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。     

犬肺静脉肌袖电生理随龄性改变

目的对比研究老龄和成年犬肺静脉肌袖电生理特性.方法采用经导管房间隔穿刺技术,应用程序刺激和短阵快速起搏分别对正常自然老龄和成年实验犬肺静脉、上腔静脉、左房、右房、以及冠状静脉窦的有效不应期、激动传导及心房颤动诱发阈值进行标测.结果老龄犬的左、右心房,上腔静脉,冠状静脉窦和肺静脉的有效不应期较成年犬均有不同程度的缩短,其中左心房,上腔静脉和肺静脉有效不应期的随龄性变化有统计学差异(P＜0.01).老龄犬的肺静脉不应期较其左房的不应期明显缩短,而成年犬肺静脉与左房的不应期则无显著性差异.老龄犬的肺静脉和上腔静脉内激动传导呈显著递减性传导.在多数老龄犬的肺静脉、左心房和上腔静脉,快速短阵起搏及程序刺激能诱发持续时间＞30s的房颤.结论老龄犬肺静脉肌袖有易于房颤发生的电生理变化,提示心脏老龄化可能是房颤发生的潜在基质.     

心脏脂肪垫在肺静脉引发房颤中的作用

目的探讨窦房结-心房脂肪垫(SAFP)在右上肺静脉灶性放电引发阵发性房颤(PAF)中的作用。方法12条新疆家养犬,苯巴比妥钠麻醉,经右侧开胸暴露右侧肺静脉。将1根8极标测电极导管固定在右上肺静脉,给予S1S1600bpm起搏刺激,另将1根8极(1.5×1.5cm)电极板固定在心外膜窦房结-心房脂肪垫上。术中监测II和aVR导联、血压和体温。以1～4V电压、1000bpm频率刺激窦房结-心房脂肪垫30～60s。结果12条家养犬在给予S1S11000ppm窦房结-心房脂肪垫刺激,随着电压从1增加到4V,心率从142±20bpm减少到75±30bpm(p<0.05),同时出现房性早搏、房性心动过速(房速)和房颤,同时予以右上肺静脉S1S1600ppm刺激,诱发房颤的房性早搏数随着刺激电压1～4V的增加从7个减少到2个,并以S1S1300ms,S1S2稍长于右上肺静脉不应期的早搏右上肺静脉刺激。S1S1600ppm刺激下房颤诱发率从基础状态的49.86%提高到70.59%,S1S2早搏刺激下从3.78%提高到16.6%(p<0.05)。7条狗在4%利多卡因4ml注射到窦房结-心房脂肪垫局部阻滞神经后,6条狗在同样右上肺静脉刺激诱发房颤电压的条件下不能诱发房颤,其中3条狗在电压增加大于9V时诱发房颤。房颤诱发的有效刺激部位在窦房结-心房脂肪垫2～3mm的范围内。结论有效部位窦房结-心房脂肪垫刺激,能够诱发慢频率依赖性阵发性房颤,刺激窦房结-心房脂肪垫增加右上肺静脉阵发性房颤的诱发率,局部神经阻滞降低或消除阵发性房颤的诱发.提示:增强窦房结-心房脂肪垫的自发神经放电,可能是临床右上肺静脉灶性放电转变成房颤的基础,消融窦房结-心房脂肪垫可能预防阵发性房颤的诱发。     

慢性快速肺静脉起搏建立犬持续性心房颤动模型

目的探讨利用慢性快速刺激肺静脉的方法,建立犬持续性心房颤动(简称房颤)模型。方法在15只犬的左上肺静脉放置自制的环状起搏电极,并在左房游离壁缝合一片状标测电极。将肺静脉起搏电极在体外连接自制的脉冲发生器,持续快速起搏(1200次/分)肺静脉。每隔三天进行心房程序电刺激和burst刺激,分析电生理指标,直至房颤维持超过24h。超声心动图测量基础状态和起搏结束后左右房面积等指标。结果11只犬完成研究。在28.2±3.0天内诱发出持续超过24h的房颤,4只不需刺激诱发即发生自发性房颤,5只经程序刺激可发生房颤,2只经burst刺激可发生房颤,持续时间大于24h。超声心动图测量显示起搏结束后心房面积明显扩大(左房:6.9±1.1cm2vs11.7±1.6cm2;右房:4.3±0.8cm2vs7.0±1.2cm2,P均<0.001)。结论慢性快速刺激犬肺静脉建立持续性房颤模型的方法临床模拟性好,可靠易行。     

