阵发性心房颤动患者心房复极离散度的研究

目的　通过记录阵发性心房颤动 (房颤 )患者心房单相动作电位 (MAP) ,分析心房复极离散度与房颤发生的关系。方法　特发性阵发性房颤患者与无自发房颤病史的阵发性室上性心动过速患者各 1 5例 ,均接受心内电生理检查和 /或导管射频消融治疗。两根 MAP电极于右心房共取 4～ 1 0个不同部位进行同步的窦性心律基础刺激 (S1)及期前刺激 S2 时的 MAP记录。测量、计算心房复极离散度(RTd)及动作电位时限和局部冲动时间的离散度 (APDd、ATd)。　结果　窦性心律时房颤组最大 RTd显著大于对照组 (1 2 3 .69± 54.67) ms比 (64 .2 5± 2 3 .2 9) ms,(P<0 .0 1 )。其差异主要来源于 APDd(1 1 5.0 0± 4 6.90 ) ms比 (57.56± 3 3 .57) ms,(P<0 .0 1 ) ,ATd差异无显著性。随 S1、S2 的加入 ,各组局部激动时间和离散度逐渐增大 ,而动作电位时限逐渐缩短 ,且房颤组的这种改变程度显著大于对照组。在S1时无房颤发生 ,加入期前刺激时 ,大多数房颤组患者均多次诱发出短阵房颤。其诱发率及次数均显著高于对照组。　结论　研究结果表明 ,MAP记录技术是临床观察、分析心房复极离散度及其在阵发性房颤中的作用的较佳方法。心房复极离散度的增加是阵发性房颤发生的重要因素。期前刺激时动作电位时限的缩短和离散以及传导障碍在     

胺碘酮对人在体心室复极离散度的影响

目的使用单相动作电位技术评价静脉推注胺碘酮对人在体心室复极离散度的影响。方法使用铂电极导管记录29例无器质性心脏病患者应用胺碘酮前后右室心尖部和右室流出道的单相动作电位图形,测量各标测点的激动时间(AT)、动作电位时程(APD_(90))、复极时间(RT)、舒张期基线和平台期峰点之间的电位差幅度(AMP),计算各指标的离散度ATd、APDd、RTd。结果 29例患者静脉推注胺碘酮20 min前后,右室心尖部的AT、APD_(90)、RT分别为(16.8±6.1)ms vs (24.3±5.5)ms、(248.3±10.6)ms vs (265.0±13.8)ms、(265.0±13.6)ms vs (282.1±17.3) ms(P均0.01),而右室流出道的AT、APD_(90)、RT分别为(19.1±5.7)msvs (26.2±6.6)ms、(260.0±18.6)ms vs (270.0±15.4)ms和(275.4±16.5)ms vs (294.7±16.4)ms(P均0.01)。而AMP、ATd、APDd、RTd值较用药前差别无统计学意义(P0.05)。结论静脉推注胺碘酮可延长不同部位AT、APD_(90)及RT,但对人在体心室复极离散度各指标无明显影响。     

四氢巴马汀对在体犬跨室壁复极离散度的影响

从跨室壁复极离散度(TDR)的角度研究左旋四氢巴马汀(L-THP)的电生理作用。采用自制电极同步记录在体犬左室三层心肌细胞的单向动作电位(MAP),观察静脉注射L-THP前后动作电位时程(APD)、振幅(APA)、TDR及各层心肌有效不应期(ERP)的变化。结果:应用L-THP后三层心肌的动作电位复极90%的时程均延长(内、中、外层心肌分别为189.67±23.29msvs182.83±23.70ms、194.67±24.12msvs192.17±24.49ms和185.08±24.53msvs173.42±22.06ms,P均<0.01),内、外层心肌ERP显著增加(分别为164.54±20.53msvs159.08±20.08ms、161.60±21.28msvs150.99±18.93ms,P<0.01)、TDR降低(9.58±2.94msvs18.75±3.77ms,P<0.01),对APA无明显影响。结论:L-THP降低心室肌的TDR,延长心室内、外膜心肌细胞的ERP。     

