左上肺静脉脂肪垫对犬心房颤动的影响

目的观察射频消融左上肺静脉脂肪垫(left superior pulmonary vein fat pad,LSPV-FP)对心房颤动(AF)的影响。方法 12只健康杂种犬,麻醉插管后持续心电监测;于双侧颈部暴露迷走神经干,左右侧第4肋间开胸并暴露LSPV-FP;分别测量基础、刺激迷走神经、消融LSPV-FP、刺激迷走神经+消融LSPV-FP 4种状态下的心房及左上肺静脉有效不应期(ERP)和有效不应期离散度(dERP)、AF诱发率、AF时心室率。结果基础状态下,刺激左侧或右侧迷走神经干可明显缩短心房ERP[(84.44±29.50)ms vs(129.7±15.83)ms,(85.42±26.11)ms vs(129.7±15.83)ms,P<0.05]、增大dERP[(71.67±14.03)ms vs(34.17±18.32)ms,(57.5±24.17)ms vs(34.17±18.32)ms,P<0.05]、增大左上肺静脉近端与远端ERP的差异(P<0.05)、增加AF的诱发率[(5.33±1.231)次vs(0.75±0.96)次,(4.67±1.155)次vs(0.75±0.96)次,P<0.05]及降低AF时心室率[(143.6±22.42)次/min vs(226.3±28.50)次/min,(146.4±30.72)次/min vs(226.3±28.50)次/min,P<0.05]。消融LSPV-FP可以逆转刺激左侧迷走神经干所致的上述变化(P<0.05),但对右侧迷走神经刺激干所致的电生理变化无显著影响。结论左侧迷走神经干纤维部分通过LSPV-FP对心房颤动的触发或维持发挥作用。     

心房颤动电生理重构的实验研究

目的 :研究心房颤动 (atrialfibrillation ,AF)时心房肌的电生理重构。方法 :快速持续起搏犬右心房 8～ 10周 ,制备持续性AF模型。比较对照犬 ( 8只 )与起搏犬 ( 10只 )的有效不应期 (effectiverefractoryperiod ,ERP)和心房颤动波周长 (atrialfibrillationcyclelength ,AFCL)的变化来分析心房肌的电生理重构。结果 :起搏组P波时间和PA间期比起搏前明显延长 (P波时间 90 5± 10 5对 5 3 6± 8 3ms ;PA间期 5 9 6± 8 8对 3 8 6± 11 4ms ,P <0 0 5 )。经程序刺激ERP较对照组明显缩短 (S1S13 0 0ms 115± 2 3对 15 0± 2 1;S1S14 0 0ms 10 5± 2 7对 15 4± 2 4ms ,P <0 0 5 )。同一心房不同部位的ERP和AFCL也存在差异。结论 :心房率的长期变化可引起ERP和AFCL的变化 ,即心房肌发生电生理重构 ,而且不同部位心房肌电生理重构是不同的。     

Electro-anatomic mapping of the right atrium: anatomic abnormality is an important substrate

Previousstudieshavesuggestedthattypicalatrialflutter(AF)isamacroreentrywiththecircuitconstrainedbetweentheanteriorborderofthetricuspidannulusandposteriorborderconsistingofthecristaterminalis (onthefreewallandEustachianvalve/ridgeontheseptumandthatcavotricuspidisthmus (CTI)isaprotectedcriticalslowconductionzonethatistheelectrophysiologicaldeterminantoftheinductionofcounterclockwiseandclockwiseisthmusdependentAFinhumans 1 5　Althoughslowconductionlocatedinthelowrightatrialisthmuswasinvestigate…     

快速起搏心房对家兔心房NPR-A受体表达及心房钠尿肽含量的影响

[目的]建立家兔快速心房起搏模型,探讨快速心房起搏早期心房NPR-A受体表达水平及血浆中心房钠尿肽(ANP)含量的变化与心房颤动发生的关系.[方法]由右侧颈外静脉穿刺置入电极于右心房,以600次/min的频率诱导心房颤动,利用放射免疫分析技术和免疫组织化学方法观察起搏前、起搏8 h和假手术组血浆中ANP含量和心房NPR-A表达水平.[结果]起搏8 h组血浆中ANP含量与起搏前和假手术组相比明显升高,且心房NPR-A表达水平明显增高.[结论]在快速起搏早期,血浆中ANP含量和心房NPR-A受体表达水平均升高,其主要机制可能是心房颤动早期代偿性和保护性效应.     

