心脏脂肪垫在肺静脉引发房颤中的作用

目的探讨窦房结-心房脂肪垫(SAFP)在右上肺静脉灶性放电引发阵发性房颤(PAF)中的作用。方法12条新疆家养犬,苯巴比妥钠麻醉,经右侧开胸暴露右侧肺静脉。将1根8极标测电极导管固定在右上肺静脉,给予S1S1600bpm起搏刺激,另将1根8极(1.5×1.5cm)电极板固定在心外膜窦房结-心房脂肪垫上。术中监测II和aVR导联、血压和体温。以1～4V电压、1000bpm频率刺激窦房结-心房脂肪垫30～60s。结果12条家养犬在给予S1S11000ppm窦房结-心房脂肪垫刺激,随着电压从1增加到4V,心率从142±20bpm减少到75±30bpm(p<0.05),同时出现房性早搏、房性心动过速(房速)和房颤,同时予以右上肺静脉S1S1600ppm刺激,诱发房颤的房性早搏数随着刺激电压1～4V的增加从7个减少到2个,并以S1S1300ms,S1S2稍长于右上肺静脉不应期的早搏右上肺静脉刺激。S1S1600ppm刺激下房颤诱发率从基础状态的49.86%提高到70.59%,S1S2早搏刺激下从3.78%提高到16.6%(p<0.05)。7条狗在4%利多卡因4ml注射到窦房结-心房脂肪垫局部阻滞神经后,6条狗在同样右上肺静脉刺激诱发房颤电压的条件下不能诱发房颤,其中3条狗在电压增加大于9V时诱发房颤。房颤诱发的有效刺激部位在窦房结-心房脂肪垫2～3mm的范围内。结论有效部位窦房结-心房脂肪垫刺激,能够诱发慢频率依赖性阵发性房颤,刺激窦房结-心房脂肪垫增加右上肺静脉阵发性房颤的诱发率,局部神经阻滞降低或消除阵发性房颤的诱发.提示:增强窦房结-心房脂肪垫的自发神经放电,可能是临床右上肺静脉灶性放电转变成房颤的基础,消融窦房结-心房脂肪垫可能预防阵发性房颤的诱发。     

心脏血管内迷走神经丛刺激与阵发性心房颤动的动物模型制作

探讨心脏血管内迷走神经丛刺激与阵发性心房颤动 (简称房颤 )的动物模型制作。 32条Mongrel狗活体心脏大血管 :冠状窦、左右肺动脉、左房、上下腔静脉等处插入 7F蓝状电极进行迷走神经丛刺激 ,刺激频率为 2 0Hz,刺激间期 0 .1ms,刺激电压 1～ 4 0V ,刺激时间 30～ 5 0s。为了避免神经丛刺激直接对心房的影响 ,于刺激迷走神经丛的同时在P波后发放 2 0 0Hz、2 0～ 5 0ms的PS2 心房高频刺激 ,使迷走神经刺激落入心房的不应期。在这些心脏血管迷走神经丛刺激时减慢窦性心律 ,且减慢速度呈电压依赖。在一定的刺激强度下 ,窦性心律能够达到最大减低 (从75 0± 10 2ms至 15 6 0± 2 30ms) ,心房肌不应期显著缩短 (从 175± 13ms缩至 96± 2 3ms) ,同时出现房性早搏、房性心动过速和房颤 ,且重复性很好。应用 β 阻断剂 (esmolol1mg/kg)时 ,提高了房颤诱发域值 ;迷走神经阻断剂 (atropine1～ 2mg/kg)可以完全阻断房颤的诱发。结论 :蓝状电极非常有利于快速在静脉血管腔内找到迷走神经丛刺激位点 ;心脏大血管处存在迷走神经丛 ,刺激这些神经丛能够复制出与临床灶性阵发性房颤非常类同的房颤 ,迷走神经阻断剂可阻断这类房颤的诱发。     