缺血心肌复极离散及迷走神经的保护作用

探讨急性心肌缺血后 ,迷走神经刺激对心室肌不同部位复极时程和复极离散的影响 ,及其对缺血心肌的保护作用。结扎兔冠状动脉左室支 (LVB) ,制备急性心肌缺血模型。分离、结扎并剪断双侧颈迷走、心交感神经 ,电刺激迷走神经外周端。心室复极时程以心外膜电图 (EPG)的QT间期及采用玻璃微电极技术记录的心肌细胞动作电位时程 (APD)表示。分别测定迷走神经刺激前后及缺血前后LVB支配区 (缺血区 )及非支配区 (非缺血区 )的QT间期及APD值。结果 :迷走神经刺激使正常心室肌不同部位的QT间期、APD均有明显缩短 (P <0 .0 5 )。急性心肌缺血后 ,缺血区与非缺血区的QT间期分别是 14 8.6 7± 10 .4 4vs 15 9.5 0± 14 .71ms(P <0 .0 5 ) ;APD90 分别是 :12 8.75±17.84vs 138.0 0± 11.2 2ms(P <0 .0 5 ) ;APD50 分别是 :74 .6 7± 12 .15vs 85 .0 0± 6 .78ms(P <0 .0 5 )。迷走神经刺激后 ,缺血区与非缺血区QT间期、APD差值明显缩小 ,分别是 ,QT间期 :5 .5 8± 1.0 1vs 12 .83± 4 .34ms(P <0 .0 5 ) ;APD904 .5 0± 0 .98vs 11.2 5± 7.0 9ms(P <0 .0 5 ) ;APD50 5 .4 1± 1.2 2vs 12 .5 0± 6 .19ms(P <0 .0 5 )。心肌缺血后心室易损期(VVP)明显延长 34± 2 2 .6 1ms,迷走神经刺激后VVP明显缩短至 11.75± 7.72m     

兔R-on-T室性早搏的时程特征与致心律失常易损窗的关系

目的观察动作电位时程异质性如何影响致心律失常易损窗,以及了解R-on-T室性早搏的时程特征与单向传导阻滞及折返激动易损窗的关系。方法采用冠状动脉灌注兔左室楔形组织块标本,同步记录内、外膜侧心肌细胞动作电位和跨壁心电图。内、外膜侧动作电位时程(APD)的差值(△APD)反映了心室壁跨壁异质性。对标本施加基础刺激(S1),刺激周长分别为2000,1000,500ms。每10次S1后施加S2。S1S2间期以1ms的步长递增,诱发单相传导阻滞和室性心律失常,并分别测量致单向传导阻滞及折返激动易损窗。结果引起单向传导阻滞的易损窗大于产生折返激动的易损窗,当进一步加大复极离散性时才可能引发折返激动。S1刺激诱发室性心动过速时,其R-on-T早搏的时程明显较单纯引起一次心室激动增宽(70.0±15msvs56.1±11ms,P<0.001)。结论单向传导阻滞及折返激动的易损窗与S1刺激所引起心室复极异质性增大有关。R-on-T室性早搏只有在更大的复极梯度状态下,才可能诱发折返激动和室性心动过速、心室颤动。     

体表心电图、腔内单极电图与单相动作电位测定心室复极离散度相关分析

目的探讨心室复极离散度测定方法的可靠性.方法对19例无器质性心脏病者,应用左、右心室内膜单相动作电位(MAP)标测、腔内单极电图(UECG)和体表12导联同步心电图(ECG)3种方法研究心室复极离散度.结果UECG测值(UQ-Td,33±7ms)大于MAP测值(RTd,27±6ms,P＜0.01),而小于体表心电图测值(Q-Td,38±7m,P＜0.01),即Q-Td＞UQ-Td＞R-Td,但UQ-Td与R-Td、UQ-Td与Q-Td、R-Td与Q-Td均呈显著线性相关(r=0.75、0.87,0.78,P均＜0.01).结论体表心电图Q-Td可以代表心室复极离散.     

