans. Results: Of the 124 subjects, 20 consenting subjects had an implantable defibrillator before follow‐up. During a 40 ± 19‐month follow‐up, 12 subjects (9.7%) reached one of the endpoints (sudden death or ventricular tachyarrhythmia). Of the 12 risk indices, a family history of sudden death, syncopal episodes, a spontaneous coved‐type ST‐segment elevation, a spontaneous change in ST segment, and LP had significant values. In multivariate analysis, a spontaneous change in ST segment had the most significance (a relative hazard, 9.2; P = 0.036). Combined assessment of this index and other significant indices obtained higher positive predictive values (43–71%). Conclusions: A spontaneous change in ST segment is associated with the highest risk for subsequent events in subjects with a Brugada‐type ECG. The presence of syncopal episodes, a history of familial sudden death, and/or LP may increase its value.     

Spontaneous T wave alternans in a patient with Brugada syndrome--responses to intravenous administration of class I antiarrhythmic drug, glucose tolerance test, and atrial pacing

Spontaneous T wave alternans in Brugada syndrome. A 43-year-old man with an episode of syncope showed ECG patterns of coved-type ST elevation in leads V1-V3 and right bundle branch block pattern. The patient had spontaneous T wave alternans at baseline, and T wave alternans diminished with distinct development of ST elevation after administration of Na+ channel blocker, and during oral glucose load and atrial pacing. Na+ channel mutation may contribute to the genesis of his ECG changes.     

Brugada type 1 electrocardiographic pattern induced by severe hyponatremia

Brugada syndrome is characterized electrocardiographically by ST segment elevation in the right precordial leads, followed by a negative T wave unrelated to ischemia, electrolyte disturbance or drug effects and prone to rapid polymorphic ventricular tachycardia capable of degenerating into ventricular fibrillation. The ECG pattern may be dynamic and is often concealed. Sodium channel blockers, drugs, electrolyte imbalances, fever and several other clinical circumstances are recognized inducers of a Brugada type 1 ECG in susceptible patients. We describe a case of a Brugada type 1 ECG pattern induced by severe hyponatremia.