射频导管消融治疗特发性室性期前收缩触发的心室颤动／多形性室性心动过速

目的：探讨特发性室性期前收缩（早搏,PVC）触发心室颤动和（或）多形性室性心动过速（VF／PVT）的临床特点及射频导管消融治疗效果。方法：313例无器质性心脏病接受射频导管消融治疗的特发性PVC患者,其中6例发生了由PVC触发的VF／PVT,分析该6例患者的临床资料及射频导管消融治疗效果。结果：该6例患者动态心电图可记录到频发PVC[（16303±5854）次／d],PVC联律间期及基础QT间期分别为（412±44）ms和（407±10）ms。这些参数值在另外307例特发性PVC患者中分别为（15570±4743）次／d、（419±36）ms和（404±8）ms,两组间无显著性差异。313例患者中,有88例记录到由PVC触发的单形态室性心动过速（VT）。PVC触发VF／PVT患者中晕厥发生率（3／6）高于由PVC触发的单形态VT患者（4／88,4．5％,P〈0．05）,PVT的周长[（235±22）ms]则短于单形态VT组[（324±29）ms,P〈0．05]。针对触发VF／PVT的PVC消融后随访的10～36个月期间,所有6例患者未再发生晕厥、VF及心脏骤停。结论：恶性VF／PVT可能由一些特发性PVC诱发,射频导管消融PVC治疗可作为一项有效的治疗选择。     

心肌梗塞后诱发室性心动过速(VT)或心室颤动(VF)的电生理特征:心室晚电位与诱发持续性VT所需的配对间期的相关性

本文探讨心梗后心室晚电位与诱发持续性室速或室颤所必需的配对间期的相关性。 对象为83例既往心肌梗塞患者,56例被证实有持续性VT发作史,15例有VF发作史,12例为不明原因晕厥。心室分级程序刺激诱发持续性单形性室速(SMVT)71例(作为VT组),诱发室颤12例(为VF组)。SMVT和VF均在SR-S_2-S_3或S_1-S_2-S-3刺激时诱发。VT组诱发VT和VF所需配对间期之和(SCI)显著长于VF组(485±59对387±36ms,P<0.001),有效不应期与第二配对间期之差小于VF组(-3±40对24±29ms,     

氯化铯诱发在体心脏触发性心律失常的实验研究

心内膜单相动作电位研究表明,单相动作电位的复极进程能够正确反映心肌细胞动作电位复极时程。狗静脉注射氯化铯后早期后除极电位(EAD)的发生率为100％,单相动作电位90％复极时程明显延长(224.4±50.6ms VS 368.4±34ms),与QT间期延长相一致。氯化铯诱发的室性心律失常发生于EAD顶峰,触发心律联律间期与EAD联律间期密切相关。硫酸镁使EAD和室性心律失常同时消失。提示该心律失常为EAD触发活性所致。     

直立倾斜试验诱发晕厥时RR和QT间期变化及其意义

目的 观察血管迷走性晕厥(VS)患者直立倾斜试验(HUT)诱发晕厥时RR和QT间期的变化。方法测定20倒VS患者HUT前平卧位时、倾斜后最快心率时和晕厥发生前或先兆晕厥最慢心率时RR和QT间期。结果 晕厥发生前或先兆晕厥最慢心率时，RR间期较试验前和卧位明显延长(1473±458ms对956±117ms，P<0．001)，而QT间期无明显变化(427±55ms对416±49ms，P>0．05)。结论 HUT诱发晕厥时．虽然迷走神经活性显著增强，交感神经活性迅速撤除，但后者对心脏的谓节作用依然存在。     