导管消融去肾交感神经抑制星状神经节刺激诱发的心房颤动

【目的】探讨经导管射频消融去肾交感神经对交感神经过度激活介导的心房颤动的影响和心房电重构机制?【方法】 16只家犬随机分为对照组(n = 8)和去肾交感神经(RSD)组(n = 8),RSD组进行经导管射频消融去肾交感神经术,对照组行不消融肾交感神经的假手术,通过左侧星状神经节电刺激(LSG) +快速心房起搏(RAP)3 h建立交感神经介导的房颤犬模型?【结果】 LSG刺激联合RAP使左心耳?右心房?左上肺静脉?左下肺静脉部位的房颤诱发率升高,有效不应期缩短(ERP),有效不应期离散度增大,均较基础值有统计学差异(P < 0.05),RSD组消融后各部位房颤诱发率降低?ERP显著延长?ERP离散度显著缩小,与对照组相比有统计学差异(P < 0.05)?LSG刺激联合RAP引起各检测部位的R-R间期?SDNN缩短,LF?HF和LF/HF降低,均较基础值有统计学差异(P < 0.05);RSD可逆转LSG刺激联合RAP引起的这些心率变异性改变,与对照组相比具有统计学差异(P < 0.05)?【结论】 交感神经过度激活使房颤易于诱发?恶化急性心房电重构,RSD可有效降低房颤的诱发率,抑制心房电重构?改善心脏自主神经功能,提示RSD对交感神经过度激活介导的房颤的发生具有潜在抑制作用?     

右美托咪定对快速心房起搏后兔心房电生理学特性及Cx43 Cx40表达的影响

目的 探讨右美托咪定对快速心房起搏后兔心房电生理学特性及Cx43、Cx40表达的影响。方法 选择成年雄兔24只,随机分为对照组（C组）、快速心房起搏组（RAP组）与快速心房起搏+右美托咪定灌流组（RAP+DEX组）,每组8只。制备Langendorff离体心脏灌注模型,通过快速心房起搏构建房颤模型。分别检测3组心房90%单相动作电位复极时程（MAPD₉₀）、心房有效不应期（ERP）、ERP与MAPD₉₀比值（ERP/MAPD₉₀）、房颤诱发率及持续时间,取心房组织,采用Western-bolt法和免疫荧光法检测Cx43、Cx40的蛋白含量和分布。结果 T₁~T₃时,3组MAPD₉₀比较,差异有统计学意义（P<0.05）。RAP组MAPD₉₀随时间的推移有逐渐下降趋势（P<0.05）,不同的处理方式和时间对MAPD₉₀有交互作用（P<0.05）。T₃时,RAP组ERP、ERP/MAPD₉₀、Cx43和Cx40蛋白含量均低于C组和RAP+DEX组,房颤诱发率高于C组和RAP+DEX组,差异有统计学意义（P<0.05）。3组房颤持续时间比较,差异无统计学意义（P>0.05）。电镜下,RAP组Cx43和Cx40分布不规律且侧面分布增多,而C组和RAP+DEX组Cx43和Cx40分布较规律且主要集中在两端。结论 右美托咪定可抑制房颤时的心房电重构,降低房颤的易感性,其机制可能与其抑制Cx43、Cx40的表达下调和再分布有关。     