射频消融心外膜脂肪垫治疗犬肺静脉左房交界处起源的心房颤动

目的探讨射频消融心外膜脂肪垫对左房-肺静脉交界触发的局灶性心房颤动(简称房颤)治疗的有效性。方法成年杂种犬10只,心外膜脂肪垫注射氯化乙酰胆碱(Ach)+左房短阵快速电刺激诱发犬左房-肺静脉交界触发的局灶性房颤模型。4极电极分别缝置于左房、右房、左肺静脉与左房交界处,记录最快激动部位。直视下射频消融心外膜脂肪垫。于房颤模型建立前后,及消融脂肪垫后测量左、右房有效不应期(ERP),肺静脉-左房交界处ERP、计算房颤诱发率。术毕处死实验犬行组织学检查。结果所有犬均能通过脂肪垫注射氯化Ach+左房短阵快速电刺激诱发出左房-肺静脉交界触发的局灶性房颤,建模后左房、右房、肺静脉-左房交界处的ERP均较建模前显著缩短(分别为94±33 ms vs 139±9 ms,104±17 ms vs 137±9 ms,104±17 ms vs 137±9 ms;P均<0.01)。脂肪垫消融后房颤诱发率与消融前比较显著降低(45%±16%vs 86%±4%,P均<0.01);左房、右房ERP无变化,肺静脉-左房交界处不应期显著延长(137±8 ms vs 104±17 ms,P<0.01)。组织学未发现除脂肪垫外的其它消融损伤灶。结论射频消融心外膜脂肪垫对肺静脉-左房交界触发的局灶性房颤治疗有效。     

消融犬右肺静脉脂肪垫对心房及右上肺静脉电生理特性及房颤诱发的影响

目的探讨消融右肺静脉脂肪垫对心房及右上肺静脉电生理特性及房颤诱发的影响。方法犬18只分别在颈部迷走神经未刺激和刺激的情况下,观察射频消融肺静脉脂肪垫前后心房不同部位及右上肺静脉有效不应期、房颤诱发率及房颤诱发窗口的变化。结果在刺激迷走神经的情况下,与消融前相比,消融后高位右心房有效不应期延长（P<0.05）,其余部位有效不应期无显著差异,消融后高位右心房房颤诱发率降低（P<0.01）,房颤诱发窗口变窄（P<0.05）,左心房（P<0.01）及右上肺静脉（P<0.01）房颤诱发率升高,诱发窗口增宽。同时,心房有效不应期离散度增加（P<0.01）。结论消融右肺静脉脂肪垫使高位右心房房颤诱发率降低及房颤诱发窗口变窄,却使左房、右上肺静脉房颤诱发率升高及房颤诱发窗口增宽。     

去自主神经条件下迷走神经对肺静脉不同部位房颤诱发阈值的影响

目的研究去自主神经条件下迷走神经对肺静脉不同部位房颤诱发阈值的影响。方法于2004年10月至2005年5月对北京大学人民医院心脏电生理室的10只健康杂种犬进行了电生理实验。所有动物均经切断双侧颈迷走神经干和破坏颈交感神经节，建立犬的去自主神经模型。分别在右心耳（RAA）、左心耳（LAA）、左房（LA）和四支肺静脉的近、中、远段行burst刺激，刺激周长S1S1为80ms，脉宽为0．5ms。在仅改变电压刺激强度的情况下，观察迷走神经对肺静脉不同部位房颤诱发阈值的影响。结果当行双侧颈迷走神经刺激时，在心房及肺静脉的所有部位，房颤诱发阈值均有不同程度的下降，且在4支肺静脉的远段表现为差异有显著性（P〈0．05和P〈0．01），而阿托品则可消除这种变化。结论对于肺静脉起源的房颤，迷走神经不仅参与房颤的维持，而且也可能是参与其起始的重要诱发因素。     

去自主神经条件下迷走神经对肺静脉不同部位房颤诱发阈值的影响

目的研究去自主神经条件下迷走神经对肺静脉不同部位房颤诱发阈值的影响。方法于2004年10月至2005年5月对北京大学人民医院心脏电生理室的10只健康杂种犬进行了电生理实验。所有动物均经切断双侧颈迷走神经干和破坏颈交感神经节,建立犬的去自主神经模型。分别在右心耳(RAA)、左心耳(LAA)、左房(LA)和四支肺静脉的近、中、远段行burst刺激,刺激周长S1S1为80ms,脉宽为0.5ms,在仅改变电压刺激强度的情况下,观察迷走神经对肺静脉不同部位房颤诱发阈值的影响。结果当行双侧颈迷走神经刺激时,在心房及肺静脉的所有部位,房颤诱发阈值均有不同程度的下降,且在4支肺静脉的远段表现为差异有显著性(P<0.05和P<0.01),而阿托品则可消除这种变化。结论对于肺静脉起源的房颤,迷走神经不仅参与房颤的维持,而且也可能是参与其起始的重要诱发因素。     

