犬快速心房起搏心房颤动模型肺静脉及左右心房组织细胞内钙含量变化的实验研究

目的探讨持续性心房颤动(房颤)时肺静脉及心房细胞内钙含量的变化,以期阐明房颤的发病机制。方法建立快速心房起搏式房颤模型犬8只。正常对照犬8只。实验分为6组1.房颤犬左上肺静脉组;2.房颤犬左心房峡部组;3.房颤犬右心耳组;4.正常对照犬左上肺静脉组;5.正常对照犬左心房峡部组;6.正常对照犬右心耳组。每组取相应部位心肌8块。测定细胞内钙含量。结果房颤犬肺静脉、左心房峡部和右心耳组织细胞内钙含量显著高于正常对照组(P<0.05)。房颤犬肺静脉细胞内钙含量显著高于左心房峡部(P<0.05),左心房峡部细胞内钙含量显著高于右心耳(P<0.05)。结论细胞内钙超载,可能是肺静脉和心房发生电重构的原因;肺静脉和左心房峡部,可能是房颤电重构的关键部位。     

犬快速心房起搏房颤模型肺静脉及心房组织心肌纤维化定量分析

目的：探讨持续性房颤时肺静脉及心房结构重构的变化,以期进一步阐明房颤的发病机制。方法：将18只健康杂种犬随机分为对照组（n=8）和房颤组（n=10）。房颤组犬以400次／分快速心房起搏制备房颤模型。10周后分别取两组犬的左上肺静脉（LSPV）、左房峡部（LAI）、右心耳（RAA）处心肌进行心肌纤维定量分析,并进行对照研究。结果：房颤组各部位Ⅲ型胶原含量显著高于对照组,分别为肺静脉3301．97±309．70对1404．56±178．02、左心房峡部2477．86±190．43对1479．20±187．17、右心耳2045．92±139．43对1417．07±139．43。房颤组Ⅲ型胶原的含量肺静脉组织显著高于左房峡部,左房峡部显著高于右心耳（P〈0．05）,且存在明显的梯度差。结论：快速心房起搏可导致肺静脉和心房组织纤维化程度增加,发生结构重构。肺静脉、左房峡部和右心耳心肌纤维化的程度存在显著的梯度差异,可能是结构重构的关键部位,在房颤维持过程中起重要作用。     

犬快速心房起搏房颤模型肺静脉及心房组织心肌纤维化定量分析

目的:探讨持续性房颤时肺静脉及心房结构重构的变化,以期进一步阐明房颤的发病机制. 方法:将18只健康杂种犬随机分为对照组(n=8)和房颤组(n=10).房颤组犬以400次/分快速心房起搏制备房颤模型.10周后分别取两组犬的左上肺静脉(LSPV)、左房峡部(LAI)、右心耳(RAA)处心肌进行心肌纤维定量分析,并进行对照研究. 结果:房颤组各部位Ⅲ型胶原含量显著高于对照组,分别为肺静脉3301.97±309.70对1404.56±178.02、左心房峡部2477.86±190.43对1479.20±187.17、右心耳2045.92±139.43对1417.07±139.43.房颤组Ⅲ型胶原的含量肺静脉组织显著高于左房峡部,左房峡部显著高于右心耳(P＜0.05),且存在明显的梯度差. 结论:快速心房起搏可导致肺静脉和心房组织纤维化程度增加,发生结构重构.肺静脉、左房峡部和右心耳心肌纤维化的程度存在显著的梯度差异,可能是结构重构的关键部位,在房颤维持过程中起重要作用.     

