程序电刺激时心室复极离散度的研究

了解程序电刺激 (PES)时心室复极离散度的变化 ,探讨PES诱发室性快速心律失常 (VTA)的可能机制。采用单相动作电位 (MAP)标测技术测定 10例无器质性心脏病的阵发性室上性心动过速患者接受PES时的心室复极离散度。结果 :S1 S1 刺激 ( 5 0 0ms)时的动作电位时程 (APD)的离散度 (APDd)与窦性心律时无明显差异 ( 34± 10msvs38± 9ms ,P >0 .0 5 )。随S1 S2 间期缩短 ,各标测点S2 的APD逐渐缩短 ,且与S1 S2 间期呈正相关 ,但激动时间 (AT)及其离散度 (ATd)、APDd、复极时间离散度 (RTd)逐渐延长 ;S1 S2 间期缩短至有效不应期 (ERP) +30ms后 ,S2 的APDd、RTd大于窦性心律及S1 S1 刺激时 (APDd :5 1± 8msvs 38± 9ms或 34± 10ms,P <0 .0 5 ;RTd :39± 10msvs2 4± 7ms,P<0 .0 5 ) ,但ATd无明显增大。心室内各点有效不应期离散度为 31± 14ms,ERP APD平均为 0 .89± 0 .0 8。认为在无器质性心脏病者PES可使心室复极离散度增大 ,但不增加传导差异 ,不易诱发VTA     

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.     

Monophasic action potential mapping in human subjects with normal electrocardiograms: direct evidence for the genesis of the T wave

T wave concordance in the normal human electrocardiogram (ECG) generally is explained by assuming opposite directions of ventricular depolarization and repolarization; however, direct experimental evidence for this hypothesis is lacking. We used a contact electrode catheter to record monophasic action potentials (MAPs) from 54 left ventricular endocardial sites during cardiac catheterization (seven patients) and a new contact electrode probe to record MAPs from 23 epicardial sites during cardiac surgery (three patients). All patients had normal left ventricular function and ECGs with concordant T waves. MAP recordings during constant sinus rhythm or right atrial pacing were analyzed for activation time (AT) = earliest QRS deflection to MAP upstroke, action potential duration (APD) = MAP upstroke to 90% repolarization, and repolarization time (RT) = AT plus APD. AT and APD varied by 32 and 64 msec, respectively, over the left ventricular endocardium and by 55 and 73 msec, respectively, over the left ventricular epicardium. On a regional basis, the diaphragmatic and apicoseptal endocardium had the shortest AT and the longest APD, and the anteroapical and posterolateral endocardium had the longest AT and the shortest APD (p less than .05 to less than .0001). RT was less heterogeneous than APD, and no significant transventricular gradients of RT were found. In percent of the simultaneously recorded QT interval, epicardial RT ranged from 70.8 to 87.4 (mean 80.7 +/- 3.9) and endocardial RT ranged from 80 to 97.8 (mean 87.1 +/- 4.4) (p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

犬短QT综合征发生心室颤动的电生理机制研究

目的：研究犬短QT综合征模型易发致命性心室颤动的电生理机制.方法：应用吡那地尔建立比格犬短QT综合征模型,利用篮状电极标测左室心内膜心肌电位.比较静脉推注吡那地尔（负荷剂量0.5 mg/kg,维持剂量每小时0.5 mg/kg）前后,QT间期、T波峰末间期（Tp-Te）、心肌细胞复极90％的动作电位（APD90）及激动恢复时间（ARI）、心室颤动周长（VF-CL）等参数的变化. 结果：与基础状态相比,吡那地尔显著缩短窦性心律和300 ms起搏时的QT间期,分别为（264±17） ms对（240±15） ms,P＜0.01;（247±7）ms对（229±10） ms,P＜0.01.应用吡那地尔后,APD90、ARI和VF-CL均较基础值显著降低,分别为（175±11） ms对（164±11） ms,P＜0.01;（156±11） ms对（147±10） ms,P＜0.01;（104±9） ms对（95±7）ms,P＜0.01.同时,Tp-Te间距较基础状态延长19％,即（35.8±3.4） ms对（44.1±1.4） ms,P＜0.01. 结论：不应期缩短和不应期心室跨壁离散度增加可能是吡那地尔诱导短QT综合征并发致命性室性心律失常的电生理基础.     