窦房结脂肪垫对犬右上肺静脉电生理特性影响的研究

目的研究不同水平刺激窦房结脂肪垫(SANFP)对右房(RA)及右上肺静脉(RSPV)的有效不应期(ERP)及心房颤动(简称房颤)诱发率的影响,探讨SANFP对房颤发生维持的作用。方法6只犬麻醉后经右侧开胸暴露RSPV及SANFP,以0.6～2,5,8mV三种不同电压强度水平、60ms频率刺激SANFP,同时以S1S2刺激观察三种水平下RA游离壁远、中、近端及RSPV远、中、近端ERP的变化;同样方法刺激SANFP以S1S1和S1S2程序刺激诱发房颤,测定房颤的诱发率。结果以5mV电压刺激窦房结脂肪垫RSPV近端ERP较基础时明显缩短(90±24msvs109±16ms,P<0.05),其房颤诱发率50%;以5,8mV电压刺激SANFP时RA游离壁近端、中端ERP变化较基础时明显缩短(96±20msvs117±14ms,65±20msvs117±14ms,P均<0.05),其房颤诱发率100%。结论窦房结脂肪垫可能在肺静脉起源的房颤的诱发和维持中起了重要作用。     

序列消融犬窦房结脂肪垫和房室结脂肪垫对迷走神经介导心房颤动诱发的影响

目的 研究旨在探索序列消融窭房结脂肪垫(sinus atrial node fat pad,SANFP)和房室结脂肪垫(atrialventricular node fat pad,AVNFP)对迷走神经介导的心房颤动(房颤)诱发的影响.方法 18只健康成年家犬分为二组,每组9只.A组优先消融SANFP,再联合消融SANFP+ AVNFP;B组优先消融AVNFP,再联合消融SANFP+ AVNFP.高频电刺激左、右侧迷走神经干制作迷走神经介导的房颤模型,测定消融前、后的房颤诱发率及心房和肺静脉不同部位有效不应期(effective refractory period,ERP).结果 (1)迷走神经干刺激可显著增加房颤的诱发率,且右侧迷走神经干刺激下的房颤诱发率高于左侧迷走神经干[(60.0±0.0)％比(18.4±22.1)％].(2)优先消融SANFP可显著降低左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别降低了67.0％和72.0％),联合消融SANFP+ AVNFP可进一步降低2V电压的左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别较消融前降低了100％和95.5％).而优先消融AVNFP也可显著降低2V电压的左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别降低了95.7％和96.3％),但联合消融SANFP+ AVNFP并不进一步显著降低左侧迷走神经干或右侧迷走神经干刺激下的房颤诱发率(分别较消融前降低了98.0％和100％).(3)优先消融SANFP或AVNFP均可显著抑制迷走神经干刺激引起的右房、左房及右上肺静脉部位的ERP缩短效应.与单独消融SANFP相比,联合消融SANFP+AVNFP可进一步抑制迷走神经干刺激引起右房ERP的缩短效应,而联合消融AVNFP+ SANFP对迷 走神经干刺激引起左、右心房及肺静脉ERP的缩短效应的抑制作用与单独消融AVNFP比较差异无统计学意义.结论 心外膜脂肪垫消融可改变迷走神经干刺激对房颤诱发及心房肌、肺静脉ERP的影响,其中AVNFP是迷走神经干支配心房的汇聚点和主控区,因此AVNFP可能是房颤神经消融更有效的靶点.     