起源于左心室游离壁的单形室性心动过速和早搏的射频导管消融

目的 起源于左心室游离壁的室性心动过速(ventricular tachycardia, VT)及早搏(premature ventricular contraction, PVC)是较少见的心律失常,本文报道对其进行标测及射频导管消融的初步经验。方法 11例患者(男性9例,女性2例),平均年龄(37.3±17.2)岁。其中7例有持续性VT,4例为短阵非持续性单形VT和/或频发PVC,体表心电图均为右束支阻滞(RBBB)和心电轴右偏。3例患者伴明显的左心室扩大及充血性心力衰竭。对全部患者进行了左心室电生理标测,其中6例采用了心内非接触式标测。在标测到的最早激动部位进行温度控制下的射频导管消融。结果 11例患者均标测到自发的单形VT或PVC。其室性心律的平均周长(443.3±76.6)ms。全部室性心律均起源于左心室游离壁,其中2例位于偏前的高位近二尖瓣环处,2例位于后外侧游离壁中、高位,6例源于游离壁中高位,1例位于游离壁中下部。VT或PVC最早电位平;啕领先体表心电图(31.8±11.8)ms。全部患者的消融均获得即时成功,且不再服用抗心律失常药物,平均随访(11.8±8.0)个月,仅1例VT患者有单形PVC(<1000次/24h),3例左心室增大者均有明显缩小,其中1例基本恢复正常。结论 单形VT或PVC可发生于无缺血性心脏病的患者,表现为右束支阻滞和心电轴右偏,其频率较慢,可被射频导管消融消除。     

反复单形房性心动过速的电生理特点和射频消融结果

目的报道反复单形房性心动过速(房速)的电生理特点和射频消融结果.方法对8例反复单形房速患者进行心内电生理检查和射频消融治疗.结果反复单形房速的发作方式与反复单形室性心动过速相似.房速时心电图PP间期和心内电图AA间期极不规则(200～450)ms,平均最大与最小AA间期的差值为(169±75)ms,但P波形态和心房激动顺序恒定.房速的病理机制为非折返性.成功消融8例患者的房速,其中7例的成功消融靶点位于肺静脉开口部或肺静脉内.平均随访(10±2)个月,无1例复发.结论反复单形房速是一种不同于阵发性或慢性房速的少见房性快速心律失常,能被射频消融术所根治.     

房性早搏始动的阵发性心房颤动的动态心电图分析

了解房性早搏 (简称早搏 )与阵发性心房颤动 (简称房颤 )的关系。通过 2 4h动态心电图分析 2 4例阵发性房颤患者 ,观察其 2 4h房颤的发作阵数 ,房早的发作情况 ,诱发和未诱发房颤的房早的联律间期、房早前周长、房早前12 0s房早频率等。结果 :诱发房颤的房早比未诱发房颤的房早显著提前 (35 5 .9± 32 .8msvs 4 0 8.4± 4 1.7ms,P <0 .0 1) ,房早是否诱发房颤还与房早前周长长 (85 4± 10 6msvs 74 2± 113ms ,P <0 .0 1)及房早前 12 0s的房早频率快 (2 1.7± 15 .3次 /分vs9.79± 7.92次 /分 ,P <0 .0 1)有关。结论 :房早是否始动阵发性房颤不仅与房早的联律间期有关 ,而且与房早前周长及其前 12 0s房早的频率有关。     

急性心肌梗死QT间期测量的导联选择及QT离散度分析

目的探讨急性心肌梗死测定最大QT间期的导联选择及分析心肌梗死急性期QT离散度与恶性以律失常的相关性。方法研究41例急性心肌梗死患者发病一周内的常规12导联体表心电图,1.比较最大QT间期的所在导联;2.比较室速/室颤患者无室速/室颤的QT离散度。结果在常规12导联体表心电图上,最大QT间期导联在V1～V3;室速/室颤患者的QT离散度(83±25ms)显著大于无室速/室颤的QT离散度(65±20ms),P<0.01。结论在急性心肌梗死患者中进行QT间期测定和QT离散分析时,正确的选择应在胸前导联测量最大QT间期。而心肌梗死急性期QT离散度增加可作为恶性心律失常发生的危险信号。     

