有预防心房颤动程序的双腔频率应答型起搏器的抗心房颤动作用

目的：观察具有预防心房颤动程序的DDDR型起搏器（Vitatron 900E)预防阵发性心房颤动的机制及效果。方法：对10例阵发性心房颤动分3段（每段2周），第1段启动起搏器进入房性心律失常记录状态，DDD60次／min，探查心房颤动的诱发因素；第2段为起搏治疗段1，DDD85次／min，观察超速起搏的抗心房颤动作用；第3段为起搏治疗阶段Ⅱ，DDD70次／min，据第1阶段获悉的心房颤动的触发因素，启动4个预防心房颤动程序中相关的项目。结果：10例均可控制心房颤动，3例用心房超速起搏控制，7例仅通过启动“房性期前收缩后反应”及／或运动后心率控制程序，其中3例尚需用可达龙0．2g/天。结论：抗心房颤动起搏器有防治阵发性心房颤动作用，尤其适用于合并病态窦房结综合征的患者。     

起搏器的休息频率功能对房性心律失常的近期影响

目的探讨起搏器的休息频率功能对房性心律失常的近期影响,评估其临床疗效和安全性。方法选择植入Identity Adx DDD 5286型双腔起搏器的病态窦房结综合征患者39例。起搏器植入后不打开休息频率,保持起搏器出厂设置;术后3个月随访时程控为在双腔起搏模式下打开休息频率,共随访6个月。比较起搏器植入前后及打开心房滞后模式后心房起搏百分比及房性心律失常的发生情况。结果与术前比较,术后3个月24 h动态心电图显示,房性期前收缩次数和房性心动过速、心房颤动阵数增加(U=4.19、4.28和4.39,均为P<0.05),相应的发作例数也增加(χ2=4.57、4.61和4.96,均为P<0.05)。与未打开休息频率模式比较,打开后心房的起搏百分比明显降低[56%(40%⁷3%)比84%(64%73%)比84%(64%⁹7%),P=0.03];24 h动态心电图显示,房性期前收缩次数和房性心动过速、心房颤动阵数明显减少(P<0.01),相应的发作例数也减少(P<0.01)。结论休息频率模式可以减少心房起搏的比例,减少房性心律失常的发生;打开休息频率模式安全可靠。     

兼有APP和PMOP功能的起搏器抗房性心律失常的临床观察

目的评价兼有心房优先起搏(atrial preference pacing,APP)和模式转换后的超速起搏(post mode switch overdrive pacing,PMOP)功能的起搏器预防房性心律失常的临床效果。方法具有起搏器适应证伴房性心律失常30例患者植入了兼有APP和PMOP功能的起搏器。术后1个月为空白期,关闭抗房性心律失常(atrial arrhythmia,ATA)功能,从而进行参数观察调试;术后2～7个月为诊断期,关闭抗ATA功能;术后8～13个月为治疗期,打开抗ATA功能;比较治疗前后房性心律失常事件发作频率,持续时间、心脏彩色超声检查等变化。结果 (1)治疗期的左心房内径、左心室舒张末径、右心房内径、左心室射血分数较诊断期无明显改变,差异无统计学意义(P 0. 05);右心室内径较诊断期有所减少,差异有统计学意义(t=2. 31,P 0. 05)。(2)治疗期的24小时动态心电图房性心动过速(阵/次)、房性期前收缩、阵发性心房颤动24小时次数、阵发性心房颤动持续时间等指标较诊断期有所减少,差异有统计学意义(t=1. 85～3. 37,P 0. 05)。(3)治疗期的心房起搏比率、心房颤动百分比较诊断期有所减少,差异有统计学意义(Z=3. 26、3. 59,P 0. 05)。结论 (1)伴发阵发性心房颤动或房性心动过速的接受起搏的患者植入抗心房颤动起搏器可以减少心房颤动和房性心动过速的复发。(2)在短期观察中,APP和PMOP的工作模式不会使得患者心功能恶化。     

阵发性心房颤动的动态心电图特征研究

目的 探讨阵发性心房颤动发生的动态心电图特征. 方法 对38例阵发性心房颤动患者和24例非阵发性心房颤动患者的动态心电图进行分析,测定和计算房性期前收缩偶联间期和房性期前收缩指数. 结果 阵发性心房颤动共发作291次,其中221次由房性期前收缩诱发（75.95%）.诱发心房颤动的房性期前收缩与未诱发心房颤动的房性期前收缩比较,偶联间期较短,期前收缩指数较小,差异有统计学意义（P〈0.05）.心房颤动发作前1h房性期前收缩和短阵房性心动过速频率增加.35.75%阵发性心房颤动发生时出现明显的长短周期现象. 结论 房性期前收缩是阵发性心房颤动发生的主要因素,长短周期现象是阵发性心房颤动发生的重要电生理机制.     

