心力衰竭犬心房电生理特性的研究

为观察心力衰竭 (简称心衰 )犬心房肌电生理特性的改变 ,探讨充血性心衰时心房颤动 (AF)发生机制。选择14只犬随机分为起搏组 (n =7)和假手术组 (n =7) ,在左、右房各缝植 4对电极 ,电极尾端经皮下由犬背部穿出。假手术组犬埋置起搏器后不起搏。起搏组犬置入实验用VOO型起搏器快速心室起搏 (2 2 0次 /分 ) 6周 ,建立心衰犬模型 ,分别于起搏前、起搏 6周后 ,测定心房有效不应期 (AERP)、AERP离散度 (AERPd)、房内和房间传导时间及心房肌传导速度 ,记录AF诱发情况。结果 :①假手术组犬术前与术后比较 ,心功能和心房电生理特性均无明显变化。②心室快速起搏 6周犬AERP较起搏前略延长 ,但差异无显著性。起搏 6周犬AERPd较起搏前明显增大 (4 0 .4±15 .6msvs 2 2 .6± 10 .2ms,P <0 .0 5 )。与起搏前比较 ,起搏 6周犬房内及房间传导时间明显延长 (CTRA5 4 .7± 7.2msvs 33.1± 9.5ms ;CTLA5 2 .3± 8.9msvs 31.7± 6 .3ms ;CTRA LA6 9.7± 8.2msvs 4 2 .8± 7.9ms,P均 <0 .0 5 ) ,心房肌传导速度显著减慢 (CVRA5 4 .8± 7.9cm/svs 90 .7± 8.4cm/s ;CVLA5 7.4± 9.6cm/svs 94 .6± 10 .2cm/s,P均 <0 .0 5 )。③心衰犬AF诱发率、诱发次数、AF持续时间较起搏前明显增加。假手术组犬术前、术后比较AF诱发情况无?     

异氟醚预处理对体外循环后QT离散度的影响

观察体外循环心脏停跳心内直视手术过程中异氟醚预处理对患者QT离散度 (QTd)的影响并探讨其意义。2 0例瓣膜置换术患者 (ASA2～ 3级 ) ,随机分为预处理组和对照组。分别于麻醉后 (T1)、主动脉开放后 15min(T2 )、2h(T3 )、2 4h(T4)时间点取血样 ,检测血清心钠素 (ANP)、心肌钙蛋白I(cTnI)浓度 ;另于术前、术后第 1,3天记录同步 12导联心电图 ,测量QTd和校正QTd(QTcd)。结果 :术后两组QTd和QTcd较术前显著增加 (P <0 .0 1) ,其中对照组增加尤为显著 ,且第 1天时QTd和QTcd值大于预处理组 (70 .38± 8.34msvs 6 0 .84± 9.15ms,89.94± 7.6 5msvs81.6 8± 8.2 3ms,P均 <0 .0 5 ) ;两组ANP于T2 、T3 时有显著升高 (P <0 .0 1) ,且T3 时预处理组明显高于对照组 (5 5 7.89± 84 .0 3pg/mlvs 4 82 .38± 73.4 4 pg/ml,P <0 .0 5 ) ;T3 、T4时 ,对照组cTnI显著高于预处理组 (0 .19± 0 .0 5ng/mlvs0 .13± 0 .0 2ng/mL ,0 .2 4± 0 .0 7ng/mlvs 0 .18± 0 .0 4ng/ml,P <0 .0 1或 0 .0 5 )。结论 :异氟醚预处理能缩短QTd和QTcd ,其机制可能与其减少心肌损伤有关。     

