电刺激和起搏在心房颤动动物模型中的运用

心房颤动(AF)的模型建立中离不开电刺激和起搏的应用。电刺激包括短阵快速刺激(burst刺激)和程序期前刺激,其既可作为急性AF模型的建立,亦可作为慢性AF模型的建立,还可作为慢性AF模型中的诱发方式使用。快速起搏主要用于慢性AF模型的建立。自主神经电刺激可以直接或间接增加AF的诱发成功率;乙酰胆碱、苯肾上腺素使用、一些因素致心脏结构或组织病变后电刺激易诱发AF。电刺激和起搏在制作AF动物模型中,既可短期运用作为触发因素,也可长期运用作为引起电生理和解剖异常而出现AF致AF。     

心脏血管内迷走神经丛刺激与阵发性心房颤动的动物模型制作

探讨心脏血管内迷走神经丛刺激与阵发性心房颤动 (简称房颤 )的动物模型制作。 32条Mongrel狗活体心脏大血管 :冠状窦、左右肺动脉、左房、上下腔静脉等处插入 7F蓝状电极进行迷走神经丛刺激 ,刺激频率为 2 0Hz,刺激间期 0 .1ms,刺激电压 1～ 4 0V ,刺激时间 30～ 5 0s。为了避免神经丛刺激直接对心房的影响 ,于刺激迷走神经丛的同时在P波后发放 2 0 0Hz、2 0～ 5 0ms的PS2 心房高频刺激 ,使迷走神经刺激落入心房的不应期。在这些心脏血管迷走神经丛刺激时减慢窦性心律 ,且减慢速度呈电压依赖。在一定的刺激强度下 ,窦性心律能够达到最大减低 (从75 0± 10 2ms至 15 6 0± 2 30ms) ,心房肌不应期显著缩短 (从 175± 13ms缩至 96± 2 3ms) ,同时出现房性早搏、房性心动过速和房颤 ,且重复性很好。应用 β 阻断剂 (esmolol1mg/kg)时 ,提高了房颤诱发域值 ;迷走神经阻断剂 (atropine1～ 2mg/kg)可以完全阻断房颤的诱发。结论 :蓝状电极非常有利于快速在静脉血管腔内找到迷走神经丛刺激位点 ;心脏大血管处存在迷走神经丛 ,刺激这些神经丛能够复制出与临床灶性阵发性房颤非常类同的房颤 ,迷走神经阻断剂可阻断这类房颤的诱发。     

心房颤动动物模型建立的方法学

心房颤动动物模型的建立围绕触发和维持两个方面。触发因素为局灶的异常放电,可能来自心房肌、自主神经、肺静脉心肌袖,由相应部位的电刺激模拟。维持因素为时间依赖性的心房结构和电生理重构,研究病因学时可由疾病模型模拟,探讨机制时则多由起搏模型模拟,心房、心室、肺静脉、迷走神经干或神经结是可供选择的起搏刺激部位。在起搏模型中联合各种化学药物,包括神经递质、离子通道阻滞剂,可用于探讨心房颤动促进和终止因素。     

迷走神经刺激对心房颤动影响的双重作用

迷走神经刺激（VNS）可通过缩短心房有效不应期（AERP）和动作电位时程（APD）、增加AERP和APD离散度、促进心房电重构等机制诱发和维持心房颤动（简称房颤）,但最近有实验表明VNS除了致房颤作用外,在一定条件下具有治疗作用,低强度VNS可以抑制房颤的诱发,选择性房室结VNS可以控制房颤时快速心室率,但VNS治疗房颤的作用还面临着一些问题,仍需进一步研究。     

起搏器植入患者合并心房颤动的程控管理策略

心脏起搏器是治疗各类缓慢性心律失常的常用有效手段.心脏起搏器植入患者通过起搏器的诊断功能可以提高心房颤动(简称房颤)的检出率,同时最小化心室起搏、保持房室同步起搏以及生理性起搏部位可以减少房颤的发生.随着起搏技术的不断进步,越来越多的算法可用于预防和终止房颤发作.对于起搏器植入合并房颤患者而言,优化程控管理策略,合理应...     

