肺静脉节段性消融治疗阵发性心房颤动

肺静脉内的折返是促使心房颤动（房颤）发作的最可能机制，肺静脉在房颤的发生和维持机制中起重要作用。在实时左心房三维标测系统（Carto）指导下，肺静脉环状射频消融电隔离治疗阵发性房颤已成为可能。这里我们评价术前16排螺旋CT指导下肺静脉节段性消融治疗顽固性阵发性房颤的临床效果。     

肺静脉在心房颤动机制中的作用

心房颤动是最为常见的异常心脏节律。起搏电生理研究表明大多数心房颤动均为源自肺静脉壁内心肌组织(即肌袖)的异位搏动病灶所触发。但是,心房颤动肺静脉起源的机制尚未完全阐释,目前认为与肺静脉内心肌自律性升高,触发活动及折返有关。对心房颤动发生、发展及维持机制的研究,对于指导心房颤动的临床治疗具有重要的意义。     

环肺静脉电隔离术后左心房-肺静脉折返性心动过速诊断与治疗

目的:探讨心房颤动(房颤)环肺静脉电隔离术后左心房-肺静脉折返性心动过速的心电生理学特征及其消融策略.方法:环肺静脉电隔离术后复发节律规整的心动过速患者9例,三维指引下拖带标测左心房、肺静脉,明确环肺静脉消融线遗留的缝隙,消融缝隙并随访.结果:9例左心房-肺静脉折返性心动过速患者平均年龄(57.9±11.1)岁(42～72岁),心动过速周长(300.1±29.4)m,(264～318 ms),其中持续性心动过速7例,阵发性心动过速2例.所有患者环肺静脉线性消融后电传导恢复,心动过速时左心房与肺静脉之间1:1传导,三维标测显示5例最早心房激动位于右肺静脉前庭、2例位于左肺静脉前庭、1例位于左肺静脉干、1例位于右肺静脉干.拖带标测显示心动过速与左心房、肺静脉以及环肺静脉消融遗留的两个缝隙[间距(34.4±4.1)mm]构成的折返环路有关,单一传导路径消融可以终止心动过速,心动过速终止后消融缝隙,随访15.1 ±411.1(6～32)个月无复发.结论:左心房-肺静脉折返性心动过速与左心房、肺静脉以及环肺静脉电隔离线上遗留的两个缝隙相关,可根据左心房和肺静脉内拖带标测明确诊断,消融缝隙可以根治此类心动过速.     

犬左上肺静脉电传导的特性

目的研究肺静脉电传导的特性,探讨肺静脉异位兴奋灶诱发心房纤颤的具体机制。方法选用25只犬,将自制的18导联环状标测电极置于左上肺静脉外膜上,从左心房、冠状窦远端、肺静脉远端采取S1S1、S1S2两种刺激方案,记录肺静脉18导联外膜标测电图。结果肺静脉内存在类文氏和类莫氏传导阻滞和肺静脉-左心房传导速度逐渐加快电生理现象,后一现象发生在房颤启动前,导致短配对间期或短长周期的心房激动;电活动从心房向肺静脉远端传导时肺静脉各个部位激动较一致,而电活动从肺静脉远端向心房传导时肺静脉各个部位激动不一致;肺房传导时间显著长于房肺传导时间[（46.6±14.4）msvs（17.8±9.3）ms,P<0.01]。结论正常肺静脉具有传导阻滞、传导延迟及各向异性传导的特性,有利于肺静脉内折返的形成;而肺静脉异位兴奋灶快速电活动使肺静脉和心房发生电重构,导致肺静脉-左心房传导速度逐渐加快,最终诱发出心房纤颤。     

心房颤动和胸静脉

胸静脉包括上腔静脉、肺静脉、Marshall静脉（vein of Marshall VOM）、下腔静脉、上腔静脉、冠状静脉和奇静脉。人类奇静脉无肌袖，但可于犬中发现。冠状静脉周围的肌袖是心律失常潜在起源点，但其激动很难和左心房的激动区分开来，临床对其研究甚少。最近研究观察到阵发性心房颤动（房颤）时可被肺静脉的反复快速激动（repetitive rapid activities RRAs）所启动。在心房颤动时，Marshall静脉和肺静脉比左心房的激动周长更短，而左心房的激动周长比右房短，提示胸静脉是维持心房颤动的反复快速激动的来源。     