2008 Obstetrics & Gynecology Symposium in China

Background CartoXP and CartoMerge have been used to treat atrial fibrillation （AF） for several years. Our randomized prospective study compared clinical outcomes of these two versions of three dimensional electroanatomic mapping system in guiding catheter ablation for paroxysmal atrial fibrillation （PAF）. Methods Eighty-one patients with symptomatic, drug refractory PAF were randomly assigned to CartoMerge group （n=-42, mean age （54.5 ＋ 13.1） years, history of AF = 3.2 years） or CartoXP group （n=39, mean age （59.8 ± 15.6） years, history of AF = 2.9 years）. All patients underwent 64-slice computed tomography （MSCT） 1 to 3 days prior to ablation procedure. Using CartoMergeTM Image Integration Module, 3D anatomical images of the left atrium （LA） and pulmonary veins （PVS） derived from MSCT of CartoMerge group were established and merged with the electroanatomical map. The integrated images were used to guide the procedure of circumferential pulmonary vein isolation （CPVl）. In the other group, CPVl was guided just by CartoXP. The endpoint of CPVl in both groups was abolition or dissociation of pulmonary vein potentials （PVPs）. Results Mapping points to establish the electroanatomical model of the LA/PVs were 48.7＋13.4 in CartoMerge group and 62.5±15.7 in CartoXP group （P〈0.001）. Mean distance between mapping points and the MSCT surfaces in CartoMerge group was （1.59±0.33） mm. Accomplishment of abolition or dissociation of PVPs was achieved 95.2% in CartoMerge group and 92.3% in CartoXP group. Durations of procedure and exposure to X-ray were （156±25） minutes, （179±21） minutes （P〈0.001） and （19.6±7.5） minutes, （28.5±12.8） minutes （P 〈0.001）, respectively. After a follow-up with duration of （11.9＋3.1） months vs （12.4±3.6） months post the first ablation procedure, patients free of AF were 33 （78.6%） in CartoMerge group and 29 （74.4%） in CartoXP group （P〉0.50）. No patient suffered pulmonary vein stenosis,     

持续性快速右心房起搏犬肺静脉-左心房连接处自主神经重构的研究

目的 定量研究持续性快速右心房起搏后犬肺静脉-左心房(PV-LA)连接处自主神经重构的情况。方法 12只健康成年杂种犬,随机分为对照组和起搏组,每组各6只,起搏组以400次/min的速率快速起搏犬右心房,持续4周。起搏结束后立即测定所有犬左上肺静脉-左心房(LSPV-LA)连接处的有效不应期,并收集所有PV-LA连接处直径为1cm内的组织。用酪氨酸羟化酶(TH)及乙酰胆碱转移酶(ChAT)分别标记交感与副交感神经,并通过免疫组化染色及Western blotting进行神经定量研究。结果 起搏组LSPV-LA连接处有效不应期较对照组显著缩短［(83.33±16.33) vs (111.67±20.41)ms, P<0.05］。起搏组2只犬发生自发性房颤,而对照组无房颤发生。免疫组化染色显示,起搏组LSPV-LA连接处TH及ChAT的平均密度及分布不均一程度均显著高于对照组(P<0.01)。Western blotting显示,起搏组的4个PV-LA连接处TH和ChAT总表达量显著增加(P<0.01)。结论 持续性快速右心房起搏后犬PV-LA连接处发生了自主神经重构,可能与房颤的发生相关,并在房颤的射频消融治疗中具有重要意义。     

羊持续心房颤动心房有效不应期变化的时间进程及其逆转观察

目的：探讨持续心房颤动（AF）心房有效不应期（ERP）变化的时间进程及其逆转过程.方法：采用起搏方法建立AF模型,在起搏前和起搏后的第1 d,3 d,5 d,7 d对左、右心耳的有效不应期（ERP）进行测定.采用S1S2程序刺激,基础起搏周长（PCL）分别为400 ms,350 ms,300 ms,250 ms,200 ms,S2为200 ms,以5 ms的步长递减.程序刺激结合Burst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0 h,3h,5 h,24 h左、右心耳的ERP进行测定.结果：各个基础起搏周长下左、右心耳的ERP在AF后1 d,3 d,5 d,7 d逐渐缩短,且较AF前明显缩短（P＜0.05）;AF终止后左、右心耳的ERP逐渐延长,但AF终止0 h,3 h,5 h ERP与AF前相比仍有明显缩短（P＜0.05）;AF终止后24 h ERP基本恢复到AF前水平,两者相比差异无统计学意义（P＞0.05）;随着AF持续时间的延长,左、右心耳AF的诱发率逐渐增高,与AF前相比,AF后1 d、3 d、5 d、7 d AF的诱发率明显增高（P＜0.05）.结论：随着AF持续,心房的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.     

