射频消融心外膜脂肪垫治疗犬肺静脉左房交界处起源的心房颤动

目的探讨射频消融心外膜脂肪垫对左房-肺静脉交界触发的局灶性心房颤动(简称房颤)治疗的有效性。方法成年杂种犬10只,心外膜脂肪垫注射氯化乙酰胆碱(Ach)+左房短阵快速电刺激诱发犬左房-肺静脉交界触发的局灶性房颤模型。4极电极分别缝置于左房、右房、左肺静脉与左房交界处,记录最快激动部位。直视下射频消融心外膜脂肪垫。于房颤模型建立前后,及消融脂肪垫后测量左、右房有效不应期(ERP),肺静脉-左房交界处ERP、计算房颤诱发率。术毕处死实验犬行组织学检查。结果所有犬均能通过脂肪垫注射氯化Ach+左房短阵快速电刺激诱发出左房-肺静脉交界触发的局灶性房颤,建模后左房、右房、肺静脉-左房交界处的ERP均较建模前显著缩短(分别为94±33 ms vs 139±9 ms,104±17 ms vs 137±9 ms,104±17 ms vs 137±9 ms;P均<0.01)。脂肪垫消融后房颤诱发率与消融前比较显著降低(45%±16%vs 86%±4%,P均<0.01);左房、右房ERP无变化,肺静脉-左房交界处不应期显著延长(137±8 ms vs 104±17 ms,P<0.01)。组织学未发现除脂肪垫外的其它消融损伤灶。结论射频消融心外膜脂肪垫对肺静脉-左房交界触发的局灶性房颤治疗有效。     

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。     

犬快速肺静脉起搏心房颤动模型中CalpainⅠ在肺静脉肌袖及左心房的表达及意义

目的模拟肺静脉自行发放高频脉冲建立心房颤动的动物模型,研究肺静脉及左心房的CalpainⅠ重构情况,以期阐明CalpainⅠ的变化在持续性房颤的发生和维持中的重要作用。方法30只犬随机分为实验组和对照组,建立犬快速肺静脉起搏持续性心房颤动模型,取组织标本,标本共分4组:①正常犬左心房后壁组;②正常犬左上肺静脉肌袖组;③房颤犬左心房后壁组;④房颤犬左上肺静脉肌袖组。用RT-PCR和W estern印记法分别检测各组的CalpainⅠmRNA和蛋白的表达情况。结果正常犬左心房和肺静脉肌袖的CalpainⅠ的mRNA和蛋白表达水平无明显差异;房颤犬肺静脉和左心房的CalpainⅠ的mRNA和蛋白表达均高于对照组（均P<0.05）,房颤犬肺静脉肌袖CalpainⅠ的mRNA和蛋白表达高于左心房后壁部（均P<0.05）。结论在犬快速肺静脉起博心房颤动模型中,CalpainⅠ肺静脉肌袖和左心房中出现重构,参与了房颤的发生和维持。     

犬左上肺静脉电刺激诱发心房颤动的电生理机制探讨

为探讨肺静脉异位电活动诱发心房颤动 (简称房颤 )的机制 ,选用 2 5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 ,从肺静脉远端采取S1S1、S1S2 两种刺激方法诱发房颤 ,记录房颤从发生到结束的全过程。结果 :2 2只犬完成试验。S1S1连续刺激、S1S2 程序刺激均可诱发房颤 ,在 2min内 3,10只犬分别被诱发 ;S1S2 诱发房颤的肺静脉标测图的特点是S2 较短 (15 2 .5± 6 .3ms) ;在S1S1持续刺激 19只犬诱发的 2 1次房颤事件中 ,有三类特征性肺静脉标测图 ,所占比例分别为 14 .2 9%、9.5 2 %、2 3.81% ,其共同点是肺静脉 左房传导速度突然递增。第一类是传导速度的递增造成心房激动的联律间期不断缩短 ,肺静脉异位刺激本身诱发房颤 ,第二、三类是传导速度的递增造成心房激动的长间歇 ,长间歇之后肺静脉异位刺激之外的逸搏或异位刺激诱发房颤。结论 :肺静脉异位刺激可使肺静脉和心房发生电重构 ,来自于肺静脉异位刺激或之外的激动可诱发房颤。     