心室偏心性除极时复极离散度指标的应用

目的　评价显性预激综合征时心室复极离散度指标 ( QTd和 JTd)的临床价值 ,以阐明偏心性心室除极是否导致心室复极离散度异常。方法　选择 4 6例成人显性预激综合征患者行射频消融术 ,观察射频消融前后的心室复极离散度指标 ( QTd和 JTd)的变化。结果　射频消融后最大 QRS时间较消融前缩短 ( 4 6± 2 8) ms,随着预激波消失和 QRS的“正常化”,消融后的 QTd[( 3 0± 13 ) ms]和 QTcd[( 3 7± 19) ms]较消融前的 QTd[( 5 1± 2 3 ) ms]和 QTcd[( 60± 2 7) ms]明显缩短( P值均 <0 .0 5 ) ,而消融后的 JTd[( 2 5± 10 ) ms]和 JTcd[( 2 8± 10 ) ms]与消融前的 JTd[( 2 7± 12 )ms]和 JTcd[( 3 2± 12 ) ms]相比无明显变化 ( P值均 >0 .0 5 )。消融前的预激 QRS波群导致消融前后 QTd和 QTcd的差别。由于消融前后 JTd和 JTcd并无差异 ,表明心室偏心除极不导致复极离散度异常。结论　在显性预激存在时 ,测定心室复极离散度使用 JTd和 JTcd优于 QTd和 QTcd;同时 ,预激时的心室偏心除极不导致复极离散度异常 ,即心室偏心除极不是导致复极离散度异常的机制。     

LQT2模型室性心律失常电生理机制研究

为探讨心室肌跨壁复极离散度 (TDR)和心脏兴奋的恢复性质在长QT综合征 (LQTS)室性心律失常发生过程中的作用 ,应用冠状小动脉灌流的兔左室肌楔形组织块标本 ,分模型组和对照组 ,采用浮置玻璃微电极法同步记录心室肌内、外膜心肌细胞动作电位和跨壁心电图。模型组以 30 μmol/L的d sotalol台氏液灌流 ,制备LQT2模型。对照组以标准台氏液灌流。结果 :模型组和对照组比较TDR有显著性差异 (83.6± 14 .0msvs 4 8.6± 5 .3ms,P <0 .0 1,n =10 )。模型组内、外膜动作电位时程 (APD)恢复曲线最大斜率均大于 1,而对照组均小于 1,两组间APD恢复曲线最大斜率比较有显著性差异 (P <0 .0 1,n =2 0 )。模型组在S1S2 程序刺激下尖端扭转型室性心动过速的发生率为70 %。对照组无 1例发生室性心律失常。结论 :心脏兴奋的恢复性质和心室肌TDR均参与了LQT2室性心律失常的发生。     

兔心肌心室间复极离散的电生理学机制研究

目的观察生理和缺血状态下兔心室间复极离散,探讨临床缺血心肌发生室性心律失常的电生理机制。方法酶解法急性分离兔心室肌细胞,采用细胞膜片钳技术,分别观察对照组(正常心室内膜动作电位时程)和缺血组(缺血心室内膜动作电位时程)在不同刺激频率下[即基础循环周长(basic cycle length,BCL)=2000、1000、500及250 ms]左右心室肌心内膜细胞的动作电位时程变化。结果对照组生理心肌的室间离散分别为(47.70±7.89)ms,(45.50±7.00)ms,(40.30±7.33)ms,(37.90±6.45)ms;缺血后心室间离散则分别为(91.90±7.67)ms,(91.40±7.62)ms,(88.60±7.78)ms,(89.20±6.91)ms。结论生理状态的心肌左右心室间存在复极离散,缺血状态下心室间复极离散增大。这种心室间的复极异质性可能是缺血心肌发生室性心律失常的电生理机制之一。     

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。     

正常心室肌复极离散度初步研究

目的     

Upstream stimulation versus downstream stimulation: arrhythmogenesis based on repolarization dispersion in the human heart