山羊心房不同部位有效不应期与心房颤动诱发的关系

目的:测定心房不同部位的有效不应期(ERP),并探讨其与心房颤动(AF)发生的相互关系.方法:山羊15只,运用程序刺激(S1S2程序刺激,基础起搏周长(PCL)分别为400 ms、350 ms、300 ms、250 ms、200 ms;S2为200 ms,以5 ms的步长递减)测定正常左心耳、右心耳、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.程序刺激结合Burst刺激对上述心房部位进行AF诱发,记录AF的发生率.结果:左心耳、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差异无统计学意义(P＞0.05);上述部位的ERP较右心耳ERP短(P＜0.05),AF发生率较右心耳高(P＜0.05).结论:左心房及肺静脉固有的电生理特点可能是AF主要来源于左心房的一个重要因素.     

心房颤动犬心房肌细胞骨架重构及贝那普利的干预作用

目的 观察快速心房起搏心房颤动(房颤)犬心房肌细胞骨架重构及贝那普利的干预作用.方法 采用慢件快速左心房起搏建立房颤犬模型,分为假手术组(6只)、房颤组(7只)、干预组(6只).房颤组应用固定频率型起搏器,600次/min起搏6周;干预组于起搏前1周开始每日服贝那普利(1 mg/kg).实验结束时取材,HE染色测定心房肌细胞直径;Masson染色进行心房肌纤维化定量分析;免疫组织化学法检测结蛋白心脏原位蛋白分布及表达;RT-PCR方法测定心房肌组织β-微管蛋白、结蛋白mRNA表达水平.结果 假手术组、房颤组、干预组左心房肌细胞直径分别为(19.6 ±2.9)μm、(27.9 ±3.8)μm、(25.1 ±3.4)μm,右心房分别为(18.7 ±2.6)μm、(26.8 ±3.2)μm、(25.2 ±3.5)μm,房颤组、干预组左、右心房肌细胞直径均明显长于假手术组(均P＜0.01);左心房胶原容积分数(CVF)分别为(9.2±0.9)%、(16.9 ±1.1)%、(11.3 ±0.8)%,右心房CVF分别为(9.3±0.8)%、(15.7 ±2.3)%、(10.9 ±0.8)%,房颤组左、右心房CVF均高于假手术组(均P＜0.01),干预组均明显低于房颤组(均P＜O.01).免疫组化示房颤组结蛋自在细胞质内表达增多,而闰盘处表达不明显,房颤组左、右心房肌结蛋白吸光度值均高于假手术组(均P＜0.01),干预组均明显低于房颤组(均P＜0.01).房颤组左、右心房肌结蛋白、微管蛋白mRNA表达均高于假手术组(均P＜0.01);干预组房颤组(均P＜0.01).结论 快速心房起搏房颤犬心房肌细胞骨架发生重构且贝那普利对其有干预作用.     

快速心房起搏诱导猪持续性房颤心房组织ACE2表达及替米沙坦干预的影响

目的 探讨猪心房颤动（房颤）心房肌组织中血管紧张素转换酶2（ACE2）的表达和替米沙坦干预的作用.方法 18只健康小猪随机分为3组,分别为正常对照组（假手术组）、快速心房起搏组（RAP组）、替米沙坦干预组（起搏＋替米沙坦,ARB组）,每组各6头猪.对照组安置起搏器（AOO）但不行起搏刺激,其余各组安置起搏器,给予500次/min的快速右心房起搏2周,制成慢性房颤实验模型.各组均给予相同饲料喂养.替米沙坦（1.5 mg·kg^-1·d^-1）混于饲料中,并提前3天应用于ARB组;2周后处死所有实验猪,免疫组化染色方法 观察心房组织ACE2蛋白表达及定位;Western Blot检测心房组织ACE2的表达变化.结果 免疫组化染色可见：RAP组心房组织ACE2阳性染色较正常对照组明显减少,ARB干预组ACE2阳性染色较RAP组明显增加,接近正常对照组.与正常对照组比较,RAP组ACE2蛋白表达明显降低（P〈0.05）,替米沙坦干预组ACE2蛋白表达较RAP组明显增加（P〈0.05）.结论 房颤心房肌组织中ACE2表达下调,替米沙坦对房颤的效应可能与其上调ACE2有关.     

