与Cibenzoline转复山羊持续性心房颤动相关的电生理现象分析

目的 :在持续性心房颤动 （房颤 ）山羊模型上 ,分析 类抗心律失常药 Cibenzoline使房颤转复为窦性心律时出现的电生理现象 ,探讨房颤转复的机制。方法 :给 7只山羊的左心房游离壁、左心耳、Bachmann氏束 （ BB）、右心耳及右心房游离壁缝合心外膜电极。用自动房颤刺激器维持房颤 ,待房颤持续 4周后 ,静脉滴注 Cibenzoline（ 0 .1mg·kg-1· min-1 ） ,直至房颤终止。分析房颤转复前单极电图的形态特点、房颤周长 （ AFCL）的变化 ,并通过测量房颤周长的标准差 （ AFCLSD） ,分析心房激动均一性变化。结果 :在房颤转复前最后 2次心搏的平均 AFCL有跳跃性延长（ P<0 .0 5 ） ,正常电位的百分率显著增加 （ P<0 .0 5 ）。房颤转复前最后 1个 AFCLSD在除 BB外的心房各部位内明显缩小 （ P<0 .0 5 ） ,在整个心房内的变化不显著。结论 :在房颤转复前的最后 2次激动 ,房颤波激动的规律性明显增加 ,支持 类抗心律失常药通过延长心房可兴奋间期而起作用的学说     

Ic类抗心律失常药Cibenzoline 转复山羊持续性心房颤动过程中心房异常电位的变化

目的 :在山羊持续性心房颤动 (房颤 )模型上分析Ic类抗心律失常药cibenzoline对心外膜单极心房电图形态的影响。　　　方法 :在 7只山羊的心房外膜分别缝合 83个电极。用自动房颤刺激器维持房颤 ,待持续性房颤持续 4周后 ,静脉滴注cibenzoline[0 1mg/ (kg·min) ] ,直至房颤终止。记录用药后房颤周长 (AFCL)的变化 ,分析AFCL分别延长 2 0、40、60、80ms和房颤转复前各 16s的间期内 ,心房各部位异常电位的百分率和左心房传导速度的变化。结果 :在静脉滴注cibenzoline后 ,平均AFCL逐渐延长 ,心房传导速度逐渐下降 ,异常电位的百分率逐渐减少 ,与静脉滴注前比均有显著性差异 (P均 <0 0 5 )。结论 :Ic类抗心律失常药cibenzoline延长AFCL ,减慢房颤波的传导速度 ,减少房颤时异常电位的比例。提示该抗心律失常药物可能增加房颤的可兴奋间期从而使房颤转复为窦性心律。     

山羊心房颤动进展过程中心房电图形态的演变

目的利用山羊模型研究心房颤动(简称房颤)在由阵发性向持续性转变过程中,心房/肺静脉外膜电图形态的演变。方法在山羊的左房(LA)游离壁外膜和左上肺静脉(LSPV)根部缝合电极片,利用自制的房颤刺激器于体外发放50Hz的刺激,刺激左房,刺激时程1s,每次间隔2s,诱发出自发维持时间超过24h的持续性房颤。将心房/肺静脉外膜电图形态分为单电位(SP)、双电位(DP)和碎裂电位(FP)。分析在基础状态下和房颤维持不同时间时各电位在所有激动中所占比例和动态变化。结果在窦性心律时LA和LSPV全为SP,随着房颤持续时间的延长,两部位的SP比例逐渐减少,DP和FP的比例逐渐增加。房颤刚开始和持续24h后SP的比例在LA分别为94.2%±5.0%和68.4%±6.0%(P<0.01),在LSPV则分别为74.2%±3.3%和40.1%±7.3%(P<0.01)。在房颤自发持续24h后,LA各种形态的电位交替出现,而LSPV可见连续的反复快速激动。结论心房和肺静脉外膜电图的碎裂程度增加,以及肺静脉出现连续的反复快速激动与房颤的持续有关。     