OBJECTIVE: The purpose of this study was to test the hypothesis that a ventricular tachycardia (VT) induction site has a shorter action potential duration (APD) and effective refractory period (ERP) than a noninducing site, resulting in collision against longer ERP ("upstream") as opposed to shorter ERP ("downstream," no collision). BACKGROUND: Induction of sustained VT is often feasible at one stimulation site while application of an identical pacing protocol to another site fails to provoke VT. METHODS: Sixty-nine patients undergoing programmed stimulation for VT inducibility had monophasic action potential recording/pacing catheters placed in the right ventricular outflow tract (RVOT) and right ventricular apex (RVA) simultaneously. Up to three extra-stimuli were introduced in 5 to 10 ms decrements until ERP was reached. Upon completion of a drive cycle at one stimulation site, it was repeated at the other. RESULTS: Thirty-eight patients had inducible VT, nine exclusively by RVA pacing and nine exclusively by RVOT pacing. Action potential duration and ERP at the induction site were significantly shorter (12 +/- 15 ms, p <0.05 and 22 +/- 14 ms, p < 0.01, respectively, at 600 ms basic cycle length) than at the noninduction site. Dispersion of repolarization between corresponding APD at the two sites was 58 +/- 41 ms during baseline stimulation (S1) at the inducing site but only 37 +/- 23 ms at the noninducing site (p < 0.05). Dispersion increased during extra-stimulus application (p < 0.05), reaching a maximum of 75 +/- 45 ms during VT induction, but only 53 +/- 33 ms during extra-stimulation at the noninduction site. CONCLUSIONS: Site specificity of VT induction underscores the role of dispersion of repolarization and refractoriness in facilitating re-entry arrhythmias. Upstream stimulation at a site with short repolarization produces larger dispersion and facilitates VT induction.     

Two-Dimensional Vector Analysis of Beat-to-Beat Dynamics of Ventricular Repolarization

Objective: Duration of ventricular repolarization is a result of complex interaction between autonomic modulation and heart rate (HR). Methods: To study the dynamics of ventricular repolarization of the human right ventricle, beat-to-beat variability of ventricular repolarization was measured by plotting the duration of each monophasic action potential at the 90% phase of repolarization (APD₉₀) as a function of the previous APD90 both in sinus rhythm and during steady-state atrial pacing (cycle length of 600 rns) in 12 subjects without structural heart disease. Results: Quantitative analyses of APD₉₀ and RR interval variability in sinus rhythm showed that the total standard deviation (SD) of APD90 was only 8% of the SD of all RR intervals. Both longterm, continuous variability (SD2) of APD90 (3.9 ± 1.5 ms) and instantaneous beat-to-beat variability (SD1) of APD₉₀ (1.2 ± 0.3 ms) were smaller than the SD2 and SD1 of RR intervals (46 ± 17 ms and 15 ± 9 ms, respectively) (P < 0.001 for both), but the shapes of the APD₉₀ and RR interval plots and the SD1/SD2 ratio did not differ. SD1 of APD90 correlated well with the SD1 of RR intervals (r = 0.64, P < 0.05) but no significant correlation was observed between the SD2 of APD₉₀ and SD2 of RR intervals (r = 0.32, NS). During steady-state atrial pacing, only minimal instantaneous beat-to-beat variability in APD₉₀ (0.9 ± 0.3 rns) was observed but the SD2 was larger than the SD2 of RR intervals (2.3 ± 1.0 ms vs. 1.6 ± 0.8 ms, P < 0.001). Conclusion: The results suggest that instantaneous beat-to-beat variability of ventricular repolarization is mainly due to beat-to-beat fluctuation of HR, but the long-term dynamics of repolarization are partly influenced by other factors than the HR variability.     

The repolarization-excitability relationship in the human right atrium is unaffected by cycle length, recording site and prior arrhythmias.

