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     

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。     

心房肌急性电重构的临床研究

目的探讨快速心房激动对心房电生理特性的影响.方法以150～200ms起搏周长(PCL)对21例射频消融术后患者右心房进行S1S1刺激诱发心房颤动,心房快速刺激前、后均以400ms周长分别对高位右心房(HRA)、低位右心房(LRA)、希氏束周围(HB)、右心耳(RAA)等多部位进行S1S2扫描,测定心房有效不应期(ERP)、有效不应期空间离散度(ERPd)、右心房内及心房间传导时间(CT)的变化;以350ms、400ms和450ms3个不同周长随机对RAA进行S1S2扫描,观察有效不应期频率自适应性(ERPA)的变化.结果快速心房激动后ERP较刺激前有明显缩短,HRA的ERP[(193.2±25.5)msvs(179.7±23.3)ms,P=0.001、LRA的ERP [(198.0±30.8)msvs(182.0±22.5)ms,P=0.026]、HB的ERP[(195.0±26.6)ms vs(182.0±16.8)ms,P=0.018]、RAA的ERP(194.0±20.1)msvs(180.0±29.0)ms,P=0.014].而ERPd则无明显变化[(25.0±17.8)ms vs(28.0±16.9)ms,P=0.576];3个不同周长下RAA的ERP均较心房快速激动前有显著缩短,S1S1为350ms、400ms和450ms.心房快速激动前后ERP分别为[(186.2±24.4)ms vs(168.7±30.9)ms,P=0.006]、[(194.0±20.1)ms vs(180.0±29.0)ms,P=0.014]和[(191.2±33.1)ms vs(170.0±28.3)ms,P=0.0001];心房快速激动前、后ERP与PCL相关系数分别为(rb=0.998,P=0.041;ra=0.397,P=0.74),心房激动前斜率接近正常0.058,激动后斜率为0.015.房内房间CT无明显变化,HRA-HB[(46.5±12.5)msvs(48.4±12.0)ms,P=0.125]、HB-CSD[(47.0±14.2)ms vs(49.6±14.8)ms,P=0.153].结论快速心房激动使右心房同一周长不同部位、同一部位不同起搏周长下ERP缩短,ERPA下降;ERPd及右心房内房间传导速度无明显改变.快速心房刺激使人心房肌发生电重构,ERP缩短、ERPA下降可能是心房颤动发生、维持和发展的重要原因.     

左房快速起搏对肺静脉口及心房肌电重构的影响

目的探讨左房快速起搏对肺静脉口、左右心耳电重构的影响。方法运用快速起搏左心耳的方法建立心房颤动(AF)模型,在起搏前及起搏后的第1,3,5,7d对左、右心耳;左上、左下肺静脉口;右上、右下肺静脉口的有效不应期(ERP)、ERP频率适应性、ERP离散度及心房间的传导时间进行测定。采用S1S2程序刺激,基础起搏周长(PCL)分别为400,300,200ms,S2为200ms,以5ms的步长递减。程序刺激结合Burst刺激对上述心房部位进行AF的诱发,记录AF的发生率。在第8天关闭起搏器,采用上述相同方法对起搏停止后即刻;2,4,6,24h的上述各部位的ERP进行测定。结果起搏1d后各个基础起搏周长下各部位的ERP明显缩短,ERP频率适应性降低,ERP离散度增大(P<0.05),而心房间传导时间无明显变化(P>0.05);起搏终止后各部位的ERP逐渐延长,但起搏终止后6hERP与快速起搏前相比仍有明显缩短(P<0.05);24h后ERP基本恢复到起搏前水平,两者相比无明显差异(p>0.05);随着起搏时间的延长各部位AF的诱发率逐渐增高(P<0.05)。结论快速心房起搏不仅引起心房肌电重构,亦引起肺静脉电重构。     

