肺静脉电隔离对犬急性心房电重构影响的实验研究

目的肺静脉电隔离（PVI）是治疗心房颤动（房颤）的重要手段，心房电重构是房颤发生和维持的重要因素。本研究旨在研究PVI对急性心房电重构的影响并揭示其可能机制。方法选取成年杂种犬18只，随机分为对照组和PVI组。应用硫代巴比妥钠麻醉后分离并结扎双侧颈交感迷走神经干。两组犬均行房间隔穿刺并以600次／min起搏右心房30min构建急性心房电重构模型，PVI组穿间隔后即行环肺静脉口部电隔离。快速心房电刺激前后于右心耳（RAA）及左心耳（LAA）处测量基础状态下（非迷走神经刺激）及颈部迷走神经干刺激时的心房有效不应期（ERP）和房颤易感窗口（VW）。结果（1）对照组快速心房电刺激后基础状态下（RAA处P〈0．01，LAA处P〈0．001）和迷走神经刺激时（RAA处P〈0．05，LAA处P〈0．05）测得的ERP均明显缩短。快速心房电刺激前后基础状态下均不能诱发房颤；快速心房电刺激后，RAA（P〈0．01）和LAA处（P〈0．05）的VW在迷走神经刺激时明显增宽。（2）PVI组快速心房电刺激后基础状态下（RAA处P=0．451，LAA处P=0．197）和迷走神经刺激时（RAA处P=0．104，LAA处P=0．231）测得的ERP较快速心房电刺激前无明显变化。快速心房电刺激前后基础及迷走神经刺激下均不能诱发房颤。（3）对照组快速心房电刺激后ERP缩短值较PVI组明显增加（基础状态时LAA处P〈0．05，RAA处P〈0．05；迷走神经刺激时LAA处P〈0．01，RAA处P〈0．05）。结论心房电重构伴随着迷走神经对心房电生理特性调节活动增强，肺静脉电隔离能减轻心房电重构，其机制可能为心房去迷走神经效应。     

右心室流出道间隔部起搏与右心室心尖部起搏随机对照研究

目的应用组织多普勒方法随机对照研究右心室流出道间隔部（right ventficular outflow tract septum,RVOTS）起搏与右心室心尖部（fight ventricul arapical,RVA）起搏心脏同步性和心功能变化,探讨右心室流出道间隔部在主理性起搏中的临床意义。方法128例缓慢心律失常患者按单双数字随机分为两组,对病态窦房结综合征房室功能正常患者,起搏器植入术后根据心电图PR间期时间将起搏器AV间期调整,暂时关闭AV搜索功能以保证心室起搏。所有患者起搏器植入术后1、3、6个月定期随访,观察起搏参数、累积心室起搏百分比,同时行超声心动图检查。结果RVOTS起搏组与RVA起搏组电极导线植入时间、X线曝光时间差异有统计学意义（P〈0．01）,主动固定电极导线植入15min与植入即刻比较起搏阈值明显下降,分别为（0．76±0．21）mV和（1．13±0．25）mV（P〈0．01）。RVOTS起搏组和RVA起搏组QRS时限分别为（0．14±0．04）S、（0．16±0．03）S（P〈0．01）。随访6个月起搏参数两组之间差异无统计学意义。全部患者未出现植入并发症,随访6个月无电极导线移位、阈值增高。6个月RVOTS起搏组左心室同步指标明显优于RVA起搏组（P〈0．01）。左心室收缩末内径及舒张末内径两组比较无显著变化,左心室射血分数在RVA起搏组有所降低（P〈0．05）,心脏做功指数（Tei）、RVOTS起搏组与RVA起搏组比较差异有统计学意义（P〈0．05）,在RVA起搏组随访6个月与1个月比较差异有统计学意义（P〈0．01）。结论RVA起搏导致心脏收缩不同步,损害左心室功能。RVOTS起搏保持良好心脏收缩同步性、保护左心室功能,是较好的右心室起搏部位。     