心房颤动肺起源的电生理机制研究进展

心房颤动（简称房颤）是最常见的心律失常之一。房颤的肺静脉起源学说被认为是阵发性房颤研究方面最具突破性的进展，但是房颤肺静脉起源的电生理机制尚未完全阐明，近年来的电生理学研究显示自律性增高和触发活动可能是肺静脉肌袖电活动产生的机制。但是由于肺静脉的解剖和电生理特点造成的肺静脉内传导阻滞的存在，生理情况下，肺静脉电位很少能够激动心房导致房颤的发生。快速心房起搏(rapid atrial pacing,RAP)已经被证实是房颤研究中一种非常有价值的方法，在RAP或房颤后，诱发肺静脉电重构和心房电重构，有利于房颤的发生与维持。     

心房颤动射频导管消融的策略及疗效评估

射频导管消融(下称消融)已发展成为心房颤动最有效的根治手段.与抗心律失常药物(AAD)不同,消融针对的是心房颤动的发病与维持机制,因而使根治成为可能.研究表明,肺静脉及其周围左心房后壁为心房颤动发病及维持的关键部位.因而,这一区域也是所有心房颤动消融策略的共同干预靶区.目前,在有经验的电生理中心,以肺静脉及左心房后壁为干预目标的心房颤动消融术后随访成功率在80%以上.     

室上性心律失常与心房颤动关系再认识

心房颤动(atrial fibrillation,AF)是室上性心律失常常见的合并症。与普通人群相比,阵发性室上性心律失常患者AF发生率显著升高,且一般表现为阵发性AF。但迄今为止,AF发生的电生理机制并不十分明朗,其机制有多种学说,如多子波折返学说、异常自律性增高学说、主导转子学说、局灶触发学说等。但不管何种学说,AF的发生必须依赖两个因素,即发生机制和维持机制,两者缺一不可。目前越来越多的证据表明,AF的机制很可能是局灶驱动伴向周围的颤动样传导,多发子波折返仅仅是AF时心房激动的一种表现形式,而不是其维持的关键因素[1]。驱动AF的局部兴奋可以使一个或多个局灶的自律性升高或触发活动,但更可能是位于心房某个固定解剖部位(特别是肺静脉前庭部位)具有完整折返环路的折返激动。本文就室上性心律失常,包     

心房颤动递进式线性消融后的左心房扑动

目的旨在探讨心房颤动（房颤）递进式线性消融术中出现的房性心律失常的电生理特点及消融的结果。方法对80例房颤消融中出现规律的房性心律失常进行非接触激动顺序标测,判断电生理机制并指导消融。结果共146阵心动过速,4阵为左心房房性心动过速（房速）,周长为（225±49）ms,其余142阵为左心房扑动,左心房激动时间占心动过速周长的100％,周长为（205±37）ms,均与房颤“7”字消融线上的缝隙有关。根据缝隙的位置将心房扑动的折返环分为3类：Ⅰ类（n=68）,缝隙位于左心耳-左上肺静脉间的嵴部,Ⅱ类（n=50）,缝隙位于左心房顶部,Ⅲ类（n=24）,缝隙位于二尖瓣环峡部。其中130阵消融成功,其余16阵因消融反应欠佳后经药物或体外电转复为窦性心律。随访（16．2±6．7）个月,82．5％（66／80）的患者可维持窦性心律。结论房颤递进式线性消融术中出现的房性心律失常多为大折返机制,且与“7”字消融线上的缝隙有关,这些缝隙主要位于左心耳-左上肺静脉间的嵴部。非接触标测技术能快速准确地识别这些缝隙并指导消融。     

肺静脉前庭的组织解剖学特点与心房颤动

肺静脉前庭是肺静脉和左房相延续的区域，胚胎发育中由肺静脉与左房融合、吸收逐渐形成，该处肌纤维走行复杂，可呈环形、纵行或斜行排列，不同肌纤维相互交错、各向异性明显，激动在此处传导时存在明显延缓或阻滞。肺静脉及其前庭组织与心房颤动的发生、维持密切相关，深入认识肺静脉前庭区域的组织解剖学特点，对理解心房颤动发生、维持机制，进而指导临床治疗具有重要意义。     

