风湿性心脏病心房颤动电生理机制的研究

报告２１例风湿性心脏病（简称风心病）慢性心房颤动（简称房颤）患者（ＣＡｆ组）的心外膜标测及心电生理结果，并与１４例非风心病阵发性房颤（ＰＡｆ组）和１２例无房颤者（正常对照组）进行对照，以对房颤机制进行研究进而为房颤外科术式的改良提供依据。ＣＡｆ组右房传导时间延长发生率（８０．０％）显著高于ＰＡｆ组（４２．９％）和正常对照组（８．３％），Ｐ＜０．０５和＜０．０００１。ＣＡｆ组和ＰＡｆ组窦性心律时的房间传导时间显著长于正常对照组（分别为１０３．０±２４．５和１１３．３±２６．１ｍｓｖｓ７８．７±１８．１ｍｓ，Ｐ均＜０．０１）。ＣＡｆ组和ＰＡｆ组的高位右房有效不应期均显著短于正常对照组（２２５．９±２２．２和２１０．０±３９．３ｍｓｖｓ２４８．８±３１．４ｍｓ，Ｐ＜０．００１和＜０．０１）。ＣＡｆ组和ＰＡｆ组易损性发生率（均为５０％）显著高于正常对照组（０），Ｐ均＜０．０１。ＣＡｆ组心外膜标测房颤时的波长指数显著小于房扑时的波长指数（１．４２±０．２７ｖｓ２．４２±０．４１，Ｐ＜０．０１）。右房多为细密的颤动波，左房多为规则的扑动波，但激动模式多变。表明右房传导时间延长、有效不应期短、易损性高是风心病ＣＡｆ的     

MS-551对麻醉犬心肌的电生理作用及血液动力学影响

为研究１，３二甲基－６［２－（Ｎ－２羟乙基－３－４硝苯丙氨基）乙氨基］－２，４（１Ｈ，３Ｈ）－盐酸嘧啶二酮即ＭＳ－５５１（简称ＭＳ）对麻醉犬心肌的电生理作用和血液动力学影响，采用自身前后对照的方法测定用药（５ｍｉｎ内每公斤体重静脉注射ＭＳ０．５ｍｇ，继以每公斤体重静脉滴注０．５ｍｇ持续３０ｍｉｎ）前后麻醉犬（ｎ＝８）有关电生理参数及心输出量、肺毛细血管楔嵌压等变化。结果表明ＭＳ：①使心房有效不应期和心室有效不应期显著延长，分别为２７．１±６．８，２０．７±５．２ｍｓ，Ｐ均＜０．０１。②使自发性窦性周期、窦房结恢复时间和校正的窦房结恢复时间均显著延长，分别为４１．４±８．０，５０．０±９．８，８．６±３．４ｍｓ，前两者Ｐ＜０．０１，后者Ｐ＜０．０５。但对窦房传导时间无明显影响（３．６±１．８ｍｓ，Ｐ＞０．０５）。③对ＡＨ、ＨＶ、ＰＱ间期及ＱＲＳ波群时限无明显影响，显著延长ＱＴ间期，明显降低文氏点（调搏周长延长）。④轻度减低心输出量，但无统计学意义（变化值：－０．５６±０．２３Ｌ／ｍｉｎ，Ｐ＝０．０６１），对肺毛细血管楔嵌压无显著性影响。结论：ＭＳ延长心肌不应期，对心内传导影响不明显，有良好的血液动力学特性，可?     

心内膜导管射频消融致心律失常作用的研究

通过分别比较１０条犬右房和左室导管射频消融前后的电生理检查结果和８０例房室旁道病人射频消融前后的电生理检查、心电监测和晚电位检查结果，探讨心内膜导管射频消融是否具有近期致心律失常作用。１０条犬消融前和消融后７日右房有效不应期分别为１４３±２５和１４１±２８ｍｓ（Ｐ＞０．０５），左室有效不应期分别为２３１±５６和２３７±７４ｍｓ（Ｐ＞０．０５），均未诱发出房性心动过速、心房扑动、心房颤动、室性心动过速、心室颤动等心律失常。８０例病人消融后即刻电生理检查没有诱发出上述快速心律失常；消融后随访３个月，共行２４小时心电监测３次均未发现新的心律失常，晚电位检查均为阴性。表明采用导管射频消融术治疗室上性快速心律失常没有近期的致心律失常作用，是一种相对安全的介入性治疗方法。     

