改良Brugada四步法诊断室性心动过速价值初探

为评价改良的Brugada四步法诊断室性心动过速（VT）的价值，对心电图表现为宽QRS波（QRS时限＞110ms），心动过速行射频消融术的连续病例24例（其中经心脏电生理检查证实VT19例，室上性心动过速5例）进行回顾性分析，结果显示改良的Brugada四步法对VT的敏感性为94．7％，特异性为80％，阳性预告值为94．7％。     

与室性心动过速有关的心电学改变

目的　观察在动态心电图中，室性心动过速（室速）发生前，心电学指标的改变。方法　７ 例在动态心电图中有持续性室速或频发非持续性室速的患者被列入观察。结果　与无室速时的ＱＴｃ差值（７．３±１．９ｍ ｓ）相比，室速前１０ 分钟的ＱＴｃ差值（３０．６±２４．２ｍ ｓ）较大（Ｐ＝ ０．０４９）。结论　心室复极的不稳定参与了室速的形成。     

反复性室性心动过速

心电快递专栏编辑 :我有一份短阵室速心电图 ,有些现象不能肯定 ,恳请指教。患者女 ,55岁 ,临床诊断冠心病 ,图 1为 1 2导联同步心电图 ,可见室性早搏伴完全性代偿间期 ,室早呈左束支阻滞伴电轴不偏。图中还有短阵室速 ,其QRS波形态与室早完全相同。图 2为 II导联的连续记录 ,可见偶发房早 ( * ) ,频发室早呈三联律 ,还可见到多次的短阵室速。室速每阵持续 8～ 1 1跳 ,因有明显的房室分离 ,室速的诊断可以肯定。仔细测量后可见每阵室速前室早的代偿期均比其他室早的代偿期长 ,室早的发生与较长的代偿期是否形成了长短周期现象 ?除此 ,图 2…     

动态心电图检出短阵室性心动过速的临床和心电图分析

一般认为器质性心脏病发生Lown分级Ⅲ级以上的室性心律失常易引发心室颤动而致猝死,故属恶性心律失常.本文收集经24h动态心电图检出的短阵室性心动过速32例,就其临床和心电图作一初步分析,旨在探讨动态心电图检出短阵室性心动过速的临床意义和发生机制.临床资料本组32例均为住院患者.用英国牛津公司产 Prima型动态心电图仪24h监测,其中男性23例,女性9例,年龄43～84(65.41±8.02)岁,经询问病史及各项检查明确诊断.基础心脏病为冠心病23例,高血压心脏病5例,肺源性心脏病3例,扩张型心肌病1例.其中3例为急性心肌梗死,6例为陈旧性心肌梗死,11例合并脑出血或脑梗死.X线胸片、超声心动描记术提示20例有不同程度心房、心室或全心扩大,5例有     

房性心动过速和室性心动过速并存1例

患者,女性,65岁,因反复胸闷、心悸10余年,加重1个月求诊。3年前心脏超声示:左心室肥大,左心房肥大,肥厚性心肌病(心尖肥厚性)。临床诊断为肥厚性心肌病。常规心电图(图略):窦性心律,左心房肥大,左心室肥大,心室内传导阻滞,ST-T     

24小时动态心电图检出室性心动过速分析

对５７例２４ｈ动态心电图检出的３１６阵室性心动过速进行分析发现，发生在日间活动中最多，共２１２阵，占６７％；发生在睡眠中１０４阵，占３３％。有１５４阵室性心动过速发生前有ＳＴ段压低或上抬，提示室性心动过速发生与心肌缺血有关。３１２阵室性心动过速中提前指教大于或等于１．０（占９８．７％），说明室性心动过速的发生大多数不是由＂Ｒ波重叠Ｔ波＂现象激发；易损指数无一阵大于１．０，提示动态心电图监测的室性心动过速不具有高的易损指数。３１６阵室心动过速无一例发展为心室扑动或心室颤动。     

Syncope and polymorphic ventricular tachycardia in the setting of a febrile illness

An asymptomatic woman with no clinical history consulted for pneumonia-induced fever; she then presented episodes of syncope due to polymorphic ventricular tachycardia and ECG alterations compatible with Brugada syndrome. Genetic studies showed no alterations in the SCN5A gene but other polymorphisms were observed. Further genetic studies are required to elucidate the pathophysiological mechanisms of fever and the function of sodium channels.     

