快速起搏兔右房致自主神经电活动改变和重构的研究

目的研究自主神经系统(ANS)在心房颤动(AF)发生和维持中的作用。方法成年新西兰大白兔20只,随机分为假手术组(n=10)和模型组(n=10)。模型组给予24h快速心房起搏。以自主神经放电活动变化作为快速起搏后神经重构的参考指标,统计指标是放电积分幅度(AID),放电时程(TCD),放电间隔时程(TCDI)。并应用荧光免疫技术研究自主神经生长相关蛋白(GAP43),乙酰胆碱转移酶(ChAT),酪氨酸羟化酶(TH)的分布密度和再生。结果与假手术组比较,模型组迷走神经AID增加(P<0.001);而TCD和TCDI无延长(P均>0.05);模型组交感神经AID降低(P=0.002);而TCD延长,TCDI缩短(P=0.000)。GAP43、ChAT和TH假手术组依次呈阳性、弱阳性、弱阳性。而模型组依次呈强阳性、阳性、阳性。结论24h快速心房起搏后,心脏神经纤维存在形态、分布及密度的改变,即神经重构。     

胺碘酮对右房快速起搏兔肺静脉心肌袖细胞Kir3.1、KvLQT1、HERG基因表达的影响

目的观察胺碘酮对右房快速起搏兔肺静脉心肌袖细胞膜钾通道亚型(Kir3.1、KvLQT1、HERG)基因表达的影响。方法新西兰兔30只,随机分为对照组、快速心房起搏组(起搏组,600次/分频率起搏7天)及心房快速起搏+胺碘酮组(胺碘酮组,快速起搏+胺碘酮灌胃7天),每组10只。剪取3组兔肺静脉心肌袖组织,应用逆转录-聚合酶链反应技术测定肺静脉心肌袖细胞Kir3.1、KvLQT1、HERG的mRNA表达水平。结果起搏组Kir3.1mRNA的表达低于对照组42.8%(P<0.01),胺碘酮组低于对照组46.4%(P<0.01);HERG mRNA的表达起搏组与对照组无差异(P>0.05),胺碘酮组比对照组高28.8%(P<0.05);KvLQT1三组无差异。结论快速心房起搏可引起兔肺静脉心肌袖细胞钾通道基因表达变化,胺碘酮对其亦有影响。     

Efficacy and tolerability of continuous overdrive atrial pacing in atrial fibrillation.

Overdrive right atrial pacing has been used to prevent atrial fibrillation, but its efficacy in atrial fibrillation prevention and the patient tolerability and quality of life during high rate pacing remain uncertain. The objective of this study was to test the effects of a consistent atrial pacing algorithm that automatically paced the atrium at 30 ms shorter than the sinus P-P interval for atrial fibrillation prevention. Fifteen patients with sick sinus syndrome implanted with a Thera DR (model 7940 or 7960, Medtronic Inc.) were randomly programmed to rate adaptive dual chamber pacing (DDDR) or DDDR + consistent atrial pacing mode, each for an 8-week study period. The efficacy of consistent atrial pacing was assessed by the number of automatic mode switching and the number of premature atrial complexes. Symptoms and quality of life were assessed by the SF-36 quality of life questionnaire and an atrial fibrillation symptom checklist. The percentage of atrial pacing increased from 57 +/- 32% to 86 +/- 28%. Overall, there was no significant difference in the number of automatic mode switching episodes between DDDR and DDDR + consistent atrial pacing (47 +/- 90 vs 42 +/- 87, P > 0.05), but a significant reduction in premature atrial complexes by 74.7% (P < 0.001). There was no undue increase in atrial rate by the DDDR + consistent atrial pacing mode versus DDDR (63 +/- 13 vs 70 +/- 7 bpm). There was no significant difference in quality of life scores and symptom severity on frequency between the two modes of pacing, but a trend towards a lower frequency of symptoms in the DDDR + consistent atrial pacing mode compared with baseline (29.5 +/- 10.2 vs 25.1 +/- 9.7, P = 0.07). An algorithm that provides consistent atrial overdrive pacing can suppress atrial fibrillation triggering premature atrial complexes without the need to increase the overall atrial rate compared with conventional pacing. The algorithm appears to be well-tolerated, but further studies are needed to address the clinical impact of this atrial fibrillation prevention algorithm.     