心室起搏对后间隔旁道与快径逆传的诊断价值

通过右室心尖部和基底部两个不同部位的起搏，比较１５例房室结折返性心动过速（对照组）和８例隐匿性后间隔旁道参与的房室折返性心动过速患者（观察组）的室房传导时间（ＶＡＩ）。结果显示：①心尖部起搏时对照组ＶＡＩ为１７４±３４ｍｓ，与观察组１８６±３８ｍｓ相比无显著性差异（Ｐ＝ＮＳ）。②基底部起搏时观察组ＶＡＩ为１５３±２４ｍｓ，明显短于对照组１９９±３４ｍｓ，两者比较有显著性差异（Ｐ＜０．０１）。③两个部位（心尖部与基底部）ＶＡＩ的差值对照组≤０（－５０～０，平均－２４±１６ｍｓ）与观察组≥１５ｍｓ（１５～７５，平均３４±１９ｍｓ）比较有非常显著性差异（Ｐ＜０．００１）。提示右室心尖部与基底部连续起搏可快速、准确地鉴别室房传导是经快径路还是后间隔旁道     

房室结传导的加速性、疲劳性对房室结功能不应期的影响

房室结传导的加速性、疲劳性对心室免于各种类型的室上性心动过速包括心房颤动的影响起决定作用，但对房室结功能不应期（ＡＶＮ－ＦＲＰ）的影响不明。旨在通过对离体兔心施以多种方案电生理刺激以阐明两者的相互关系。实验结果表明：①房室结传导的加速性使ＡＶＮ－ＦＲＰ缩短（Ｂ方案１４６±３．３ｍｓｖｓＡ方案１５９±３．５ｍｓ，Ｐ＜０．０１，ｎ＝６），疲劳性使ＡＶＮ－ＦＲＰ延长（Ｃ方案１８７±４．９ｍｓｖｓＡ方案１５９±３．５ｍｓ，Ｐ＜０．０１，ｎ＝６）；②加速性和疲劳性诱导的ＡＶＮ－ＦＲＰ的变化是在１１房室传导范围内产生的，并在快速频率下达到它的最大效应（１００％频率下，Ｂ方案１５４±６．０ｍｓ、Ｃ方案１８７±８．３ｍｓ分别与Ａ方案１６８±６．９ｍｓ相比，Ｐ均＜０．０１，ｎ＝６）。结论：ＡＶＮ－ＦＲＰ受房室结传导之加速性、疲劳性相互作用的共同影响，ＡＶＮ－ＦＲＰ的变化可以用来反映房室结的传导功能     

不同起搏方式对病窦综合征患者远期效果的影响

为了解不同起搏方式对病窦综合征特别是慢－快综合征患者心功能及房性心律失常的影响，利用超声心动图、体表心电图及Ｈｏｌｔｅｒ检查，对２１１例病窦综合征患者采用自身对照方法进行回顾性分析。结果发现：生理性起搏（ＡＡＩ／ＤＤＤ）组术后左室射血分数（ＬＶＥＦ）、心输出量（ＣＯ）明显增加（ＡＡＩ：５３．５±６．１％ｖｓ４７．２±７．８％，４．９５±０．５７Ｌ／ｍｉｎｖｓ４．２０±０．６２Ｌ／ｍｉｎ；ＤＤＤ：５２．５±６．８％ｖｓ４４．３±０．１％，５．１２±０．７１Ｌ／ｍｉｎｖｓ４．４１±０．３８Ｌ／ｍｉｎ；Ｐ均＜０．０１），左房内径（ＬＡＤ）无明显变化；ＤＤＤ组Ｅ／Ａ比值明显增加（０．９８±０．０９ｖｓ０．８７±０．１５，Ｐ＜０．０１），ＡＡＩ组Ｅ／Ａ比值呈增加趋势（Ｐ＝０．０５７）。房性心律失常发生率明显减少（１５．９％ｖｓ５０％，Ｐ＜０．０１）。非生理性起搏（ＶＶＩ）组术后ＬＶＥＦ、ＣＯ明显下降（４４．１±４．７％ｖｓ４８．３±４．３％，３．７７±０．４２Ｌ／ｍｉｎｖｓ４．１７±０．８５Ｌ／ｍｉｎ，Ｐ均＜０．０１），ＬＡＤ明显增大（３９．２６±２．３７ｍｍｖｓ３６．８１±２．３５ｍｍ，Ｐ＜０．０１），Ｅ／Ａ比值呈?     