心外膜室性心动过速的心电图特征

心外膜室速的心电图有其共同表现：QRS 时限≥200 ms,但也有部分时限≤120 ms;起始部有假性Δ波≥34 ms;电轴多数左偏,胸前导联移行在 V2以后;V2导联 R 波达峰值时间延长≥85 ms;最短 RS 时间≥121 ms。识别左心室起源的心外膜室速：Ⅰ导联呈 Q 波的基底、心尖部室速;Ⅱ、Ⅲ、aVF 导联无 Q 波的基底部室速;Ⅱ、Ⅲ、aVF 导联呈 Q 波的基底上部、心尖部室速;最大转折指数可识别左室流出道心外膜室速,当最大转折指数≥0．55可识别远离主动脉窦的心外膜室速。识别右心室起源的心外膜室速：Ⅰ导联呈 Q 波且右室前壁导联呈 QS,预示心外膜室速可能性大;Ⅱ、Ⅲ、aVF 导联起始 Q 波,可在同步电生理标测时观察到位于右心室心外膜起源的室速。但不同部位及不同病因的室速又有其特殊性,术前通过体表心电图进行较为精确的定位对室速消融有一定的指导意义。     

Pilsicainide-induced Brugada-type ECG and ventricular arrhythmias originating from the left posterior fascicle in a case with Brugada syndrome associated with idiopathic left ventricular tachycardia.

The patient was a 50-year-old male in 2002, who was first suspected of having a Brugada-type electrocardiogram (ECG). A drug challenge test using pilsicainide was performed and unmasked a typical coved type ST elevation followed by ventricular arrhythmias (VAs) manifesting a QRS pattern with a right bundle branch block and left axis deviation. Three years later, he was transferred to the emergency room due to a wide QRS tachycardia with the same QRS morphology as the VA that previously occurred in the drug challenge test. An ECG just after the recorded termination of the tachycardia exhibited a typical Brugada-type ECG. In an electrophysiological study, ventricular fibrillation could be easily induced with reproducibility. Since the clinical tachycardia could not be sustained by an isoproterenol infusion, mapping and catheter ablation targeting the pilsicainide-induced VAs was performed. The successful ablation site was the left mid-lower septal wall where a Purkinje potential was recorded and a false tendon was attached just to it.     

Evaluation of new self-learning techniques for the generation of criteria for differentiation of wide-QRS tachycardia in supraventricular tachycardia and ventricular tachycardia

This study presents a comparison of three different methods for differentiating between supraventricular and ventricular tachycardias with wide-QRS complex. One set of criteria, derived using classical statistical techniques, was compared with two new self-learning computer techniques: the artificial neural networks and the induction algorithm approach. By analyzing the results obtained in an independent test set, using these new techniques, the criteria defined by the classical method could be improved.     

经食管心房调搏在特发性室速诊断中的应用

目的探讨经食管心房调搏在特发性室性心动过速(室速)中的应用价值。方法回顾分析30例特发性室速患者的经食管心房调搏资料。结果经食管心房调搏基础刺激诱发心动过速6例(20%),静脉滴注异丙肾上腺素激发后刺激诱发12例(40%),心动过速时通过食管心电图证实QRS波群与P波非1∶1关系,且心室率>心房率而确诊为室速26例(86.67%)。心动过速自行终止5例(16.67%),药物或其它方法终止19例,经食管心房调搏超速刺激法终止6例(20%)。结论经食管心房调搏对诱发和确诊室速有较大的帮助,经食管心房调搏终止室速成功率不高。     

Mapping for ventricular tachycardia

Mapping strategies for ventricular tachycardia (VT) have evolved significantly in the past 2 decades. This review discusses mapping techniques that can help in successful VT ablation. The electrocardiogram (ECG) remains a vital component of VT mapping and can help to identify the chamber of origin of VT. The ECG morphology of VT, however, is influenced by orientation of heart and location of the scar. Activation mapping during VT is an important technique that can help in further localization. Care has to be exercised to ensure that small signals are not ignored and far-field signals are recognized. Pace-mapping to mimic the VT is another way to map exit site for scar based reentrant VT or the site of origin of triggered and automatic VT in the absence of structural heart disease. For the latter group, this technique is widely used in determining the site of ablation. It is important to ensure a complete ECG match (12 out of 12 leads) of the pace-map to the clinical arrhythmia in these patients. In patients with structural heart disease, entrainment mapping remains the gold standard for defining the protected isthmus and other components of the VT circuit. Using this technique, successful ablation of reentrant VT can be achieved in 60–90% of patients. In order to perform entrainment mapping, the VT has to be hemodynamically tolerated; this is not the case in 25% of pts with scar based reentrant VT. The development of 3-dimensional mapping systems allows for more anatomically based linear ablation in patients with poorly tolerated uniform VT. Despite these advances, there are still about 10–20% VTs that cannot be ablated successfully with the above described techniques, especially in patients with structural heart disease. Other recent advances such as percutaneous closed chest epicardial mapping technique and cooled tip ablation catheter technology have the potential to enhance mapping and successful ablation of VT.     

Syncopal monomorphic ventricular tachycardia with pleomorphism, sensitive to antitachycardia pacing in a patient with Brugada syndrome.

Polymorphic ventricular tachycardia and ventricular fibrillation are the most common arrhythmias in Brugada syndrome, causing syncope or sudden death. Sustained monomorphic ventricular tachycardias are rare in this context. We report the case of a 41-year-old man with repetitive syncopal episodes and an ajmaline-induced characteristic Brugada ECG pattern, in whom episodes of monomorphic ventricular tachycardia with pleomorphism and response to ventricular pacing were documented.