肌袖性房性心律失常3例分析

肌袖性房性心律失常是由大静脉驱动或触发心房肌所引起,包括肌袖性房性期前收缩（PAS）、肌袖性房性心动过速、肌袖性心房扑动、肌袖性心房颤动。下面报告3例。     

心房颤动的电学治疗进展

心房颤动即心房呈无序激动和无效收缩的房性节律 ,是最常见的心律失常之一。尽管心房颤动的药物治疗具有一定的疗效 ,但大多数患者的症状和由心房颤动带来的后果未能得到理想的改善 ,有一定的致残率和病死率。近来心房颤动的非药物治疗即电学治疗得到了较广泛的研究。一、预防性心房多部位起搏心房起搏预防心房颤动发作是一个较新的概念。一些临床观察结果提示人们应用心房起搏方法来预防 ［１～３］:(１)在长期随访中发现 ,病态窦房结综合征患者单独心房起搏 (ＡＡＩ)或单独心室起搏 (ＶＶＩ)的３～５年中 ,前者发生心房颤动者仅为５ %～７…     

病态窦房结综合征

病态窦房结综合征的临床表现包括:(1)持久而不能解释的窦性心动过缓;(2)窦性静止,无逸搏或房性或连接处性节律;(3)继发于颈动脉窦过敏的严重窦性心动过缓;(4)电击复律、阵发性心动过速或心房调搏后无窦房结功能;(5)窦房传出阻滞;(6)心动过缓一心动过速综合征——窦性心动过缓与阵发性房性心动过速、房性心动过速、心房扑动、心房颤动、连接处性心动过速或心室颤动相交替。窦房结功能不全的原因主要有二:(1)起搏失效,可产生窦性心动过缓及窦性静止。     

预防病态窦房结综合征心房颤动的心脏起搏模式探讨

目的 :观察何种心脏起搏模式能有效预防病态窦房结 (病窦 )综合征心房颤动 (房颤 )的发作。方法 :对 4 5例安置心房按需起搏器 (AAI)及房室顺序起搏器 (DDD)的病窦综合征房颤患者进行了平均 3.3年的随访观察。结果 :4 5例病窦患者仅 1例出现房颤 (2 .2 % )。对 5个典型病例进行分析的结果提示 ,超速持续心房起搏可以抑制病窦患者房颤的发生。结论 :心脏起搏抑制房颤发生的机制可能与快频率起搏加速心房内传导、抑制了房性期前收缩、消除了窦性心动过缓和心脏长 短间歇有关。双心房或AA起搏方式可能是一种比较理想的预防房颤的方法     

窦房结功能不良与传导阻滞患者植入双腔起搏器后动态心电图的表现及其意义

目的 探讨窦房结功能不良与传导阻滞患者植入双腔起搏器后动态心电图的表现及临床意义。 方法 分析植入DDD型双腔起搏器的160例患者的动态心电图,其中窦房结功能不良组80例,传导阻滞组80例,比较2组患者植入双腔起搏器后的动态心电图表现、主要的工作模式、心室起搏情况、自身心律失常及起搏器所致的心律失常。 结果 窦房结功能不良组与传导阻滞组起搏比例≥60%者均多于起搏比例<60%者（82%比18%、85%比15%）,组间差异无统计学意义。窦房结功能不良组心房按需起搏工作模式显著高于传导阻滞组（31%比2%,P<0.01）,而心室按需起搏/心房同步心室起搏工作模式显著低于传导阻滞组（19%比50%,P<0.01）;组间比较,双腔按需起搏工作模式检出率二者无统计学差异（50%比48%）。窦房结功能不良组心室安全起搏检出率显著高于传导阻滞组（25%比12%,P<0.05）,而心室起搏融合波的检出率则显著低于传导阻滞组（35%比51%,P<0.05）。窦房结功能不良组起搏介导性心动过速及感知房性心动过速触发快速型心室起搏的检出率显著高于传导阻滞组（12%比2%,24%比11%,P<0.05）,房性心动过速和频发房性早搏的检出率亦显著高于传导阻滞组（38%比18%,22%比4%,均P<0.05）。 结论 窦房结功能不良与传导阻滞患者植入双腔起搏器后对应的主要工作模式可以通过动态心电图的各种表现进行识别,全面了解起搏器的工作状态,为起搏器的合理程控以及自身心律失常提供可靠的依据。     