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     

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。     

快速右心房起搏对实验犬心房胶原纤维分布的影响

目的 实验探讨切除上腔静脉中部和主动脉根部脂肪垫(简称脂肪垫)对快速右心房(RA)起搏实验犬的心房胶原容积分数(CVF)的空间分布变化意义.方法 24只成年健康杂种犬雌雄不限,随机分为切除脂肪垫组、保留脂肪垫组和假手术组,每组8只.RA心外膜起搏6周,按左心房(LA)、RA、左心耳(LAA)、右心耳(RAA)、房间隔(AS)5个部位取材,Masson染色测算CVF,荧光定量聚合酶链反应技术检测缝隙连接蛋白(Cx)40和Cx43mRNA表达.结果 (1)假手术组和切除脂肪垫组CVF在部位分布上差异无统计学意义;保留脂肪垫组胶原增生明显,见于LAA和AS,P＜0.01.(2)假手术组Cx40mRNA含量分布在LA、RA、RAA、AS间差异无统计学意义;Cx40mRNA表达在切除脂肪垫组与保留脂肪垫组以LA、LAA增多且组间差异有统计学意义(P＜0.01).(3)假手术组Cx43mRNA含量优势表达于RA、RAA,P＜0.01;而在切除脂肪垫组LA、RA、RAA、AS其含量增多,在保留脂肪垫组的相应部位,其含量减少,P＜0.01.结论 快速RA起搏所致心房间质纤维增生具有空间各异向性,去迷走神经能抑制此效应.迷走神经效应影响起搏后Cx40mRNA与Cx43mRNA在心房与心耳间含量的表达.     

犬慢性快速心房起搏心房颤动模型的建立

报道犬慢性快速心房起搏心房颤动 (简称房颤 )模型的建立方法。取杂种犬 13只 ,安置实验用埋藏式高频率心脏起搏器快速起搏 ( 3 70～ 4 0 0次 /分 )心房 8～ 10周。于起搏前及起搏 8～ 10周后行经胸超声心动图、心房程序电刺激和burst刺激。 10只犬完成实验。快速起搏前所有犬均未能用心房程序刺激诱发出持续性房颤 ( >15min) ,2只 ( 2 0 %)可用burst刺激诱发出非持续性房颤。起搏 8～ 10周后 ,3只 ( 3 0 %)犬不需诱发即出现房颤。 8只 ( 80 %)可经程序刺激诱发出持续性房颤 ,其平均持续时间为 5 3± 11min。 10只犬 ( 10 0 %)均可用burst刺激诱发出持续性房颤。超声心动图检查显示快速起搏后犬心房面积显著增大 (左房 :6.4± 1.3cm2 vs 11.1± 1.8cm2 ;右房 :4 .2± 1.1cm2 vs 7.8± 1.3cm2 ,P均 <0 .0 0 1)。结论 :犬慢性快速心房起搏房颤模型具有房颤诱发率高、持续时间长、重复性好等特点。     

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。     

环孢霉素A干预钙调神经磷酸酶信号通路对持续心房起搏犬心房Cx40/Cx43表达的影响

目的: 观察钙调神经磷酸酶抑制剂环孢霉素A（CsA）对持续心房起搏（atrial tachypacing,ATP）模型犬心房中Cx40/Cx43表达分布的影响,探讨CsA抑制钙调神经磷酸酶信号通路（CaN）激活是否具有一定的抗心房重构的作用。方法: 健康杂种犬18只,随机分为对照组（sham组）、心房快速起搏组（ATP组,植入固律型单腔起搏器,以400次/min持续起搏8周）及CsA干预组(在快速心房起搏组处理因素的基础上,喂食CsA 8周),每组6只。8周后,处死所有实验犬,采用免疫荧光染色法及蛋白印迹法,检测各组实验犬心房组织中Cx40/Cx43表达及分布的情况。结果: 持续快速心房起搏8周,可导致犬左右心房中Cx40的表达明显增加（P<0.01）,但CsA干预组Cx40表达增加的程度明显小于ATP组（P<0.05）。Cx40的分布方式,ATP组和CsA干预组均呈现出明显的异质性,均有端端连接减少,侧侧连接增加的现象。Cx43蛋白表达的趋势与Cx40不同:快速起搏8周后,犬左右心房组织中Cx43的表达均明显减少（P<0.01）,但减少的程度CsA干预组小于ATP组（P<0.05）。Cx43的分布方式,ATP组及CsA干预组均表现为异质性增加,端端连接减少,侧侧连接增加。结论: CsA可减少ATP导致的Cx40/43表达的重构性变化,提示CsA可能具有一定的抑制心房重构的作用。     