白藜芦醇对快速起搏右心房诱发的持续性心房颤动猪心房结构重构的影响

目的 观察快速起搏猪右心房制备持续性心房颤动（AF）的效果,探讨白藜芦醇（RES）干预对持续性AF猪的心房结构重构的影响.方法 18只小家猪（雌雄不拘）按完全随机设计的分组方法（采用动物编号和随机分组表）分为起搏组（ATP组）、假手术组（Sham组）和RES干预组各6只,采用Seldinger血管穿刺技术送入双极电极至右心房并连接实验用起搏器（AOO）,ATP组和RES干预组的右心房快速起搏（500次/min）2周,制备持续性AF实验模型.3组猪分别于起搏前和起搏2周后进行电生理和经胸壁超声心动图检查,以检测AF的持续时间、左右心房大小及左心房收缩末面积.RES干预组猪于起搏前1周开始服用RES（2.5 mg·kg-1·d-1）.起搏2周后取各组猪的左右心房组织标本,观察心房组织形态学和间质纤维化的改变,用免疫组织化学分析软件计算胶原容积分数（CVF）来反映间质纤维化程度.结果 （1）起搏2周后,ATP组AF的发生率较RES干预组明显升高（100％比66.7％,x2=10,P＜0.01）、持续时间延长[（26.41±9.89）min比（9.56±1.36） min,F=10.7,P=0.01].（2）起搏2周后,ATP组和RES干预组猪的左右心房明显比起搏前增大;但RES干预组的左心房收缩末面积明显低于ATP组[（599.2±8.7） mm2比（744.3±29.9） mm2,F=130.61,P＜0.01].（3）RES干预组左右心房组织CVF明显低于ATP组（56％±6％比73％±7％;59％±6％比75％±7％,均为P＜0.01）.结论 快速起搏猪右心房可成功制备持续性AF模型;RES干预可以明显抑制快速起搏右心房诱发的持续性AF猪的心房结构重构,减少AF的发生.     

钾通道阻断剂对心房快速起搏兔右心耳场电位时限的影响

目的应用微电极阵列（MEA）研究钾通道阻断剂对快速起搏（RAP）兔右心耳场电位时限（fAPD）的变化。方法成年新西兰大白兔40只,体重2．5～3．0kg,雌雄不拘,由新疆医科大学动物实验中心提供,动物质量属于一级标准。随机分为3组,对照组（non．pace,n=8）,起搏＋钾通道阻断剂组（TEA、4-AP和BaCl2,每组n=8）,起搏＋胺碘酮组（n=8）。RAP24h后,迅速开胸取心脏,剪下右心耳,随即切片（厚度500um）,将标本固定在MEA记录系统。分别记录正常对照组,给予阻断剂及胺碘酮组MEA形态和fAPD改变。结果对照组右心耳fAPD为（188．33±18．29）ms,起搏组fAPD为（173．91±6．83）ms。给予20mmol／LTEA阻断Ix,fAPD由（176．67±8．66）ms延长到（196．11±10．76）ms（P=0．012）,5mmol／L4-AP阻断Ito,fAPD由（169．38±10．56）ms延长到（188．56±13．82）ms（P=0．005）。10～mol／L BaCl2阻断IKir,fAPD由（182．22±12．87）ms延长到（191．11±13．09）ms（P=0．039）。2×10-6mmol／L胺碘酮使fAPD由（167．38±13．67）ms延长到（185．00±15．14）ms（P=0．002）。结论应用MEA技术可真实客观反映心肌组织切片的电生理特性。24hRAP后,以阻断Ito,IKur IK1和IKs为主的钾通道阻断剂延长右心耳fAPD。胺碘酮可有效逆转或阻止右心耳fAPD的延长。     

No incremental benefit of multisite atrial pacing compared with right atrial pacing in patients with drug refractory paroxysmal atrial fibrillation