心房颤动电重构的实验研究

目的 :研究犬心房颤动 (Af)模型心房有效不应期 (ERP)的变化 ,验证Af电重构这一假说的正确性。方法 :采用快速心房起搏的方法建立犬的Af模型 (起搏组 ,n =13) ,用程序刺激测量心房的ERP ;观察P波时限和PA间期的变化 ,并与假手术组 (对照组 ,n =7)作比较。结果 :持续快速起搏 9～ 10周后 ,心房ERP明显缩短 ,当S1S1为 30 0ms时 ,对照组与起搏组分别为 (15 0± 2 1)ms与 (115± 2 3)ms(P<0 .0 1) ;S1S1为 4 0 0ms时分别为(15 4± 2 4 )ms与 (10 5± 2 7)ms(P <0 .0 1)。起搏组P波时限和PA间期明显长于对照组。结论 :持续心房快速刺激可使ERP明显缩短 ,使心房发生电重构。心房电重构可促进Af的发生和发展     

心房肌易损性与阵发性心房颤动的发生机制

目的探讨左、右心房肌复极,及其易损性与阵发性心房颤动(AF)的发生与维持机制。方法应用单相动作电位(MAP)技术记录14只犬左、右心房肌的复极达90%动作电位时程(APD90),通过S1S2程序刺激,同时记录心房有效不应期(ERP)及相对不应期(RRP),观察反复心房激动(RAF,在S1S2的早搏刺激后,发生2个以上的连续心房活动,从心房刺激到RAF第一个激动的间期必须小于250 ms)及AF的诱发。结果14只犬S1S2间期递减至130±32 ms时,可出现RAF,随后当S1S2间期缩短为110±28 ms时AF发作。AF发作前大多数可记录到RAF(66.7%);共诱发出15阵RAF,左房11阵,右房4阵,左房RAF的发生率明显多于右房(P<0.05);共诱发出18阵AF,左房诱发出12阵,右房诱发出6阵。左房的AF诱发率明显多于右房(P<0.05)。结论AF发作前多伴有RAF发作;RAF是易发生阵发性AF的特征性表现,代表心房的易损性;左右心房易损性不同。     

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     

阵发性房室结及房室折返性心动过速导致的人心房有效不应期的变化

目的 :探讨阵发性房室结折返性心动过速 （AVNRT）和房室折返性心动过速 （AVRT）对人心房有效不应期（ERP）的影响。方法 :对 86例住院进行电生理检查和 （或 ）导管射频消融术中出现自发或诱发的 AVNRT和 AVRT患者 ,分别于 AVNRT和 AVRT发生前及发生终止后在 5 0 0 ,4 0 0和 30 0 ms等不同基础周长下测量心房 ERP。结果 :阵发性 AVNRT和 AVRT持续时间分别为 14± 6 m in及 14± 7min。AVNRT和 AVRT终止后即刻心房 ERP缩短 ,与各自心动过速前相比均 P<0 .0 1。该缩短改变可以在 5 m in内恢复。结论 :阵发性 AVNRT和 AVRT可以使人心房 ERP缩短 ,造成短暂心房电重构     

大鼠心房肌电生理特性的增龄性变化

目的探讨年龄对心房肌单相动作电位(MAP)和有效不应期(ERP)的影响,及其与心房颤动(房颤)的关系。方法选取Wistar大鼠40只分为青年组、成年组、中年组和老年组4组。Langendorff体外灌流心脏。分别测量各组心房肌在400ms刺激周长下MAP复极到90%、50%及20%时的时程(MAPD90、MAPD50、MAPD20)和ERP,以及其他不同刺激周长下的MAPD。结果在400ms刺激周长下,4组大鼠右心房肌MAPD90随年龄增长而逐渐延长〔(75±5)(、123±8)(、140±11)和(140±14)ms,均为P<0.01〕;而左心房肌青年组至中年组延长分别为〔(60±4),(120±3),(139±7)〕,老年组缩短〔(102±14)ms,均为P<0.01〕。心房肌ERP的增龄性变化规律与MAPD90相同。刺激周长从400ms缩短到250ms,右心房肌MAPD90缩短程度从青年组到老年组逐渐增加;左心房肌以老年组缩短程度最小。结论左右心房肌电生理特性增龄性变化规律不同。老年期心房电生理变化可能有利于房颤的发生。     