Comparison of QT dispersion during atrial fibrillation and sinus rhythm in the same patients, at normal and prolonged ventricular repolarization.

AIMS: Drug-induced increase in QT dispersion has been associated with increased risk of ventricular proarrhythmia. The aim of the present study was to compare QT dispersion during atrial fibrillation and sinus rhythm in the same patients at normal and prolonged ventricular repolarization. METHODS AND RESULTS: Sixty-one patients who had had chronic atrial fibrillation for 8 +/- 14 months received a 6 h infusion of the Ikr-blocker almokalant, the first 90 min of which are used for this analysis. The following day, after conversion to sinus rhythm, by almokalant (n = 19) or direct current cardioversion (n=42), an identical 90 min infusion was administered. Prior to infusion, there was no difference in precordial QT dispersion between atrial fibrillation and sinus rhythm (29 +/- 12 vs 36 +/- 17 ms, P=ns). During infusion, at prolonged repolarization, the increase in QT dispersion was greater during sinus rhythm than during atrial fibrillation (58 +/- 49 vs 30 +/- 15 ms, P=0.0011, after 30 min infusion). No correlation was found between QT dispersion and the QT or RR interval. CONCLUSION: QT dispersion during atrial fibrillation does not differ from QT dispersion during sinus rhythm during normal repolarization. while measurement of QT dispersion during prolonged repolarization, induced by an Ikr-blocker, yielded larger values during sinus rhythm than during atrial fibrillation.     

Dispersion of atrial repolarization in patients with paroxysmal atrial fibrillation.

To study the role of the dispersion of atrial repolarization (DAR) in the genesis of atrial fibrillation (AF), monophasic action potentials (MAP) were recorded simultaneously from a catheter at the high lateral right atrium (HLRA) and a catheter moving around the high, middle and low lateral right atrium (RA) the high, anterior and posterior septal RA and the RA appendage in 15 patients with paroxysmal AF and 15 patients with atrioventricular nodal re-entry tachycardia (AVNRT) or concealed Wolff-Parkinson-White syndrome (WPW) without history of AF. After recordings during sinus rhythm (SR), MAPs were recorded during programmed stimulation (PS) via the HLRA catheter at a drive cycle length (CL) of 500 ms. Thus, MAPs were recorded simultaneously from 2 sites at a time and sequentially from 4 to 12 sites during SR, drive pacing and PS. Taking the MAP at the HLRA as reference, the dispersion of repolarization time (dispersion of RT) and its two components, the dispersions of activation time (dispersion of AT) and MAP duration (dispersion of MAP duration) among the 4 to 12 sites were calculated and taken as parameters of DAR. RESULTS: During SR and PS, the maximal dispersion of RT was significantly greater in AF than in control patients, 113+/-49 ms vs 50+/-28 ms (P<0.001) and 114+/-56 vs 70+/-43 ms (P<0.05) respectively. The increased dispersion of RT in the AF group was caused by increases in both dispersion of MAP duration and dispersion of AT. CONCLUSION: During SR and PS, DAR increased in patients with paroxysmal AF due to increases in dispersion of MAP duration and dispersion of AT, which suggests the involvement of both repolarization and conduction disturbances in the development of paroxysmal AF.     