肺静脉在犬持续性心房颤动发病机制中的作用

探讨肺静脉在犬持续性心房颤动 (简称房颤 )发病机制中的作用。选用成年健康杂种犬 13条 ,通过持续快速心房起搏制备持续性房颤模型。将 12对心外膜电极分别缝于犬的左、右房游离壁和肺静脉等部位。心外膜标测犬自发持续性房颤 (>15min)的起源部位及自发和诱发的持续性房颤发作过程中心房不同部位的房颤波周长(AFCL) ,比较电学隔离肺静脉前、后持续性房颤的诱发率。 10只犬完成实验。总计记录到 3次自发出现的持续性房颤 ,心外膜标测显示其均起源于肺静脉。持续性房颤维持过程中心房的AFCL呈梯度分布 :右房游离壁 >左房游离壁 >肺静脉。电学隔离肺静脉后持续性房颤的诱发率显著降低 (P <0 .0 1)。结论 :肺静脉是犬持续快速心房起搏模型持续性房颤发作的关键部位     

射频消融治疗心房肌肌袖相关的房性心动过速

目的研究房性心动过速(房速)的临床和电生理特点.方法病例为1998年1月～2001年4月在我院因房速[部分伴心房颤动(房颤)]而行心内电生理和射频消融的患者.比较不同部位起源房速的临床特点和心内激动差异.结果共19例,年龄(46.8±18)岁.尝试消融治疗16例,房速起源右房侧11例,分别为希氏束上方4例,上腔静脉、右心耳各2例,下腔静脉、冠状窦口、终末嵴各1例.起源于左房侧5例,分别为肺静脉4例,左心耳1例.消融成功13例(81%),不成功者分别为希氏束旁2例,肺静脉1例.左房起源和上腔静脉起源房速心电图aVL导联P波呈负相,不同之处是后者Ⅰ导联P波呈正相.左上肺静脉、左心耳和上腔静脉起源的房性早搏(房早)和房速冠状窦远端心房激动早于或等于冠状窦口.而右上肺静脉房早和房速的冠状窦口激动早于远端.左上肺静脉、冠状窦口和下腔静脉的房早和房速时的冠状窦口激动早于右房上部.其他起源房早和房速时的右房上激动早于冠状窦口.成功消融部位电位提前体表心电图的P波(37.6±16.6)ms.但肺静脉和上腔静脉心动过速病例中各有1例经消融隔离心动过速起源的远端而成功.虽然多数患者的心动过速起源于易形成肌袖的心房和血管交界部位,但是肺静脉起源房速[AA间期(230.8±58.O)ms]的频率显著快于其他部位者[AA间期(342.6±86.5)ms,P=0.015],且更易出现房颤(4例全部出现).成功病例随访1～30(10±10)个月,无复发.结论局灶房速好发于心房与其他结构交界的部位,可能与该部位心房肌肌袖的存在有关,常规心内电生理检查有助于初步定位房速起源部位,射频消融成功率高.     

左心房在犬迷走神经介导性心房颤动中作用的研究

目的 研究犬肺静脉口周围的左心房组织在迷走神经介导的心房颤动(房颤)中的作用.方法 杂种犬7只,刺激颈部迷走神经干并诱发出持续性房颤.依次在心外膜进行肺静脉根部隔离、环肺静脉口"C"形左心房线性消融及完整的左心房线性消融.分别比较在刺激迷走神经时,肺静脉根部隔离前后、"C"形及完整的左心房线性消融后左、右心房的有效不应期(AERP),房颤波周长(AFCL),房颤的诱发率和持续时间的变化.结果 肺静脉根部隔离后,左、右心房AERP、AFCL较隔离前明显延长(P＜0.05),但可诱发出持续性房颤;"C"形左心房线性消融后,与肺静脉隔离前相比,左、右心房AERP、AFCL明显延长(P＜0.05),左、右心房AERP差异无统计学意义(P＞0.05),仍可诱发出持续性房颤;在完整的左心房线性消融后,与"C"形消融后相比,左、右心房AERP、AFCL及左、右心房AERP差异无统计学意义,诱发房颤持续(13.1±8.6)s.结论 肺静脉口周围左心房组织在迷走性房颤的维持上起决定性的作用.     