地尔硫(艹卓)、普罗帕酮和胺碘酮对短阵心房快速除极诱发的心房有效不应期变化的影响

目的　研究地尔硫、普罗帕酮和胺碘酮对短阵心房快速除极诱发的心房有效不应期(ERP)变化的影响。方法　 6 9例室上性心动过速消融成功后的自愿者 ,被随机分为对照组、地尔硫组、普罗帕酮组和胺碘酮组。以 4 0 0ms起搏周长 (PCL)分别对高位右心房、低位右心房、希氏束周围等部位进行S1S2 程序刺激 ,另以 3个不同PCL(35 0、4 0 0和 4 5 0ms)对右心耳进行S1S2 程序刺激 ,应用双极记录法测定各组在基础状态、心房快速除极前、后心房ERP和ERP频率自适应性 (ERP RA)的变化 ,同时观察心房快速除极后程序刺激过程中意外诱发继发性心房颤动 (AF)的情况。结果　基础状态下 ,各组 4 0 0ms周长下心房各部位ERP差异不显著 ;心房快速除极前 ,对照组和地尔硫组心房各部位ERP无明显改变 ,而普罗帕酮组和胺碘酮组心房各部位ERP均明显延长 ;心房快速除极后 ,地尔硫组心房各部位ERP较除极前无明显缩短 ,对照组、普罗帕酮组和胺碘酮组心房各部位ERP较除极前均明显缩短。对照组、普罗帕酮组和胺碘酮组心房快速除极后斜率均值较除极前明显下降 ,地尔硫组心房快速除极后斜率均值较除极前无明显变化。地尔硫组、普罗帕酮组和胺碘酮组心房快速除极后继发AF发生阵数明显低于对照组。结论　预先给予地尔硫可以阻止心     

快速心房激动对心房肌电生理特性的影响

比较快速心房起搏与急性心房颤动 (简称房颤 )诱发心房电生理特性的变化。以 15 0～ 2 0 0ms起搏周长(PCL)对 4 5例成功射频消融后 (RFCA)病人右房进行S1S1刺激诱发急性房颤 ,据能否诱发急性房颤分为非房颤组和急性房颤组 ;再以 4 0 0msPCL对心房快速激动前后高位右房、低位右房、His束周围等多部位进行S1S2 扫描 ,测定心房有效不应期 (ERP)、ERP离散度 (ERPd)、右房内及房间的传导时间的变化 ;另以 35 0 ,4 0 0和 4 5 0ms三个PCL随机对RAA进行S1S2 扫描 ,观察ERP频率自适应性的变化。两组心房快速激动后 4 0 0msPCL下右房各刺激部位及三种不同PCL右心耳ERP均较心房快速激动前有明显的缩短 ,并且缩短的程度相同。两组病人心房快速激动前后房内和房间传导时间及ERPd没有明显改变。两组心房快速激动前后斜率均值均较激动后明显下降 ;心房快速激动前、后斜率均值两组间无显明差别 (P >0 .0 5 )。结论 :两种方式的心房快速激动可诱发相似的心房电重构现象。     

地尔硫卓对心房急性电重构影响的临床研究

探讨地尔硫卓对心房快速激动诱发心房急性电重构的影响。将 31例导管射频消融成功的室上性心动过速患者随机分为两组 ,对照组 2 1例、地尔硫卓组 10例 ,以 15 0～ 2 0 0ms起搏周长 (PCL)诱发急性心房颤动 (AF)。以4 0 0msPCL分别在高位右房 (HRA)、低位右房 (LRA)、His束区 (HIS)等部位进行S1S2 扫描 ,测定基础状态、干预后和心房快速激动后心房有效不应期 (AERP) ;以三种不同PCL (35 0 ,4 0 0和 4 5 0ms)随机对右心耳 (RAA)进行S1S2 扫描 ,观察AERP频率自适应性的变化。对照组心房快速激动后HRA、LRA、HIS和RAA的AERP较基础状态、给盐水后有明显缩短 ;而地尔硫卓组心房快速激动后上述指标变化无显著性差异。将RAA处AERP与相应PCL进行曲线拟合 ,对照组基础状态下斜率为 0 .0 5 8、给盐水后斜率为 0 .0 6 8和心房快速激动后斜率为 0 .0 15。地尔硫卓组则分别为0 .0 30 ,0 .0 7和 0 .0 6 0。对照组诱发继发AF 13例 (13/2 1,6 1.9% ) ,明显高于地尔硫卓组 3例 (3/10 ,30 .0 % ) ,继发AF平均时限两组无明显差别。结论 :预先给予地尔硫卓可以阻止心房快速激动诱发的心房急性电重构的发生     