钙激活蛋白酶Ⅰ抑制剂对快速起搏犬心房结构重构的影响

目的观察钙激活蛋白酶Ⅰ（calpainⅠ）抑制剂对长期心房快速起搏致心房颤动犬的心房结构重构的影响。方法杂种犬15只,分为假手术组、起搏组、抑制剂组各5只。于犬右心耳缝置电极,起搏3周（600次／min）。起搏后抑制剂组每日给以calpain Ⅰ抑制剂N-Acetyl-Leu-Leu-Met（ALLM）1．0nag·kg^-1·d^-1静脉注射,起搏组和假手术组给予等量溶剂二甲亚砜。采用荧光光度法测定心房肌calpain Ⅰ活性,光镜观察肌溶解程度,电镜观察超微结构的变化,Western blot技术测定心肌肌钙蛋白T蛋白含量,超声测定左心房容积的变化。结果起搏3周后,起搏组calpain Ⅰ活性增加至假手术组的2．3倍（P〈0．01）,抑制剂组calpain Ⅰ活性为假手术组的1．1倍（P〉0．05）;起搏组左心房肌溶解的比率为（76．7±5．9）％,抑制剂组左心房肌溶解的比率为（20．8±8．1）％,两组比较,P〈0．01。calpain Ⅰ活性与肌溶解的比率呈高度正相关（r=0．89）。肌钙蛋白T蛋白含量在抑制剂组高于起搏组（P〈0．01）。抑制剂组左心房容积的变化较起搏组显著减轻。结论ALLM通过抑制心房快速起搏犬心肌calpain Ⅰ活性,防止了心房肌结构的改变,为心房颤动后心肌的保护提供了一种可能的有效途径。     

Effects of pulmonary vein ablation on regional atrial vagal innervation and vulnerability to atrial fibrillation in dogs

INTRODUCTION: Pulmonary vein (PV) isolation has proven to be an effective therapy for atrial fibrillation (AF). However, clinical evidence suggests that suppression of AF after PV isolation could not be fully attributed to the interruption of electrical conduction in and out of the PVs. Furthermore, little is known regarding the effects of ablation around the PVs on the atrial electrophysiological properties. We aimed to study the changes in atrial response to vagal stimulation (VS) after PV ablation (PVA). METHODS: We studied 11 adult mongrel dogs under general anesthesia. Bilateral cervical sympathovagal trunks were decentralized. Propranolol was given to block sympathetic effects. Multipolar catheters were placed into right atrial appendage (RAA), distal and proximal coronary sinus (CSD, CSP), and left atrial free wall (LAFW). PVA was performed via trans-septal approach. Atrial effective refractory period (AERP) and vulnerability window (VW) of AF were measured with and without VS before and after ablation to isolate the PVs. RESULTS: After ablation, AERP shortening in response to VS significantly decreased in the left atrium (43.64 +/- 21.57 vs 11.82 +/- 9.82 msec, P < 0.001 at LAFW; 50.91 +/- 26.25 vs 11.82 +/- 14.01 msec, P < 0.001 at CSP; 50 +/- 31.94 vs 17.27 +/- 20.54 msec, P < 0.005 at CSD), while the response to VS did not change significantly at RAA (58.18 +/- 28.22 vs 50.91 +/- 22.12 msec, P = 0.245). After ablation, atrial fibrillation VW during VS narrowed (20.63 +/- 11.48 vs 5.63 +/- 8.63 msec, P < 0.03 at LAFW; 26.25 +/- 12.46 vs 5.00 +/- 9.64 msec, P = 0.001 at CSP; 28.75 +/- 18.47 vs 6.88 +/- 7.53 msec, P < 0.02 at CSD, and 33.75 +/- 24.5 vs 16.25 +/- 9.91 msec, P = 0.03 at RAA). CONCLUSIONS: Ablation around the PV ostia diminishes left atrial response to VS and decreases the atrial VW. The attenuated vagal response after ablation may contribute to the suppression of AF.     