采用心内非接触式标测的右心室流出道室性心动过速的射频消融

目的 右心室流出道(right ventricular outflow tract,RVOT)的解剖结构使得对该部位的室性心动过速(ventricular tachyeardia,VT,室速)标测定位的难度较大,远期成功率也较低,为此,采用心内非接触式标测指导导管消融。方法 20例患者(男性12例,女性8例),年龄14～59(35.1±12.3)岁。其中6例有晕厥或黑矇史,7例既往曾接受射频消融未获成功。全部患者均在RVOT内放置EnSite3000标测导管,在窦性心律下进行疤痕标测和心动过速时进行最早激动标测,并根据标测结果使用EnSite 3000导管的导航功能指导消融定位。消融前并进行起搏标测。结果 20例患者共诱发出22种RVOT室速,其中3例还伴其它起源的室性早搏(室早)。疤痕标测提示,13例患者有电学意义上的疤痕区域,且有11例室速起源于该疤痕区域。25个室速或室早起源点中1例起源于近肺动脉瓣口部,10个位于间隔侧,其余均偏游离壁,其中7个偏RVOT后壁中、下部,4个偏前壁中、下部,3个位于游离壁侧;病变基质的直径为6～42 mm,平均(16.8±9.2)mm。非接触式标测所确定的最早激动处电位平均领先体表20～62(41.0±13.8)ms;与自发的室性心动过速相比,起搏标测下14例的12个导联QRS形态完全一致,11/12个导联一致的为10例,1例有10/12导联一致。全部室速和室早均消融成功。在标测确定的     

短联律间距室性早搏引发的多形性室性心动过速或/和心室颤动五例临床分析

报道5例短联律间距室早引发的多形性室速或/和室颤,临床表现与常见的QT间期延长综合征引起的扭转室速不同,其特点有:单一或触发室速的室早联律间距极短(240～320ms);窦律时QT间期及T/U波形态正常;无明显心脏病证据;利多卡因对此治疗无效,而异搏定、心律平、硫酸镁有效。     

Electrocardiographic determinants of the polymorphic QRS morphology in idiopathic right ventricular outflow tract tachycardia

Coupling Intervals and Polymorphic QRS Morphologies . Introduction: Premature ventricular contractions (PVCs) arising from the right ventricular outflow tract (RVOT) can trigger polymorphic ventricular tachycardia (PVT) or ventricular fibrillation (VF) in patients with no structural heart disease. We aimed to clarify the ECG determinants of the polymorphic QRS morphology in idiopathic RVOT PVT/VF. Methods and Results: The ECG parameters were compared between 18 patients with idiopathic PVT/VF (PVT‐group) and 21 with monomorphic VT arising from the RVOT (MVT‐group). The coupling interval (CI) of the first VT beat was comparable between the 2 groups. However, the prematurity index (PI) of the first VT beat was smaller in the PVT‐group than in the MVT‐group (P < 0.001). Furthermore, the QT index, defined as the ratio of the CI to the QT interval of the preceding sinus complex, was also smaller for the PVT/VF in the PVT‐group than that for the VT in the MVT‐group (P < 0.01). In the PVT‐group, the CI of the first VT beat was comparable between that of VT and isolated PVCs, but the PI of the first VT beat was shorter for VT than isolated PVCs (P < 0.05). The PI was the only independent determinant of the polymorphic QRS morphology (odd ratio = 2.198; 95% confidence interval = 1.321–3.659; P = 0.002). Conclusion: The smaller PIs of the first VT beat may result in a polymorphic QRS morphology. (Cardiovasc Electrophysiol, Vol. 23, pp. 521‐526, May 2012)     