Atrial fibrillation in patients with Wolff-Parkinson-White syndrome: role of pulmonary veins

AF in WPW Syndrome. Aim: We aimed to characterize electrophysiological properties of pulmonary veins (PVs) in patients with Wolff–Parkinson–White (WPW) syndrome and atrial fibrillation (AF), and to compare them to those in patients with WPW without AF. Methods and Results: A total of 31 patients (mean age 40 ± 15 years, 23 males) with WPW were recruited: 16 patients with (AF group) and 15 without (controls) a history of AF. The basic electrophysiological (EPS) and echocardiographic data were not different between the 2 groups. Effective refractory periods (ERPs) of PVs were significantly shorter in the AF group compared to controls: left superior (LS) PV ERP 185±29 versus 230 ± 24 ms, P = 0.001; left inferior PV ERP 198 ± 25 versus 219 ± 26 ms, P = 0.04; right superior (RS) PV ERP 207 ± 25 versus 236 ± 19 ms, P = 0.001; right inferior PV ERP 208 ± 30 versus 240 ± 19 ms, P = 0.003. Maximal veno‐atrial conduction delay (i.e., the maximal prolongation of interval from stimulus delivered at PV ostia to proximal coronary sinus after extrastimulus compared to the basic drive cycle) was longer in the AF group when pacing from LSPV (69.3 ± 37.9 vs 32.6 ± 16.1 ms, P = 0.01) and RSPV (74.1 ± 25.9 vs 50.2 ± 26.5 ms, P = 0.04). During EPS, AF was induced more often in the AF group (n = 7) compared to controls (n = 1; P = 0.04). Follow‐up revealed that AF recurred in 3 patients in the AF group and none of the controls. Conclusion: Patients with WPW syndrome and AF have shorter ERPs of PVs and greater maximal veno‐atrial conduction delay compared to patients with WPW without AF. These findings suggest a potential role of PVs in the development of AF in patients with WPW. (J Cardiovasc Electrophysiol, Vol. 23 p. 280‐286, March 2012.)     

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     

Atrial conduction: effects of extrastimuli with and without atrial dysrhythmias

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Postcardioversion atrial electrophysiologic changes induced by oral verapamil in patients with persistent atrial fibrillation

OBJECTIVES: The aim of our study was to verify the effect of oral administration of verapamil on atrial electrophysiologic characteristics after cardioversion of persistent atrial fibrillation (AF) in humans. BACKGROUND: Discordant findings have been reported regarding the efficacy of verapamil in preventing the electrical remodeling induced by AF. METHODS: We determined the effective refractory periods (ERPs) at five pacing cycle lengths (300 to 700 ms) and in five right atrial sites after internal cardioversion of persistent AF (mean duration 238.1+/-305.9 days) in 19 patients. Nine patients received oral verapamil (240 mg/day) starting four weeks before the electrophysiologic study, whereas the other 10 patients were in pharmacologic washout. RESULTS: The mean ERPs were 202.0+/-22.7 ms in the washout group and 189.3+/-18.5 ms in the verapamil group (p < 0.0001). The degree of adaptation of refractoriness to rate was similar in the two groups (mean slope value in the washout group and verapamil group: 0.07+/-0.03 and 0.08+/-0.05, respectively), showing a normal or nearly normal adaptation to rate in the majority of the paced sites in both groups. The mean ERP was slightly longer in the septum than in the lateral wall and in the roof, both in the washout and verapamil groups. CONCLUSIONS: In patients with persistent AF, long-term administration of verapamil before internal cardioversion resulted in 1) shortening of atrial ERPs; 2) no change in refractoriness dispersion within the right atrium; and 3) no change in atrial ERP adaptation to rate.     