增龄对犬心房和肺静脉电生理学特性的影响

目的研究增龄对犬心房和肺静脉电生理学特性影响。方法17只杂种犬按年龄分为两组,成年犬7只,老年犬10只,做12导联同步心电图,测量P波平均时限和P波离散度;放置冠状静脉窦电极,左、右心耳电极,左上、左下、右上、右下肺静脉电极,测量各部位有效不应期（ERP）、ERP离散度及频率适应性。结果与成年犬相比,老年犬的P波平均时限延长,P波离散度增大;右心耳和冠状静脉窦近端ERP延长,左心耳和冠状静脉窦远端以及左上肺静脉ERP缩短;心房各部位及肺静脉ERP离散度增大;左心耳和冠状静脉窦远端及左上肺静脉频率适应性减低。结论增龄对心房和肺静脉电生理影响主要是左心房和左上肺静脉ERP缩短和频率适应性减低,心房及肺静脉ERP离散度增大。     

肌袖性房性心律失常--一种独特的房性心律失常?(Ⅱ)

四、肌袖性房性心律失常的解剖与电生理机制 肌袖性房性心律失常命名的提出,归功于近年来局灶性心房颤动（房颤）的解剖和电生理机制的研究进展。局灶性房颤表现为频发单形房性早搏（房早）、短阵房性心动过速（房速）和阵发性房颤,这些房性心律失常起源于同一个异位兴奋灶,多位于肺静脉开口或肺静脉内（95％）,部分位于腔静脉内,极少位于右心房的界嵴、游离壁、冠状静脉窦口和左心房游离壁。进而,人们就把关注的目光集中于产生这种特殊电生理现象的解剖基础——肺静脉和腔静脉的肌袖组织。 （一）肺静脉的解剖与电活动的关系 目前公认肺静脉的特殊结构是产生异常兴奋并触发局灶性房颤最常见的解剖基础。但是此处局灶性电活动具体发作的原因,以及电生理机制仍不完全清楚。 研究发现肺静脉内的心肌袖位于血管外膜并与血管平滑肌间有脂肪组织分隔,同时肌袖远端的肌纤维明显萎缩,且有结缔组织纤维包绕,提示有产生兴奋,向心房传导兴奋,以及发生微折返的解剖基础。而且也观察到肺静脉的平滑肌并不存在电活动,肺静脉的电活动来自延续到肺静脉的心房肌,并向心房传导。     

消融犬右肺静脉脂肪垫对心房及右上肺静脉电生理特性及房颤诱发的影响

目的探讨消融右肺静脉脂肪垫对心房及右上肺静脉电生理特性及房颤诱发的影响。方法犬18只分别在颈部迷走神经未刺激和刺激的情况下,观察射频消融肺静脉脂肪垫前后心房不同部位及右上肺静脉有效不应期、房颤诱发率及房颤诱发窗口的变化。结果在刺激迷走神经的情况下,与消融前相比,消融后高位右心房有效不应期延长（P<0.05）,其余部位有效不应期无显著差异,消融后高位右心房房颤诱发率降低（P<0.01）,房颤诱发窗口变窄（P<0.05）,左心房（P<0.01）及右上肺静脉（P<0.01）房颤诱发率升高,诱发窗口增宽。同时,心房有效不应期离散度增加（P<0.01）。结论消融右肺静脉脂肪垫使高位右心房房颤诱发率降低及房颤诱发窗口变窄,却使左房、右上肺静脉房颤诱发率升高及房颤诱发窗口增宽。     