OBJECTIVES: The goal of this study was to determine the relationship between repolarization and excitability in the human atrium under various conditions. BACKGROUND: Action potential duration (APD) measurements from monophasic action potential (MAP) recordings provide a surrogate for measuring the effective refractory period (ERP) in human ventricle. The relationship between repolarization and refractoriness in human atrium and the effect of prior atrial fibrillation/flutter on the ERP/APD correlation are unknown. METHODS: Seven patients with sinus rhythm and 15 patients after conversion of atrial flutter or fibrillation were evaluated. Monophasic action potentials were recorded at multiple right atrial sites and during different basic cycle lengths from 300 to 700 ms, while ERPs were determined by extrastimulus technique using the MAP recording-pacing combination catheter. RESULTS: There was a close correlation between ERP and APD at 70% repolarization (APD70, r = 0.97; p < 0.001) and 90% repolarization (APD90, r = 0.98; p < 0.001), respectively. Refractoriness occurred at a repolarization level of 72 +/- 8%. The ERP/APD70 and ERP/APD90 ratios averaged 1.06 +/- 0.10 and 0.86 +/- 0.08, respectively. These ratios were nearly constant over the entire range of basic cycle lengths, between different sites in individual patients and between different patients. Patients cardioverted from atrial fibrillation or flutter exhibited no significant differences in the ERP/APD relationship compared with patients with sinus rhythm. CONCLUSIONS: Effective refractory period and APD are closely related in the human right atrium. Using the MAP recording technique, atrial ERPs can be assessed by measurement of APDs. Effective refractory period is most closely reflected by APD70. Thus, MAP recordings allow investigation of the local activation and repolarization time course beat by beat, visualizing the excitable gap.     

Novel electrophysiologic parameter of dispersion of atrial repolarization: comparison of different atrial pacing methods

INTRODUCTION: Heterogeneity of ventricular repolarization plays a major role in reentrant tachyarrhythmias in cardiac tissue. However, the role of atrial repolarization added activation time (AT) to refractoriness in atrial vulnerability has not been investigated in detail. METHODS AND RESULTS: The study population consisted of 34 patients: 18 with atrial fibrillation (AF) and 16 without AF (control group). The effective refractory periods (ERPs) in the right atrial appendage, low lateral right atrium, high right septum, and distal coronary sinus, and ATs from P wave onset to each electrogram during sinus rhythm and right atrial appendage, low lateral right atrial, high right septal, distal coronary sinus, and biatrial pacing were measured. Atrial recovery time, defined as the sum of AT and ERP, and its dispersions during sinus rhythm, right atrial appendage, low lateral right atrial, high right septal, distal coronary sinus, and biatrial pacing were calculated. Both ERP dispersion and atrial recovery time dispersion during sinus rhythm were significantly greater in the AF group than in the control group. Atrial recovery time dispersion during distal coronary sinus, high right septal, or biatrial pacing was significantly smaller than that during right atrial appendage or low lateral right atrial pacing in each group. In particular, atrial recovery time dispersion during distal coronary sinus pacing was the smallest of the five pacing methods in the AF group. P wave duration during biatrial or high right septal pacing was significantly shorter than during right atrial appendage, low lateral right atrial, or distal coronary sinus pacing in each group. CONCLUSION: Atrial recovery time dispersion is suitable as an electrophysiologic parameter of atrial vulnerability. Distal coronary sinus pacing may prevent AF by increasing homogeneity of atrial repolarization, whereas biatrial and high right septal pacing contribute not only homogeneity of atrial repolarization but also improvement of atrial depolarization.     