心房颤动时山羊肺静脉反复快速激动形成原因的研究

目的利用心房颤动(房颤)山羊模型探讨肺静脉局部反复快速激动(repetitiverapidac-tivations,RRA)的产生机理。方法在8只山羊的左心房(LA)游离壁外膜和左上肺静脉(LSPV)根部缝合电极片,利用自制的房颤刺激器于体外发放50Hz的冲动刺激左心房,刺激时限1s,每次间隔2s,在(9.3±4.6)d(6~16d)内诱发出自发维持时间超过24h的持续性房颤。分析窦性心律下以及左心房起搏时肺静脉电位(PVP)的特点以及房颤持续过程中RRA的变化。结果在窦性心律时PVP不明显,左心房刺激可显示出PVP,随着基础刺激周长的缩短,LA-PVP的间距加大,PVP间出现分裂,并可诱发房颤。房颤刚发作时的肺静脉电图形态,与心房快速刺激时一致。在房颤刚被诱发时,肺静脉就可出现短暂的局部的RRA,但在房颤时限中所占的比例很低,为3.3%±4.0%。随着刺激时间/房颤持续时间的延长,RRA的比例逐渐增加;在房颤持续24h后,肺静脉RRA的持续时间占总激动时间的91.8%±6.7%(P<0.05)。结论在本模型肺静脉RRA的产生与其复杂的组织结构有关,而与局部自律性增高和触发激动无关。房颤逐渐稳定过程中,RRA的比例增加与心房/肺静脉的电重构进展有关。     

心房可兴奋间期对山羊心房颤动稳定性的影响

目的研究山羊心房可兴奋间期(EP)在心房颤动(房颤)稳定过程中的作用。方法在10只山羊的左心房游离壁外膜缝合电极片,利用自制的房颤刺激器于体外发放50HZ的刺激1S,每次间隔2S,诱发维持时间超过24H的持续性房颤。定期终止刺激,记录房颤自发持续时间,计算平均房颤波周长(AFCL),并在房颤持续过程中利用感知房颤波发放刺激夺获心房的方法测量房颤时心房有效不应期(ERPAF),计算EP(EP=AFCL-ERPAF)。结果8只山羊完成实验,均在6~16(9·3±4·6)D内诱发出持续超过24H的持续性房颤。在房颤自发维持达3~10MIN和24H时的AFCL分别为98·3MS±11·0MS与84·9MS±5·2MS,P<0·05;ERPAF分别为90·5MS±13·2MS与63·0MS±4·8MS,P<0·05;EP分别为7·8MS±2·4MS与21·9MS±3·5MS,P<0·05。结论心房ERPAF的缩短大于AFCL的缩短,使得EP持续性增宽,可能在房颤的稳定过程中起重要作用。     

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。     

风湿性心脏病心房颤动患者心房细胞外信号调节蛋白与纤维化的关系

探讨风湿性心脏病 (简称风心病 )心房颤动 (简称房颤 )患者心房组织细胞外信号调节激酶 (ERK)与心房纤维化的关系。 33例风心病二尖瓣病变患者行心脏外科手术时取右心耳组织。通过逆转录 聚合酶链反应和免疫组织化学技术 ,测量ERK2 mRNA和激活的ERK2 蛋白相对表达量 ,测定心房组织血管紧张素Ⅱ (AngⅡ )含量和胶原纤维容积分数 (CVF)。结果 :阵发性和慢性房颤患者的心房组织CVF、AngⅡ均明显高于窦性心律患者 (10 .4 4 %±1.83% ,15 .0 1%± 2 .30 %vs 7.4 8%± 1.2 6 % ;10 .17± 1.73,12 .13± 1.95vs 6 .6 9± 1.18ng/mg,P均 <0 .0 1) ,而慢性房颤患者的CVF、AngⅡ又明显高于阵发性房颤患者 (P <0 .0 1,P <0 .0 5 ) ;阵发性和慢性房颤患者的心房组织ERK2mRNA表达量显著高于窦性心律患者 (1.2 0 9± 0 .2 85 ,1.30 5± 0 .2 6 3vs 0 .92 3± 0 .2 71;P <0 .0 5 ,P <0 .0 1) ,而阵发性和慢性房颤患者之间无明显差别 (P >0 .0 5 ) ;阵发性和慢性房颤患者的心房间质细胞激活的ERK2 蛋白表达量显著高于窦性心律患者 (0 .2 5 2± 0 .0 75 ,0 .2 88± 0 .0 6 3vs 0 .175± 0 .0 74 ;P均 <0 .0 1) ,而阵发性和慢性房颤患者之间无明显差别 (P >0 .0 5 )。结论 :心房间质ERK途径的激活是风心病房颤患者心房纤维     

