房室结双径路顺传及逆传有效不应期研究

目的：研究房室结双径路（DAVNP）快径、慢径的顺传及逆传有效不应期。方法：通过心内电生理方法对25例房室结折返性心动过速的病人行心房、心室程序刺激,测定快径、慢径的顺传及道传文氏点、有效不应期（ERP）、跃增值。结果：快径与慢径的顺传ERP有极显著性差异（P＜0．001）。未分组时顺传及逆传文氏点、快径ERP、慢径ERP、跃增值比较无显著性差异。根据顺传快径ERP是否大于逆传快径ERP分为两组,再分别比较顺传快径ERP和逆传快径ERP,发现有非常显著差异,P均＜0．001。结论：DAVNP快径的顺传ERP和逆传ERP截然不同,可能存在快径顺传优势型和快径逆传优势型两种类型,其机制尚不清楚。     

A波延迟电位在慢径消融靶点定位中的应用

为了探讨A波延迟电位在慢径消融靶点定位中的应用价值 ,对传统下位法和A波延迟电位引导下的慢径消融两组病例的靶点的电生理特征进行了研究。结果 :延迟电位引导下的慢径消融在提高成功率、减少试放电方面明显优于下位法。有效靶点的突出特征是A波宽度 >6 8ms、A波终末具延迟电位 ,A/V比例不能作为预测靶点的指标。A波延迟电位有四种形态 ,分别为单弓状延迟电位、双弓状延迟电位、穗状电位及A波终末的高频电位 ,其中以前两种最为常见。当程序刺激遇快径不应期而经慢径传导时 ,靶点正传的A波更加延迟 ,逆传A波更加领先是成功靶点的特征。结论 :在慢径消融的靶点定位中应用A波延迟电位和程序刺激可提高成功率、减少盲目性 ,A波延迟电位引导慢径消融方法优于传统的消融方法慢径消融方法优于传统的消融方法     

隐匿性拖带时起搏后间期与慢径消融成功靶点的关系

评价应用隐匿性拖带方法对准确靶点消融的有效性及探讨常规慢径靶点部位与房室结折返性心动过速(AVNRT)折返环的关系。可反复诱发的持续性典型AVNRT的患者 34例 ,消融导管在后或中间隔标测到A/V≤ 0 .5处 ,然后诱发心动过速 ,在高位右房 (HRA)和冠状窦口 (CSO)超速起搏产生隐匿性拖带 ,并按常规方法进行慢径消融。比较隐匿性拖带时靶点部位起搏后间期与心动过速周长的差值 (PPI-TCL值 )在成功靶点与不成功靶点区别。结果 :HRA超速起搏发生隐匿性拖带时 ,His束记录部位A波均为逆向夺获。而CSO超速起搏拖带时 ,32例His束记录部位A波为顺向夺获 ,另 2例为逆向夺获。在这 32例中共记录 5 4个靶点 ,成功靶点的PPI-TCL值明显小于不成功靶点 (12 .4± 5 .8msvs 32 .1± 18.6ms,P <0 .0 1)。PPI-TCL值≤ 2 0ms对靶点成功消融的敏感性和特异性分别为 84%、81%。结论 :本研究提示常规慢径消融成功部位作为房室结外的后部延伸组织参与组成AVNRT折返环或距其非常近。在可持续发作和诱发的AVNRT患者中 ,CSO部位起搏拖带顺向心房夺获时 ,靶点部位测出的PPI-TCL值≤ 2 0ms,可作为一种新的慢径路电生理定位消融方法     

射频消融术后复发原因分析

目的 了解射频消融治疗各种心律失常复发原因。方法 通过1108例射频消融治疗病例进行回顾性总结,对其中40例复发患者从诊断、消融部位、靶点图形、功率、即刻成功时间和术中是否诱发心动过速及术后心电生理情况以及消融技术开展时间等方面进行临床分析,总结复发原因。结果 ①总复发率为3.7%,其中房室折返性心动过速3.1%,房室结折返性心动过速2.6%;②对诊断复杂,右侧旁道,靶点V-Q间期小于10 ms,消融功率大于25 W,即刻成功长于5秒,消融时AV波稳定性差及术中未诱发心动过速的房室折返性心动过速患者容易复发（P＜0.01）;③对消融功率大于30 W才出现结性心律,术中未诱发心动过速及术后仍存在心房回波和A-H跳跃现象的房室结折返性心动过速也容易复发（P＜0.01）;④对V-Q间期短于20 ms的室性期前收缩也易复发;⑤复发病例多集中在消融技术开展的第2～5年。结论诊断是否明确,对消融靶点的掌握,消融部位及功率的选择,即刻成功时间,术中是否诱发心动过速及消融技术开展时间是引起射频消融治疗心律失常复发的主要原因。     

Coronary Sinus Obstruction after Atrioventricular Canal Defect Repair

The coronary sinus can become obstructed with any instrumentation at or near the ostium such as in atrioventricular canal defect repairs. This complication may lead to a wide range of consequences including dyspnea, angina, myocardial infarction, and sudden death. The following report illustrates the importance of careful perioperative echocardiographic evaluation of the coronary sinus in procedures that may affect the sinus and its ostium.     