房室结折返性心动过速患者房室结功能曲线连续性的电生理分析

分析房室结折返性心动过速 (AVNRT)中房室结功能曲线呈连续性者的电生理特点。将AVNRT分为房室结功能曲线连续组 (Ⅰ组 )及房室结功能曲线不连续组 (Ⅱ组 ) ,行慢径消融 ,进行消融前后和组间的电生理比较 ,分析房室结功能曲线呈连续性者的特点。结果 :I组心房程序刺激对AVNRT的诱发率仅 42 % (5 / 12 ) ,低于Ⅱ组的 6 6 %(2 3/ 35 )。Ⅰ组房室结前传有效不应期 (ERP AVN)消融前后无显著变化 (2 18.2± 2 9.3msvs 2 5 3.3± 80 .3ms,P >0 .0 5 ) ;心房程序刺激最长A2 H2 间期 (AHmax)消融前后无显著变化 (2 2 5 .8± 71.8msvs 175 .4± 41.9ms,P >0 .0 5 )。Ⅱ组ERP AVN消融后显著延长 (2 78.9± 5 8.9msvs 2 35 .8± 39.6ms,P <0 .0 5 ) ;AHmax消融后显著缩短 (172 .0± 6 7.1msvs 331.6± 86 .6ms ,P <0 .0 5 ) ;消融后房室结快径前传有效不应期 (ERP FP)显著缩短 (2 78.9± 5 8.9msvs 330 .0±5 5 .3ms,P <0 .0 5 )。消融前Ⅰ组AHmax短于Ⅱ组 (P <0 .0 5 ) ,Ⅰ组心动过速时A2 H2 间期 (AHSVT)与消融前AHmax比较差异无显著性 (P >0 .0 5 ) ;Ⅱ组AHSVT短于消融前AHmax(P <0 .0 5 )。结论 :房室结功能曲线连续性者较难经常规心房程序刺激诱发心动过速 ;慢径消融后曲线“尾巴”消失可作为消融终点的一项指     

腹主动脉结扎引起高血压大鼠心房结构和电生理变化

目的研究腹主动脉结扎大鼠心房结构和电生理特征变化,探讨高血压相关性房颤的发病机制.方法雄性SD大鼠随机分为非手术组(对照组,n=12)和腹主动脉结扎组(实验组,n=12),两组喂养时间均为4周.4周后动物麻醉,描记I导体表心电图,经左侧颈总动脉插管测量收缩压和舒张压.在心脏体外灌流条件下,采用心房短阵刺激评价房间传导时间(IACT)和心房对刺激的反应.取心房组织制作切片,Masson染色,测量纤维组织占总区域的百分比.结果实验组血清 Ang Ⅱ水平较对照组明显升高[(1.76±0.5 vs 0.97±0.4)ng/mL,P＜0.01], P波持续时间和IACT也较对照组延长[分别为(27.8±5.1 vs 23±4.5)ms, P＜0.05和(37.3±5 vs 23.1±3.3)ms,P＜0.01],在实验组诱发出4例AF;对照组没能诱发出AF.组织学发现实验组心房纤维组织明显增加,纤维化程度与AF的诱发有相关性(OR=5.75,P＜0.01).结论腹主动脉结扎大鼠心房纤维化程度增加,P波时限增宽,IACT延长,心房有效不应期没有改变.心房纤维化程度增加可能是AF诱发率升高的原因.     

房间隔起搏对阵发性心房颤动患者最大P波时限和P波离散度的影响

观察房间隔起搏对阵发性心房颤动 (AF)患者最大P波时限 (Pmax)及P波离散度 (Pd)的影响 ,探悉房间隔起搏防治AF发作的电生理机制。对 2 1例阵发性AF患者和 2 6例室上性心动过速行射频消融术无阵发性AF患者 ,分别进行右心耳和房间隔起搏 ,比较不同部位起搏对阵发性AF和无阵发性AF患者的Pmax和Pd影响。结果 :阵发性AF患者较无阵发性AF患者Pmax和Pd值明显大 (分别为 1 35± 1 5vs 1 1 9± 1 4ms ,P <0 .0 5 ;36 .5± 9.2vs 1 9.7± 7.1ms ,P <0 .0 1 ) ;房间隔起搏使阵发性AF患者Pd、Pmax显著下降 (分别为 2 3 .4± 8vs 36 .5± 9.2ms ,1 2 0± 1 1vs1 35± 1 5ms,P均 <0 .0 5) ;右心耳起搏使无阵发性AF患者Pmax和Pd明显增加 (分别为 1 32± 1 2vs 1 1 9± 1 4ms,2 5 .5± 8.5vs 1 9.7± 7.1ms ,P均 <0 .0 5)。结论 :右心耳起搏能够使无阵发性AF患者Pmax和Pd值增加。房间隔起搏能够明显降低阵发性AF患者Pmax、Pd ,纠正房内或房间传导延缓 ,改善心房内电活动的各向异性 ,防治AF发作     