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 )     

抗心房颤动起搏器的应用初探

为评价心房程序起搏治疗阵发性心房颤动 (简称房颤 )的有效性 ,1 1例阵发性房颤患者中 1 0例置入Selec tion90 0E(AF2 .0 )型起搏器、1例置入IntegrityTMAFXDR5346型起搏器。对患者进行术前 1个月和术后 1 ,2个月阵发性房颤事件和SF 36生活质量调查。结果 :患者术后 1 ,2个月较术前 1个月在有症状阵发性房颤事件数和生活质量评分有明显降低 (1 3 .0 1± 8.51 ,9.81± 5 .91vs 2 7.0 0± 1 3 .2 1 ;62 .82± 2 1 .57,55 .73± 1 8.48vs 1 1 0 .0 0± 1 6 .57,P值均<0 .0 5) ,术后 2个月较术后 1个月有症状阵发性房颤事件数 (9.81± 5 .91vs 1 3 .0 1± 8.51 )、阵发性房颤总数 (2 1 0 .0 0± 2 69.59vs 30 9.82± 41 8.1 4 )、房颤总持续时间 (6 .0 0± 4 .1 4dvs 7.87± 4 .2 6d)、房颤负荷 (2 0 .0 1 %± 1 3 .80 %vs 2 6 .2 4 %± 1 4 .2 0 % )及生活质量评分 (55 .73± 1 8.48vs 62 .82± 2 1 .57)均降低 (P值均 <0 .0 5)。结论 :心房程序起搏能够减少阵发性房颤事件的发生 ,降低房颤负荷 ,有望成为阵发性房颤药物治疗的重要辅助手段     

干预犬左心房峡部对心房颤动诱发率的影响及其机制研究

阐明干预左心房峡部对犬心房颤动 (简称房颤 )诱发率的影响及其与电学隔离Marshall韧带的关系。左心房峡部干预指经开胸手术自左下肺静脉下缘中点沿垂直于冠状静脉窦方向切割至冠状静脉窦上缘 ,切割后缝合关闭切口。共对 19只犬经心外膜途径对Marshall韧带进行标测和对左心房峡部干预。根据干预左心房峡部后Mar shall韧带电位是否消失分为A组 (Marshall韧带电位消失 ,n =12 )和B组 (Marshall韧带电位不消失 ,n =7)。A组干预后房颤诱发率明显降低 (16 .7%vs 83.3% ,P <0 .0 5 ) ;B组干预后房颤诱发率无明显变化 (77.4 %vs 85 .7% ,P >0 .0 5 )。干预左心房峡部后A组房颤诱发率显著低于B组 (16 .7%vs 77.4 % ,P <0 .0 5 )。干预左心房峡部前后左心房峡部传导时间A组 (98.33± 3.2 0msvs 97.5 8± 2 .81ms ,P >0 .0 5 )和B组 (96 .14± 2 .6 1msvs 97.4 2± 3.10ms,P >0 .0 5 )均无明显变化。结论 :干预犬左心房峡部可降低房颤诱发率 ,其机制可能是因电学隔离了Mar shall韧带。     