OBJECTIVE—To evaluate the incremental antifibrillatory effect of multisite atrial pacing compared with right atrial pacing in patients with drug refractory paroxysmal atrial fibrillation paced for arrhythmia prevention alone.
METHODS—In 20 of these patients (mean (SD) age 64 (8) years; 14 female, six male), a single blinded randomised crossover study was performed to investigate the incremental benefit of one month of multisite atrial pacing compared with one month of right atrial pacing. Outcomes included the number of episodes of paroxysmal atrial fibrillation, their total duration obtained from pacemaker Holter memory, and quality of life using a cardiac specific questionnaire (the modified Karolinska questionnaire).
RESULTS—Comparing right atrial with multisite atrial pacing, there was no significant change in either the number of paroxysmal atrial fibrillation episodes (mean (SD): right atrial pacing 77 (98) episodes v multisite pacing 52 (78) episodes, NS) or their total duration (right atrial, 4.8 (5.4) days v multisite, 6.3 (9.8) days, NS). Quality of life scores compared with baseline status were equally improved by either pacing strategy (mean percentage improvement: right atrial, 38%, p = 0.003; multisite, 44%, p = 0.003). There was no significant difference in life scores comparing the two pacing modes.
CONCLUSIONS—Multisite atrial pacing has no incremental antiarrhythmic effect compared with right atrial pacing in patients paced for drug refractory paroxysmal atrial fibrillation. Quality of life is equally improved with either pacing strategy, with no differences between them.


Keywords: multisite atrial pacing; atrial fibrillation; pacing     

No evidence of automatic atrial overdrive pacing efficacy on reduction of paroxysmal atrial fibrillation.

AIMS: Paroxysmal atrial fibrillation (PAF) is frequently encountered in pacemaker patients, most commonly in sick sinus syndrome. The combination of site-specific pacing in conjunction with an overdrive algorithm combined with antiarrhythmic drugs on the incidence of PAF in patients with a conventional indication for pacing is unknown. METHODS AND RESULTS: Patients with pacemaker indication and PAF received a DDDR-pacemaker, which included an automatic atrial overdrive (AO) algorithm. The atrial lead was implanted in either the right atrial appendage (RAA) (n = 83) or the right low-atrial septum (LAS) (n = 94). The algorithm was switched on or off in a 3 month, single blind crossover design and antiarrhythmic drugs were kept stable. A control group of 96 patients (LAS, n = 14; RAA, n = 84) without PAF served as controls to assess any proarrhythmic effect of overdrive pacing. Atrial fibrillation (AF) burden defined as cumulative time in mode switch was not reduced during automatic AO from either the RAA or from the LAS. The reduction was not effective both for AF of short (<24 h) and long (> or =24 h) duration. There was no atrial proarrhythmia induced by the overdrive algorithm in the control group. CONCLUSIONS: We could not demonstrate a reduction of AF burden defined as cumulative time in AF by the AO algorithm, in patients who are paced for standard indications and PAF, neither from the RAA nor from the LAS.     

Septal atrial pacing for the prevention of atrial fibrillation.

AIMS: Atrial fibrillation (AF) produces significant morbidity and mortality. The current method of permanent pacing of the right atrium (RA) may cause delayed interatrial conduction and predispose to AF. We hypothesized that atrial septal pacing would reduce AF compared with high RA pacing. METHODS AND RESULTS: The patients were randomized into two groups. After randomization, patients received a dual-chamber rate-responsive device capable of mode-switching with advanced telemetry features. Devices were programmed in a standardized manner. To be eligible, the patients were required to have a conventional indication for a permanent pacemaker and recurrent paroxysmal AF. Group 1 was paced from high RA and Group 2 was paced from the atrial septum. Analysis of 43 patients who have completed 6 months of follow-up and 22 patients who completed 12 months of follow-up showed no significant differences in the number of mode-switching episodes or in AF burden between groups (P = NS by Mann-Whitney) although there was a trend for less AF with septal pacing. There were no differences in thresholds, sensing, or lead impedance. Lead parameters remained stable over time and there were no displacements of the electrodes after implantation. No patient experienced lead-related complications. A significant variability in AF burden was noted in this patient population. CONCLUSIONS: Implantation of an atrial-active fixation lead on the atrial septum is safe and feasible. However, this study showed no significant difference between septal pacing and high atrial pacing, using the endpoints of AF duration and number of AF episodes.     