老年人急性心肌梗塞后心室颤动与QTc离散度关系的探讨

回顾性单盲分析老年人急性心肌梗塞发病２４小时内首次心电图ＱＴｃ离散度（ＱＴｃｄ）。心室颤动（简称室颤）组（ｎ＝１０）ＱＴｃｄ为７５．１±４５．２ｍｓ，非室颤组（ｎ＝６０）则为３２．０±１５．３ｍｓ，健康对照组（ｎ＝２０）为２７．２±７．１ｍｓ。室颤组与后两组比较，差异有高度显著性（Ｐ＜０．０１）。前壁心肌梗塞者（ｎ＝３０）ＱＴｃｄ为３６．３±３１．１ｍｓ，下壁心肌梗塞者（ｎ＝４０）则为３９．５±２２．５ｍｓ。ＱＴｃｄ≥４０ｍｓ２５例，发生室颤９例（３６％），而ＱＴｃｄ＜４０ｍｓ且ＱＴｃ＜４４０ｍｓ的２９例中，无一例发生室颤。结果提示老年人急性心肌梗塞后室颤的发生与ＱＴｃｄ明显增加有关。     

急性心肌梗塞患者心率变异性及其临床意义

采用心率变异性（ＨＲＶ）时域指标──２４ｈ心电图中全部窦性Ｒ－Ｒ间期标准差（ＳＤＮＮ），研究急性心肌梗塞（ＡＭＩ）患者ＨＲＶ改变及其与肌酸激酶同功酶（ＣＫ－ＭＢ）、心功能和住院期间病死率的关系。结果显示：ＡＭＩ后２～３ｄ的ＳＤＮＮ（６０．５３±２０．６０ｍｓ）较正常对照组（１３０．２０±３０．４１ｍｓ）显著降低（Ｐ＜０．００１），并与ＣＫ－ＭＢ峰值呈显著负相关（ｒ＝－０．４８，Ｐ＜０．０５）；服用美多心安者的ＳＤＮＮ显著高于未服者（６１．２７±１３．４４ｍｓＶＳ４７．５３±１１．２５ｍｓ，Ｐ＜０．０５）；心功能Ⅱ～Ⅳ级者ＳＤＮＮ显著低于Ⅰ级者（４９．７１±１８．１０ｍｓＶＳ６８．５２±１８．８０ｍｓ，Ｐ＜０．０１）；住院期间死亡者ＳＤＮＮ显著低于存活者（４２．２５±６．４５ｍｓＶＳ６２．５６＋２０．６３ｍｓ，Ｐ＜０．０１）；ＳＤＮＮ＜５０ｍｓ者的住院病死率显著高于＞５０ｍｓ者（３１％ＶＳ０，Ｐ＜０．０５）。提示ＡＭＩ早期心脏交感神经活动增强而迷走神经活动受抑制，其改变的程度与心功能损害和梗塞面积相关；ＡＭＩ早期测定ＨＲＶ可获得重要临床信息和有助于对患者作早期危险性的分层。     