心外膜左心耳起搏建立山羊心房颤动模型

目的探讨开胸置入高频起搏器建立山羊心房颤动(AF)模型的方法和可行性。方法山羊12只,随机分为实验组(6只)与对照组(6只)。开胸后于左心耳底部置入起搏电极,以400±10次/分连续起搏12周,诱导AF。记录山羊体表心电图变化。连续起搏12周采用光学显微镜、电镜观察左、右房游离壁心肌组织学、超微结构的变化。结果1只山羊术中死亡;5只经连续起搏12周后,出现AF心电图改变。左房游离壁较右房游离壁心肌细胞直径变细;左房游离壁较右房游离壁心肌纤维排列紊乱,润盘受损,心肌纤维溶解明显,线粒体增多、体积变大,内质网模糊、有的出现空泡样等改变更加明显。正常对照组左、右房心肌纤维排列规整。结论心外膜左心耳起搏建立AF动物模型是可靠而易行的方法。     

心房颤动与线粒体功能障碍

线粒体作为心房肌细胞供能物质,在心房肌细胞的能量代谢、氧化应激、信号传导、细胞凋亡等方面有重要作用.研究表明,心房颤动时线粒体发生生物合成异常、线粒体DNA改变、能量代谢受损、心肌细胞和线粒体多种离子通道稳态失衡、氧化应激与活性氧的产生、线粒体形态结构改变等.     

心房颤动与心房结构重构

心房颤动 (AF)时心房肌结构发生改变 ,即出现结构重构 (SR)。主要表现为 :①出现类似胎儿心肌或“冬眠”心肌的组织学特征 ;②尽管细胞结构发生明显改变 ,但细胞仍存活 ,且无细胞退化和凋亡迹象 ,可被称为程序性细胞存活。它使得心房肌细胞能够在缺血或被动延展等病理情况下存活。钙超载可能是引起AF时心房SR的主要原因。     

甲状腺机能亢进与心房颤动

心房颤动（简称房颤）是甲状腺机能亢进（简称甲亢）患者常见心律失常之一。血清甲状腺素水平长期升高使心房电生理特性、结构特性和自主神经分布发生改变，即出现电重构、结构重构和自主神经重构，这些可能是甲亢引起房颤发生并持续的主要原因。     

植入型心房除颤器治疗心房颤动的临床应用

目的 评估入型心房除颤器（ｉｍｐｌａｎｔａｂｌｅ ａｔｒｉａｌ ｄｅｆｉｂｒｉｌｌａｔｏｒ,ＩＡＤ）治疗阵发性和持续性心房颤动（房颤）患者的有效性和安全性。方法 １１例患者（８例阵发性房颤,３例持续性房颤）安装了ＩＡＤ,型吨Ｍｅｔｒｉｘ＾ＴＭ３０００和Ｍｅｔｒｉｘ＾ＴＭ３０２０。所有的患者在室功能正常,４５％存在高血压等基础心脏病。ＩＡＤ在识别房颤和心室同步化后,通过右房－冠状静脉窦电流路线,发放     

特殊心房起搏程序预防和治疗阵发性心房颤动的临床效果

目的评价特殊心房起搏程序预防和治疗阵发性心房颤动(PAF)的临床效果。方法12例病窦综合征合并PAF患者植入Vitatron Selection 900E(AF2.0、DDDR)型双腔起搏器,比较患者术后不同阶段PAF的发作总数、持续时间、AF负荷和心房起搏比率。结果除1例外,其余11例术后第2个月和第6个月(起搏预防阶段)比术后第1个月(监测阶段)的PAF事件数[80(25;215),57(12;102)vs 203(86;425)],房颤总持续时间[1.9 d(0.6d;5.3 d),1.5 d(0.3 d;6.1 d)vs 2.9 d(0.8 d;9.8 d)],AF负荷[6.3%(2.0%;17.7%),5.0%(1.0%;20.6%)vs 9.6%(2.7%;32.8%)]均减低(P均<0.05),心房起搏比率增加[60%(40%;80%),54%(42%;84%)vs46%(26%;54%),P<0.05]。结论预防性心房起搏程序可以减少PAF事件的发生,降低AF负荷,改善患者的症状,具有短期的疗效。     