Substrate of complex fractionated atrial electrograms: evidence by pathologic analysis

Background  Ablation of complex fractionated atrial electrograms (CFAE) is an important adjunctive therapy in atrial fibrillation (AF). The present study was to elucidate the substrate underlying CFAE.

Methods  Nine adult mongrel dogs were involved in the present study. AF was induced through rapid atrial pacing with vagosympathetic nerve stimulation. CFAE was recorded during AF. Ablation was performed at CFAE sites. Based on the location of the ablation scar, the atrial specimens were divided into CFAE and non-CFAE sites. Serial sections of the atrium were stained respectively with hematoxylin-eosin (HE) and the general neural marker protein gene product 9.5 (PGP9.5). We compared the characteristics of the myocardium and the ganglionated plexus (GPs) distribution between the CFAE and non-CFAE sites.

Results  The myocardium of non-CFAE sites was well-organized with little intercellular substance. However, the myocardium in the CFAE site was disorganized with more interstitial tissue ((61.7±24.3)% vs. (34.1±9.2)%, P <0.01). GPs in the CFAE site were more abundant than in non-CFAE sites ((34.45±37.46) bundles/cm² vs. (6.73± 8.22) bundles/cm², P <0.01).

Conclusion  The heterogeneity of the myocardium and GPs distribution may account for the substrate of CFAE and serve as a potential target of ablation.

     

犬心房与肺静脉交感神经分布与阵发性心房颤动的关系

目的 探讨犬交感神经末梢在心房与肺静脉分布的特点及其与房颤诱发的相关性.方法 16只健康杂种犬,全麻、左右侧开胸.刺激双侧迷走交感干,分别于右心耳、左心耳、左心房及四支肺静脉行S1S1猝发刺激及S1S2程序刺激,观察心房及肺静脉不同部位房颤的诱发率.随后,处死动物,行心房、肺静脉交感神经抗酪氨酸羟化酶(TH)抗体染色,计算心房及肺静脉各部位交感神经密度,比较交感神经密度与房颤诱发之间的关系.结果 14只犬完成全部试验.除右下肺静脉房颤诱发率较低外,余各部位房颤诱发率无明显差异;心房和心耳TH染色阳性的神经密度分别为高于肺静脉内的神经密度[(128±65)/mm2,(76±29)/mm2,P=0.02];能诱发房颤的犬的TH染色阳性的神经密度高于未能诱发房颤(P＞0.05).结论 心房、心耳的交感神经分布比肺静脉的交感神经分布的密度大;房颤诱发与心房和肺静脉内交感神经分布的密度有一定关系.     

高甲状腺素时快速心房激动对心房电生理特性的影响

目的：研究高甲状腺素水平时快速心房激动对心房电生理特性的影响。方法：将实验兔随机分为正常对照组（n=10）、起搏组（n=10）、甲亢组（n=14）和甲亢起搏组（n=12）。在基础状态和快速心房起博后2、4、6h，分别测定各组基础起搏周长为200ms、150ms、130ms时的心房有效不应期（AERP）。结果：起搏组快速起搏2、4、6h后的AERP明显小于基础状态和对照组（P〈0．01），甲亢组的AERP明显小于对照组（P〈0．01），甲亢起搏组快速起搏2、4、6h后的AERP明显小于基础状态（P〈0．01）和甲亢组（P〈0．05）。起搏组快速起搏2、4、6h后的AERP200-150和AERP200-130明显小于基础状态和对照组（P〈0．01），甲亢组和甲亢起搏组的AERP200-150和AERP200-130均明显小于对照组（P〈0．01），但甲亢组和甲亢起搏组的AERP200-150和AERP200-130无显著性差异（P〉0．05）。结论：高甲状腺素水平及在此基础上的短时间快速心房激动可引起心房电生理重构。     