QT离散度对X综合征的临床价值探讨

分析经冠状动脉造影证实的 1 82例冠心病、94例正常人及 3 8例X综合征者活动平板运动试验前及运动高峰时QT离散度 (QTd)的变化。X综合征组运动前QTd明显小于冠心病组 (2 9.41± 1 5 .1 1msvs 5 4.3 0± 9.2 2ms ,P <0 .0 1 )、而与正常组 2 5 .3 0± 1 3 .2 1ms相似(P >0 .0 5 ) ;X综合征组运动高峰时QTd明显大于正常组 (4 9.92±1 0 .2 3msvs 2 3 .5 2± 1 4.3 2ms,P <0 .0 1 )。结论 :X综合征者运动时QTd明显增加 ,提示运动高峰时较大的QTd可反映冠状动脉微血管病变所致心肌缺血     

人类自发的阵发性心房颤动导致的心房有效不应期及其频率适应性的变化

探讨人类自发的阵发性心房颤动 (AF)导致的心房有效不应期 (ERP)及其频率适应性的变化。对 12例在我院进行心腔内电生理检查和 或射频消融术且术中出现阵发性AF的患者 ,于AF发生前及AF终止后分别以基础周长 5 0 0 ,40 0和 30 0ms的刺激测量心房ERP。结果 :AF持续时间为 8.9± 2 .0min ,以周长为 5 0 0 ,40 0和 30 0ms行S1 S1 刺激 ,在AF发生前 ,ERP分别为2 2 3± 39,2 13± 33和 2 0 1± 2 1ms ,AF终止后 ,ERP分别为 189± 32 ,186± 35和 180± 2 3ms ,其缩短率分别为 15 .5 %± 4.0 % ,12 .9%± 3.1%和 10 .8%± 3.0 % ,与AF发生前相比 ,P均 <0 .0 1。心房ERP在低频率时的缩短程度大于在高频率时 ,各起搏周长下ERP缩短的程度比较具有显著统计学差异 (P <0 .0 5 )。AF终止后 10minERP恢复至AF前水平。结论 :人类几分钟的阵发性AF可使ERP缩短 ,并且可造成ERP频率适应不良     

人类自发的阵发性心房颤动导致的心房有效不应 …

探讨人类自发的阵发性心房颤动 (AF)导致的心房有效不应期 (ERP)及其频率适应性的变化。对 12例在我院进行心腔内电生理检查和 或射频消融术且术中出现阵发性AF的患者 ,于AF发生前及AF终止后分别以基础周长 5 0 0 ,40 0和 30 0ms的刺激测量心房ERP。结果 :AF持续时间为 8.9± 2 .0min ,以周长为 5 0 0 ,40 0和 30 0ms行S1 S1 刺激 ,在AF发生前 ,ERP分别为2 2 3± 39,2 13± 33和 2 0 1± 2 1ms ,AF终止后 ,ERP分别为 189± 32 ,186± 35和 180± 2 3ms ,其缩短率分别为 15 .5 %± 4.0 % ,12 .9%± 3.1%和 10 .8%± 3.0 % ,与AF发生前相比 ,P均 <0 .0 1。心房ERP在低频率时的缩短程度大于在高频率时 ,各起搏周长下ERP缩短的程度比较具有显著统计学差异 (P <0 .0 5 )。AF终止后 10minERP恢复至AF前水平。结论 :人类几分钟的阵发性AF可使ERP缩短 ,并且可造成ERP频率适应不良     