间隔起搏对快速性心律失常和心力衰竭的治疗作用

目的:探讨间隔起搏对快速性心律失常和心力衰竭的临床疗效。方法:对62例病态窦房结综合征和(或)高度/Ⅲ度房室传导阻滞患者行房间隔和(或)室间隔起搏,术前和术后1周内查24h动态心电图(DCG)及二维超声心动图(2-DE),并跟踪随访32～660(346.29±196.08)d。结果:62例患者均顺利完成起搏器安置术,未发生任何并发症。与术前相比:DDD和AAI间隔起搏手术后房性期前收缩次数P50(P25、P75)为[290.00(14.00;3114.00)∶6.00(0.00;124.50),P=0.000]、房性心动过速阵数[13.50(1.75;112.75)∶1.00(0.00;7.50),P=0.002]和阵发性心房扑动/颤动阵数[2.00(1.00;5.25)∶0.00(0.00;0.25),P=0.048]以及房性期前收缩发作例数(23∶14,P=0.048)均明显减少,房性心动过速和阵发性心房扑动/颤动发作例数均有减少趋势(均P>0.05);DDD和VVI间隔起搏术后室性期前收缩次数明显减少[25.50(3.75;123.00)∶7.00(1.00;30.75),P=0.003],室性心动过速...     

心房颤动患者心房纤维化研究进展

心房颤动的发生和维持与心房重构有关。心房纤维化是心房颤动患者心房结构重构最突出的表现,目前被认为是发生心房颤动的结构基础,是心房颤动发生、维持的一个重要因素。现综述心房颤动患者心房纤维化及其发生机制。通过对心房颤动患者心房纤维化结构改变及肾素-血管紧张素系统、转化生长因子、基质金属蛋白酶等在心房纤维化的发生和心房颤动发生、维持中的作用等的全面阐述,,探讨了心房颤动患者心房纤维化的研究进展。防治心房颤动新的策略取决于对心房纤维化机制更好的理解。     

Effects of High-Frequency Atrial Pacing in Atypical Atrial Flutter and Atrial Fibrillation

Atypical atrial flutter has, hitherto, been relatively refractory totermination by rapid atrial pacing. High-frequency pacing (HFP) in theatrium, for termination of atrial flutter or atrial fibrillation (AF), andthe electrophysiologic effects related to it have not been examined. Weexamined the clinical efficacy, safety, and electrophysiologic mechanisms ofHFP using 50-Hz bursts at 10 mA applied at the high right atrium in patientswith atypical atrial flutter (group 1) or AF (group 2), using a prospectiverandomized study protocol. Four burst durations (500, 1000, 2000, and 4000ms) were applied at the high right atrium repetitively in random sequence in22 patients with spontaneous atrial flutter or AF. Local and distant rightand left atrial electrogram recordings were analyzed during and after HFP.HFP resulted in local and distant right and left atrial electrogramacceleration in 8 of 10 patients (80%) in group 1 but caused lessfrequent local atrial electrogram acceleration (6 of 12 patients) and nodistant atrial electrogram effects in group 2 (p < .05 versus group 1).The HFP protocol was effective in arrhythmia termination in 6 of 10patients in group 1 but in no patient in group 2 (p < .05 versus group1). Standard HFP protocol applied at the high right atrium can frequentlyalter atrial activation in both atria and can terminate atypical atrialflutter. Efficacy in AF is limited, probably due to limitedelectrophysiologic actions beyond the local pacing site.     

Atrial Tachycardias Following Atrial Fibrillation Ablation

One of the most important proarrhythmic complications after left atrial (LA) ablation is regular atrial tachycardia (AT) or flutter. Those tachycardias that occur after atrial fibrillation (AF) ablation can cause even more severe symptoms than those from the original arrhythmia prior to the index ablation procedure since they are often incessant and associated with rapid ventricular response. Depending on the method and extent of LA ablation and on the electrophysiological properties of underlying LA substrate, the reported incidence of late ATs is variable. To establish the exact mechanism of these tachycardias can be difficult and controversial but correlates with the ablation technique and in the vast majority of cases the mechanism is reentry related to gaps in prior ablation lines. When tachycardias occur, conservative therapy usually is not effective, radiofrequency ablation procedure is mostly successful, but can be challenging, and requires a complex approach.     