Thoracic veins and the mechanisms of non-paroxysmal atrial fibrillation

OBJECTIVE: The purpose of this article is to review the importance of thoracic veins in the maintenance of sustained (non-paroxysmal) atrial fibrillation (AF). METHODS: Thoracic veins, including the pulmonary veins (PVs), vein of Marshall (VOM) and the superior vena cava (SVC), have muscle sleeves that connect to the atria. It is well known that electrical activities can be recorded within these venous structures. In some incidences, these thoracic veins may serve as the trigger and/or the substrate for paroxysmal AF. The importance of thoracic veins in chronic (sustained) AF is less well appreciated. Therefore, we review the literature to determine if thoracic veins are important in the maintenance of sustained AF. RESULTS: Our recent study demonstrated that repetitive rapid electrical activities are present in the PVs and in the VOM during pacing-induced sustained AF in dogs. Because of these repetitive rapid activities, these thoracic veins have shorter activation cycle lengths than that of the left atrium, which, in turn, has shorter cycle lengths than that of the right atrium. Others have demonstrated that PV isolation in humans can result in a cure of sustained human AF in >80% of patients undergoing concomitant surgery. CONCLUSION: These findings suggest that repetitive rapid activities within the thoracic veins may be responsible for the maintenance of non-paroxysmal (sustained) AF.     

左房快速起搏对肺静脉口及心房肌电重构的影响

目的探讨左房快速起搏对肺静脉口、左右心耳电重构的影响。方法运用快速起搏左心耳的方法建立心房颤动(AF)模型,在起搏前及起搏后的第1,3,5,7d对左、右心耳;左上、左下肺静脉口;右上、右下肺静脉口的有效不应期(ERP)、ERP频率适应性、ERP离散度及心房间的传导时间进行测定。采用S1S2程序刺激,基础起搏周长(PCL)分别为400,300,200ms,S2为200ms,以5ms的步长递减。程序刺激结合Burst刺激对上述心房部位进行AF的诱发,记录AF的发生率。在第8天关闭起搏器,采用上述相同方法对起搏停止后即刻;2,4,6,24h的上述各部位的ERP进行测定。结果起搏1d后各个基础起搏周长下各部位的ERP明显缩短,ERP频率适应性降低,ERP离散度增大(P<0.05),而心房间传导时间无明显变化(P>0.05);起搏终止后各部位的ERP逐渐延长,但起搏终止后6hERP与快速起搏前相比仍有明显缩短(P<0.05);24h后ERP基本恢复到起搏前水平,两者相比无明显差异(p>0.05);随着起搏时间的延长各部位AF的诱发率逐渐增高(P<0.05)。结论快速心房起搏不仅引起心房肌电重构,亦引起肺静脉电重构。     

Response of pulmonary vein potentials to premature stimulation

INTRODUCTION: Pulmonary vein potentials reflect depolarization of muscle fascicles within the myocardial sleeves that surround the pulmonary veins. The response of pulmonary vein potentials to premature stimulation has not been described. METHODS AND RESULTS: In 31 patients with paroxysmal atrial fibrillation referred for segmental isolation of the pulmonary veins, programmed stimulation with a single atrial extrastimulus was performed from the coronary sinus. Bipolar and unipolar electrograms were recorded with a decapolar Lasso catheter positioned sequentially within the left superior, left inferior, and right superior pulmonary veins, near the ostium. Premature stimulation often resulted in greater separation of the atrial and pulmonary vein potentials recorded within the pulmonary veins, fractionation of the pulmonary vein potentials, a change in the circumferential activation sequence of the pulmonary vein potentials, and dropout of pulmonary vein potentials. CONCLUSION: In response to premature stimulation, the muscle fascicles within the myocardial sleeves that surround the pulmonary veins display a greater degree of decremental conduction than do the myocardial fibers in the adjacent left atrium, and they display heterogeneity in conduction properties and refractoriness. Discrimination of pulmonary vein potentials from atrial electrograms is facilitated by premature stimulation.     

阵发性心房颤动患者心房及肺静脉不应期离散度的变化

目的探讨阵发性房颤患者房颤相关组织的电生理特性改变情况。方法选取阵发性房颤患者10例(房颤组)和无房颤病史的左侧旁路有显性预激波患者15例(对照组)。将大头电极分别放置在两组患者左上肺静脉、左下肺静脉、右上肺静脉、右下肺静脉开口及左心房顶壁、前壁、后壁、高位右心房,分别测定各部位有效不应期(EPR)。结果①房颤组心房及肺静脉EPR离散度指数(DI)为0.117±0.028,对照组为0.074±0.029,两组比较,P<0.05。②房颤组左心房ERP为(234.00±28.72)ms,肺静脉ERP为(230.75±32.69)ms;对照组左心房ERP为(248.00±25.99)ms,肺静脉ERP为(244.33±26.78)ms,两组比较,P均<0.05。结论阵发性房颤患者DI明显增大,左心房、肺静脉ERP显著缩短。     