快速心房刺激对P波时限及离散度的影响

目的分析快速心房刺激对P波时限及离散度的影响.方法在74例射频消融术及82例经食管心房调搏检查中,用180ppm的S1S1刺激心房3min,在刺激前后立刻记录12导联同步心电图,通过心电图测出刺激前后的最大P波时限、最小P波时限及P波离散度,然后进行比较.结果射频消融组最大P波时限在心房刺激后比刺激前有显著性延长（p=0.002）,最小P波时限及P波离散度无显著性差异,食管心房调搏组最大P波时限及P波离散度在心房刺激后比刺激前有显著性增加（p=0.001）,最小P波时限无显著性差异.结论快速心房刺激能引起心房传导时间延长,非均质电活动的离散程度增加.最大P波时限及P波离散度是可以用来评价心房电重构的简便而无创的指标.     

Atrial pacing for suppression of early reinitiation of atrial fibrillation after successful internal cardioversion.

AIMS: To evaluate the efficacy of atrial pacing in the suppression of early reinitiation of atrial fibrillation after successful internal cardioversion. METHODS AND RESULTS: The efficacy of atrial pacing in suppressing early reinitiation of atrial fibrillation was studied in 12 of 45 (29%) patients with early reinitiation of atrial fibrillation after successful cardioversion. These patients were randomized to undergo either repeated defibrillation alone or repeated defibrillation followed by high right atrial pacing at 500 ms in a crossover fashion. In patients with persistent early reinitiation of atrial fibrillation despite atrial pacing at 500 ms and repeated defibrillation, atrial pacing at 300 ms was tested. Lastly, if early reinitiation of atrial fibrillation persisted, administration of intravenous sotalol (1.5 mg. kg(-1)) was tested. Atrial pacing at 500 ms after defibrillation prevented early reinitiation of atrial fibrillation in five of 12 (42%) patients, and was significantly more effective than repeated defibrillation (0/9 patients, 0%, P<0.05). During atrial pacing at 500 ms, the density of atrial premature depolarizations (APDs) was significantly decreased (2.4+/-2.4 APDs. min(-1)vs 16.4+/-9.8 APDs. min(-1), P<0. 05) and the coupling interval of atrial premature depolarization was significantly increased (420+/-32 ms vs 398+/-19 ms, P<0.05) as compared to no pacing. In the remaining seven (58%) patients, atrial pacing at 500 ms failed to prevent early reinitiation of atrial fibrillation, but significantly decreased the density of atrial premature depolarization (3.4+/-2.4 APDs. min(-1)vs 14.2+/-4.8 APDs. min(-1), P<0.05) and delayed the onset of early reinitiation of atrial fibrillation (33+/-17s vs 11+/-11 s, P<0.05). Atrial pacing at 300 ms decreased the coupling interval of atrial premature depolarization as compared to no pacing and during atrial pacing at 500 ms (P<0.05), but without early reinitiation of atrial fibrillation suppression. Administration of intravenous sotalol was effective in preventing early reinitiation of atrial fibrillation in five of seven (71%) patients where pacing failed to suppress early reinitiation of atrial fibrillation. CONCLUSION: The results of this study suggest that atrial pacing can be useful when combined with transvenous defibrillation in patients with early reinitiation of atrial fibrillation.     

双房同步起搏预防和治疗房性快速性心律失常

目的 观察双房同步起搏技术对伴有房间传导阻滞的阵发性快速性房性心律失常的疗效。方法 病态窦房结综合征合并房间传导阻滞的阵发性快速性房性心律失常患者7例，男4例、女3例，年龄58～78岁。其中4例行双房起搏(AAT)，3例行双房右室三腔起搏(DDD)，经穿刺左锁骨下静脉插入右房、右室和冠状静脉窦起搏电极导线，分别用于起搏右房、右室和左房。结果 起搏器及电极导线均顺利植入，未发生任何并发症。冠状静脉窦电极顶端距冠状静脉窦口2．5—3．5cm，P波振幅为1．6—5．5mV、阻抗624—808Ω,、单极起搏阈值0．5—0．7V。随访2—31个月，7例均健在，房性心律失常的临床发作得到明显控制。结论：双房同步起搏技术是房间传导阻滞合并快速房性心律失常的有效预防和治疗方法。     