去自主神经条件下迷走神经对肺静脉不同部位房颤诱发率的影响

目的 探讨去自主神经条件下迷走神经对肺静脉不同部位房颤诱发率的影响。方法 10只健康杂种犬,经切断双侧颈迷走神经干和破坏颈交感神经节,建立动物的去自主神经模型。分别在右心耳、左心耳、左心房和四支肺静脉的近、中、远段行S1S1及S1S2程序刺激,在基础刺激及伴有双侧颈迷走神经同时刺激或阿托品作用的情况下,观察心房及肺静脉不同部位房颤诱发率的变化。结果 基础状态下,在心房及肺静脉的所有部位给予S1S2程序刺激,几乎均可诱发出房性早搏或短阵房速,而较少诱发出房颤。当同时伴有迷走神经刺激时,房颤的诱发频率明显增加;当行S1S1刺激的同时伴有双侧颈迷走神经刺激时,在心房及肺静脉的所有部位,其房颤诱发率均较基础刺激时明显升高（右心耳22．2％vs59．3％,左心耳14．8％vs55．6％,左心房18．5％vs51．9％,左上肺静脉上段33．3％vs66．7％,P〈0．05,P〈0．01）。与基础刺激比较,阿托品作用并不影响肺静脉的房颤诱发率（均P〉0．05）。结论 对于肺静脉起源的房颤,迷走神经也可能是参与其起始的重要诱发因素。     

Calpain I inhibition prevents atrial structural remodeling in a canine model with atrial fibrillation

Background Atrial fibrillation （AF） is accompanied by atrial structural remodeling. Calpain activity is induced during AE To test a causal relationship between calpain activation and atrial structural changes, N-acetyI-Leu-Leu-Met （ALLM）, a calpain inhibitor, was utilized in a canine AF model. Methods Fifteen dogs were randomly divided into 3 groups： sham-operated group, control group and calpain inhibitor group; each with 5 dogs. Sustained AF was induced by rapid right atrium pacing at 600 beats per minute for 3 weeks. ALLM was administered at a dosage of 1.0 mg-kg-l-d1 in the calpain inhibitor group. Three weeks later, the proteolysis, protein expression of TnT and myosin, calpain I localization and expression and structural changes were examined in left atrial free walls, right atrial free walls and the interatrial septum respectively. Atrial size and contractile function were also measured by echocardiography. Results Long-term rapid atrial pacing induced marked structural changes such as enlarged atrial volume, myolysis, degradation of TnT and myosin, accumulation of glycogen and changes in mitochondrial shape and size, which were paralleled by an increase in calpain activity. The positive correlation between calpain activity and the degree of myolysis （rs=0.90 961, P〈0.0001） was demonstrated. In addition to structural abnormalities, pacing-induced atrial contractile dysfunction was observed in this study. The pacing-induced atrial structural alterations and loss of contractility were partially prevented by the calpain inhibitor ALLM. Conclusions Activation of calpain represents key features in the progression towards overt structural remodeling. Calpain inhibitor, ALLM, suppressed the increased calpain activity and reversed structural remodeling caused by sustained atrial fibrillation in the present model. Calpain inhibition may therefore provide a possibility for therapeutic intervention in AE     