四氢巴马汀对家犬在体心脏单相动作电位和有效不应期影响的研究

利用单相动作电位 (MAP)技术 ,研究在整体条件下四氢巴马汀 (THP)对家犬在体心脏MAP和有效不应期(ERP)的影响 ,从而探讨THP在整体条件下的抗心律失常机制。家犬 8只 ,体重 12 .5± 3.0 ( 10～ 15 )kg。同时记录家犬右室心尖部的MAP和体表Ⅱ导联心电图 (ECG) ,比较在窦性心律下用药前和用药后 10 ,2 0 ,30min的ERP、MAP复极 5 0 %时程 (MAPD5 0 )和复极 90 %时程 (MAPD90 )以及MAP振幅 (MAPA)的变化。结果 :用药后 10min ,各参数均无明显变化 (P >0 .0 5 ) ;用药 2 0min后 ,ERP、MAPD5 0 和MAPD90 与用药前相比 ,均明显延长 (分别为 139± 18msvs 12 4±18ms,12 6± 16msvs112± 15ms ,16 4± 2 5msvs 140± 16ms,P均 <0 .0 1) ,但用药前后ERP MAPD90 的比值无显著性变化 (P >0 .0 5 )。结论 :THP通过延长动作电位 2相和 3相时程 ,使ERP和MAPD90 平行延长 ,但不改变用药前后ERP MAPD90 比值 ,从而具有增加心肌电稳定性的作用 ,推测此是其具有抗室性心律失常的作用的可能机制     

慢性充血性心力衰竭时K_(ATP)通道与心室肌电生理特性变化的关系

探讨慢性充血性心力衰竭 (CHF)时三磷酸腺苷敏感性钾通道 (KATP通道 )在心室肌电生理特性改变和室性心律失常发生中的意义。采用阿霉素制作CHF兔模型。 2 9只兔分为健康对照组 (HC组 )和CHF实验组 ,后者包括CHF对照组 (CHFC组 )、CHF +KATP通道开放剂组 (P组 )、CHF +KATP通道阻断剂组 (G组 )、CHF +KATP通道开放剂和阻断剂组 (P +G组 )四个亚组。每组均予心房快速起搏 30min ,分别测定起搏前后 90 %单相动作电位时程(MAPD90 )、心室有效不应期 (VERP)及其离散度和兴奋时间 (AT)离散度 ,测定毕程序刺激诱发室性心动过速或心室颤动。结果 :快速起搏使MAPD90 、VERP延长 ,在CHFC组较HC组显著 (11.82± 10 .2 0vs 8.18± 6 .97ms,P <0 .0 5和14 .95± 12 .82vs 9.0 7± 8.79ms,P <0 .0 1) ,而G组和P +G组的MAPD90 、VERP延长更明显。各组快速起搏均未引起MAPD90 、VERP离散度变化 ,但CHFC组和P组都有AT离散度显著增大 (2 8.5 3± 8.6 3vs 36 .80± 6 .97ms ,P <0 .0 1和 2 6 .33± 5 .82vs 33.80± 9.5 0ms,P <0 .0 5 ) ,阻断剂可对抗AT离散度的增大。结论 :快速心房起搏可开放CHF心室肌KATP通道 ,一方面阻止MAPD90 、VERP的延长 ,另一方面又加大AT的非同步性 ,使室性心动过速易于诱发。     

Trans-esophageal stimulation of the heart: electrophysiological properties of the heart of healthy subjects IV

The aim of the study to compare left atrial and ventricular electrophysiological properties determined by transesophageal stimulation with those of right atrium and ventricle measured by other authors using transvenous cardiac stimulation. 45 healthy persons (13 females and 32 males) with average age 37 years underwent the study. Transesophageal pacemaker SP-5 made by TEMED and an universal diagnostic electrode for atrial as well as ventricular stimulation were used to obtain ++noise-free recordings. ECG was recorded by 6-channel Mingograph 61 (Simens-Elema) with a paper speed - 100 mm/s. Left atrial effective refractory period (ERP LA), left ventricular effective refractory period (ERP LV), ERP of a-v conduction system measured from atrium and ventricle (ERP AVCS A, ERP AVCS R) were determined basing on generally acceptable criteria. Parameters were measured during sinus rhythm as well as atrial and ventricular stimulation with a pacing cycle length of 700 and 500 ms. There were also determined maximal antero- and retrograde 1:1 conduction via a-v node and a-v conduction time in both directions during atrial and ventricular pacing with a cycle length of 600 ms. No retrograde a-v conduction was stated in 33% of patients. Shortening of left atrial and ventricular effective refractory periods was respective to shortening of pacing cycle length from 700 to 500 ms: ERPLA-256-245-235 ms, for ERPLV-278-248-241 ms for ERP AVCS A-301, 405, 360 ms and for ERP AVCS R during sinus rhythm-312 ms. Maximal anterograde 1:1 a-v conduction was 162/min and retrograde one 156/min.(ABSTRACT TRUNCATED AT 250 WORDS)     