慢性快速心房起搏心房颤动犬内皮型一氧化氮合酶mRNA表达变化的研究

为研究慢性快速心房起搏心房颤动(简称房颤)犬模型中心内膜内皮型一氧化氮合酶(eNOS)mRNA表达的变化,探讨其与心房结构重构、血栓形成的关系。13只健康犬随机分为假手术组和起搏组,应用埋藏式高频率心脏起搏器快速起搏心房(400次 /分) 6周,取左、右心房,左、右心耳及主动脉内膜。通过逆转录 聚合酶链反应 (RT PCR),以β actin为内参照,测定犬心内膜eNOSmRNA表达的变化,同时检测血浆NO代谢产物硝酸盐 (NOx)的含量。结果:正常犬心脏eNOSmRNA表达存在差异,左房、左心耳明显高于右房、右心耳;起搏 6周后左房、左心耳eNOSmRNA表达起搏组明显低于假手术组,而右房、右心耳、主动脉无明显差别,血浆NOx起搏组亦明显低于假手术组。结论:正常犬心脏eNOS基因表达是不平衡的,左房明显高于右房。房颤犬eNOSmRNA表达降低可能是心房结构重构,血栓形成的重要因素之一。     

Differential densities of muscarinic acetylcholine receptor and I(K,ACh) in canine supraventricular tissues and the effect of amiodarone on cholinergic atrial fibrillation and I(K,ACh)

BACKGROUND: Vagal nerve plays an important role in the induction and maintenance of atrial fibrillation (AF). This study investigated the differential densities of M2 receptor and acetylcholine-induced inward rectifier K+ current (I(K,ACh)) in atrial appendage, atrium, pulmonary vein (PV) and super vena cava (SVC) to discuss the role of atrial appendage and PV in cholinergic AF. METHODS AND RESULTS: In 10 dogs, action potential duration was determined at 24 sites during bilateral cervical vagal stimulation and amiodarone administration. AF could be induced at first in right atrial appendage (RAA) and right atrium (RA) without left atrial appendage (LAA) and left atrium (LA). Amiodarone decreased the initiation of AF in vivo. Western blot and patch clamp were used to determine M2 receptor and I(K,ACh) in RAA, LAA, RA, LA, PV and SVC. The densities of M2 receptor and I(K,ACh) in LAA, RAA and LA were higher than that in RA, PV and SVC (21.34 +/- 0.92 vs. 8.24 +/- 0.45 pA/pF, p < 0.05). Furthermore, the densities of the M2 receptor and I(K,ACh) in LAA and RAA were higher than that in LA (21.34 +/- 0.92 vs. 14.17 +/- 0.65 pA/pF, p < 0.05). After amiodarone administration, densities of I(K,ACh) in LA and RA were not different, but densities of I(K,ACh )were also less in atrium than in atrial appendage. CONCLUSIONS: Densities of the M2 receptor and I(K,ACh) are higher in atrial appendage than other sites. Atrial appendage perhaps plays an important role in initiation of cholinergic AF. However, PV and SVC less often play an important role in vagotonic paroxysmal AF. Reduced dispersion of I(K,ACh) is the mechanism for amiodarone to therapy AF.     

迷走神经刺激和乙酰胆碱灌注对心房肌电生理特性的影响

研究在体情况下迷走神经刺激(VNS)和乙酰胆碱(Ach)灌注对心房肌不同部位的电生理影响,并探讨其诱发心房颤动(AF)的机制。10只杂种犬自身随机对照,运用单相动作电位(MAP)记录技术,同步记录10只开胸犬的右心耳(RAA)、高位右房(HRA)、低位右房(LRA)、左心耳(LAA)、高位左房(HLA)、低位左房(LLA)的MAP,分别给予切断迷走神经、VNS、Ach灌注(分别做为对照组、VNS刺激组、Ach灌注组)后,观察诱发AF的情况和动作电位时程APD50、APD90和APD离散(dAPD)的变化。结果:10只犬在VNS刺激和Ach灌注同时,右心耳单一刺激分别有7只和6只犬诱发AF;VNS明显缩短APD50、APD90,其中RAA缩短最明显(APD50从72±5ms到19±4ms,APD90从136±7ms到43±5ms,P<0.001);Ach灌注也明显缩短APD50和APD90,与VNS相比,LLA的APD90缩短更明显(47±6msvs62±8ms,P<0.01);VNS明显升高心房肌APD50和APD90的离散(17±5msvs7±3ms,25±7msvs8±5ms,P<0.01)。结论:VNS和Ach灌注可引起APD缩短和离散升高,但影响的部位和程度稍有差异,都易诱发AF。     