消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动的影响及机制

目的探讨消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动(简称房颤)的影响及机制。方法成年杂种犬14条,随机分为实验组8条,对照组6条。实验组首先测量左肺静脉和左心耳的有效不应期,继而刺激心房左后脂肪垫诱发房颤。消融Marshall韧带上段后和下段后重复上述步骤。对照组除不干预Marshall韧带外,其它电刺激方案与实验组相同,同时对该组犬的心脏进行迷走神经染色。结果①实验组消融Marshall韧带后,左肺静脉和左心耳的有效不应期均显著延长(P0.05)。②和消融前比较,实验组消融Marshall韧带上段后的房颤诱发率有下降趋势(70.8%vs87.5%,P0.05);消融Marshall韧带全程后房颤诱发率显著下降(33.3%,P0.001)。对照组三次电刺激所测得的不应期和房颤诱发率无差异。③Marshall韧带与左下肺静脉、心房左后脂肪垫、左心耳之间存在迷走神经的直接联系。结论消融犬Marshall韧带可显著降低刺激心房左后脂肪垫所致房颤的诱发率。     

Impact of atrial fibrillation duration on postcardioversion recurrence

BACKGROUND: "Begetting," a mechanistic tenet of atrial fibrillation (AF), stipulates that the rate of recurrence of AF after cardioversion is proportional to the preceding arrhythmia duration. However, recent reports suggest that, for brief durations, the incidence of early recurrence of AF (ERAF) is inversely proportional to duration. These reports were based on potentially biased data. OBJECTIVES: We performed a prospective study to examine the impact of AF duration on postcardioversion recurrence. METHODS: Forty-four patients underwent placement of an implantable cardioverter-defibrillator (ICD) capable of delivering patient-elicited AF cardioversion shocks. Subsequently, in the ambulatory setting, the timing of shocks in relationship to perceived AF onset was randomly assigned within individuals to early (as soon as possible) or delayed (1 day later). RESULTS: During a follow-up averaging 199 days per patient, a total of 61 AF episodes among 17 patients occurred for which a patient-elicited cardioversion shock was delivered. Twenty-three shocks were delivered using early protocol (mean 6.8 hours after AF onset), and 38 shocks were delivered using delayed protocol (mean 34.7 hours after AF onset). The incidence of ERAF was significantly lower using the delayed protocol. CONCLUSION: A strategy of approximately 24-hour delay in cardioversion shock timing decreased the incidence of ERAF, relative to a shock delivered within a few hours of AF onset. This observation has important mechanistic and therapeutic implications.     

Effect of periodontitis on susceptibility to atrial fibrillation in an animal model

Background

Inflammation is implicated in the pathophysiology of atrial fibrillation (AF). Periodontitis causes a general inflammatory response. Whether periodontitis is related to AF is unknown.

Objective

The aim of the study was to test the hypothesis that inflammation facilitates AF.

Methods

Twenty-two adult mongrel canines of either sex were used for this study. Periodontitis was induced in 12 dogs (periodontitis group) by tying 2-0 silk ligatures at the second premolar of mandibula. Ten healthy dogs were used as controls. Before the ligation procedure and on the day 30, 60, and 90 after ligation, an electrophysiologic evaluation was performed to measure atrial refractoriness and AF inducibility by delivering a single atrial extrastimuli in the high right atrium, atrial septum (AS), and coronary sinus (CS), respectively. Before each electrophysiologic study, blood samples were taken for determining the levels of C-reactive protein (CRP) and tumor necrosis factor-α (TNF-α). Animals were killed after 90 days. The hearts and mandibulae were harvested for morphological study, and the periodontal disease severity was quanti?ed.