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     

心肌缺血对心室颤动的诱发和除颤效率的影响

近来埋藏式心律转复除颤器（ＩＣＤ）已成为抗心律失常药物治疗无效的高危病人的优先选择。由于大多数需要ＩＣＤ治疗的病人常伴有缺血性心脏病,因此急性心肌缺血对ＩＣＤ病人的除颤失败和心脏猝死可能起一定作用。本文在离体灌流兔心脏标本上测定了急性心肌缺血对单相动作电位（ＭＡＰ）各参数以及心室颤动（ＶＦ）诱发和除颤的影响。结果表明,心肌缺血１５ｍｉｎ缩短ＭＡＰ时程（复极达９０％,ＡＰＤ９０）（１５４±８ｍｓｖｓ１０２±１８ｍｓ,Ｐ＜０．００１）和复极时间（ＲＴ９０）（１８５±６ｍｓｖｓ１３８±１３ｍｓ,Ｐ＜０．００１）;使激活时间（ＡＴ）增加（３１±５ｍｓｖｓ３６±８ｍｓ,Ｐ＜０．０１）;同时使ＲＴ９０弥散明显增加（３７±１６ｍｓｖｓ６９±２９ｍｓ,Ｐ＜０．０１）。心肌缺血对易损性上限（ＵＬＶ）和除颤阈值（ＤＦＴ）稍有影响,但无统计学意义（ＵＬＶ：２７４±５３Ｖｖｓ２９４±４４Ｖ,Ｐ＝ＮＳ;ＤＦＴ２６８±４２Ｖｖｓ２７１±３３Ｖ,Ｐ＝ＮＳ）;却使易损窗（ＶＷ）的宽度增加三倍（对照２５±２２ｍｓ,缺血１５ｍｉｎ时７５±２６ｍｓ,Ｐ＜０．００１）。复极时间与ＶＷ边界的相关分析表明,ＶＷ左边界和１０个ＭＡＰ中最短的ＲＴ９０高度?     

Activation and repolarization of the normal human heart under complete physiological conditions

Knowledge of normal human cardiac excitation stems from isolated heart or intraoperative mapping studies under nonphysiological conditions. Here, we use a noninvasive imaging modality (electrocardiographic imaging) to study normal activation and repolarization in intact unanesthetized healthy adults under complete physiological conditions. Epicardial potentials, electrograms, and isochrones were noninvasively reconstructed. The normal electrophysiological sequence during activation and repolarization was imaged in seven healthy subjects (four males and three females). Electrocardiographic imaging depicted salient features of normal ventricular activation, including timing and location of the earliest right ventricular (RV) epicardial breakthrough in the anterior paraseptal region, subsequent RV and left ventricular (LV) breakthroughs, apex-to-base activation of posterior LV, and late activation of LV base or RV outflow tract. The repolarization sequence was unaffected by the activation sequence, supporting the hypothesis that in normal hearts, local action potential duration (APD) determines local repolarization time. Mean activation recovery interval (ARI), reflecting local APD, was in the typical human APD range (235 ms). Mean LV apex-to-base ARI dispersion was 42 ms. Average LV ARI exceeded RV ARI by 32 ms. Atrial images showed activation spreading from the sinus node to the rest of the atria, ending at the left atrial appendage. This study provides previously undescribed characterization of human cardiac activation and repolarization under normal physiological conditions. A common sequence of activation was identified, with interindividual differences in specific patterns. The repolarization sequence was determined by local repolarization properties rather than by the activation sequence, and significant dispersion of repolarization was observed between RV and LV and from apex to base.     

胺碘酮对电击诱发心室颤动和除颤阈值的影响

目的研究胺碘酮对单、双相电击的易损窗、易损上、下限以及除颤阈值（ＤＦＴ）的影响。方法在离体Ｌａｎｇｅｎｄｏｒｆ灌流兔心脏上记录单相动作电位以测量激活时间、动作电位时程（ＡＰＤ９０）、９０％复极恢复时间及其离散度。结果与对照组相比，胺碘酮延长ＡＰＤ９０和９０％复极时间（Ｐ＜００５），但并不改变激活时间离散度和９０％复极时间离散度；使单、双相电击的易损窗都显著右移（Ｐ＜００１），但对易损窗的宽度无影响；对单相电击的易损下限无影响，但显著抬高双相电击的易损下限；对易损上限和ＤＦＴ无影响。结论胺碘酮将单、双相电击的易损窗都右移并提高双相电击的易损下限，但在该模型中对两种电击的易损上限、ＤＦＴ和易损窗宽度均无直接影响。