Prevention of chronic atrial fibrillation by pacing in the region of Bachmann's bundle: results of a multicenter randomized trial

INTRODUCTION: Atrial pacing locations that decrease atrial activation and recovery time may be preferable in patients with a history of atrial arrhythmias. This multicenter prospective randomized study compared the efficacy of Bachmann's bundle (BB) region pacing to right atrial appendage (RAA) pacing in patients with recurrent paroxysmal atrial fibrillation (AF). METHODS AND RESULTS: Patients with standard pacing indications (n = 120, 70+/-11 years) were randomized to atrial pacing in either the RAA (n = 57) or BB region (n = 63). Implantation time was similar between groups (88+/-36 min [n = 38] for BB vs 83+/-34 min [n = 34] for RAA). No differences in pacing threshold, impedance, or sensing between BB and RAA groups were observed at implantation or after the 6-week, 6-month, and 1-year follow-up periods. Average length of follow-up was 12.6+/-7.4 months for the BB group and 11.8+/-8.0 months for the RAA pacing group. The percentage of atrial pacing was similar between groups (61%+/-34% RAA vs 65%+/-31% BB at 2 weeks after implant). BB atrial pacing significantly (P < 0.05) shortened p wave duration compared with sinus rhythm (123+/-21 msec vs 132+/-21 msec, n = 50) 2 weeks after implant. In contrast, p wave duration was longer during atrial pacing from the RAA position compared with sinus rhythm (148+/-23 msec vs 123+/-23 msec, n = 37). Additionally, p wave duration was shorter during BB pacing than during RAA pacing. Patients with BB pacing had a higher (P < 0.05) rate of survival free from chronic AF (75%) compared with patients with RAA pacing (47%) at 1 year. CONCLUSION: BB region pacing is safe and effective for attenuating the progression of AF.     

Gap junctional remodeling in relation to stabilization of atrial fibrillation in the goat

OBJECTIVE: It has been postulated that high atrial rate induced changes at the level of the gap junctions ('gap junctional remodeling', i.e. changes in distribution, intercellular orientation and expression of gap junction proteins), could be part of the vicious circle of electrophysiologic and structural changes leading to sustained atrial fibrillation (AF). To obtain experimental evidence in favour of such a postulate the timing of this remodeling process was studied in relation to the development of sustained AF in a goat model. METHODS AND RESULTS: Thin sections from the left (LAA) and right atrial appendage (RAA) from goats in sinus rhythm (SR) or AF, induced through programmed endocardial burst pacing for time periods between 0 and 16 weeks, were immunolabeled with antibodies against connexin(Cx)40 and Cx43 and analysed by immunofluorescence and confocal laser scanning microscopy. During SR the distribution pattern for Cx43 was completely homogeneous (LAA and RAA) and for Cx40 mostly homogeneous (LAA: all five goats, RAA: three out of five goats). The distribution pattern for Cx43 remained stable during AF, while the Cx40 distribution pattern became increasingly heterogeneous, both in the LAA and RAA, with increasing duration of pacing. This increase in heterogeneity in Cx40 distribution correlated (Spearman rank order) with an increase in stability of AF and the occurrence of structural changes (myolysis) in atrial myocytes. The Cx40/Cx43 immunofluorescence signal ratio in both the LAA and RAA appeared to be significantly lower in AF (1-16 weeks) as compared to SR (0 weeks); going from 0 to 16 weeks average ratios decreased 54.5% (n=5; P=0.026) in the LAA and 35.8 (n=5; P=0.034) in the RAA. Western blot analyses revealed similar decreases in the total Cx40/Cx43 protein ratio, on average 50.0% (n=5; P=0.008) and 47.8% (n=5; P=0.02) in the LAA and RAA, respectively. No changes were measured in the levels of Cx40 or Cx43 mRNA, as was assessed through RT-PCR. CONCLUSION: The time course of changes in the distribution and content of Cx40 gap junctions as observed during endocardial burst pacing of the goat atrium suggests that Cx40 gap junctional remodeling might be involved in the pathogenesis of sustained atrial fibrillation.     