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。     

心房起搏阈值的随访分析

对３３例植入心房电极者进行起搏阈值的随访，结果表明：起搏阈值峰值为１．４４±０．７４Ｖ／０．５ｍｓ，出现在植入后两周内；慢性期起搏阈值为１．２２±０．４０Ｖ／０．５ｍｓ；伴器质性心脏病患者慢性期起搏阈值（１．７０士０．３７Ｖ／０．５ｍｓ）明显高于不伴器质性心脏病者（１．１６±０．３７Ｖ／０．５ｍｓ），Ｐ＜０．０１；激素电极的起搏阈值峰值（１．１２±０．２９Ｖ／０．５ｍｓ）和慢性期起搏阈值（０．７７±０．１７Ｖ／０．５ｍｓ）均显著低于非激素电极（１．８０±０．６８Ｖ／０．５ｍｓ和１．４０±０．３３Ｖ／０．５ｍｓ），Ｐ＜０．０５及０．００１。提出在非特殊情况下，将出厂时的电能由５．０Ｖ／０．５ｍｓ降至２．５Ｖ／０．５ｍｓ既可保证有效起搏，又可节省电能，从而延长起搏器的使用寿命。     

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?     

Oral vanoxerine prevents reinduction of atrial tachyarrhythmias: preliminary results

Vanoxerine, A New Cardiac Multichannel Blocker. Background: Vanoxerine is a promising, new, investigational antiarrhythmic drug. The purpose of this study was to test the hypothesis that oral dosing of vanoxerine would first terminate induced atrial flutter (AFL) and atrial fibrillation (AF), and then prevent their reinduction. Methods: In 5 dogs with sterile pericarditis, on the fourth day after creating the pericarditis, we performed electrophysiologic (EP) studies at baseline, measuring atrial excitability, refractoriness (AERP), and conduction time (CT) when pacing from the right atrial appendage, Bachmann's bundle (BB), and the posteroinferior left atrium at cycle lengths (CLs) of 400, 300, and 200 ms. Then, after induction of AFL or AF, all dogs received hourly oral doses of vanoxerine: 90 mg, followed by 180 mg and 270 mg. Blood was obtained to determine plasma vanoxerine concentrations at baseline, every 30 minutes, when neither AFL nor AF were inducible, and, finally, 1 hour after the 270 mg dose. Then we repeated the baseline EP studies. Results: Four dogs had inducible, sustained AFL, and 1 dog only had induced, nonsustained AF. In 4 AFL episodes, oral vanoxerine terminated the AFL and then rendered it noninducible after an average of 111 minutes (range 75–180 minutes) after the first dose was administered. The mean vanoxerine plasma level at the point of noninducibility was 84 ng/mL, with a narrow range of 76–99 ng/mL. In the dog with induced, nonsustained AF, it was no longer inducible at a drug level of 75 ng/mL. Vanoxerine did not significantly (1) prolong the AERP except at BB, and then only at the faster pacing CLs; (2) change atrial excitability thresholds; (3) prolong atrial conduction time, the PR interval, the QRS complex or the QT interval. Conclusions: Orally administered vanoxerine effectively terminated AFL and rendered it noninducible. It also suppressed inducibility of nonsustained AF. These effects occurred at consistent plasma drug levels. Vanoxerine's insignificant or minimal effects on measured electrophysiologic parameters are consistent with little proarrhythmic risk. (J Cardiovasc Electrophysiol, Vol. pp. 1‐8)     

Antiarrhythmic and Electrophysiologic Effects of Intravenous Ibutilide and Sotaloi in the Canine Sterile Pericarditis Model