Left atrial posterior wall and pulmonary vein refractory periods are associated with atrial fibrillation inducibility in a swine model

INTRODUCTION AND OBJECTIVES: Ectopic activity originating inside the pulmonary veins has been associated with paroxysmal atrial fibrillation in some patients. However, the roles played by the pulmonary veins and the posterior wall of the left atrium in maintaining atrial fibrillation are not well understood. METHODS: Our aim was to determine whether there is a correlation between the refractory period of either the lateral wall of the right atrium, the lateral wall of the left atrium, the posterior wall of the left atrium, or the pulmonary veins, and the inducibility of atrial fibrillation in an experimental swine model. We assessed atrial fibrillation inducibility using programmed atrial stimulation before and after intravenous administration of a high dose of methacholine in 20 pigs. RESULTS: Atrial fibrillation was induced in 17 out of the 20 pigs. Univariate analysis showed that there were negative correlations between all refractory periods and atrial fibrillation inducibility. A short refractory period was associated with greater inducibility. In the multivariate analysis, only the refractory periods of the posterior wall of the left atrium and the pulmonary veins were associated with inducibility. We also investigated the relationship between the local atrial fibrillation cycle length and refractory period; the only significant correlation was with the refractory period of the lateral wall of the right atrium (Pearson correlation coefficient 0.97). CONCLUSIONS: In an experimental swine model, the inducibility of atrial fibrillation was found to be associated with the refractory periods of both the pulmonary veins and the posterior wall of the left atrium.     

Influence of new III class antiarrhythmic drug Niferidil (RG-2) on bioelectrical activity of rat pulmonary veins myocardium

Myocardial cells in pulmonary veins are thought to play a major role in the initiation and maintenance of atrial arrhythmias, including atrial fibrillation. In experiments on rat pulmonary veins, antiarrhythmic drug niferidil (RG-2) produced increase of APD90% and functional refractory period and decrease of action potential amplitude and slope of APD restitution curve. Thus niferidil (RG-2) exerts stronger action on pulmonary veins than left atrium. This can take important part in Niferidil (RG-2) antiarrhythmic activity.     

Contemporary approach to ablation of paroxysmal atrial fibrillation

Pulmonary veins have been shown to play an important role in the initiation and maintenance of paroxysmal atrial fibrillation. Seg-mental ostial isolation of the pulmonary veins results in cure in about 2/3 of the patients. This approach does not address non-pulmonary venous triggers of atrial fibrillation or the importance of the left atrium itself. Left atrial circumferential ablation has also been shown to be efficacious in patients with paroxysmal atrial fibrillation. This approach seems to address not only the various triggers of atrial fibrillation but also the left atrial substrate. Recently, a randomized study compared the 2 strategies and showed that left atrial ablation is superior to segmental ostial isolation. This review will highlight the anatomy and electrophysiology of the pulmonary veins, and the possible mechanisms by which they initiate and maintain paroxysms of atrial fibrillation. Segmental ostial isolation of the pulmonary veins and left atrial ablation will be compared as well.     

Percutaneous ablation of atrial fibrillation: for whom and how?

Recent developments in our understanding of atrial fibrillation (AF) have focused on the key role of pulmonary vein initiators of multiple wavelet reentry in the atria. Percutaneous catheter ablation of atrial fibrillation is commonly performed by electrical disconnection of pulmonary vein myocardium from the left atrium. As a result, pulmonary vein foci can no longer drive the atria into fibrillation. At present, the procedure is offered to patients with paroxysmal atrial fibrillation refractory to multiple antiarrhythmic agents. For patients with persistent atrial fibrillation, supplementary linear lesions in the left atrium may be necessary. Success rates (AF elimination) are 90% without drugs in case of paroxysmal atrial fibrillation and 80% for persistent atrial fibrillation. Complications including pulmonary vein stenosis are uncommon.     