快速心房激动对心房肌电生理特性的影响

比较快速心房起搏与急性心房颤动 (简称房颤 )诱发心房电生理特性的变化。以 15 0～ 2 0 0ms起搏周长(PCL)对 4 5例成功射频消融后 (RFCA)病人右房进行S1S1刺激诱发急性房颤 ,据能否诱发急性房颤分为非房颤组和急性房颤组 ;再以 4 0 0msPCL对心房快速激动前后高位右房、低位右房、His束周围等多部位进行S1S2 扫描 ,测定心房有效不应期 (ERP)、ERP离散度 (ERPd)、右房内及房间的传导时间的变化 ;另以 35 0 ,4 0 0和 4 5 0ms三个PCL随机对RAA进行S1S2 扫描 ,观察ERP频率自适应性的变化。两组心房快速激动后 4 0 0msPCL下右房各刺激部位及三种不同PCL右心耳ERP均较心房快速激动前有明显的缩短 ,并且缩短的程度相同。两组病人心房快速激动前后房内和房间传导时间及ERPd没有明显改变。两组心房快速激动前后斜率均值均较激动后明显下降 ;心房快速激动前、后斜率均值两组间无显明差别 (P >0 .0 5 )。结论 :两种方式的心房快速激动可诱发相似的心房电重构现象。     

犬肺静脉急性电重构及其对心房颤动诱发的影响

观察短阵(10min)快速刺激肺静脉对肺静脉有效不应期(PVERP)及经肺静脉诱发心房颤动(简称房颤)的影响。20条成年杂种开胸犬在左上肺静脉根部血管外膜处放置自制环状电极,双极针状刺激电极固定在肺静脉远端血管外表面。测量基础状态下起搏周长(PCL)分别为300,400ms时PVERP。于肺静脉远端以1∶1起搏肺静脉的最快频率刺激肺静脉10min。分别于刺激终止即刻、5min、10min重复测量PVERP。完成以上试验后观察短阵10min快速刺激肺静脉对经肺静脉诱发房颤的影响。采用S1S1快速刺激S1S2程序刺激肺静脉的方法诱发房颤。结果:PVERP及其频率适应性在短阵刺激后即刻,5min时与刺激前相比有显著差异(P<0.05),10min时与刺激前相比无显著差异(P>0.05)。短阵快速刺激后房颤诱发率增加(55%vs20%,P<0.05),房颤持续时间延长(24.6minvs4.1min,P<0.05)。结论:短阵快速刺激肺静脉可以导致肺静脉发生急性电重构,急性电重构后经肺静脉更易诱发房颤且房颤持续时间更长。     

肺静脉在犬持续性心房颤动维持中的作用

目的探讨快速起搏肺静脉建立持续性心房颤动(简称房颤)犬模型的电生理特性以及射频消融隔离肺静脉对其影响。方法选杂种犬15只,以20Hz的固定频率行肺静脉持续起搏,建立持续时间>24h的房颤的动物模型。对该模型的左、右房游离壁,左上、下肺静脉,右上、下肺静脉进行心外膜标测,测量各标测部位的有效不应期(ERP)和平均房颤波周长(AFCL)。对肺静脉电隔离,观察电隔离前后房颤的诱发以及各部位ERP和AFCL的变化。结果11只犬完成实验,在28.2±3.0d内诱发出持续超过24h的房颤。肺静脉电隔离前,ERP和AFCL分布呈明显的梯度分布,自短至长依次为:肺静脉,左、右房游离壁;肺静脉隔离后,8只犬转变为窦性心律,3只犬先转变为房性心律失常后,在60min内转变为窦性心律,再进行快速心房起搏刺激仅能诱发出小于60s的阵发性房颤,各部位ERP和AFCL也明显延长(P<0.05)。结论肺静脉的快速电活动可能在持续性房颤的维持中起关键作用。     