右室心尖部起搏对完全性房室传导阻滞高龄患者心功能的影响

目的探讨心脏永久起搏器在心功能基本正常的高龄患者中的应用,评价右室心尖部(RVA)起搏对高龄患者心功能的影响。方法43例年龄≥75岁的完全性房室传导阻滞患者分为两组,VVI型起搏器23例,DDD型起搏器20例,心房电极置于右心耳,心室电极置于右室心尖部。术后平均随访12个月,了解患者自觉症状、运动耐量(6min步行距离试验)、起搏器功能情况及左室射血分数(LVEF)和脑利尿钠肽(BNP)水平。结果所有患者随访期间起搏器功能正常,新发生心房颤动5例;与术前相比,术后6分钟步行距离有改善[(368.58±65.74)mvs(377.47±57.72)m,P<0.01],LVEF无改变[(52.05±4.71)%vs(51.86±4.77)%,P>0.05],血浆BNP升高[(234.93±151.86)ng/Lvs(262.07±122.53)ng/L,P<0.05];术后随访期间,6分钟步行距离、LVEF和全血BNP,VVI组和DDD组相比无差别。结论高龄患者完全RVA起搏改善症状,未观察到加重心功能损害状况。     

直流电消融房室交界区及其诱发心律失常的实验研究

本研究采用细电极导管,1～3次电击,对犬房室交界区进行消融。结果5只犬有4只术后1小时仍为完全性房室传导阻滞(CAVB),仅1只形成慢性CAVB。所有犬均见心律失常出现。病理显示,病损广泛而不均匀,界限不清,伴明显水肿;慢性期病变进展,新旧病变共存,可能是构成心律失常发生的基础。本研究表明,直流电击消融房室交界区损伤广泛而不易控制,急慢性心律失常影响消融的效果和预后。     

Pharmacological analysis of the activity of the adenosine uptake inhibitor,dipyridamole, on the sinoatrial and atrioventricular nodes of the guinea-pig

1. Dipyridamole potentiates the effects of adenosine on the heart by inhibiting adenosine uptake. The effects of dipyridamole on both adenosine and N-ethylcarboxamidoadenosine (NECA) concentration-effect (E/[A]) curves were compared on the AV node, in guinea-pig isolated perfused hearts, and on the SA node, in isolated right atria, by measuring dromotropic and chronotropic responses, respectively. In the absence of dipyridamole, adenosine was significantly more potent on the AV node than SA node (AV p[A]₅₀=4.95±0.10, SA p[A]₅₀=3.62±0.10). In contrast, NECA and adenosine in the presence of dipyridamole were approximately equiactive in the two assays (NECA: AV p[A]₅₀=7.07±0.07; SA p[A]₅₀=7.30±0.08; adenosine: AV p[A]₅₀=6.49±0.08; SA p[A]₅₀=6.27±0.05). Dipyridamole was significantly more potent in enhancing the effects of adenosine on the SA node than on the AV node (pK_i values estimated by Kenakin''s method (1981): AV node=8.18±0.14; SA node=8.75±0.08).
2. The difference in pK_i values did not appear to be due to dipyridamole expressing other actions because concentrations of dipyridamole which saturated the adenosine transporter had no effect on the NECA E/[A] curves in either assay. However, the test of another assumption of Kenakin''s method, that adenosine taken up into cells is pharmacologically inactive, failed on the AV node assay because a significant potentiating interaction was found between adenosine and NECA. The interaction was concentration-dependent, reciprocal to the extent that pre-incubation with either agonist potentiated the other and was concluded to be due to an intracellular action of adenosine as the potentiation disappeared in the presence of dipyridamole.
3. An explanatory model was developed to account for the data obtained using existing pharmacological concepts of ligand action in isolated tissue bioassays. In the model, adenosine, but not NECA, was assumed to be subject to saturable agonist uptake, an uptake which was competitively blocked by dipyridamole. Adenosine and NECA were assumed to act extracellularly at adenosine A₁-receptors. In the AV node, but not the SA node, the adenosine transported into the cells was assumed to potentiate the effects of adenosine A₁-receptor activation. For the AV node assay, the model predicted that potentiation of adenosine by uptake blockade is offset by a simultaneous decrease in potentiation due to the intracellular action of adenosine. All of the experimental data obtained in the study could be accounted for by the model including the apparent differences in potency of adenosine in the absence of dipyridamole and the pK_i values for dipyridamole.

     

菸酰胺治疗房室传导阻滞的疗效观察

本文报道应用菸酰胺治疗8例房室传导阻滞患者,其中4例是高度房室传导阻滞患者,实践提示应用此药治疗本症是一种满意的方法。