长期右心室心尖部起搏对心室重构的影响

目的探讨长期右心室心尖部（RVA）起搏对心室重构的影响。方法回顾性分析1997年6月至1998年11月,92例因病态窦房结综合征首次植入双腔起搏器的患者。对照组共有45例患者入选。起搏器植入术前行12导联心电图和超声心动图检查,术后随访时记录未起搏的心电图和超声心动图。结果传统双腔起搏组患者平均心室累积起搏比例为（90．1±4．0）％,平均随访时间为（3．3±0．5）年。起搏组患者自身QRS时限由术前（874-9）ms增加到随访时的（94±10）ms（P〈0．001）。左心室舒张末内径（LVEDD）由（464-3）mm增加到（50±4）mm（P〈0．001）,左心室射血分数（LVEF）由0．63±0．04降低到0．57±0．05（P〈0．001）。Logistic回归分析显示,起搏器植入时老龄（〉65岁）（OR3．41,95％CI1．07～10．90,P=0．04）、长期RVA起搏（OR3．91,95％CI1．10～13．89,P=0．03）和冠心病史（OR7．33,95％CI1．09～50．29,P=0．04）是QRS时限增宽（〉7ms）的独立预测因素。对照组各指标随访前后差异无统计学意义。结论长期RVA起搏可能引起自身QRS时限增宽,提示RVA起搏引起心脏特殊传导系统和／或心室肌传导功能损害。起搏器植入时老龄、RVA起搏和冠心病史是自身QRS时限增宽的独立预测因子。     

右心室流出道间隔部起搏对完全性房室传导阻滞患者心功能的影响

目的：比较右心室流出道间隔部（RVS）起搏与右心室心尖部（RVA）起搏对左右心室间收缩同步性、左室重构及心功能的影响。方法：①入选Ⅲ度房室传导阻滞患者61（男39,女22）例,随机分入RVS部起搏组（RVS组,n=33）和RVA部起搏组（RVA组,n=28）。②比较两组患者植入术中及术后12月心室电极导线参数（起搏阈值、R波感知及阻抗）的差异。③观察两组患者术前及术后12月QRS波时限;术后应用组织多普勒同步图（TSI）分别测定两组左、右心室侧壁基底部收缩达峰时间差（△Ts）。评价心室间不同步的程度。④行多普勒超声心动图（UCG）检查,观察两组术前及术后12月左室舒张末期内径（LVEDD）及左室射血分数（LVEF）的变化,比较不同起搏部位对心功能的影响。结果：①两组患者测试的起搏阈值、R波感知及导线阻抗无统计学差异。②两组患者术后QRS波时限均较术前延长（均P〈0．01）,RVA组较RVS组延长更为明显（P〈0．01）。RVS组与RVA组ATs分别为（27±14）ms和（90±22）ms,有统计学差异（P〈0．01）。③术后12／了＇月两组LVEDD均较术前增加,RVA明显大于RVS组[（54±5）mm阮（51±5）mm,P〈0．05]。RVA组术后12月LVEDD较术前明显增加[（54±5）mmvs．（50±4）mm,P〈0．05],术后12月两组LVEF均较术前降低[RVS组：（0．58-4-0．14）傩．（0．63±0．09）,P〈0．01;RVA组：（0．51±0．12）伽．（0．64±0．13）,P〈0．01],组间比差异不显著。结论：RVS起搏对心室问同步性、左室重构的影响要优于RVA起搏。     

经食管心房起搏对房室结加速传导的电生理观察

目的 初步探讨房室结加速传导的电生理特性及临床意义。方法 采用经食管心房起搏检出具有房室结加速传导特征病人20例（观察组）与房室结正常传导病人20例（对照组）的房室交界区相对不应期、功能不应期、有效不应期、心房有效不应期、房室传导1：1点、文氏点相比较。结果 与对照组比较，房室结加速传导的房室交界区相对不应期、有效不应期、心房有效不应期明显缩短，差异有统计学意义（P〈0．01或P〈0．001），房室传导1：1点减小（P〈0．001），文氏点明显增大或消失。结论 房室结加速传导病人的房室交界区不应期明显缩短，递减传导功能减小或消失，心室率反应增快。     

双腔起搏器房室结优先功能与心电图

<正>双腔起搏器房室结优先功能是指通过调整心脏起搏器的房室(AV)间期或转换起搏模式,保证自身心房激动能通过房室结顺传至心室,以获得正常的心室除极和收缩顺序的功能。1房室结优先功能的必要性窦房结功能不良患者置入双腔起搏器后,右心室心尖部(RVA)起搏会导致心室激动顺序异常,心室内与心室间收缩失同步,二尖瓣反流;长期RVA起搏进一步导致心室机械重构,非对称性左心室肥厚和扩张,左心室射血分数降低,甚至抵消双腔起搏的房     