原发性高血压患者与正常人心率变异性的比较

目的　研究原发性高血压 (EH)患者与正常人心率变异性 (HRV)的比较。方法　 5 0例EH患者和 5 0例健康成人 (对照组 )行 2 4h动态心电图检查各 1次 ,分析心率时域和频域指标。结果　EH患者与对照组比较 ,代表心率总变异程度的SDNN〔(10 8 4± 33 2 )msvs (130 6± 35 6 )ms,P <0 0 1)〕、SDANN〔(96 2± 2 5 5 )msvs (118 3± 2 4 7)ms,P <0 0 1)〕和SDNNI〔(41 2± 16 3)msvs (5 4 1± 17 6 )ms,P <0 0 1)〕明显下降 ;代表迷走神经功能的RMSSD〔(2 8 4±10 3)msvs (32 8± 11 2 )ms,P <0 0 5 )〕和PNN5 0〔(6 1±1 5 )msvs (7 2± 1 8)ms ,P <0 0 5 )〕也有下降 ;频域指标VLF〔(186 2 7± 82 1 6 )Hzvs (15 34 8± 738 5 )Hz,P <0 0 5 )〕和LF〔(472 3± 2 6 5 8)Hzvs (396 2± 113 6 )Hz ,P <0 0 5 )〕升高 ,HF〔(112 5± 86 4 )Hzvs (2 0 3 6± 94 7)Hz,P <0 0 1)〕明显下降。结论　分析EH患者HRV有助于预测心脏功能受损的程度和预后     

60例2型糖尿病病人的BAEP变化

目的　观察 2型糖尿病患者BAEP的变化。方法　随机选取 60例 2型糖尿病患者检查其BAEP ,根据其有无周围神经损害分为A、B两组 ,另设 3 0例非 2型糖尿病患者作为对照组。结果　 2型糖尿病患者的BAEP的Ⅲ、Ⅴ波潜伏期为 4.0 5± 0 .2 1ms ,6.0 8± 0 .2 4ms。对照组BAEP的Ⅲ、Ⅴ波潜伏期为 3 .83± 0 .18ms ,5 .87± 0 .2 1ms。两者比较有显著性差异 (P <0 .0 0 1)。I-Ⅲ、Ⅲ -Ⅴ、I-Ⅴ峰间期在 2型糖尿病患者与正常组分别为 2 .2 8± 0 .19msvs 2 .0 4± 0 .2 5ms,2 .0 7± 0 .2 5msvs 1.84± 0 .2 1ms ,4.3 1± 0 .2 1ms,vs 4.12± 0 .2 6ms,两者相比有显著性差异 (P <0 .0 0 1)。在糖尿病患者中有周围神经损害的BAEP测值各参数 ,均明显高于无周围神经损害患者 ,P <0 .0 5～ 0 .0 0 1。结论　 2型糖尿病患者的BAEP的Ⅲ、Ⅴ波潜伏期与正常组相比明显延长 ,且有周围神经损害比无周围神经损害的 2型糖尿的患者的BAEP异常率明显增高     

依那普利干预肾素-血管紧张素系统对老龄鼠心房颤动诱发率的影响

目的研究依那普利对老龄鼠心房颤动(简称房颤)诱发率的影响。方法雄性老龄Wistar大鼠(12月龄)随机分为对照组(n=12)和实验组(n=13),对照组常规饲养,实验组加喂依那普利。3个月后,描记体表Ⅰ导联心电图,测量心率和P波时限。在体研究右房有效不应期(ERP)、房间传导时间(IACT)和心房对刺激的反应。用放免法测量血浆和心房组织血管紧张素Ⅱ(AngⅡ)浓度。取心房组织制作切片,测量纤维组织占总区域的百分比。结果实验组较对照组P波时限和IACT缩短(P均<0.01)。实验组房颤诱发率较对照组低[30.8%(4/13)vs75%(9/12),P=0.027]。实验组左、右房组织匀浆AngⅡ浓度较对照组降低(P均<0.01)。实验组大鼠左房和右房纤维化程度均较对照组明显减轻(P均<0.01)。结论老龄鼠长期应用依那普利后房颤诱发率降低,这可能是由于依那普利降低了心房纤维化程度,改善了心房传导。     