特发性右室流出道心律失常患者J波的发生率及其临床特征

目的 调查J波在特发性右室流出道室性心动过速或室性早搏（RVOT-VT/PVCs）病人的发生率及其临床特征。方法 该研究纳入143例特发性 RVOT-VT/PVCs的患者和285例年龄和性别匹配的健康体检者作为对照组。 评估、比较两组间 J-波的发生率。 依据J波的存在与否,将患者分为伴有J波的 RVOT-VT/PVCs组（J-VT/PVCs组）和不伴有J波的 RVOT-VT/PVCs组（non-J-VT/PVCs组）,对两组的临床和电生理数据进行比较。 结果 与对照组比较,J波在特发性 RVOT-VT/PVCs患者中更为常见（39. 9% vs 16. 1% ,P〈0. 01）。 与 non-J-VT/PVCs组比较,J-VT/PVCs组持续性VT、晕厥有较高的发生率,分别为24. 6% vs 4. 7% ;26. 3% vs 2. 3% ,P均〈0.01。 而且VT的周期更短[（304±56）ms vs（350±56）ms,P〈0. 01]。 两组中无心室颤动或心脏猝死发生。 结论 特发性RVOT-VT/PVCs患者,有较高的J波发生率;有J波的患者伴随有较严重的心律失常 。     

射频消融治疗室性早搏触发特发性室性心动过速／心室颤动的病例分析

目的探讨射频消融治疗在室性早搏（室早）触发特发性室性心动过速／心室颤动（室速／室颤）中的作用。方法总结3例由室早触发室速／室颤的治疗经验,1例对室早进行射频消融（RF—CA）并植入心律转复除颤器（ICD）,另1例经射频消融未完全消除室早而选择植入ICD,第3例经射频消融成功消除室早,未再发室颤。结果随访2年,3例患者均存活,ICD未再记录到室速／室颤。结论在室早触发室速／室颤病例中,应分析室早与室速／室颤的相关性,给予个体化治疗,射频消融室早可以消除／减少晕厥和室颤的发作。     

低能量放电下标测无室性早搏的流出道室性心动过速

目的 本文报道11例非频发室性早搏(室早)的流出道室性心动过速(室速)伴反复晕厥病例经导管射频消融成功的体会,并由此介绍一种新的针对这类患者的标测方法.方法 11例患者,全部为女性,年龄(39.9±13.7)岁,全部曾使用2种以上抗心律失常药物治疗,治疗期间均有晕厥或黑矇病史1～3年.结果 (1)所有11例患者在术中经过各种方法均可记录到至少1次室早、室速发作心电图,其中6例经程序刺激不能诱发的通过静脉滴注异丙肾上腺素能诱发室早、室速.(2)所有患者先在右心室流出道预测起源区以15～20 W低能量放电下微调消融电极导管位置和方向,在诱发出与所记录、冻结的室早完全一致的位点时,加大能量至35～50 W,反复巩固2～3次,直至室早、室速不再出现.然后以此点为中心,向周围微移动电极导管约5 mm,最终消融出大约1 cm2的面积.所有11例患者,采用这种方法全部都诱发出与记录室早12/12导联完全一致的室速.(3)11例患者中有10例达到消融终点,其中9例在右心室流出道间隔部及后壁,1例在右冠窦基底部.另1例未达到消融终点的患者,在消融开始时用异丙肾上腺素仅可诱发极少的室早,但在低能量消融后诱发频发的短阵室速,激动标测提示最早激动点位于左冠窦中下部,该处放电诱发出与自发室早一致的图,但反复放电室早、室速不能完全消除,考虑为靠外膜区室早而放弃.(4)术后所有患者经电话、预约门诊随访3～14个月,没有1例主诉再发黑矇和晕厥者.结论 低能量放电标测完全可作为一种新的标测手段在实际工作中配合使用,尤其对那些反复黑矇、晕厥但室早、室速发作较少的患者,常规标测方法几乎无用,此时低能量放电标测就显得更加实用.     