依那普利、厄贝沙坦和血管紧张素（1-7）对快速心房起搏犬心房肌钠通道重构的干预作用

目的观察依那普利、厄贝沙坦和血管紧张素（1-7）[Ang（1-7）]对快速心房起搏犬心房肌细胞钠通道电流（INa）的干预作用。方法普通杂种犬30只随机分为5组,每组6只。单纯心房起搏组（C组）、心房起搏＋依那普利组（EN组）、心房起搏＋厄贝沙坦组（IB组）和心房起搏＋Ang（1-7）组（A组）犬行心房快速起搏（500次／min）2周;假手术组（S组）不行起搏刺激。应用膜片钳技术检测心房肌细胞,INa电流密度及通道激活和失活特性。结果c组INa电流密度较s组明显降低（P〈0．05）;EN组、IB组和A组,INa电流密度较c组明显升高（P〈0．05）。与s组相比,起搏对INa的电压依赖性激活没有影响（P〉0．05）;与C组和s组相比,在EN组、IB组和A组,钠通道半激活电位更加超极化（P〈0．05）。与s组相比,快速心房起搏以及3种干预因素对INa的电压依赖性失活没有明显影响（P〉0．05）。结论依那普利、厄贝沙坦和Ang（1-7）通过加快INa的激活过程而增加心房肌INa电流幅度,有助于提高心房肌传导速度,从而抑制快速起搏所致的电重构。     

螺内酯对心力衰竭犬心房颤动的影响

目的探讨螺内酯对心力衰竭犬心房颤动（房颤）的影响及其作用机制。方法21只犬随机分为3组：假手术组（n=7）、起搏组（n=7）和螺内酯组（n=7）。采用心室快速起搏建立心力衰竭犬模型。假手术组植入起搏器后不起搏;起搏组和螺内酯组以220次／min快速起搏心室6周;螺内酯组起搏前1周给予螺内酯至起搏后6周。通过缝置于左、右心房的4对电极测定房颤诱发次数及持续时间,超声心动图测定心房、心室结构和功能变化,Masson染色测定心房胶原容积分数,Westernblot半定量分析心房肌基质金属蛋白酶．9（MMP-9）、转化生长因子-β1（TGF-β1）及血小板衍生生长因子（PDGF）蛋白含量。结果（1）心室快速起搏6周后,起搏组犬房颤诱发率和持续时间显著增加（P〈0．01）,螺内酯组房颤诱发率显著降低、持续时间显著缩短（P〈0．05）。（2）与假手术组相比,起搏组犬左心室最大容积（LVVmax）及左心房最大容积（LAVmax）显著增加（P〈0．01）,左心房射血分数（LAEF）及左心室射血分数（LVEF）显著降低（P〈0．01）,螺内酯组犬LVVmax、LAVmax显著缩小（P〈0．01）,LAEF及LVEF显著升高（P〈0．01）。（3）与假手术组相比,起搏组犬心房胶原容积分数显著升高（P〈0．01）,TGF-β1、PDGF、MMP-9蛋白质表达量显著增加（P〈0．05）;与起搏组相比,螺内酯组胶原容积分数显著降低（P〈0．01）,TGF-β1、PDGF、MMP-9蛋白表达量显著减少（P〈0．01）。结论螺内酯可以减少心力衰竭后房颤的发生,其机制可能与抑制心房肌PDGF、TGF-β1表达有关。     

伴连续房室结功能曲线的房室结折返性心动过速的电生理特点

目的：探讨不存在房室结双径路特性的房室结折返性心动过速（AVNRT）的电生理特点。方法：102例AVNRT患分为3组：A组15例,存在连续房室结功能曲线,心房递增起搏时无AH间期跳跃（≥5ms)延长;B组21例,存在连续房室结功能曲线,心房递增起搏时有AH间期跳跃（≥50ms）延长;C组64例,存在不连续房室结功能曲线。比较3组患射频消融前后心房递增起搏时最大AH间期[AHmax(WCL)]、心房期前刺激时最大AH间期[AHmax(ERP)]、房室结前向和逆向传导有效不应期（ERP）、保持房室1：1传导的心房／心室起搏周长和心动过速周长。结果：3组患消融后AHmax(WCL)和AHmax（ERP）均明显短于消融前（P＜0．01）。B组和C组的消融后房室结前向ERP明显增加,而组无明显变化。A组消融前AHmax和房室结逆向ERP、消融后AHmax下降程度以及心动过速周长均小于B组和C组患。结论：伴连续房室结功能曲线的AVNRT患,心房刺激可表现或不表现房室结双径路的电生理特性,射频消融后心房刺激时AHmax明显缩短提示已成功根治了AVNRT。     