血管紧张素Ⅱ对大鼠心房纤维化及Cx40重构的影响

目的采用大鼠肾上腹主动脉部分结扎的模型,探讨血管紧张素Ⅱ(AngⅡ)对心房纤维化和缝隙连接蛋白(Connexin,Cx)40重构的影响。方法将40只雄性Wistar大鼠随机等分为对照组(C组)、腹主动脉结扎组(AB组)、结扎+贝那普利组(B组)、结扎+缬沙坦组(V组)。B组给予贝那普利20mg/kg治疗,V组给予缬沙坦40mg/kg治疗。喂养8周后处死,用放射免疫法测血浆及心肌组织AngⅡ含量,用Masson染色法和免疫组化方法检测大鼠心房纤维化程度及Cx40的分布特征,半定量分析心房纤维组织含量和Cx40的分布密度。结果与C组相比,AB组和V组血浆、心肌AngⅡ含量均明显升高(P均<0.01),而B组则无明显变化(P>0.05)。AB组心房纤维组织含量较C组明显升高(P<0.01),而Cx40分布密度减低(P<0.01),且向侧边分布增加;B组和V组纤维组织含量较AB组显著降低(P均<0.01),而两组Cx40含量较AB组增加(P均<0.01),且分布不均一程度减轻。结论AngⅡ长期升高可能是导致心房纤维化和Cx40重构的重要机制之一;贝那普利及缬沙坦可有效减轻心房纤维化和Cx40的重构。     

腹主动脉结扎大鼠心房纤维化的实验研究

高血压患者有较高心律失常的发生率，房性心律失常可能与左房扩大或心房纤维化有关。为观察压力负荷增高大鼠中心房纤维化的发生情况，将Ｗｉｓｔａｒ大鼠随机分成假手术组和手术组，手术组大鼠行肾上腹主动脉部分结扎。术后４，８，１２周分别测定大鼠颈动脉压及心房胶原容积分数（ＣＶＦ），结果发现：①手术组左室舒张压明显高于假手术组（４，８，１２周分别为１８．５±２．５ｋＰａｖｓ１５．７±１．９ｋＰａ，１８．６±２．７ｋＰａｖｓ１５．３±１．３ｋＰａ，１９．６±３．１ｋＰａｖｓ１５．２±１．９ｋＰａ，Ｐ＜０．０５或０．０１）。②手术组心房ＣＶＦ明显高于假手术组（４，８，１２周左、右房分别比较：４．２３±０．７６％ｖｓ２．９３±０．８７％，４．６５±１．４５％ｖｓ３．１１±１．０７％，５．６２±１．６２％ｖｓ３．２３±１．２８％；３．８８±１．１５％ｖｓ２．５１±０．８４％，４．２４±１．６５％ｖｓ２．５１±０．８４％，５．３４±１．３２％ｖｓ２．３３±１．１４％；Ｐ＜０．０５或０．０１），手术组心房ＣＶＦ有逐渐上升趋势。③左房ＣＶＦ与左室舒张压之间无直线相关关系（ｒ＝０．１６９１，Ｐ＞０．０５）。提示在高血压大鼠模型中存在心房?     