Site-specific arrhythmogenesis in patients with Brugada syndrome

INTRODUCTION: It has been believed that electrophysiologic abnormality of the epicardial region of the right ventricular free wall may play an important role in arrhythmogenesis of phase 2 reentry in Brugada syndrome, but clinical evidence of the occurrence of ventricular arrhythmias at the right ventricular free wall has not been evaluated. In this study, we evaluated the site-specific inducibility of ventricular fibrillation (VF) and the origin of spontaneous premature ventricular contractions (PVCs) in patients with Brugada syndrome. METHODS AND RESULTS: Forty-five patients with Brugada-type ECG were enrolled in this study. Spontaneous PVCs were recorded in 9 patients. Programmed electrical stimulation (PES) was performed at the right ventricular apex (RVA), the free wall and septal region of the right ventricular outflow tract (RVOT), and the left ventricle (LV). The inducibility of PVT/VF was evaluated at each ventricular site, and the origin of PVC was determined by pace mapping. Sustained VF was induced in 17 patients. VF was induced in all 17 patients by PES at RVOT. Although PES at the septal region of the RVOT induced VF in only 5 patients (29%), PES at the free-wall region of the RVOT induced PVT/VF in 13 patients (76%). PES at RVA induced VF in only 2 patients (12%), and PES at LV failed to induce any arrhythmic events. Ventricular pace mapping showed that 64% of PVCs occurred at the free-wall region of the RVOT, 18% at the septal region of the RVOT, 9% at RVA, and 9% at LV. CONCLUSION: VF in patients with Brugada syndrome frequently is induced at the free-wall region of the RVOT area. The origin of PVC appears to be related to the site of PVT/VF induction by PES.     

Idiopathic ventricular arrhythmias arising from the pulmonary artery: Prevalence, characteristics, and topography of the arrhythmia origin

BACKGROUND: The characteristics of idiopathic ventricular tachycardias (VTs) or idiopathic premature ventricular contractions (PVCs) arising from the pulmonary artery (PA) have not been sufficiently clarified. OBJECTIVE: The purpose of this study was to clarify the prevalence, characteristics, and preferential sites of idiopathic VT/PVCs arising from the PA (PA-VT/PVCs). METHODS: Data obtained from 276 patients with idiopathic VT/PVCs who underwent radiofrequency (RF) catheter ablation were analyzed. RESULTS: Twelve VT/PVCs (4%) were PA-VT/PVCs, and their onset (34 +/- 14 years) was the youngest among all subgroups. Because those QRS morphologies were similar to VT/PVCs arising from the right ventricular outflow tract (RVOT-VT/PVC) and the earliest ventricular activation was from the RVOT, an initial ablation was performed in the RVOT in all patients. However, RF catheter ablation at the RVOT resulted in a QRS morphology change in all patients, so thereafter PA mapping and ablation was performed. A characteristic potential during sinus rhythm and/or the arrhythmia was recorded at the successful PA ablation site in all patients. A perfect or good pace map was obtained in 7 (70%) of 10 patients. The successful ablation site was the septal side of the PA close to the posterolateral attachment in 9 patients (75%) and the septal side close to the anterior attachment in the remaining 3 (25%). No PA-VT/PVCs recurred during follow-up of 27 +/- 13 months. CONCLUSION: PA-VT/PVCs should always be considered when the ECG suggests RVOT-VT/PVCs and RF catheter ablation in the RVOT results in both a failed ablation and a change in QRS morphology. PA-VT/PVCs often originate from the septal side of the PA.     

Characterization of premature ventricular contraction initiating ventricular fibrillation