Ibutilide, Sotalol, and Atrial Flutter. Introduction: Atrial arrhythmias are a frequent clinical complication following open heart surgery. We compared the Class III agents d,I-sotalol and ibutilide fumarate in an intravenous cross-over study using the canine atrial sterile pericarditis model. Methods and Results: We studied pacing-induced sustained atrial flutter over a 7-day post-surgical period in conscious dogs, alternating analysis of ibutilide (1.0 to 30.0 μg/kg) and d,I-sotalol (0.1 to 3.0 mg/kg). Ibutilide significantly increased atrial flutter cycle length (AFL CL) II ± 2 msec and atrial effective refractory period (AERP) 13 ± 2 msec, and terminated atrial flutter in all cases (n = 12) following a mean dose of 6 ± 2 μg/kg. Plasma concentrations of ibutilide were 53 ± 13 ng/mL. Ventricular effective refractory period (VERP) was not signiflcantly affected (4 ± 2 msec). Following termination with ibutilide, atrial flutter could he reinitiated in 1 of 12 trials, and was nonsustained (40-sec duration). Sotalol significantly increased AFL CL 23 ± 3 msec and terminated atrial flutter in 8 of 12 trials following a mean dose of 1.5 ± 0.4 mg/kg. AERP and VERP were significantly increased 20 ± 6 and 12 ± 2 msec, respectively. The incidence of reinduced atrial flutter was 9 of 12 trials (P ≥ 0.05 vs ibutilide) (7 nonsustained 57 ± 7 sec duration, and 2 sustained). Sotalol failed to terminate atrial flutter in two dogs on days 1 and 5, despite increases in AFL CL (21 ± 8 msec) and AERP (16 ± 9 msec), whereas on day 3, ibutilide (20 ± 7 μg/kg) terminated atrial flutter in those two dogs while increasing AFL CL and AERP 18 ± 6 and 15 ± 0 msec, respectively. Conclusion: Both sotalol and ibutilide terminate atrial flutter in this model. Ibutilide converted atrial flutter in dogs in which sotalol was not successful. Following atrial flutter termination, ibutilide had a lower incidence of reinduced arrhythmias compared to sotalol. Ibutilide produced atrial antiarrhythmic effects while having no significant electrophysiologic effects on the ventricle.     

Vanoxerine,a New Drug for Terminating Atrial Fibrillation and Flutter

Vanoxerine Terminates AF and AFL. Background: Vanoxerine produces potent block of cardiac hERG, sodium, and L‐type calcium channels. Block is strongly frequency dependent, is unassociated with transmural dispersion of repolarization, and occurs at concentrations safe in humans. Therefore, we proposed that vanoxerine might be antiarrhythmic. In these studies, we tested the hypothesis that vanoxerine would terminate induced atrial fibrillation (AF) and atrial flutter (AFL) in dogs with sterile pericarditis (SP). Methods and Results: In 9 SP dogs, 11 episodes each of sustained (>10 minutes) AF and AFL were induced. Electrophysiological studies were performed before and after infusion of vanoxerine, which effectively terminated AF and AFL in 19 of 22 episodes. Simultaneous multisite mapping during 3 AF and 3 AFL episodes demonstrated that termination of each arrhythmia occurred with termination of the driver (a reentrant circuit) following an increase in tachycardia CL. Except for conduction in an area of slow conduction in the driver's reentrant circuit, vanoxerine did not significantly affect intraatrial or atrioventricular conduction time, QRS duration, or QT/QTc intervals. Ventricular refractoriness prolonged minimally during ventricular pacing at 400 and 333 ms (176 ± 16 ms to 182 ± 16 ms; 173 ± 11 ms to 178 ± 18 ms, respectively). Vanoxerine minimally increased (mean 0.7 mA) atrial stimulus threshold for capture. Conclusions: Vanoxerine effectively terminated induced, sustained AF and AFL in the canine SP model, and produced insignificant or minimal changes in refractoriness, conduction time, or stimulus threshold, consistent with little proarrhythmic risk. (J Cardiovasc Electrophysiol, Vol. 21, pp. 311–319, March 2010)     

房间隔单线消融防治犬实验性心房颤动的研究

为探讨房间隔单线消融治疗心房颤动 (AF)的可行性 ,选用 13只犬 ,在静脉滴注乙酰甲胆碱下 ,用心房快速起搏诱发持续性 AF(持续时间 >15 min)。经皮穿刺静脉 ,在 X线透视下用 7F温控 4极同步导管介导射频能量线性消融卵圆窝前方的宽厚房间隔。观察消融前、后 AF的诱发率及电生理参数变化。结果显示消融前所有犬均可诱发持续性 AF。消融前 2只犬死亡。间隔消融后 8只犬不再诱发 AF,1只犬诱发持续性心房扑动 (AFL) ,再消融三尖瓣环和下腔静脉间心肌后 AFL消失。另 2只仍可诱发 AF。消融后卵圆窝心房有效不应期 (ERP)较消融前延长(113± 9ms vs67± 7ms,P<0 .0 5 ) ,其余部位消融前后 ERP无显著性差异。结果初步提示房间隔单线消融能够防治实验性 AF的发生 ,对于临床上有相似特点的 AF消融房间隔可能有效。     