起搏器窦房结节律优先功能与心电图

<正>起搏器发展至今已有60多年的历史,从早期的单纯右室起搏发展到心房、心室双腔起搏,起搏器逐步向接近心脏生理传导系统的方向发展。窦房结节律优先(sinus preference),便是其中一种起搏器的特殊功能。1理论基础众所周知,正常的心脏传导系统是通过窦房结先激动,起搏心房,之后传导到房室结,再沿左右束支传导,激动左右心室。因此,除非是持续性房颤患者,一般普通起搏适应证患者都是在心房也置入电极     

快速右心房起搏致犬心房迷走神经重构的研究

目的 通过对快速心房起搏犬的神经相关因子的研究,观察右心房快速起搏48 h是否引起神经重构及其在心房颤动(房颤)中的作用.方法 健康杂种犬12只,随机分为房颤组(6只)和对照组(6只).右心房起搏600次/min、持续48 h.通过一种在发芽轴突生长丘中表达的蛋白质(GAP-43)和乙酰胆碱转移酶(CHAT)来了解心脏神经萌发和迷走神经的重构.结果 在房颤犬的左心房、左心耳、右心房和右心耳,GAP-43和CHAT的神经密度同对照组相比明显增高,差异均有统计学意义(P<0.05).此外,房颤犬的右心房GAP-43和CHAT的神经密度与左心房有明显差异(P<0.05),显微镜下显示每个样点心脏神经不均匀分布.结论 48 h持续起搏犬右心房形成阵发性房颤,可见明显的神经萌发和迷走神经重构且不均一分布.     

Future easy and physiological cardiac pacing

The right atrial appendage (RAA) and right ventricular apex (RVA) have been widely considered as conventional sites for typical dual-chamber atrio-ventricular cardiac (DDD) pacing. Unfortunately conventional RAA pacing seems not to be able to prevent atrial fibrillation in DDD pacing for tachycardia-bradycardia syndrome, and the presence of a left bundle branch type of activation induced by RVA pacing can have negative effects. A new technology with active screw-in leads permits a more physiological atrial and right ventricular pacing. In this review, we highlight the positive effects of pacing of these new and easily selected sites. The septal atrial lead permits a shorter and more homogeneous atrial activation, allowing better prevention of paroxysmal atrial fibrillation. The para-Hisian pacing can be achieved in a simpler and more reliable way with respect to biventricular pacing and direct Hisian pacing. We await larger trials to consider this "easy and physiological pacing" as a first approach in patients who need a high frequency of pacing.     

Effects of omapatrilat on cardiac nerve sprouting and structural remodeling in experimental congestive heart failure

BACKGROUND: Congestive heart failure (CHF) results in decreased cardiac sympathetic innervation. OBJECTIVES: The purpose of this study was to test the hypothesis that therapy with the vasopeptidase inhibitor omapatrilat (OMA) attenuates cardiac neuronal remodeling in CHF. METHODS: We induced CHF in dogs with rapid ventricular pacing for 5 weeks with (CHF+OMA group, n = 8) or without (CHF group, n = 10) concomitant OMA treatment (10 mg/kg twice daily). Cardiac catheterization and echocardiography were performed to determine cardiac structure and hemodynamic parameters. Myocardial nerve density was determined by immunocytochemical staining with anti-growth associated protein 43 (GAP43) and anti-tyrosine hydroxylase (TH) antibodies. Seven normal dogs were used as histologic controls. RESULTS: In the CHF group, ascites developed in 3 dogs and 4 dogs died, compared with no ascites or death in the CHF+OMA group (P = .07). In the 6 CHF dogs that survived, all had atrial fibrosis, severely depressed left ventricular systolic function, and increased atrial and ventricular chamber size. OMA treatment decreased the atrial and ventricular chamber sizes and the degree of atrial fibrosis. Most CHF dogs showed severe myocardial denervation, although some showed normal or abnormally high nerve counts. OMA treatment prevented heterogeneous reduction of nerve density. The left ventricular TH-positive nerve densities were 128 +/- 170 microm(2)/mm(2), 261 +/- 185 microm(2)/mm(2), and 503 +/- 328 microm(2)/mm(2) (P < .05), and the atrial GAP43-positive nerve densities were 1,683 +/- 1,365 microm(2)/mm(2), 305 +/- 368 microm(2)/mm(2), and 1,278 +/- 1,479 microm(2)/mm(2) (P < .05) for the control, CHF, and CHF+OMA groups, respectively. CONCLUSION: CHF results in heterogeneous cardiac denervation. Long-term OMA treatment prevented the reduction of nerve density and promoted beneficial cardiac structural remodeling.     