急性心房颤动缝隙连接蛋白40和43重构及蝙蝠葛碱的干预作用

采用快速心房起搏致家兔急性心房颤动 (简称房颤 )模型 ,观察心房肌缝隙连接蛋白 4 0和 4 3(Cx4 0、Cx4 3)含量和分布的改变以及钙通道阻滞剂蝙蝠葛碱干预的防治效果。 36只家兔随机等分为 3组 :对照组、房颤组和蝙蝠葛碱组。经颈内静脉将电极置入右房 ,对照组不予快速心房起搏 ,另两组以 6 0 0次 /分行快速起搏以诱发房颤。蝙蝠葛碱组于快速起搏前 30min按 5mg /kg静脉注射进行干预 ,另两组给予等容量的生理盐水。连续刺激并且房颤 8h后 ,开胸取右心耳组织 ,用Westernblot检测Cx4 0和Cx4 3的含量 ,用免疫荧光抗体标记激光共聚焦显微镜检测Cx4 0和Cx4 3的分布。结果 :房颤组心房肌组织Cx4 0和Cx4 3含量较对照组降低 (P均 <0 .0 1) ,端端分布减少 ,侧侧分布相对增加 ,以细胞间端端连接减少为主 ,二者均呈现不均一分布。蝙蝠葛碱组Cx4 0和Cx4 3的含量较对照组降低但差异无显著性 (P均 >0 .0 5 ) ,较房颤组升高且差异有显著性 (P均 <0 .0 5 ) ,二者分布不均一程度较房颤组减轻。结论 :快速心房起搏致急性房颤可引起缝隙连接蛋白 4 0和 4 3重构 ,快速起搏前用蝙蝠葛碱干预能有效减轻急性房颤时的缝隙连接蛋白重构。     

Clinical significance of prolonged P wave width after right atrial appendage pacing in sick sinus syndrome.

The present study investigated both the clinical significance of atrial fibrillation (AF) before right atrial appendage (RAA) pacing and the influence of prolonged P wave on AF occurrence in RAA-paced patients with sick sinus syndrome (SSS). Fifty-seven patients (age 68+/-10 years; 19 men, 38 women) with SSS who underwent RAA pacing were divided into 2 groups: 23 patients without AF before pacing (I + II; Rubenstein I or II) and 34 patients with AF before pacing (III; Rubenstein III). The P wave duration in intrinsic rhythm and with RAA pacing were measured on the standard electrocardiography in leads II and V(1) with the use of a digitizing tablet. Group III was further subdivided into 2 groups: 20 patients (IIIb) with a paced P wave >130 ms in both leads II and V(1) and the other 14 patients (IIIa). The duration of the intrinsic P wave in leads II and V(1) was significantly greater in group III than in group I + II (119+/-20 vs 108+/-21 ms, p=0.0417, 106+/-16 vs 95+/-21 ms, p=0.0258, respectively). During the follow-up of 40+/-21 months, AF recurrence was significantly higher in group IIIb than in groups IIIa and I + II (17/20 vs 5/14 vs 2/23 p<0.0001). A few occurrences of AF were observed by conventional RAA pacing in patients without AF before pacing. However, SSS with AF before pacing caused a significant intra-atrial conduction disturbance and a high incidence of AF recurrence after implantation of RAA pacing, especially in patients with a prolonged paced P wave, in whom new pacing modalities may be needed to shorten paced P wave duration and prevent AF.     