Electrophysiologic actions of dl-sotalol in patients with persistent atrial fibrillation

OBJECTIVES: We sought to determine the electrophysiologic actions of sotalol in the remodeled atrium of humans. BACKGROUND: In experimental studies, sotalol has limited class III action in the electrically remodeled atrium and did not prevent atrial fibrillation (AF) induction. METHODS: We determined the effective refractory periods (ERPs) at three pacing cycle lengths (400, 500, and 600 ms) in the high right atrium (HRA) and distal coronary sinus (DCS) before and after intravenous infusion of dl-sotalol in 10 patients with persistent AF who underwent internal cardioversion. The same protocols were performed in 10 control subjects in sinus rhythm. RESULTS: In the HRA and DCS, the atrial ERPs at different drive cycle lengths were significantly shorter in patients with AF than in control subjects (p < 0.05). In patients with AF, the atrial ERP's adaptation to rate was nearly normal in the HRA, but was poor in the DCS. In both groups, dl-sotalol significantly increased the atrial ERPs at both the HRA and DCS, as compared with baseline (p < 0.05). However, the prolongation of atrial ERPs was significantly less at a drive cycle length of 600 ms in patients with AF versus control subjects (p < 0.05). After infusion of dl-sotalol, the atrial ERP's adaptation to rate at both the HRA and DCS was poor in patients with AF, and AF was still easily inducible in the majority of them, but not in control subjects. CONCLUSIONS: The results of the present study demonstrate that the electrophysiologic actions of dl-sotalol are significantly attenuated in the chronically remodeled human atrium, and these changes might represent a probable explanation for the low efficacy of dl-sotalol to prevent early AF recurrence after electrical cardioversion.     

Unequal Atrial Stretch in dogs Increases Dispersion of Refractoriness Conducive to developing Atrial Fibrillation

Atrial Stretch Precipitates Atrial Fibrillation. Introduction: We have shown previously that acute atrial dilation prolonged atrial refractoriness. We hypothesized that this increase in refractoriness might be heterogeneous and could create an electrophysiologic substrate leading to atrial fibrillation. The purpose of the present study was to test that hypothesis. Methods and Results: We studied 23 anesthetized open chest dogs. Bipolar plunge electrodes were placed in the medial free wall of the right atrium (thin region) and in the lower crista terminalis of the right atrium (thick region). Two bipolar plunge electrodes were also placed in the left ventricular apex to stimulate and record. Atrial effective refractory period (ERP) was measured in a group of nine dogs using the atrial extrastimulus method (A1A2) in two ways: during atrial pacing (AP) and during simultaneous atrioventricular (AV) pacing that achieved an AV interval of 0 msec (AV = 0). One liter/hour of normal saline was infused intravenously to elevate right atrial pressure and produce right atrial stretch. Atrial ERPs were measured before and after the normal saline infusion. To compare the extent of atrial stretch produced by volume overload, two pairs of sonomicrometer transducers were implanted in the thick and thin regions in a separate group of six dogs. The area encompassed by sonomicrometers was measured before and after saline infusion. The inducibility of atrial fibrillation was compared before and after saline infusion using rapid AP in another group of five dogs. Atrial pressure during sinus rhythm increased from 5.1 ± 0.96 mmHg to 6.3 ± 0.93 mmHg after normal saline infusion (P < 0.01). ERP increased in the thin free wall from 151 ± 14.3 to 172 ± 14.7 msec (AV = 0), and from 149 ± 12.0 to 170 ± 14.3 msec (AP). ERP increased in the thick crista terminalis from 134 ± 9.9 to 147 ± 10.2 msec (AV = 0), and from 133 ± 7.9 to 146 ± 9.8 msec (AP) (P < 0.01). The increase in ERP in the thin free wall exceeded that in the thick crista terminalis (P < 0.01), increasing the dispersion of atrial ERP. After 500-mL saline infusion for 30 minutes, the increase of area in the thin region was 12.8%± 3.7%, and that in the thick was 3.5%± 3.2%. The increase of the area in the thin region after 1000 mL for 1 hour was 18.8%± 6.2%. and that in the thick region was 6.3%± 5.1% (P < 0.01). Atrial fibrillation was not induced in any dog before saline infusion, hut induced in all five dogs after saline infusion. Conclusions: Atrial ERP in the thin right atrial free wall exceeds the ERP of the thick cristaterminalis, and an increase in atrial pressure produced by saline infusion exaggerates this ditterence by stretching thin segments of the atrial myocardium more than it stretches thick regions. Thus, atrial stretch, by increasing the dispersion of atrial ERP, may be conducive to the development of atrial fibrillation.