心房电重构与房颤关系的基础研究

目的检查观测心房电生理改变与房颤（AF）发生和持续的关系,探讨心房电重构与房颤的内在联系。方法健康成年杂种犬14只（雌雄不拘,体重10．0～12．5kg）,随机分为2组：对照组（A组）和起搏组（B组）。右侧开胸将电极置于右心房,以400次／min的频率快速起搏右心房（A组只手术不起搏）,分别于实验开始及起搏6h后对每只犬进行电生理检查,测定心房有效不应期（AERP）。起搏开始及起搏后测定burst刺激诱发房颤的频率和持续时间。结果A组在整个时间内AERP无变化,B组心房快速起搏后,AERP明显缩短。A、B两组起搏前房颤的频率和持续时间差异无统计学意义。A组起搏前、后房颤的频率和持续时间无变化,B组心房快速起搏后房颤的频率增多,持续时间延长。结论快速心房起搏可以引起心房有效不应期缩短,即心房电重构。心房电重构造成的心房有效不应期等电生理变化促进了房颤的发生和维持,是心房电重构与房颤关系的基础。     

普罗帕酮在短期电重构后山羊心房的抗心律失常作用研究

为研究普罗帕酮对短期电重构后清醒山羊心房的电生理特性的影响,探讨其抗心律失常作用的可能机制,在7只山羊的左房游离壁外膜缝合4对电极,经皮下隧道将电极导线引至颈部皮肤外。术后2周测量不同基础刺激周长(BCL)时的心房有效不应期(AERP)、BCL为200ms时的心房传导速度(CV)并计算心房波长(WL)。心房快速刺激维持心房颤动(简称房颤)6h后静脉滴注(简称静滴)生理盐水,重复上述指标测量。2天后,在房颤6h后静滴普罗帕酮,重复上述测量。结果:①在基础状态下,AERP表现出频率适应性;②6h的房颤后,在静滴生理盐水时,AERP的频率依赖特性丧失。BCL为200ms时,AERP及WL均缩短,CV变化不显著;③在静滴普罗帕酮时,AERP显示使用依赖特性。BCL为200ms时,与基础状态时比较,AERP延长,CV及WL缩短;但与静滴盐水时相比,WL无明显变化。结论:在经过6h的电重构后,普罗帕酮使AERP表现为使用依赖特性。快速心房刺激时,普罗帕酮使AERP明显延长,CV明显缩短。     

犬急性心房颤动电重构现象的实验研究

目的 观察短阵心房颤动(房颤)的电重构现象及其恢复过程，探讨电重构与房颤再发及维持的关系。方法 15只健康成年犬于左、右心房外膜7个部位缝合双极记录电极，自心耳给予600次／min起搏诱发2h房颤，其中5只犬每间隔10min测量左、右心耳的心房有效不应期(AERP)，观察其恢复过程；另10只犬在房颤前后分别测量在起搏周长350ms、250ms、200ms时7个部位的AERP并记录电生理检查时房颤的诱发率及其持续时间。结果 2h房颤后心房各点AERP显著缩短，对心率适应不良，AERP离散度增高，继发性房颤诱发率增高、持续时间延长。AERP缩短可持续30min，60-80min后恢复。左心耳AERP恢复过程慢于右心耳。可诱发房颤的部位AERP更短，与继发性房颤的平均持续时间呈显著性负相关。可诱发房颤的心房其AERP离散度明显增高，但与继发性房颤的持续时间无关。AERP心率适应不良部位继发性房颤的诱发率高于生理性AERP心率适应性部位。低位右心房及左心耳部位的期前兴奋易于诱发房颤。结论 2h诱发的房颤足以使健康心房发生类似持续性房颤的电重构，电重构使房颤易于再发。AERP离散度与房颤的诱发有关，AERP缩短与房颤的持续性有关，房性早搏的发生部位与房颤的易患性有关。     