心内膜标测指导下射频消融右房治疗心房颤动的实验研究

目的 探讨优先消融心房无序电活动区域治疗某些类型心房颤动(房颤)的可行性。方法实验犬17只，消融组12只，假性消融组5只。房颤持续过程中行激动标测．发现如下激动特征之一的部位视作优先消融靶区(简称优先区)：①电激动无序性特征最为显著的部位；②平均FF间期(AFI100)最短的部位；③最早出现F波(可重复3次以上)且超前其它导联20ms以上的部位。消融终点为用术前相同诱发方法不能诱发房颤或房颤持续对间不超过1min。结果标测发现消融组12只犬有10只存在优先区，优先区相对局限的7只犬实施单一线径消融(单线组)；优先区较为广泛的3只犬、未能标测到优先区的2只犬以及单线组未能达到消融终点的2只犬实施多线消融(多线组)。具有优先区的10只犬中8只(80%)术后即刻达到消融终点，单、多线组各4只(4／7vs 4／7)。未标测到优先区的2只犬均未达消融终点。达到消融终点的4只犬中，3只于术后14天及处死前均未诱发出持续性房颤。假性消融对房颤的发生和持续无明显影响。结论(1)心内膜标测指导下优先消融心房无序电活动区有望在不降低成功率的同时减少心房肌损伤：(2)右房RFCA可能是根治某些类型房颤的有效方法之一。     

阵发性心房颤动大静脉电隔离后肌袖内自发电活动的特点

目的　总结阵发性心房颤动 (房颤 )患者大静脉 (肺静脉和 /或上腔静脉 )电隔离治疗后肌袖内自发电活动的特点 ,探讨其临床意义。方法　顽固性特发性房颤患者 ,在环状标测电极导管指导下行心内电生理标测以及肺静脉和 /或上腔静脉肌袖的射频导管消融电隔离治疗 ,电隔离后继续留置环状标测导管 10～ 2 0min ,观察自发电位发生情况。结果　电隔离前心内标测显示 32例患者的 36根大静脉肌袖有自发电活动。以心房 大静脉传入阻滞为终点行大静脉口部消融后 ,16根 (4 4 % )记录到大静脉内自发电活动 ,其中 2根呈偶发的单一电活动 ,11根呈平均频率 (38± 12 )次 /min的缓慢节律 ,3根呈偶发的由 3～ 6个电位组成的短阵快速节律。 15根示大静脉内电活动与心房完全分离 (93 8% ) ,1根左上肺静脉存在大静脉 心房单向传导。结论　射频导管消融电隔离大静脉后 ,出现心房 大静脉传入阻滞时多同时伴有大静脉 心房传出阻断 ,心房 大静脉传入阻滞后大静脉内的电活动频率明显变慢、减少或消失 ,说明窦性心律时的心房 大静脉传导是引起大静脉内电活动不稳定的重要原因 ,射频导管消融技术即使只阻断心房 大静脉单向传导也可通过稳定大静脉内电活动而减少或控制房颤的发作。     

持续快速肺静脉起搏对犬心房结构及心电生理特性的影响

目的探讨快速起搏肺静脉(PV)建立持续性心房颤动(房颤)犬模型的心房结构及心电生理特性。方法 30只犬随机分为实验组和对照组,实验组以20Hz的固定频率行肺静脉持续起搏,建立持续时间24h的房颤动物模型。超声心动图测量实验组基础状态和起搏结束后左右心房面积,对所有犬的左右心房游离壁、左上肺静脉、左下肺静脉、右上肺静脉和右下肺静脉进行心外膜电生理标测,测量各标测部位的有效不应期(ERP)和平均房颤波周长(AFCL),观察肺静脉起搏对心房面积的影响以及各部位ERP和AFCL的变化。结果实验组11只犬完成实验,在(28.2±3.0)d内诱发出持续超过24h的房颤。超声心动图测量显示起搏结束后心房面积明显扩大(P0.05);与对照组相比,左右心房及各肺静脉的ERP明显缩短(P0.05);实验组各部位ERP和AFCL呈明显的梯度分布,自短至长依次为:肺静脉、左房游离壁和右房游离壁。结论在犬快速肺静脉起搏房颤模型中,心房面积的增大及各部位电生理特性的变化可能是持续性房颤诱发和维持的发生机制。     

Mechanisms of the preventive effect of pilsicainide on atrial fibrillation originating from the pulmonary vein.