房间隔起搏的初步临床应用经验

目的 探讨有适应证的阵发性心房颤动(房颤)患者永久性房间隔起搏的可行性和安全性。方法 先行心内电生理标测，寻找使双心房同步激动的房间隔最佳起搏点，采用主动固定方法将导线固定于该部位。结果 18例伴有房间传导阻滞的阵发性房颤患者，14例患者完成房间隔标测和永久性起搏导线植入手术，4例未能成功植入房间隔起搏导线。结论 在伴有房间传导阻滞的阵发性房颤患者中永久性房间隔起搏是安全可行的。     

氯沙坦对家兔快速心房起搏心房电重构及L-型钙通道的影响

目的:通过人工心脏起搏的方法制备家兔急性心房颤动(Af)动物模型,探讨Af时心房发生电重构的机制,并观察氯沙坦对电重构的影响.方法:30只家兔,随机分为3组(每组10只):对照组、0.9%氯化钠起搏组、氯沙坦起搏组;以600次/min的频率起搏心房8 h,并分别于起搏后2、4、6、8 h测定心房有效不应期(AERP)变化及L-型钙通道的电流密度.结果:①经快速起搏8 h,0.9%氯化钠起搏组较对照组各个基础周长下的AERP均显著下降.氯沙坦起搏组较对照组AERP无明显变化.②0.9%氯化钠起搏组较对照组心房肌ICa-L降低;氯沙坦起搏组较对照组心房肌ICa-L未见显著降低;氯沙坦起搏组较0.9%氯化钠起搏组心房肌ICa-L差异无统计学意义,但ICa-L的标准差显著降低.结论:①快速心房起搏可引起AERP缩短及AERP频率适应性不良为特征的心房肌电重构,氯沙坦可以预防电重构的发生.②快速心房起搏可以导致心房肌ICa-L的降低和离散度的增高;氯沙坦可以抑制ICa-L离散度的增加从而降低Af的潜在危险.     

Incremental programming of atrial anti-tachycardia pacing therapies in bradycardia-indicated patients: effects on therapy efficacy and atrial tachyarrhythmia burden.

AIMS: Efficacy of pace-termination of atrial arrhythmias (ATP) may depend on atrial cycle length and regularity. Whether device programming of ATP therapies can improve ATP efficacy and alter atrial tachyarrhythmia burden is unknown. METHODS AND RESULTS: ATP efficacy was evaluated in 61 patients (39 males; 66 +/- 10 years) with a standard indication for pacing, 95% with a history of AT/AF. Each patient was implanted with a novel DDDRP pacemaker capable of delivering ATP therapy. ATP efficacy and AT/AF frequency and burden were compared within each patient during a period of nominal ATP programming (NP) followed by a period of aggressive incremental programming (IP). Adjusted ATP-termination efficacy was higher during IP than during NP (54.8% vs 37.9%, P < 0.05). No differences in AT/AF frequency (3.3 +/- 5.9 vs 3.2 +/- 6.9 day(-1)) or burden (18 +/- 28% vs 18 +/- 29%) were observed comparing NP with IP. The majority of episodes during both the NP (81%) and IP (77%) periods terminated within 10 min. Episodes lasting 24 h or more accounted for only 0.4% of the episodes in both groups. but accounted for 38% of the average burden during NP and 51% during IP. CONCLUSIONS: Device programming of ATP therapies can influence the number of treated episodes and the efficacy of ATP therapies although arrhythmic frequency and burden may not change. Total atrial arrhythmia burden is disproportionately influenced by long (>24 h) episodes.     