风湿性心脏病心房颤动患者血管紧张素Ⅱ受体表达

目的 探讨风湿性心脏病心房颤动(房颤)患者心房重构的相关分子机制的表达情况.方法 取39例风湿性二尖瓣疾病换瓣手术患者的心房组织标本.其中房颤患者25例、窦性心律患者14例.应用RT.PCR技术测定左、右心房组织中血管紧张素Ⅱ1型受体(AT1)和2型受体(AT2)mRNA的表达水平,应用免疫组化技术检测AT1和AT2的蛋白表达水平.结果 与窦性心律组相比,房颤患者组左心房内径明显增大.房颤组左心房的AT1 mRNA及蛋白表达水平均显著高于窦性心律组(P<0.05),而AT2 mRNA及蛋白表达水平却无显著差别.右心房AT1和AT2的mRNA及蛋白表达水平在两组患者间无显著差别.即房颤患者左心房AT1表达明显上调,而AT2表达并未受明显影响.结论 肾素.血管紧张素系统参与了房颤过程.由AT1激活介导的一系列效应可能是心房重构的相关分子机制之一.     

Thyroid Hormone Replacement Therapy Attenuates Atrial Remodeling and Reduces Atrial Fibrillation Inducibility in a Rat Myocardial Infarction–Heart Failure Model

BackgroundHeart failure (HF) is associated with increased atrial fibrillation (AF) risk. Accumulating evidence suggests the presence of myocardial tissue hypothyroidism in HF, which may contribute to HF development. In a recent report we demonstrated that hypothyroidism, like hyperthyroidism, leads to increased AF inducibility. The present study was designed to investigate the effect of thyroid hormone (TH) replacement therapy on AF arrhythmogenesis in HF.Methods and ResultsMyocardial infarction (MI) was produced in rats by means of coronary artery ligation. Rats with large MIs (>40%) were randomized into L-thyroxine (T₄; n = 14) and placebo (n = 15) groups 2 weeks after MI. Rats received 3.3 mg T₄ (in 60-day release form) or placebo pellets for 2 months. Compared with the placebo, T₄ treatment improved cardiac function and decreased left ventricular internal diameters as well as left atrial diameter. T₄ treatment attenuated atrial effective refractory period prolongation (45 ± 1.5 ms in placebo group vs 37 ± 1.6 ms in T₄ group; P < .01) and reduced AF inducibility (AF/atrial flutter/tachycardia were inducible in 11/15 rats [73%] in the placebo- vs 4/14 rats [29%] in the T₄-treated group; P < .05). Arrhythmia reduction was associated with decreased atrial fibrosis but was not associated with connexin 43 changes.ConclusionsTo our knowledge this is the first study demonstrating that TH replacement therapy in HF attenuates atrial remodeling and reduces AF inducibility after MI-HF. Clinical studies are needed to confirm such benefits in human patients.     

Aging-related increase to inducible atrial fibrillation in the rat model

INTRODUCTION: Aging is associated with atrial interstitial fibrosis and increased incidence of atrial fibrillation (AF). We hypothesized that aged rats are suitable for study of aging-related AF and that partial atrial cellular uncoupling induced with heptanol in young rats mimics aging-related AF. METHODS AND RESULTS: Interatrial conduction time and atrial response to burst atrial pacing were evaluated in 11 young (2-3 months) and 12 old (22-24 months) male rats (Fisher 344) in the Langendorff-perfused setting. At baseline, sustained (>30 sec) atrial tachycardia (AT) and AF were induced in 10 of 12 and in 7 of 12 old rats, respectively. No such arrhythmias could be induced in the young rats. Old rats had significantly (P < 0.01) longer interatrial conduction time and P wave durations than the young rats. Burst pacing failed to induce AT and AF in all 11 young rats studied. The effects of heptanol 2 to 10 microM were studied in both groups. Heptanol 2 to 5 microM promoted inducible AT in all 5 young rats studied; however, when its concentration was raised to 10 microM, AT could no longer be induced in any of the 5 young rats. No AF could be induced in any of the 5 young rats at heptanol concentrations of 2 to 10 microM. In the old rats, AF could still be induced during perfusion of 2 microM heptanol. However, when its concentration was raised to 5 and 10 microM, AF could not be induced in any of the 6 old rats studied. Optical mapping using a potentiometric dye showed a periodic single wavefront of activation during AT in both groups and 2 to 4 independent wavefronts propagating in different directions during AF in the old rats. Histology revealed a significant increase in interstitial atrial fibrosis (P < 0.01), atrial cell size (P < 0.05), and heart weight in old versus young rats. Fibrosis in the old rats was highly heterogeneous. CONCLUSION: The rat model is suitable for study of aging-related AF. Uniform partial atrial cellular uncoupling with heptanol perfusion in the young rats, although promoting inducible AT, does not mimic aging-related AF. The results suggest that heterogeneous atrial interstitial fibrosis and atrial cell hypertrophy might contribute to the aging-related increase in atrial conduction slowing, conduction block, and inducible AF in the old rat model.     