Investigation of pacing site-related changes in global restitution dynamics by non-contact mapping.

AIMS: The determination of dynamic changes in ventricular repolarization may provide insight into arrhythmogenic mechanisms as a consequence of pacing site. This study investigated acute pacing site effects on global characteristics of electrical restitution using high resolution, non-contact mapping (NCM). METHODS AND RESULTS: Activation-recovery intervals (ARIs) were determined from reconstructed left ventricular electrograms by the NCM system and were analysed during pacing from the right atrial appendage (RAA, intrinsic), right ventricular apex (RVA), and right ventricular septum (RVS) with extrasystoles delivered at intermediate and short coupling intervals in anesthetized swine (n = 5). Electrical restitution curves were determined by the S1-S2 pacing protocol. Activation-recovery interval restitution slopes were determined by the overlapping linear segments regression method. Global distribution of repolarization was defined as the coefficient of variation of the ARIs during restitution. The maximum ARI slopes yielded by RVA pacing were significantly greater than RAA pacing (0.44 vs. 0.32; P < 0.05) and RVS pacing (0.44 vs. 0.37; P = 0.05). There was no significant difference between RAA and RVS pacing (0.32 vs. 0.37). The global distribution of ARIs during restitution from RVA pacing was significantly greater than RAA pacing (12.0 vs. 8.1%; P < 0.05). CONCLUSION: Right ventricular apex pacing is associated with impaired global repolarization patterns compared to RAA and RVS. These observations support the hypothesis that RVA pacing may be associated with increased risk of ventricular arrhythmias compared to RVS pacing.     

右心腔不同部位起搏的慢性血流动力学对比研究

比较右心耳 (RAA)、右室流出道 (RVOT)与右室心尖部 (RVA)起搏的慢性血流动力学效果 ,评价RVOT起搏的可行性。2 9例患者 ,9例RAA起搏、8例RVOT起搏、12例RVA起搏 ,分别在术前及术后 6 .11± 4 .0 1、5 .38± 2 .92、5 .5 0± 2 .88个月 ,用多普勒超声心动图观察右心腔不同部位起搏的慢性血流动力学参数 ,包括左室射血分数(LVEF)、左室内径缩短分数 (SF)、肺动脉瓣口峰值血流速度 (PV)、二尖瓣口E峰血流速度 (E)、A峰血流速度 (A)及比值 (E/A)。结果 :RAA起搏时 ,LVEF、SF分别下降为 4 .5 6 %± 3.71% ,3.33%± 2 .83% ,P <0 .0 5。RVOT起搏时 ,LVEF、SF、E/A分别下降为 6 .38%± 4 .6 9% ,4 .13%± 2 .75 % ,1.2 9± 0 .5 1,P <0 .0 1。RVA起搏时 ,LVEF、SF、PV、E、E/A分别下降为 1.4 2 %± 5 .32 % ,7.92 %± 3.96 % ,8.5 8± 11.33cm/s,8.17± 9.6 3cm/s,0 .2 7± 0 .2 9,P <0 .0 1或0 .0 5。A则上升为 7.91± 11.2 6cm/s(P <0 .0 5 )。RVOT起搏与RVA起搏相比LVEF、SF明显改善 (P均 <0 .0 5 ) ,且临床症状明显减轻 ;与右房起搏相比 ,E/A下降 (P <0 .0 5 ) ,其他指标在随访期内未显示出统计学意义上的差别。结论 :对于心功能较好的患者 ,右心腔不同部位起搏对慢性血流动力学均有一定程度的负面影响 ;R     