Atrial Fibrillatory Wall Motion and Degree of Atrial Remodeling in Patients with Atrial Fibrillation: A Tissue Velocity Imaging Study

Introduction: The atrial fibrillation cycle length (AFCL) and the intracardiac atrial electrogram morphology may be used to characterize atrial fibrillation (AF). However, assessment of these parameters requires an invasive electrophysiological study. We assessed clinical and electrophysiological correlates of noninvasive tissue velocity imaging (TVI) of the right and left atrial myocardial fibrillatory wall motion. Methods and Results: We performed an electrophysiological study in 12 patients with AF referred for His bundle ablation. Using atrial electrograms, we determined the AFCL (AFCL‐egm) and electrophysiological AF type. Simultaneously, transthoracic echocardiography was performed. We used the TVI traces to determine the cycle length of the atrial fibrillatory wall motion (AFCL‐tvi) and atrial fibrillatory wall velocities (AFV‐tvi). AFCL‐tvi matched very well with AFCL‐egm (r²= 0.98; P < 0.001), both in the left and right atrium. Patients with permanent AF had shorter AFCL‐tvi (155 ± 15 ms vs 216 ± 23 ms; P < 0.001), higher AFCL‐tvi variability, and lower AFV‐tvi compared to patients with paroxysmal AF. Three electrophysiological AF types were found based on the morphology of the electrograms and these related to specific TVI patterns. Conclusion: TVI of the atrial fibrillatory wall motion may enhance noninvasive characterization of atrial remodeling in patients with atrial fibrillation.     

High-density activation mapping of fractionated electrograms in the atria of patients with paroxysmal atrial fibrillation

BACKGROUND: Areas of complex fractionated atrial electrograms (CFAEs) have been implicated in the atrial substrate of atrial fibrillation (AF). The mechanisms underlying CFAE in humans are not well investigated. OBJECTIVES: The purpose of this study was to investigate the regional activation pattern associated with CFAE using a high-density contact mapping catheter. METHODS: Twenty patients with paroxysmal AF were mapped using a high-density multielectrode catheter. CFAE were mapped at 10 different sites (left atrium [LA]: inferior, posterior, roof, septum, anterior, lateral; right atrium [RA]: anterior, lateral, posterior, septum). Local atrial fibrillation cycle length (AFCL) was measured immediately before and after the occurrence of CFAE, and the longest electrogram duration (CFAEmax) was assessed. RESULTS: Longer electrogram durations were recorded in the LA compared with the RA (CFAEmax 118 +/- 21 ms vs 104 +/- 23 ms, P = .001). AFCL significantly shortened before the occurrence of CFAEmax compared with baseline (LA: 174 +/- 32 ms vs 186 +/- 32 ms, P = .0001; RA: 177 +/- 31 ms vs 188 +/- 31 ms, P = .0001) and returned to baseline afterwards. AFCL shortened by >or=10 ms in 91% of mapped sites. Two different local activation patterns were associated with occurrence of CFAEmax: a nearly simultaneous activation in all spines in 84% indicating passive activation, and a nonsimultaneous activation sequence suggesting local complex activation or reentry. CONCLUSION: Fractionated atrial electrograms during AF demonstrate dynamic changes that are dependent on regional AFCL. Shortening of AFCL precedes the development of CFAE; thus, cycle length is a major determinant of fractionation during AF. High-density mapping in AF may help to differentiate passive activation of CFAE from CFAE associated with an active component of the AF process.     