BACKGROUND: It has been shown that pilsicainide terminates atrial fibrillation (AF) by pharmacologic pulmonary vein (PV) isolation. However, whether it can prevent AF induction originating from the PV by the same mechanism is still uncertain. METHODS AND RESULTS: Rapid pacing from the left superior PV (LSPV) and the right atrial free wall (RAF) was performed to induce AF during electrical stimulation of both cervical vagal nerves in 6 anesthetized dogs and during the infusion of acetylcholine (ACh) in 8 isolated atria. Rapid pacing induced AF in all dogs, regardless of the pacing site, before pilsicainide. Pilsicainide (1 mg/kg) prevented AF during rapid pacing from the LSPV, with an impulse conduction block between the LSPV and the left atrial free wall (LAF). However, the same dose of pilsicainide did not prevent AF when pacing was performed from the RAF. Pilsicainide partially restored the action potential duration shortened by ACh infusion and prevented AF with an impulse conduction block at the LSPV-left atrial junction in all isolated preparations tested. CONCLUSION: The results suggest that (1) impulse conduction block at the LSPV-LA junction is the underlying mechanism of pilsicainide-induced prevention of vagally-induced AF originating from the LSPV and (2) pilsicainide is more effective at preventing AF originating from the LSPV than that from the RA.     

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。     

经导管射频消融治疗起源于肺静脉的心房颤动(附二例报告)

报道 2例经射频消融治疗成功的起源点位于肺静脉的心房颤动 (简称房颤 ) ,均伴有频发房性早搏 (简称房早 )的阵发性房颤。电生理检查时行两次房间隔穿刺 ,将两根 10极标测导管通过长鞘送入左、右上肺静脉 ,选择性肺静脉造影证实肺静脉开口部位。静脉滴注异丙肾上腺素后 1例诱发出频发房早 ,另 1例诱发出频发房早及房颤 ,且房早及房颤开始发作时的心内电图均显示最早心房激动点位于右上肺静脉内 ,其局部电位分别较体表心电图异位 P波的起点提前 61和 96ms。在最早心房激动点处以 15～ 2 0 W的输出功率消融 60～ 180 s后房早及房颤消失 ,静脉滴注异丙肾上腺素亦未再诱发房颤。术后随访 8～ 12个月 ,房颤无复发。结论 :射频消融治疗起源于肺静脉的房颤效果较好且相对安全 ;在这类患者应用两根多极导管同步标测双上肺静脉是一种有效的标测和消融方法。     

Arrhythmogenic Potential of Pulmonary Venous Tissue: Triggers for Atrial Fibrillation Identified within the Remnant of a Vein

Background: Pulmonary veins (PVs) have frequently been identified as triggers for atrial fibrillation (AF), and higher arrhythmogenic potential of superior PVs has been attributed to their larger size, which can more rigorously support abnormalities of impulse formation and/or conduction.
Case Report: Contrary to this belief, we report our observations in a 63-year-old patient with history of lung cancer, S/P left upper lobectomy, undergoing ablation for paroxysmal AF. Circular mapping (Lasso) and ablation (ABL; 8-mm) catheters were deployed in left atrium (LA). Intracardiac ultrasound revealed separate right superior (RS) and inferior (RI) PVs and a single left PV. Segmented LA anatomy from the CT angiogram images corroborated this, although on the latter there appeared to be a "stump" at superior aspect of the left PV. This stump likely was the remnant of the left superior (LS) PV. Thus, the patent left vein was likely the dilated left inferior (LI) PV. With the Lasso and ABL deployed at the LIPV ostium and LSPV remnant, respectively, AF was reproducibly seen to initiate with earliest activity in the latter. Single radio-frequency ablation (RFA) lesion within the LSPV remnant abolished AF triggers. Additional RFA was done to isolate LI, RS, and RI PVs. Over a follow-up period of 24 months, this patient has remained free from AF off any drugs.
Conclusions: Our observations suggest that even very proximal remnants of PVs can serve as triggers for AF. Recognition of this phenomenon was facilitated by the use of advanced imaging technique and the deployment of multiple catheters.     