外源性与内源性自主神经刺激对心房颤动诱发性的影响

目的探讨心脏外源性与内源性自主神经刺激对心房颤动(房颤)诱发性的影响。方法16只成年犬静脉麻醉后,分离右颈迷走神经干(VST);再行右侧开胸手术,暴露靠近右上肺静脉的心脏脂肪垫(内含心脏自主神经丛,即GP),将1根电极导管固定贴靠于右上肺静脉,使其头端电极贴靠右上肺静脉与左房交界处,进行程序期前刺激,采用2倍、4倍、10倍阈值的刺激强度进行基础程序期前刺激(control),并测量相应的心房不应期(ARP)及房颤诱发窗宽(WOV);再分别加用VST刺激或GP刺激,测量在相应刺激条件下程序期前刺激所获得的ARP及WOV。结果平均基础心率(HR)为153±22次/min,VST刺激下HR为79±44次/min,GP刺激下HR为87±99次/min(后二者比较,P>0·05)。最短的ARP在control状态下为101±20ms、VST刺激下为90±17ms、GP刺激下为91±13ms,VST刺激下及GP刺激下均较control明显缩短(P<0·05),VST刺激下与GP刺激下的差异无统计学意义(P>0·05)。三者的累计WOV分别为control22±34ms、VST刺激下44±45ms、GP刺激下99±75ms,三者间每两者的差异均有统计学意义(P<0·05)。结论在降低心率相近的情况下,电刺激心脏内源性自主神经丛与电刺激心脏外源性自主神经引起的不应期缩短相近,但前者更容易诱发房颤。     

消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动的影响及机制

目的探讨消融犬Marshall韧带对刺激心房左后脂肪垫所致心房颤动(简称房颤)的影响及机制。方法成年杂种犬14条,随机分为实验组8条,对照组6条。实验组首先测量左肺静脉和左心耳的有效不应期,继而刺激心房左后脂肪垫诱发房颤。消融Marshall韧带上段后和下段后重复上述步骤。对照组除不干预Marshall韧带外,其它电刺激方案与实验组相同,同时对该组犬的心脏进行迷走神经染色。结果①实验组消融Marshall韧带后,左肺静脉和左心耳的有效不应期均显著延长(P0.05)。②和消融前比较,实验组消融Marshall韧带上段后的房颤诱发率有下降趋势(70.8%vs87.5%,P0.05);消融Marshall韧带全程后房颤诱发率显著下降(33.3%,P0.001)。对照组三次电刺激所测得的不应期和房颤诱发率无差异。③Marshall韧带与左下肺静脉、心房左后脂肪垫、左心耳之间存在迷走神经的直接联系。结论消融犬Marshall韧带可显著降低刺激心房左后脂肪垫所致房颤的诱发率。     

Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation

OBJECTIVES: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF). BACKGROUND: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown. METHODS: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness. RESULTS: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p /=9.3 V. CONCLUSIONS: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into 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。     

导管射频肺静脉口环状消融治疗局灶性心房颤动(附一例报告)

1例女性患者 ,33岁 ,局灶性心房颤动 (简称房颤 )的起源部位位于右上肺静脉 (RSPV)口。第一次于RSPV内行点状消融短阵房性心动过速的最早兴奋点 (较体表心电图P′波提早 5 7ms) ,即刻成功 ,但术后 3日复发。观察一周后仍有房颤发作而行第二次手术。术中因各种方法都不能诱发短阵房性心动过速与房颤 ,而行RSPV口环状消融。术后随访 3个月房颤未复发 ,患者无任何不适 ,表明手术成功。结论 :导管射频肺静脉口环状消融是相对安全的方法 ,可以提高导管射频治疗起源于肺静脉口局灶性房颤的成功率 ,降低复发率。     

Autonomic mechanism for chronic atrial electrical remodeling induced by rapid atrial pacing in ambulatory danines