Electroanatomic remodeling of the left atrium in patients undergoing repeat pulmonary vein ablation: mechanistic insights and implications for ablation

Introduction: There is limited information describing late changes in the electroanatomic characteristics of the left atrium (LA) associated with recurrence after an anatomical circumferential pulmonary vein ablation (CPVA) for atrial fibrillation (AF).
Methods and Results: Forty-seven patients (57 ± 8 years) undergoing a repeat ablation after CPVA were included. Using an electroanatomic mapping system, we measured the bipolar voltage by averaging points in the pulmonary vein (PV)-LA junction and four other LA sites. Conduction velocity and AF cycle length (AFCL) were also measured and the results are compared with the first procedure. After an initial decrease observed at the end of the first procedure, voltage and conduction velocity returned to intermediate values in all LA sites, with lower voltage at the LIPV antrum (P = 0.004), and lower conduction velocity across the LIPV and RSPV (P < 0.001). Conduction gaps were more prevalent at the septal aspect of the right PV encircling lines (85%), between the left atrial appendage (LAA) and the LSPV (70%) and lines at the posterior wall (71%). There was a nonsignificant increase in AFCL, with a more widespread distribution of organized electrograms (32.4% vs 46.6%).
Conclusion: Recurrence after CPVA is associated with a reverse process of voltage and conduction velocity increase across ablated areas, especially the PV-LA junction, and is related to the presence of conduction gaps, which are distributed mostly at the septal aspect of the lines encircling the right PVs and at the LAA-LSPV area. Organization of atrial electrograms seen during AF ablation is maintained at a repeat procedure.     

犬Marshall韧带的电生理特征实验研究

目的 评估不同电生理刺激方案对犬Marshall电位的影响.方法 成年杂种犬15只暴露Marshall韧带,Lasso电极导管置于韧带上方记录Marshall电位.分别于左心耳、右心耳处予以电生理刺激.记录Marshall电位及心房-Marshall电位间期(AM间期).随机选择10只犬组织学检查明确Marshall韧带肌束(Marshall束)与心房间解剖连接(组1为无连接,组2为有连接).余5只犬酒精消融Marshall韧带(组3).结果 组1共6只犬,1只犬窦性心律下未记录到Marshall电位,但在左心耳刺激时Marshall电位从左心房电位中分离出来.5只犬窦性心律下记录到Marshall电位,左心耳刺激时AM间期延长(＞20 ms)[(125±9)ms vs(80 ±6)ms,P=0.043,左心耳刺激=350 ms;(126±9)ms vs(80±6)ms,P=0.044,左心耳刺激=450 ms].组2共4只犬,2只犬窦性心律下未记录到Marshall电位,左心耳刺激时可见Marshall电位从左心房电位中分离出来.2只犬窦性心律下记录到Marshall电位,左心耳刺激时AM间期可延长,但亦可缩短.组3犬窦性心律或左心耳刺激下记录到Marshall电位,酒精消融Marshall韧带后,Marshall电位消失.结论 与窦性心律比较,左心耳刺激时,Marshall电位呈现多种形式,包括AM间期延长.后者对Marshall韧带消融有益.     

普罗帕酮转复山羊持续性心房颤动过程中左上肺静脉和左房外膜电图的变化

目的研究普罗帕酮转复心房颤动(简称房颤)时左上肺静脉(LSPV)和左房(LA)外膜电图的变化,分析普罗帕酮转复房颤的可能机制。方法在6只山羊的LA前壁及LSPV根部外膜缝合电极片,LA快速刺激诱发房颤,在房颤自发维持超过24h后,静脉滴注普罗帕酮直至房颤终止。分析用药前、后房颤波周长(AFCL)分别延长40,80ms和房颤转复前各16s的间期内,LSPV和LA外膜电图的变化规律。结果6只山羊在经过静脉滴注普罗帕酮后,全部转复为窦性心律。用药前的LSPV的AFCL显著短于LA(P<0.05);用药后LSPV和LA的AFCL都出现逐渐延长,在房颤转复前两者趋于一致。用药前LSPV双电位和碎裂电位的百分比显著高于LA,单电位比例显著低于LA(P<0.05);用药后,LA和LSPV单电位百分比逐渐增加,双电位和碎裂电位逐渐减少,但在LA双电位和碎裂电位的比例始终小于LSPV(P<0.05);在房颤终止前LA先于LSPV出现双电位和碎裂电位的显著减少或消失,当LSPV的双电位和碎裂电位消失后房颤才终止。结论在本模型中,普罗帕酮对左房、肺静脉电生理的影响在房颤的转复过程中起着重要的作用。