Catheter ablation of focal triggers and drivers of atrial fibrillation

It has been demonstrated that most paroxysmal atrial fibrillation (AF) is triggered by ectopic beats originating from the pulmonary veins (PVs). It has been recently reported that some AF episodes are maintained by focal drivers and AF substrates in the PVs and atrium. Left atrial ablation combined with PV isolation targeting AF triggers and drivers may be effective for eliminating atrial arrhythmias. However, multiple AF drivers in the PVs and atrium and acute conduction recovery after the PV isolation may sometimes render that technique less reliable. In this article, we describe the current status of the catheter ablation of focal triggers and drivers of AF in the PVs and atrium, illustrating with case presentations.     

Pulmonary vein electrogram characteristics in patients with focal sources of paroxysmal atrial fibrillation

INTRODUCTION: The major source of ectopic beats initiating paroxysmal atrial fibrillation (AF) is from pulmonary veins (PVs). However, the electrogram characteristics of PVs are not well defined. METHODS AND RESULTS: Group I consisted of 129 patients with paroxysmal AF. Group II consisted of 10 patients with a concealed left-sided free-wall accessory pathway. All group I patients had spontaneous AF initiated by ectopic beats, including 169 ectopic foci originating from the PVs. We analyzed PV electrograms from the 169 ectopic foci during sinus beats and ectopic beats. During AF initiation, most (70%) ectopic beats showed PV spike potential followed by atrial potential; 16% of ectopic beats showed PV fragmented potential followed by atrial potential; and 14% showed fusion potentials. The coupling interval between the sinus beat and the ectopic beat was significantly shorter in the inferior PVs than in the superior PVs (171 +/- 48 msec vs 222 +/- 63 msec, P = 0.001) and was significantly shorter in the distal foci than in the ostial foci of PVs (206 +/- 52 msec vs 230 +/- 56 msec, P = 0.01). The incidence of conduction block in the PVs during AF initiation was significantly higher in the inferior PVs than in the superior PVs (12/24 vs 37/145, P = 0.03) and was significantly higher in the distal foci than in the ostial foci of PVs (43/121 vs 6/48, P = 0.04). The maximal amplitude of PV potential was significantly larger in the left PVs than in the right PVs, and the maximal duration of PV potential was significantly longer in the superior PVs than in the inferior PVs during sinus beats in both group I and II patients. CONCLUSION: PV electrogram characteristics were different among the four PVs. Detailed mapping and careful interpretation are the most important steps in ablation of paroxysmal AF originating from PVs.     

犬快速心房起搏心房颤动模型全心房心外膜标测以及静脉胺碘酮对其心电的影响

探讨快速心房起搏心房颤动(简称房颤)模型房颤发作时肺静脉、左右心房各部位激动频率的差异以及胺碘酮对其电生理特性的影响。选健康雄性杂种犬10只,以400次/分的固定频率进行右心耳起搏,建立快速心房起搏房颤模型。10周后终止起搏,行64道全心房心外膜标测。标测部位分别为左右心房游离壁、左右心房顶部、左上肺静脉、左下肺静脉、右上肺静脉和右下肺静脉。记录以上部位的心外膜电图,测量各标测部位的平均房颤波周长(AFCL),并对不同部位心外膜标测电图进行频谱分析。静脉注射胺碘酮300mg,分析胺碘酮治疗前后各部位有效不应期(ERP)和AFCL的变化。结果:8只犬完成整个实验。在所有8只犬中,最短AFCL/ERP位于Marshall韧带的有2只,位于左下肺静脉的有6只;AFCL/ERP在心房的分布呈明显的梯度分布,自短至长依次为:肺静脉或Marshall韧带、左房游离壁和左侧Bachmann束、右侧Bachmann束和右房游离壁;频谱分析结果与AFCL分析结果一致;胺碘酮虽然可延长肺静脉和心房各部位ERP和AFCL,但是不能终止房颤的发作。结论:局灶机制可能是快速心房起搏房颤模型的发生和维持机制。