糖尿病兔心房电生理及L型钙电流的变化

目的研究糖尿病时心房电生理参数、L型钙电流(ICa,L)变化,探讨糖尿病引起心房颤动(简称房颤)的机制。方法本研究分为离体电生理实验和全细胞膜片钳实验两部分,每部分均分为糖尿病组和对照组。糖尿病兔采用四氧嘧啶诱导。每组各8只兔,饲养8周,离体电生理部分在建立Langendorff灌流的离体兔心脏模型后,测量心房间传导时间(IACT)、高位右房、高位左房、低位左房有效不应期(AERP)、AERP的离散度(AERPD)、应用Burst刺激观察房颤诱发情况;膜片钳实验采用酶解法分离单个心房肌细胞,采用全细胞膜片钳技术记录ICa,L。结果与对照组比较,糖尿病组IACT延长(37.66±8.88 ms vs 27.70±2.12 ms),AERPD增大(28.37±7.52 ms vs 11.62±5.60 ms);房颤诱发率升高(6/8 vs 1/8);心房肌细胞ICa,L最大电流密度显著增加(8.94±3.81 pA/pF vs 5.16±1.10 pA/pF),P均<0.05。结论糖尿病时存在心房电重构。     

Lengthening of intraatrial conduction time in atrial fibrillation and its relation with early recurrence of atrial fibrillation.

Intraatrial conduction delay in atrial fibrillation (AF) that is considered a component of atrial electrical remodeling has been demonstrated previously in experimental models and it is considered an important factor for the induction or stabilization of AF. However, it is not known if this phenomenon exists in human AF. The present study aimed to compare intraatrial conduction time (IACT) in patients with chronic atrial fibrillation who were converted to sinus rhythm and a matched control group, and to investigate its relation with early AF recurrence. Seventeen patients with chronic AF (mean duration of 20.71+/-16.35 months) were enrolled in the study (7 males, 10 females, 63+/-8 years). An age and sex matched control group (n=12) consisted of patients with sinus rhythm who underwent electrophysiological study (EPS). None of the patients were on any antiarrhythmic treatment during the procedures. Cardioversion was performed via external DC cardioversion. Eight patients in the control group were delivered a DC shock because of induced ventricular tachycardia during EPS. IACT was defined as the interval between the onset of P wave surface ECG and the beginning of A wave at high right atrium (IACT 1) and low right atrium (IACT 2). Additionally, the interval between A wave at high right atrium and low right atrium was measured (IACT 3). Patient characteristics such as age, sex and echocardiographic variables were not different between the AF group and the control group. Heart rate after cardioversion was found to be similar between the two groups. Total delivered energy was significantly higher in the AF group than in the control group (464.47+/-165.82 joules vs. 315.00+/-27.77 joules, p<0.001). IACT 1 (15.30+/-7.61 msec vs 8.50+/-5.29 msec, p<0.02 ), IACT 2 (45.25+/-836 msec vs 26.44+/-10.45 msec, p<0.001) and IACT 3 (26.9+/-8.26 msec vs. 18.67+/-10.05, p<0.05) significantly lengthened in the AF group after maintenance of sinus rhythm compared to the control group. There were 6 early AF recurrences during the 1 week follow-up period. Multivariate analysis, revealed IACT 2 and IACT 3 were significantly different between the control group, the patient with recurred AF and the patients with maintained sinus rhythm. Post-hoc analysis revealed that IACT 2 and IACT 3 significantly lengthened in the patients with recurred AF compared to both the control group and patients with maintained sinus rhythm. On the other hand, only IACT 2 patients with maintained sinus rhythm were found to be higher than those of the control group. The present study indicated that intraatrial conduction was disturbed in patients with AF, a finding which is consistent with those of previous experimental studies. Additionally, such a phenomenon may be a risk factor for the early recurrence of AF after cardioversion to sinus rhythm.     