Patterns of anomalous pulmonary venous drainage

All of our cases of abnormal pulmonary venous connections collected to the middle of 1965 and verified at surgery or autopsy have been reviewed by means of diagrams and tabulations, using a specially devised code to facilitate the survey. The material consisted of 52 autopsy cases (half of them obtained after surgery) and the cases of 72 patients who survived operation. The postmortem group was much younger than the surgical group and differed also from the latter by showing male preponderance as well as relatively many instances of total abnormal pulmonary venous connection and frequently associated cardiac anomalies. Partial anomalous connection of right pulmonary veins was 10 times more frequent than that of the left pulmonary veins. This was caused by (1) the frequent drainage of some of the right pulmonary veins into the junctional area between right atrium and superior vena cava in the presence of normal left pulmonary veins, and (2) the complete absence of isolated left pulmonary venous connection to the right atrium. Abnormal connection of solitary pulmonary veins was always effected to the most proximal venous structure among the four possible ones which are derived from the main embryonic channels (superior vena cava and inferior vena cava on the right side, and left superior vena cava and coronary sinus on the left side). Common pulmonary veins from one lung also drained in accordance with this proximity rule, if this may be taken to apply also to the drainage of right pulmonary veins into the right atrium. The one exception in our material was the drainage of all right pulmonary veins into the portal venous system. Total abnormal pulmonary venous connection may be found with all structures mentioned, but most frequently with the left superior vena cava, or coronary sinus, or both, usually by way of a common pulmonary vein. In a few cases however, drainage into different sites, all of them abnormal, did occur. Then again the proximity rule seemed to apply. A tentative embryological explanation is given for the patterns described.     

持续心房颤动时肺静脉口部有效不应期变化的时间进程及其逆转

为探讨持续心房颤动 (AF)肺静脉有效不应期 (ERP)变化的时间进程及其逆转 ,运用起搏方法建立AF模型 ,在起搏前和起搏后的第 1 ,2 ,3,4 ,5 ,6 ,7d对左上肺静脉口、左下肺静脉口、右上肺静脉口及右下肺静脉口的ERP进行测定。采用S1 S2 程序刺激 ,基础起搏周长 (S1 S1 )分别为 4 0 0 ,35 0 ,30 0 ,2 5 0 ,2 0 0ms,S2 为 2 0 0ms,以 5ms的步长递减。程序刺激结合猝发刺激对上述心房结构进行AF的诱发 ,记录AF的发生频率。上述相同方法对起搏停止后 1 ,2 ,3,4 ,5 ,6 ,2 4h 4个肺静脉口的ERP进行测定。结果 :各个基础起搏周长下 4个肺静脉口的ERP在AF后 1 ,2 ,3,4 ,5 ,6 ,7d逐渐缩短 ,且较AF前明显缩短 ,P <0 .0 5 ;AF终止后 4个肺静脉口的ERP逐渐延长 ,但AF终止后 0 ,1 ,2 ,3,4 ,5 ,6hERP与AF前相比仍有明显缩短 ,P <0 .0 5 ;AF终止后 2 4hERP基本恢复到AF前水平 ,随着AF持续时间的延长 4个肺静脉口AF的诱发率逐渐增高 ,与AF前相比 ,AF后 1 ,2 ,3,4 ,5 ,6 ,7dAF的诱发率明显增高 ,P <0 .0 5。结论 :随着AF持续 ,肺静脉的ERP逐渐缩短 ,AF的诱发率逐渐增高 ,AF终止后缩短的ERP逐渐延长致AF前水平。     