Correction for Heart Rate Is Not Necessary for QT Dispersion in Individuals without Structural Heart Disease and Patients with Ventricular Tachycardia

Background: It remains controversial whether QT dispersion should be corrected for heart rate, especially when the limitations of rate correction formulae are considered. We investigated whether incremental atrial pacing affects QT dispersion and the rate‐corrected values according to Bazett's formula in individuals without structural heart disease and in patients with history of sustained ventricular tachycardia. Methods: We studied 32 individuals without structural heart disease (group A), and 16 patients with a history of sustained ventricular tachycardia (group B). QT dispersion and corrected for heart rate QT dispersion using Bazett's formula (QTc dispersion) were calculated in sinus rhythm, and during continuous right atrial pacing for one minute at 100 and 120 beats/min. Results: Interobserver variability was not significant (P ≧ 0.10). QT dispersion did not differ at rest between groups A and B and did not change significantly from baseline at any heart rate in both groups. However, QTc dispersion increased significantly with atrial pacing in a similar manner in group A and group B (42 ± 19 ms at rest vs 53 ± 23 ms at 120 beats/min, P < 0.001 for group A, 39 ± 16 ms at rest vs 60 ± 19 ms at 120 beats/min, P < 0.001 for group B). Conclusions: We conclude that QT dispersion remains unchanged during atrial pacing at heart rates up to 120 beats/min in both individuals without structural heart disease and in patients with a history of sustained ventricular tachycardia. Correction by Bazett's formula results in prolongation of QTc dispersion, yielding values which may be misleading. A.N.E. 2002;7(1):47–52     

Pharmacological inhibition of SK-channels with AP14145 prevents atrial arrhythmogenic changes in a porcine model for obstructive respiratory events

Background

Obstructive sleep apnea (OSA) creates a complex substrate for atrial fibrillation (AF), which is refractory to many clinically available pharmacological interventions. We investigated atrial antiarrhythmogenic properties and ventricular electrophysiological safety of small-conductance Ca²⁺-activated K⁺ (SK)-channel inhibition in a porcine model for obstructive respiratory events.

Methods

In spontaneously breathing pigs, obstructive respiratory events were simulated by intermittent negative upper airway pressure (INAP) applied via a pressure device connected to the intubation tube. INAP was applied for 75 s, every 10 min, three times before and three times during infusion of the SK-channel inhibitor AP14145. Atrial effective refractory periods (AERP) were acquired before (pre-INAP), during (INAP) and after (post-) INAP. AF-inducibility was determined by a S1S2 atrial pacing protocol. Ventricular arrhythmicity was evaluated by heart rate adjusted QT-interval duration (QT-paced) and electromechanical window (EMW) shortening.

Results

During vehicle infusion, INAP transiently shortened AERP (pre-INAP: 135 ± 10 ms vs. post-INAP 101 ± 11 ms; p = .008) and increased AF-inducibility. QT-paced prolonged during INAP (pre-INAP 270 ± 7 ms vs. INAP 275 ± 7 ms; p = .04) and EMW shortened progressively throughout INAP and post-INAP (pre-INAP 80 ± 4 ms; INAP 59 ± 6 ms, post-INAP 46 ± 10 ms). AP14145 prolonged baseline AERP, partially prevented INAP-induced AERP-shortening and reduced AF-susceptibility. AP14145 did not alter QT-paced at baseline (pre-AP14145 270 ± 7 ms vs. AP14145 268 ± 6 ms, p = .83) or QT-paced and EMW-shortening during INAP.

Conclusion

In a pig model for obstructive respiratory events, the SK-channel-inhibitor AP14145 prevented INAP-associated AERP-shortening and AF-susceptibility without impairing ventricular electrophysiology. Whether SK-channels represent a target for OSA-related AF in humans warrants further study.