The aim of this study is to characterize the electrocardiographic features of premature ventricular contractions (PVC) from different anatomical region that trigger ventricular fibrillation (VF). METHODS AND RESULTS: 36 consecutives patients (20 males, 42+/-14 yrs) undergoing VF ablation from 7 centres were studied (22 with idiopathic VF, 4 associated with a long QT syndrome, 3 with Brugada syndrome, 4 with ischaemic cardiomyopathy and 3 associated with other substrate). Mapping of these PVC showed 2 different origins, which were then confirmed by ablation: right ventricular outflow tract (RVOT) (22%) and peripheral Purkinje network (81%). One patient had PVC from both origins (Brugada). RVOT PVC were frequent but had triggered only 5+/-5 episodes of VF for 26+/-33 months. Purkinje PVC were more likely to be present during electrical storm with 18+/-28 episodes of VF for 33+/-45 months. Right Purkinje PVC have a left bundle branch block with superior axis morphology whereas left Purkinje ones have a right bundle branch block. The axis of activation showed variation from inferior to superior depending on the area of origin from the Purkinje network and the exit site to the myocardium. However Purkinje PVC were characterized by short QRS duration (126+/-18 vs 145+/-13ms for RVOT PVC; p=0.05). In addition the coupling interval was significantly shorter compared to RVOT PVC (292+/-45 vs 358+/-37ms respectively; p=0.005). CONCLUSION: PVC initiating VF demonstrate specific electrocardiographic features that facilitate determination of their origin. Ablation of these typical PVC is feasible in order to reduce ICD shock.     

Successful catheter ablation in a patient with polymorphic ventricular tachycardia

We describe a patient with polymorphic ventricular tachycardia (PVT)/ventricular fibrillation (VF) without organic heart disease who was cured by radiofrequency catheter ablation. The patient was a 65-year-old woman with a 10-year history of recurrent syncope. There was no evidence of organic heart disease, and the QT interval during sinus rhythm was borderline normal (corrected QT interval = 0.45 sec1/2). ECG recording during syncope showed PVT. On one occasion, PVT degenerated into VF. This PVT was always induced by a premature ventricular complex (PVC) originating from the right ventricular (RV) outflow tract. Rapid pacing (220 beats/min) at the site of PVC origin reproduced polymorphic change of the QRS wave on surface ECG that was similar to PVT. This suggests that the PVT originated from a single focus in the RV outflow tract. Catheter ablation was performed at the site of PVC origin. During 18-month follow-up, PVT/VF was not documented.     

The Relation of QT Dispersion to Spontaneous Ventricular Arrhythmias During the Acute Phase of Myocardial Infarction

Background: QT dispersion is associated with ventricular arrhythmias and sudden death among patients with a previous myocardial infarction (Ml). The relationship between QT dispersion and ventricular arrhythmias during the acute phase of Ml is uncertain. Methods: Patients enrolled in the Multicenter Study of Silent Myocardial Ischemia who had first Q wave myocardial infarctions (n = 363) were screened for the presence of ventricular arrhythmias during the initial hospitalization. Twelve patients had ventricular fibrillation, and 18 patients had an episode of monomorphic ventricular tachycardia. Each patient who had ventricular arrhythmias was matched with four controls on the basis of age, peak creatine kinase, thrombolysis, and the presence of congestive heart failure. The final study population consisted of 150 patients: 12 patients with ventricular fibrillation (VF+) who were compared to 48 controls (VF—), and 18 patients with ventricular tachycardia (VT+) who were compared to 72 controls (VT–). The RR, QRS, and QT intervals were measured manually using standard 12-lead ECGs (25 mm/s) obtained after hospital admission. The maximal QT dispersion (maximum — minimum value) was calculated. Multivariate logistic regression analysis was performed to determine if QT dispersion was independently associated with ventricular arrhythmias during the acute phase of Ml. Results: QT dispersion was significantly greater in VF+ patients compared to VF— patients (89 ± 18 ms vs 66 ± 22 ms, P > 0.01). QT dispersion was similar in VT+ and VT— patients (68 ± 25 ms vs 68 ± 26 ms, P = NS). QT dispersion was the only variable that was independently associated with ventricular fibrillation (OR 1.7 for each 10-ms increment in QT dispersion; 95% Cl 1.2–2.6; P = 0.008). QT dispersion was not associated with monomorphic ventricular tachycardia (OR 1.0; 95% Cl 0.8–1.2; P = NS). Conclusion: QT dispersion is independently associated with ventricular fibrillation, but not monomorphic ventricular tachycardia, during the acute phase of Ml.