射频导管消融进行心房-肺(或上腔)静脉电隔离治疗阵发性心房颤动的并发症分析

目的总结射频导管消融进行心房 肺静脉和 /或上腔静脉 (合称大静脉 )电隔离治疗阵发性心房颤动 (房颤 )的并发症。方法顽固性阵发性房颤患者 89例 ,在环状标测电极导管指导下行大静脉的射频导管消融电隔离治疗 ,分析出现的各种并发症。结果 89例病人共接受电隔离治疗 10 3次 ,隔离大静脉 2 30根 ,其中肺静脉 2 0 7根 ,上腔静脉 2 3根。出现并发症 10例 ,其中严重迷走神经反射导致的一过性三度房室阻滞引起的晕厥发作 2例 ,脑卒中 2例 ,肺静脉狭窄 4例 (狭窄程度 >5 0 % ) ,术后少量心包积血 2例 ,并发症的总发生率为 11%。结论射频导管消融进行心房 肺和 /或上腔静脉电隔离治疗阵发性房颤可出现各种并发症 ,多数并发症可通过采取相应的措施使之减少或避免 ,其中肺静脉狭窄和脑卒中为最棘手的并发症 ,应予以高度重视。     

心房颤动上腔静脉节段性电隔离方法及安全性评估

目的:分析心房颤动(房颤)上腔静脉节段性电隔离的具体手术方法,并评估其安全性.方法:入选2017年11月至2018年9月期间我院阵发性房颤患者50例,患者常规进行肺静脉隔离后,继续行上腔静脉隔离.消融前进行上腔静脉造影,显示上腔静脉与右心房解剖关系,并在CARTO系统运用PentaRay电极导管进行上腔静脉及右心房三维...     

Effect of the stellate ganglion on atrial fibrillation and atrial electrophysiological properties and its left-right asymmetry in a canine model

OBJECTIVE:

To investigate the effect of the stellate ganglion (SG) and its left-right asymmetry on atrial fibrillation (AF) inducibility, AF duration and atrial electrophysiological properties.

METHODS:

Sixteen adult mongrel dogs were randomly assigned to three groups. The control group (n=4) underwent 6 h rapid atrial pacing (RAP) only; the right SG (RSG) group (n=6) underwent 6 h RSG stimulation plus RAP; and the left SG (LSG) group (n=6) underwent 6 h LSG stimulation plus RAP. AF induction rate, AF duration, effective refractory period (ERP) and dispersion of ERP (dERP) were measured.

RESULTS:

In the RSG group, the induction rate of AF was significantly increased in sites in the right atrium (RA) compared with baseline (P<0.05). In the LSG group, the induction rate of AF was significantly increased (P<0.05) compared with baseline in the left atrium (LA), left superior pulmonary vein and left inferior pulmonary vein, respectively. Compared with RSG stimulation, right stellate ganglionectomy markedly decreased the AF induction rate of the RA (P<0.05). Compared with LSG stimulation, left stellate ganglionectomy markedly decreased the AF induction rate of the LA, the left superior pulmonary vein and the left inferior pulmonary vein (P<0.05). In the RSG group, the ERP was significantly shortened (P<0.05) and the dERP was significantly increased (P<0.05) in RA sites (P<0.05). The ERP was significantly shortened in the LSG group (P<0.05). The dERP was significantly increased (P<0.05) in LA and pulmonary vein sites (P<0.05).

CONCLUSIONS:

Unilateral electrical stimulation of the SG in combination with RAP can successfully establish a canine model of acute AF mediated by excessive sympathetic activity. SG stimulation facilitates AF induction and aggravates electrical remodelling in sites in the atrium and pulmonary vein. Inhibiting sympathetic nerve activation through unilateral stellate ganglionectomy can reduce AF initiation.     

A Focal Source of Atrial Fibrillation in the Superior Vena Cava: Isolation and Elimination by Radiofrequency Ablation with the Guide of Basket Catheter Mapping

Although it has been reported that pulmonary veins sometimes act as a focal driver of atrial fibrillation (AF), little has been reported concerning the contribution of the superior vena cava (SVC) to the maintenance of AF. Here we report a patient with sustained AF due to focal discharges inside the SVC after pulmonary vein isolation procedure. Stepwise radiofrequency current applications with the guide of multielectrode basket catheter mapping first disconnected the arrhythmogenic SVC from the right atrium and then eliminated the tachycardia.