氯沙坦增加Akt活性对慢性心力衰竭大鼠心功能及心肌细胞凋亡的保护作用

目的研究氯沙坦对腹主动脉结扎所致慢性心力衰竭大鼠心肌细胞凋亡和心功能保护作用的可能机制。方法采用腹主动脉缩窄法制备SD大鼠心力衰竭模型,将SD大鼠随机分为模型组,治疗组,假手术组,对照组,每组10只。治疗组和对照组氯沙坦(20 mg·kg~(-1)·d~(-1))干预8周后,采用超声心动图和心室插管法评估各组大鼠心功能,计算左、右心室质量指数(LVMI),放射免疫法检测血浆和心肌组织血管紧张素Ⅱ(AngⅡ)水平,高敏ELISA检测去甲肾上腺素(NE)水平。琼脂糖凝胶电泳和TUNEL法观察心肌细胞凋亡状态,通过RT-PCR检测凋亡相关基因表达,Western blot检测磷酸化Akt(p-Akt)蛋白水平表达变化。结果与模型组比较,治疗组大鼠心功能和LVMI等指标明显好转(P<0.05),血浆NE和心肌组织AngⅡ水平降低(P<0.05),但血浆AngⅡ水平升高(P<0.05),未出现细胞凋亡特有的"DNA梯度"现象,且凋亡指数减少(P<0.05),Bax/Bcl-2基因表达比例降低(P<0.05),p-Akt蛋白水平显著升高(P<0.05)。与假手术组和对照组相比,模型组大鼠各项心功能指标明显恶化,心肌细胞凋亡较为严重(P<0.05)。结论氯沙坦通过阻断AngⅡ与AngⅡ1型受体结合抑制凋亡通路并可促进Akt信号通路活化,从而保护慢性心力衰竭大鼠心肌细胞凋亡,改善心功能。     

培哚普利与硫氮唑酮联合治疗阵发性心房颤动

为探讨培哚普利 +硫氮唑酮对控制阵发心房颤动 (简称房颤 )发作和左心房扩张的疗效 ,将阵发性房颤分为硫氮唑酮组 (Ⅰ组 )和培哚普利 +硫氮唑酮组 (Ⅱ组 ) ,二组根据左房内径大小分为左房正常组 (Ⅰa=33例、Ⅱa =33例 ) ,左房扩大组 (Ⅰb =34例、Ⅱb =31例 )。Ⅰ组给予硫氮唑酮 30mg 2次 /日或 3次 /日 ;Ⅱ组给予硫氮唑酮 30mg 2次 /日 +培哚普利 4mg 1次 /日。所有患者均治疗 3年。结果 :①各组房颤年发作次数治疗后均有显著减少 (P <0 .0 5 )。②Ⅰb、Ⅱa、Ⅱb组治疗后的房颤持续时间显著缩短 (P <0 .0 5 )。③房颤的年发作次数治疗后 1,2 ,3年间 ,Ⅰa、Ⅱa组显著高于Ⅰb、Ⅱb组 (P <0 .0 5 )。④随治疗时间的延长 ,Ⅱ组左房扩张的增幅明显低于Ⅰ组 (P <0 .0 5 )。结论 :硫氮唑酮和培哚普利 +硫氮唑酮治疗阵发性房颤均可减少房颤的发作 ,但后者优于前者 ,培哚普利 +硫氮唑酮治疗可明显减慢左房的扩张速度。