Repolarization changes underlying long-term cardiac memory due to right ventricular pacing: noninvasive mapping with electrocardiographic imaging

Background- Cardiac memory refers to the observation that altered cardiac electrical activation results in repolarization changes that persist after the restoration of a normal activation pattern. Animal studies, however, have yielded disparate conclusions, both regarding the spatial pattern of repolarization changes in cardiac memory and the underlying mechanisms. The present study was undertaken to produce 3-dimensional images of the repolarization changes underlying long-term cardiac memory in humans. Methods and Results- Nine adult subjects with structurally normal hearts and dual-chamber pacemakers were enrolled in the study. Noninvasive electrocardiographic imaging was used before and after 1 month of ventricular pacing to reconstruct epicardial activation and repolarization patterns. Eight subjects exhibited cardiac memory in response to ventricular pacing. In all subjects, ventricular pacing resulted in a prolongation of the activation recovery interval (a surrogate for action potential duration) in the region close to the site of pacemaker-induced activation from 228.4±7.6 ms during sinus rhythm to 328.3±6.2 ms during cardiac memory. As a consequence, increases are observed in both apical-basal and right-left ventricular gradients of repolarization, resulting in a significant increase in the dispersion of repolarization. Conclusions- These results demonstrate that electrical remodeling in response to ventricular pacing in human subjects results in action potential prolongation near the site of abnormal activation and a marked dispersion of repolarization. This dispersion of repolarization is potentially arrhythmogenic and, intriguingly, was less evident during continuous right ventricular pacing, suggesting the novel possibility that continuous right ventricular pacing at least partially suppresses pacemaker-induced cardiac memory.     

阿魏酸钠与胺碘酮对家兔心室肌电生理作用的频率依赖性影响

与典型的Ⅲ类抗心律失常药物胺碘酮对比 ,研究在整体条件下阿魏酸钠对家兔心室肌电生理特性频率依赖性的影响。 16只家兔随机分为阿魏酸钠组与胺碘酮组 ,应用单相动作电位 (MAP)技术和心脏电刺激方法测定电生理参数 ,比较用药前后、窦性心律及不同起搏频率下心室肌有效不应期 (ERP)、MAP复极 90 %时程 (MAPD90 )的变化。胺碘酮用药后 15min ,在窦律及 180 ,2 0 0 ,2 2 0次 /分起搏频率下 ,MAPD90 的变化率分别为 5 1.5 2± 13.99,5 2 .35±14.5 0 ,5 6 .19± 14.6 3,5 7.15± 16 .6 6 (% ) ,ERP的变化率分别为 5 6 .34± 15 .6 6 ,6 0 .32± 17.0 1,6 1.2 4± 15 .5 4,6 1.0 2±14.0 3(% ) ;阿魏酸钠用药后 2 5min ,在窦律及 2 5 0 ,2 70 ,2 90次 /分起搏频率下 ,MAPD90 的变化率分别为 18.5 3± 3.78,15 .71± 4.41,18.0 0± 6 .12 ,2 0 .48± 5 .6 2 (% ) ,ERP的变化率分别为 18.2 5± 4.6 7,19.76± 3.6 4,2 1.31± 4.18,19.2 5±4.38(% )。结果表明 :阿魏酸钠与胺碘酮作用相似 ,用药后不同起搏频率与窦律时的ERP、MAPD90 变化率及ERP/MAPD90 比值的变化差异无显著性 ,P >0 .0 5。结论 :在整体条件下 ,阿魏酸钠延长心肌复极无逆频率依赖性