Results

Atrial effective refractory period (AERP) shortened, and AF inducibility increased progressively in the periodontitis group. At a drive length of 300 milliseconds, AERP in the CS was 126.7 ± 13.0 milliseconds and 107.5 ± 9.7 milliseconds after 60 and 90 days of ligation, respectively (vs 165.8 ± 10.8 milliseconds at baseline; P < .001). By CS pacing, AF was induced in 5 and 10 of 12 dogs on day 60 and 90 after ligation, respectively (vs 1/12 at baseline; P < .05 and P < .01, respectively). Elevation of CRP and TNF-α occurred after 60 days of ligation (CRP, 13.42 ± 2.21 mg/L vs control, 1.92 ± 0.38 mg/L; P < .001; TNF-α, 9.85 ± 1.72 mg/L vs control, 3.36 ± 0.75 mg/L; P < .001) and reached the peak at the end of the study (CRP, 31.38 ± 2.69 mg/L vs control, 1.99 ± 0.40 mg/L; P < .001; TNF-α, 12.32 ± 1.07 mg/L vs control, 3.24 ± 0.53 mg/L; P < .001). There was a negative correlation between the levels of serum inflammatory factors and AERP values (P < .05). Alveolar bone level decreased in the periodontitis group (P < .001). The long axis (P < .001) of atrial cardiomyocytes including the right atrial appendage (25.50 ± 3.58 μm vs 18.14 ± 3.32 μm), AS (24.78 ± 3.45 μm vs 17.47 ± 2.57 μm), and left atrial appendage (31.90 ± 4.80 μm vs 18.78 ± 2.42 μm) from the periodontitis group was larger than the control group. The short axis of atrial cardiomyocytes was larger than the control group, too (P < .001). Inflammatory cells were more generally found in the atria of the periodontitis group (P < .001). Myolysis affected some atrial cardiomyocytes of the dogs with periodontitis.

Conclusion

Periodontitis led to inflammatory responses in the atrial myocardium, which disturbed the structural and electrophysiologic properties of the atrium and facilitated AF.     

1436例心房颤动住院患者的种族及临床特性分析

目的分析心房颤动(简称房颤)住院患者的种族及临床特性。方法收集2002年1月~2006年8月本院住院的1436例房颤患者的资料,并进行统计分析。结果1436例中,汉族967例(67.3%),维吾尔族350例(24.4%),哈萨克族58例(4.0%),回族38例(2.6%),其他族23例(1.6%)。发病年龄60.8±13.9岁。其中汉族与回族的发病年龄大于维吾尔族与哈萨克族(63.9±12.4,62.5±13.2岁vs53.7±14.9,54.0±14.3岁;P<0.05);各族别引起房颤的病因中,汉族以高血压为主,而维吾尔族与哈萨克族及回族以风湿性瓣膜病为主。回族与维吾尔族的血栓栓塞危险因素发生率高于汉族及哈萨克族(P=0.014)。各族别与缺血性脑卒中及血栓栓塞并发症之间的关系差别无显著性。结论房颤患者的病因、发病年龄及血栓栓塞的危险因素等方面存在种族差别。     

起搏术后心房颤动的影响因素及心房颤动与心钠素的关系

目的观察心脏起搏术后发生心房颤动(简称房颤)的影响因素及房颤与血心钠素(ANP)的关系。方法选择安装心脏起搏器的患者103例进行随访,分析房颤与年龄、起搏方式、心律失常类型、左房内径(LAD)、左室射血分数(LVEF)和血ANP的关系。结果①65岁以下患者房颤发生率低于65岁以上组(P<0.05)。②VVI组房颤发生率高于DDD组(P<0.05)。③慢快综合征组房颤发生率较缓慢型病窦综合征和房室传导阻滞组高(P<0.05)。④VVI房颤组术后LAD增大、LVEF下降(P<0.05),VVI房颤组术后与DDD组比较有差异(P<0.05)。⑤VVI房颤组和VVI窦性心律组ANP浓度较DDD组高(P<0.05);各组不同心功能级别(NYHA)之间ANP浓度随着心功能级别的加重而升高。结论长期心脏起搏术后房颤的发生可能与年龄大、VVI起搏、病窦综合征(慢快型)、LAD增大、LVEF降低及ANP浓度升高相关。