伊贝沙坦对快速心房起搏家兔心房电重构的影响

目的观察伊贝沙坦对心房快速起搏8h家兔心房电重构及心房肌细胞超微结构改变的影响。方法将12只家兔随机分为伊贝沙坦组和对照组。经颈内静脉将电极置入右心房,以600次/min行快速心房起搏,分别测定起搏前及起搏后0.5h、1h、4h、8h及停止起搏后10min、20min、30min,S1S1为200ms、150ms时的心房有效不应期(AERP200、AERP150);取未起搏家兔及每组起搏8h后家兔右心耳组织观察超微结构。结果①心房快速起搏8h,对照组家兔AERP缩短,起搏0.5h内AERP缩短幅度最明显;AERP频率自适应性出现了下降—逆转;停止起搏后30minAERP及AERP频率自适应性基本恢复至起搏前水平(最初10min恢复迅速)。②伊贝沙坦组家兔8h心房快速起搏过程中各时间点AERP较起搏前无明显变化。③8h心房快速起搏后对照组家兔心房肌细胞超微结构可见线粒体肿胀、脊溶解、糖原聚集,伊贝沙坦组家兔心房肌细胞超微结构基本正常。结论伊贝沙坦可阻止8h心房快速起搏所致的心房电重构和心房肌细胞超微结构改变。     

ZV1,ZV5导联心室晚电位的检出率及临床意义

用Ｘ、Ｙ、Ｚ正交导联和改良的ＺＶ１、ＺＶ５导联，对３８例室性早搏病人进行心室晚电位检测。结果显示ＺＶ１、ＺＶ５导联法晚电位阳性率明显高于Ｘ、Ｙ、Ｚ正交导联法（ｕ＝４．６９，Ｐ〈０．０１），改进、弥补了Ｘ、Ｙ、Ｚ正交导联对晚电位“稀释”的不足。用ＤＣＧ同时记录，发现ＺＶ１导联法晚电位阳性与右室起源的早搏有关；ＺＶ５导联法记录的晚电位与左室起源的早搏有关。显示改良的ＺＶ１、ＺＶ５导联与传统的Ｘ、Ｙ、Ｚ     

经心内和食管快速心房刺激对P波时限及离散度的影响

目的分析快速心房刺激对P波时限及离散度的影响。方法在74例射频消融术经电极导管起搏高位右房及82例经食管心房调搏检查者中,用180次/分的S1S1刺激心房3min,在刺激前后立刻记录12导同步心电图,通过心电图测出刺激前后的最大P波时限(Pmax)、最小P波时限(Pmin)及P波离散度(Pd),然后进行比较。结果:射频消融组Pmax在心房刺激后比刺激前有显著性延长(P<0.01),Pmin及Pd无显著性差异。食管心房调搏组Pmax及Pd在心房刺激后显著性增加(P<0.01),Pmin无显著性差异。结论:快速心房刺激能引起心房传导时间延长,非均质电活动的离散程度增加。     

动态心房超速起搏预防阵发性房颤

目的观察动态心房超速起搏预防阵发性房颤的临床疗效和安全性。方法选择病态窦房结综合症伴阵发性房颤,并需植入永久起搏器的患者8例,分别植入具有动态心房起搏功能的起搏器,PacessetterTrilogy23643例,VitatronSelectionTM900E5例;随访6个月,前3个月不打开动态心房起搏功能,后3个月打开动态心房起搏功能,根据起搏器记录到的模式转换次数和持续时间来判断其预防房颤发作的疗效。结果打开动态心房起搏功能前后,患者房颤发作的次数分别为2437±956次/月和472±135次/月(P<0.05);模式转换持续时间分别为173±105小时/月和48±25小时/月(P<0.05);房颤负荷分别为33±8%和10±7%(P<0.05)。结论动态心房超速起搏,是阵发性房颤预防治疗的有效和安全的方法之一。     

食管心房调搏诱发阵发性房颤的心房电生理特性

为了探讨食管心房调搏对阵发性房颤检查的临床价值。回顾食管心房调搏诱发２５例阵发性房颤的心房电生理特性。其结果；程序刺激，分级起搏诱发１１例房颤，均有明确的房颤 史，猝发电脉冲诱发的１４例中１０例有明确的房颤史。房颤组２５例与正常对照组２５例相比心房有效不应期缩短，相对不应期区域扩大，最大房间传导时间延长，房间传导延缓更显著，这些可能是食管心房调搏诱发房颤的重要电生理基础。认为食管心房调搏对确定临床