Objetives The mechanism for changes in the electrophysiological properties of the atria during rapid pacing induced atrial fibrillation(AF) is not well understood.We aimed to investigate the contribution of intrinsic cardiac autonomic nervous system(ICANS) in chronic atrial electrical remodeling and AF induced by rapid atrial pacing for 4 weeks. Methods Twelve adult mongrel dogs weighing 15 to 20 kg were assigned to two groups;group 1(experimental group,n= 7) and group 2(control group,n =5).All dogs were anesthetized with propofol and mechanically ventilated via endotracheal tubes.The chest was entered via bilateral mini-thoracotomy at the fourth intercostals space.Bipolar pacing electrode was sutured to the right atrial appendage.Four-electrode catheters(Biosense-Webster,Diamond Bar,CA) were secured to allow recording at the right and left atriaum.All tracings from the electrode catheters were amplified and digitally recorded using a computer-based Bard Laboratory System (CR Bard Inc,Billerica,MA).Electrograms were filtered at 50 to 500 Hz.Continuous rapid pacing(600 bpm, 2×threshold[TH]) was performed at the right atrial appendage. Ganglionated Plexi(GP) was localized by applying high frequency stimulation(HFS;20 Hz,0.1ms duration, 0.5 to 4.5 V)with a bipolar stimulation-ablation probe electrode (AtriCure,West Chester,OH).Group1 underwent ablation of bilateral GP and ligament of Marshall followed by 4-week pacing.Group 2 underwent sham operaton without ablation of GP and ligament of Marshall followed by 4-week pacing.The effective refractory period(ERP) and window of vulnerability(WOV) were measured at 2×TH before(baseline) and every week after GP ablation.WOV was defined as the difference between the longest and the shortest coupling interval of the premature stimulus that induced AF.GP consist of the anterior right ganglionated plexi(ARGP) located in the fat pad at the right superior pulmonary vein(RSPV)-atrial junction;the inferior right ganglionated plexi(IRGP) located at the inferior vena cava/right atr     

犬肺静脉急性电重构及其对心房颤动诱发的影响

观察短阵(10min)快速刺激肺静脉对肺静脉有效不应期(PVERP)及经肺静脉诱发心房颤动(简称房颤)的影响。20条成年杂种开胸犬在左上肺静脉根部血管外膜处放置自制环状电极,双极针状刺激电极固定在肺静脉远端血管外表面。测量基础状态下起搏周长(PCL)分别为300,400ms时PVERP。于肺静脉远端以1∶1起搏肺静脉的最快频率刺激肺静脉10min。分别于刺激终止即刻、5min、10min重复测量PVERP。完成以上试验后观察短阵10min快速刺激肺静脉对经肺静脉诱发房颤的影响。采用S1S1快速刺激S1S2程序刺激肺静脉的方法诱发房颤。结果:PVERP及其频率适应性在短阵刺激后即刻,5min时与刺激前相比有显著差异(P<0.05),10min时与刺激前相比无显著差异(P>0.05)。短阵快速刺激后房颤诱发率增加(55%vs20%,P<0.05),房颤持续时间延长(24.6minvs4.1min,P<0.05)。结论:短阵快速刺激肺静脉可以导致肺静脉发生急性电重构,急性电重构后经肺静脉更易诱发房颤且房颤持续时间更长。     

Pulmonary Vein Bigeminy: Electrophysiological Characteristics and Results of Catheter Ablation

Pulmonary vein bigeminy is the pair of a second, late and ectopic pulmonary vein potential following atrial far-field activation and a first passive pulmonary vein potential during sinus rhythm. The aim of this study was to determine the electrophysiological characteristics of pulmonary vein bigeminy and to evaluate its relevance as a trigger for paroxysmal atrial fibrillation. Methods and Results: Pulmonary vein bigeminy was recorded in 8 of 45 patients (18%) who underwent mapping of pulmonary veins for ablation of focal atrial fibrillation. The premature ectopic pulmonary vein potentials were conducted to the atria in 5 patients and were not conducted (concealed bigeminy) in 3 patients. The coupling interval of the ectopic pulmonary vein potential to the preceding atrial signal during sinus rhythm was significantly longer in patients with conducted bigeminy (375 ± 25 ms) than with concealed bigeminy (230 ± 17 ms). The pulmonary vein bigeminy was driven by coronary sinus pacing with the pacing cycle length at lower stimulation rates and was suppressed by overdrive pacing. Coronary sinus pacing led to a separation of the first pulmonary vein potential from the atrial signal but the interval between the atrial signal and the second pulmonary vein potential remained unchanged. Focal ablation at the site of earliest ectopic pulmonary vein activity in 5 patients induced rapid repetitive firing before elimination of the pulmonary vein bigeminy. Ostial disconnection of the arrhythmogenic pulmonary vein in 3 patients was associated with elimination of the pulmonary vein bigeminy. During the follow-up of 9 ± 5 months after ablation of the pulmonary vein bigeminy, 5 of the 8 patients (63%) were free of atrial fibrillation without antiarrhythmic medication. Conclusions: The response of pulmonary vein bigeminy to atrial pacing and ostial ablation suggests that pulmonary vein bigeminy depends on an intact electrophysiological breakthrough between the left atrium and the pulmonary vein. Ablation targeting the pulmonary vein bigeminy is a possible limited approach for this subgroup of patients with paroxysmal atrial fibrillation.     