持续快速心房起搏对犬肺静脉及心房组织连接蛋白43和Ⅲ型胶原的影响

目的　探讨持续快速心房起搏对犬肺静脉和心房组织连接蛋白 43(Cx43)和Ⅲ型胶原的影响。方法　16只杂种犬,随机分为持续快速心房起搏组(8只)和正常对照组 (8只 ),前者以 400次 /min的频率持续起搏 10周,建立心房颤动(房颤)动物模型。分别取两组犬的左上肺静脉、左房游离壁和右心耳等部位的心肌组织进行Cx43的免疫荧光半定量分析和Ⅲ型胶原纤维定量分析。结果10周后快速心房起搏组所有犬均可诱发出持续性房颤。快速心房起搏组犬肺静脉、左房游离壁和右心耳部位的Cx43水平显著高于正常对照组犬各相应的部位 (肺静脉: 3370 .91±275. 11与1405 .82±90. 38, P<0. 05;左房游离壁: 2448. 68±272 .10与 1467. 12±147 .93,P<0. 05;右心耳: 2331 .96±199 .61与 1288. 27±216 .22, P<0 .05)。快速心房起搏组犬肺静脉Cx43的水平显著高于左心房游离壁和右心耳(P<0. 05),而左心房和右心耳部位的Cx43水平差异无统计学意义 (P>0. 05)。持续快速心房起搏组犬肺静脉、左房游离壁和右心耳等部位的Ⅲ型胶原含量显著高于正常对照组犬各相应部位(肺静脉: 3301 97±309 70与 1404 56±178 02, P<0 05;左房游离壁: 2477 86±190. 43与1479. 20±187 .17, P<0 .05;右心耳: 2045 .92±139 .43与 1417. 07±139. 43,P<0 .05 )     

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。     

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.     

Difference between electrical remodelling after pulmonary veins and right atrium appendage pacing.

OBJECTIVE: Pulmonary veins (PVs) are important sources of paroxysmal atrial fibrillation (AF). Rapid atrial pacing changes atrial electrophysiology, and facilitates the induction and maintenance of AF. The purpose of our study was to evaluate the changes in atrial effective refractory period (AERP) proprieties and in ionic currents in PVs myocytes from dogs subjected to rapid atrial pacing in PVs and right atrial appendage (RAA) and to relate these changes to the ability to induce AF. METHODS: Twelve mongrel dogs in normal sinus rhythm were paced from the superior left PVs or RAA at 500 bpm for 4 h. Electrophysiological studies were conducted to determine the changes in AERP, dispersion, and rhythm. Ionic currents were evaluated using patch clamp technique in single PVs myocytes in sham-operated dogs, and the results were compared with those from PVs and RAA pacing groups. RESULTS: The presence of rapid atrial pacing was associated with a marked shortening in AERP in both PVs and RAA pacing group with a marked increase in AERP dispersion in PVs pacing. Both L-type calcium current (I(Ca,L)) and the transient outward current (I(to)) were reduced in both groups with an increased significance in PVs pacing group. The density of I(Ca,L) was decreased significantly from (-6.03 +/- 0.63) pA/pF in the control group to (-3.21 +/- 0.34) pA/pF in the PVs pacing group and (-4.75 +/- 0.41) pA/pF in the RAA pacing group (n = 6, P < 0.05), whereas the density of I(to) was decreased significantly from (8.45 +/- 0.71) pA/pF in the control group to (5.21 +/- 0.763) pA/pF in the PVs pacing group and (6.84 +/- 0.69) pA/pF in the RAA pacing group (n = 6, P < 0.05). CONCLUSION: Our findings provide likely ionic mechanisms of shortened repolarization in induced atrial tachycardia with a decrease in I(Ca,L) and I(to) densities, which is the likely mechanism for a decrease in action potential duration rate adaptation in the canine rapid pacing model more pronounced in the PVs pacing group underlying the crucial role of PVs in initiating AF.     

病态窦房结综合征心房按需起搏后双结功能的转归探讨

为了解心房按需起搏术后窦房结和房室传导功能的远期转归,观察22例植入AAI起搏器患者术后30～102个月的双结功能电生理参数,并与术前比较.结果显示:术后SACT、SNRT、CSNRT、房室传导文氏阻滞点、2:1阻滞点与术前比较差异均无显著意义(P>0.05).认为AAI起搏器植入对病态窦房结综合征患者窦房结功能和房室传功能没有显著影响,也无起搏器依赖性.