两种不同起搏模型心房颤动发生机制的比较

目的对比心房快速起搏（ATP）与心室快速起搏（VTP）诱发心房颤动（AF）起搏模型的电重构和结构重构,探讨其（特别是VTP模型）导致的充血性心力衰竭（CHF）与AF发生维持的关系.方法选择健康成年杂种犬21只,随机分为对照组、ATP组和VTP组.采用Burst刺激诱发AF,心房有效不应期（ERP）采用S1S2法,超声心动图测定左右心房收缩末期面积,Mallory三色法染色并测定纤维化百分比.结果VTP组的左室射血分数显著降低;ATP组与VTP组AF诱发率、持续性AF诱发率均明显增加,AF持续时间明显延长,ATP组ERP显著缩短且频率自适应性几乎消失,AF持续时间与ERP呈密切负相关.VTP组与对照组ERP及其频率自适应性无明显变化,但VTP组左右心房明显扩大,纤维化程度显著增高,AF持续时间和左心房收缩面积及左心房纤维化程度呈密切正相关.结论ATP模型的AF发生、维持主要与电重构有关,VTP模型导致CHF时AF发生、维持的重要因素可能是心房扩大及心房纤维化等结构性重构.     

Effects of Losartan on acute atrial electrical remodeling

Background Atrial electrical remodeling (AER) contributes to the maintainance of atrial fibrillation (AF). This study was to compare the effects of Losartan with those of Diltiazem on tachycardia-induced acute AER in rabbits.Methods Twenty-one rabbits paced with maximal atrial capture rate for 3 hours in the right atrium (RA) were randomly divided into saline group, Diltiazem group and Losartan group. After autonomic blockage, we measured atrial effective refractory period (AERP), AERP rate adapting feature, AERP dispersion and RA conduction time at basic cycle lengths (BCLs) of 200 ms and 150 ms at baseline, 0.5 hour, 1 hour, 2 and 3 hours after rapid atrial pacing. Results In the saline group, there was a prompt decrease in AERP as a result of rapid atrial pacing, and AERP200 and AERP150 were shortened sharply within 0.5 hour of pacing （30.2±10.5 ms and 24.1±9.1 ms, respectively）. The AERP did not change dramatically in the Diltiazem and Losartan groups. In the saline group, the value of （AERP200-AERP150）/50 ms in high RA was 0.17±0.08 at baseline and became significantly smaller at 0.5 hour (0.08±0.06), 1 hour (0.09±0.06), 2 hours (0.08±0.04) and 3 hours (0.09±0.05) (all P&lt;0.05), suggesting a reduction of rate adaptation of AERP. The value of （AERP200-AERP150）/50 ms in high RA did not change during the 3 hours of pacing in both Diltiazem and Losartan groups. In the saline group, AERP dispersion increased significantly at 2 and 3 hours (P&lt;0.05). However, Diltiazem could not prevent the increase of AERP dispersion at 3 hours (P&lt;0.05). During Losartan infusion, the AERP dispersion was no longer increased after rapid atrial pacing. There was no significant difference in RA conduction time among the three groups.Conclusion Like calcium antagonist Diltiazem, Losartan could prevent AERP shortening and preserve rate adaptation of AERP after rapid atrial pacing. Losartan is more effective than Diltiazem in inhibiting the increase of AERP dispersion.     

心脏CT左房参数在预测房颤患者卒中发生中的价值

目的：应用心脏CT评估房颤患者左心房、左心耳结构以及功能状况,探讨其与房颤患者卒中发生的关系。方法：回顾性分析221例房颤患者心脏CT资料,根据病程中患者有无发生卒中分成卒中组和非卒中组。以图像后处理软件测量左心房和左心耳最大、最小容积,计算左心房及心耳的射血分数。根据心耳形态将其分成鸡翅型和非鸡翅型,并观察心耳内是否存在血栓或血栓前状态。对左房各项参数进行单因素及多因素统计学分析。结果：221例中47例发生了卒中事件。卒中组患者的左心房最大容积、最小容积均较非卒中组增大（P < 0.05）,卒中组左心房射血分数较非卒中组下降（P < 0.05）。卒中组左心耳非鸡翅型的比例更高（P=0.006）;卒中组左房内存在血栓或血栓前状态的比例高于非卒中组（P=0.01）。左心房容积、左心耳分叶结构及左心耳血流动力学状态是房颤患者卒中发生的独立危险因素。结论：心脏CT获得的左房参数对房颤患者卒中发生具有一定预测价值。