Implantable Atrial Defibrillator and Detection of Atrial Flutter

The implantable atrial defibrillator (IAD) is designed to detect and treat atrial fibrillation (AF) with low energy synchronized shocks. A patient with a history of persistent AF was implanted with an IAD after ineffective treatment with procainamide and sotalol. Through four months of follow-up, the IAD performed appropriate detection and treatment of AF. During the fifth month, the patient was put on flecainide in an attempt to minimize the AF recurrence rate. On flecainide the patient experienced typical atrial flutter which required IAD reprogramming for appropriate detection and therapy delivery. This case report examines the optimization of the IAD to detect atrial flutter. Six months of follow-up after optimization the IAD has shown appropriate detection of both atrial flutter and AF. During the entire follow-up period the IAD had appropriate detection of sinus rhythm (no false positive detection, i.e. sinus rhythm as AF).     

心房颤动致心房重构分子机制研究进展

心房颤动是临床上一种常见的心律失常,心房颤动致心房重构是近年来研究发现的一个重要的电生理现象。心房颤动本身能够导致心房电生理、功能和结构的改变。本文综述了心房颤动致心房快速的电生理变化和缓慢的蛋白质表达及其分子改变机制。通过对心房电生理重构、离子重构和蛋白质重构和超微结构及其功能变化等不同方面的全面阐述,探讨了心房重构的分子机制研究进展。防治心房颤动新的策略将取决于心房重构机制更好的理解。     

Right Atrial Thrombi and Depressed Right Atrial Appendage Function After Cardioversion of Atrial Fibrillation

BACKGROUND: It has been shown that cardioversion of atrial fibrillation may result in left atrial chamber and appendage dysfunction and cause new thrombi in the left atrium. The aim of this prospective study was to investigate right atrial appendage function and assess the incidence of new right atrial thrombi after electrical cardioversion. METHODS: Transthoracic echocardiography was performed in 25 patients 4 h before and at 24 h and 7 days after electrical cardioversion to determine right and left atrial mechanical function (internal atrial defibrillation, n = 16; external electrical cardioversion, n = 9), as assessed by peak A wave velocities derived from the transtricuspid and transmitral velocity profiles. In addition, transesophageal echocardiography was performed 4 h before and 24 h after cardioversion to evaluate postcardioversion thrombus formation in the right and left atrial chambers and to assess right and left atrial appendage function. The degree of spontaneous echo contrast was noted, and peak emptying velocities of the appendages were measured before and after cardioversion. RESULTS: Peak emptying velocities of both the right atrial appendage (mean +/- SD, 0.23 +/- 0.1 vs 0.32 +/- 0.11 m/sec; P = 0.02) and the left atrial appendage (0.3 +/- 0.15 vs 0.4 +/- 0.15 m/sec; P = 0.01) were significantly lower 24 h after cardioversion compared with 4 h before cardioversion, respectively. The degree of spontaneous echo contrast increased in the left atrium after cardioversion from 1.0 +/- 1.2 to 1.9 +/- 2.1 (P = 0.02), and in the right atrium, it increased from 0.8 +/- 1.1 to 1.2 +/- 1.1 (P = 0.1) after cardioversion. Peak A wave transtricuspid velocity increased from 0.26 +/- 0.05 m/sec at 24 h to 0.38 +/- 0.06 m/sec (P = 0.001) after 7 days; respective values for transmitral peak A wave velocity were 0.39 +/- 0.15 and 0.54 +/- 0.16 m/sec (P = 0.009). No thrombi were found in either the right or left atrium before cardioversion. In two patients, new thrombi in the right atrium were detected 24 h after internal atrial defibrillation. Thrombi were located at the superior rim of the fossa ovalis in both patients with patent foramen ovale. Another patient had developed a thrombus in the left atrial appendage. CONCLUSIONS: Electrical cardioversion may not only cause left atrial chamber and appendage dysfunction and left atrial thrombi but also lead to depressed right atrial appendage function and the generation of new thrombi in the body of the right atrium.     

Atrial Fibrillation: The Role of Atrial Defibrillation

Dual defibrillator implantation represents an emerging option to treat patients with drug refractory atrial fibrillation. Atrial antitachycardia pacing and cardioversion have been demonstrated to be highly effective in treating spontaneous tachyarrhythmias and may reduce atrial fibrillation burden by preventing atrial remodeling. Device implantation has been associated to improved quality of life and reduced hospitalization rate. Patient selection and tailored device programming are critical as regard to clinical outcome. Individual psychological profile analysis as well as underlying heart disease and atrial fibrillation clinical patterns represent the main drivers for the right strategy. Controlled studies are needed in order to define the subset of patients who can benefit more from device implantation.     

胸腔静脉在心房颤动发生机制中的作用

心房颤动是临床上常见的心律失常。肺静脉、上腔静脉、Marshall静脉等在心房颤动发生中扮演重要角色,现就胸腔静脉的组织学、电生理特征及其与心房颤动关系进行综述。