低通气量犬心房颤动模型的建立

为了对心房颤动（简称房颤）进行电生理检查和治疗的研究，对２８只犬建立低通气量房颤模型。所有犬于麻醉状态下气管插管，以低于所测潮气量１０％～１５％的通气量通气３０ｍｉｎ后，经高位右房远端电极分别给予程序刺激和Ｂｕｒｓｔ刺激诱发房颤。２只犬没能诱发房颤，２６只犬被诱发，持续时间为１ｓ～３４ｍｉｎ，诱发率为９２．８６％（２６／２８）。有４只犬房颤持续在３０ｍｉｎ以上。３只犬只能被程序刺激诱发、９只犬只能被Ｂｕｒｓｔ刺激诱发，其余１４只犬两种刺激方式均可诱发。Ｂｕｒｓｔ刺激时６００ｐｐｍ最易诱发房颤，其次为７００ｐｐｍ，其余频率范围诱发率较低。程序刺激Ｓ１Ｓ２间期诱发范围８８．８２±９．２７（７０～１００）ｍｓ。窦性心律下和房颤持续时的动脉压无明显差异，但房颤时心室率却明显增快（２５９．６±２１．３ｂｐｍｖｓ１８０．７±１８．５ｂｐｍ，Ｐ＜０．０１）。结果表明：低通气量房颤模型的制作方法简便、费用低廉、诱发率高、重复性良好。     

肺静脉在犬持续性心房颤动维持中的作用

目的探讨快速起搏肺静脉建立持续性心房颤动(简称房颤)犬模型的电生理特性以及射频消融隔离肺静脉对其影响。方法选杂种犬15只,以20Hz的固定频率行肺静脉持续起搏,建立持续时间>24h的房颤的动物模型。对该模型的左、右房游离壁,左上、下肺静脉,右上、下肺静脉进行心外膜标测,测量各标测部位的有效不应期(ERP)和平均房颤波周长(AFCL)。对肺静脉电隔离,观察电隔离前后房颤的诱发以及各部位ERP和AFCL的变化。结果11只犬完成实验,在28.2±3.0d内诱发出持续超过24h的房颤。肺静脉电隔离前,ERP和AFCL分布呈明显的梯度分布,自短至长依次为:肺静脉,左、右房游离壁;肺静脉隔离后,8只犬转变为窦性心律,3只犬先转变为房性心律失常后,在60min内转变为窦性心律,再进行快速心房起搏刺激仅能诱发出小于60s的阵发性房颤,各部位ERP和AFCL也明显延长(P<0.05)。结论肺静脉的快速电活动可能在持续性房颤的维持中起关键作用。     

Effect of 60 Minutes of Rapid Atrial Pacing on Atrial Action Potential Duration in the In-Situ Canine Heart

Right atrial monophasic action potentials were recorded before and after 60 minutes of rapid atrial pacing (pacing cycle length (CL); 127 ± 10 ms) in 12 closed-chest dogs. The right atrial (RA) monophasic action potential (MAP) duration at 90% repolarization (RAMAPD) was measured at CLs of 400 ms and 250 ms. CL-dependent changes in RAMAPD (CL 400 ms – 250 ms) before and after rapid atrial pacing were 24 ± 1 ms and 16 ± 5 ms, respectively (p < 0.02). RAMAP was recorded at each atrial pacing CL starting at 240 ms decreasing by 10-ms increments. RAMAPD alternans was observed in 10 of 12 dogs at a CL of 163 ± 17 ms before and in 10 of 12 dogs at s CL of 198 ± 29 ms (p < 0.01) after rapid atrial pacing. Sustained atrial fibrillation (AF) (>5 minutes) was induced in 1 of 12 dogs at a pacing CL of 130 ms before rapid atrial pacing and in 4 of 12 dogs at a pacing CL of 135 ± 17 ms after rapid atrial pacing. Onset of AF was always preceded by the RAMAPD alternans. Sixty minutes of rapid atrial pacing leads to diminution of rate adaptation of atrial action potential duration (APD) and appearance of APD alternans of greater magnitude at longer CL, both of which may contribute to the initiation and perpetuation of AF during its early phase.