西拉普利对心房颤动犬内皮细胞功能及纤溶系统的影响

目的研究血管紧张素转换酶抑制剂西拉普利对心房颤动(房颤)犬内皮功能和纤溶系统的影响。方法应用埋藏式高频心脏起搏器快速起搏心房建立房颤犬动物模型。实验分为未起搏组、单纯起搏组和起搏 西拉普利组。采用ISO-NOP3005一氧化氮(NO)敏感电极测定心内膜NO含量;酶联免疫吸附双抗体夹心法测定血浆血管性血友病因子水平;Westernblot定量分析心房心肌纤溶酶原激活剂抑制物-1(PAI-1)和组织型纤溶酶原激活剂(tPA)蛋白表达;同时免疫组化检测蛋白表达位置。血浆PAI-1和tPA含量采用酶联免疫吸附双抗体夹心法测定。结果西拉普利能显增加房颤犬心内膜NO合成,降低血浆血管性血友病因子水平,同时显减少心房肌PAI-1蛋白表达和血浆PAI-1含量,增加心房肌tPA蛋白表达和血浆含量。结论西拉普利能明显改善房颤犬内皮细胞功能,恢复纤溶系统平衡,可能对房颤的血栓前状态有益。     

Beneficial effects of biatrial pacing on cardiac function in patients with bradycardia -- tachycardia syndrome.

BACKGROUND: Biatrial (BiA) pacing prevents atrial fibrillation. By an unknown mechanism. The purpose of this study was to use Doppler echocardiography to evaluate the hemodynamic effects during BiA pacing. METHODS AND RESULTS: The subjects were 7 patients with bradycardia - tachycardia syndrome with an implanted pacemaker. Atrial pacing sites were the right atrial appendage (RAA) and coronary sinus. P wave duration during BiA pacing (123 +/-16 ms) was significantly shorter than during either RAA pacing (167+/-19 ms, p<0.05) or sinus rhythm (148+/-12 ms, p<0.05). Doppler echocardiography revealed a greater cardiac output during BiA pacing than during RAA pacing (4.1+/-1.1 vs 3.5+/-0.7 L/min, p=0.042). The Doppler waveform of transmitral flow indicated that the left ventricular contraction interrupted the atrial filling wave during RAA pacing. The interval between the end of the atrial filling wave of transmitral flow and the mitral valvular closing sound was significantly increased by BiA pacing compared with RAA pacing (56+/-65 vs 40+/-57 ms, p=0.047). CONCLUSION: Cardiac hemodynamics were improved by BiA pacing and reduction of left atrial load may be one of the mechanisms.     

Effect of Bachmann's bundle pacing on atrial fibrillation: electrophysiologic assessment

BACKGROUND: It has recently been reported that simultaneous multisite atrial pacing, Bachmann's bundle (BB) pacing, and coronary sinus (CS) pacing are useful for preventing the induction of atrial fibrillation (AF). HYPOTHESIS: We investigated whether a simple pacing approach via BB could reduce the induction of AF by extrastimuli (S2) from the right atrial appendage (RAA). METHODS: Programmed electrical stimulation was performed from the RAA and the area of BB at the superior aspect of the atrial septum, and bipolar recordings were obtained from the RAA, BB, and CS in 14 patients. RESULTS: In five patients, AF was induced with critically timed RAA-S2 delivered during RAA pacing. However, AF was not induced in any patient when RAA-S2 was delivered during BB pacing. The duration of the P wave during BB pacing was significantly shorter than that during RAA pacing and sinus rhythm (BB 80 +/- 16 ms vs. RAA 106 +/- 36 ms vs. sinus rhythm 100 +/- 24 ms, p < 0.05). The intra-atrial conduction time to the distal coronary sinus (CSd) caused by early S2 at the RAA was significantly reduced by BB pacing (BB 114 +/- 22 ms vs. RAA 157 +/- 35 ms, p < 0.001). CONCLUSION: Bachmann's bundle pacing reduces atrial conduction time caused by RAA-S2 and may be useful for preventing the induction of AF.     

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。