The superior vena cava as a site of ectopic foci in atrial fibrillation

Radiofrequency catheter ablation of ectopic foci that trigger atrial fibrillation has been established as a curative method for patients with symptomatic paroxysmal atrial fibrillation. Although the majority of these foci are located in and around the pulmonary veins, other less common locations have been identified. Recognition that foci can lie outside the pulmonary veins is important for ensuring therapeutic success. The most frequently reported foci of ectopic activity outside the pulmonary veins are in the superior vena cava and the posterior wall of the left atrium. Here we report our experience with the ablation of ectopic foci located in the superior vena cava in patients with symptomatic paroxysmal atrial fibrillation.     

Evaluation of the Pulmonary Veins and Left Atrial Volume using Multidetector Computed Tomography in Patients Undergoing Catheter Ablation for Atrial Fibrillation

Catheter ablation is an evolving treatment option in patients with atrial fibrillation. Contrast enhanced electrocardiogram-gated multi-detector computed tomography (MDCT) has rapidly evolved over the past few years into an important tool in the diagnosis of coronary atherosclerosis. There is increasing recognition that MDCT is a useful tool to evaluate non-coronary structures, such as cardiac chambers, valves, the coronary sinus and adjacent structures including pulmonary veins. In particular, MDCT is playing an increasingly important role in the evaluation of the left atrium and the pulmonary veins in patients undergoing catheter ablation for atrial fibrillation. It provides accurate and reliable identification of the pulmonary veins and anatomical relationship between the left atrium and esophagus although the mobile esophagus may limit the value of MDCT to reduce the risk of atrio-esophagus fistula. In this article, we will review the evaluation of the left atrium and pulmonary veins using MDCT in patients undergoing catheter ablation of atrial fibrillation.     

Bronchogenic cyst causing atrial fibrillation by impinging the right inferior pulmonary vein

Atrial fibrillation is the most common sustained cardiac arrhythmia and is usually associated with underlying structural heart disease, but may also occur in isolation--the entity of "lone" atrial fibrillation. Recently, attention has been directed to the pulmonary veins as a source of the arrhythmia through identification of rapidly firing ectopic foci within the covering myocardial sleeves. We describe a 38-year-old man who presented with treatment-resistant atrial fibrillation and a posterior mediastinal mass. Electrophysiological studies demonstrated abnormal foci of electrical activity at the entrance of the right inferior pulmonary vein into the left atrium. Surgical exploration revealed a bronchogenic cyst that distorted and stretched the right inferior pulmonary vein as it traversed the posterior mediastinum towards the left atrium. Restoration of sinus rhythm without recurrence of atrial fibrillation characterized the clinical course after surgical resection of the mass. This case demonstrates that a retro-cardiac bronchogenic cyst can cause atrial fibrillation by impinging on a pulmonary vein.     

肺静脉异常电活动引起持续性心房颤动的电生理特点和消融治疗

目的　报道 4例肺静脉异常电活动引起持续性心房颤动 (房颤 )的电生理特点和消融治疗。方法　 4例患者的临床表现和心电图记录提示为持续性房颤。经股静脉和锁骨下静脉穿刺置入高位右房 (HRA)和冠状静脉窦 (CS)电极 ,并行房间隔穿刺和肺静脉造影 ,置入 10极环状电极 (Lasso电极 )进行各肺静脉标测。观察自发和诱发房颤时的心腔各部位局部电活动的周期及规则性 ,以局部异常电活动出现最早、持续异常电活动最紊乱的肺静脉作为靶肺静脉。在房颤持续时消融电隔离靶肺静脉至左房连接处 ,以房颤终止和异常电活动消失为消融终点。结果　 4例患者异常电活动起源于右上肺静脉 (3例 )和左上肺静脉 (1例 )。靶肺静脉局部电活动频率快且不规则 ,间断出现短阵性周期缩短。靶肺静脉口部消融分别于放电 1～ 18次时房颤终止 ,3例伴有异常电活动终止 ,1例肺静脉内仍显示快速异常电活动 ,经肺静脉内局灶消融后电活动终止。随访 4～ 17个月 ,无房颤复发。结论　肺静脉内异常电活动是部分持续性房颤的发生机制 ,射频消融肺静脉口部可隔离和消除异常电活动而终止房颤