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过早逸搏。完整心脏中触发活动的一种模型?

Premature escape beats. A model for triggered activity in the intact heart?

作者信息

Vos M A, Gorgels A P, de Wit B, Drenth J P, van Deursen R T, Leunissen J D, Wellens H J

机构信息

Department of Cardiology, University Hospital Maastricht, University of Limburg, The Netherlands.

出版信息

Circulation. 1990 Jul;82(1):213-24. doi: 10.1161/01.cir.82.1.213.

DOI:10.1161/01.cir.82.1.213
PMID:1694739
Abstract

In conscious dogs with complete atrioventricular block, overdrive pacing of the idioventricular rhythm normally results in overdrive suppression (OS). Frequently, however, we observed another response to overdrive, that is, QRS complex or complexes with unexpectedly short coupling intervals followed by normal OS. We have named such a QRS complex a "premature escape beat" (PEB). Based on the response of PEBs to electrical stimulation, we postulate that PEBs are based on triggered activity resulting from delayed afterdepolarizations. This hypothesis was tested in 82 experiments by 1) stimulation under control conditions and in combination with 2) subtoxic and toxic amounts of ouabain 20-50 micrograms/kg, 3) lidocaine 3 mg/kg, and 4) doxorubicin 16-24 mg/m2. The stimulation protocol, which was repeated at random five to 10 times, consisted of 10 and 50 stimuli using interstimulus intervals of 200, 400, 600, and 800 msec. This protocol was not only performed during spontaneous idioventricular rhythm but also during a continuously paced rhythm with interstimulus intervals of 800 msec. It was found that 1) the chance to induce a PEB or PEBs increased and 2) their first postpacing interval significantly decreased using short or fast drives, or both. Ouabain increased significantly and in a dose-dependent manner 1) the ability to induce PEBs and 2) the number of PEBs per stimulation-train, and also shortened their first postpacing interval. Opposite effects were seen after lidocaine, doxorubicin, and continuous pacing as follows: 1) a lower incidence of PEBs and 2) lengthening of their first postpacing interval. These results support our hypothesis that PEBs are based on triggered activity resulting from delayed afterdepolarizations.

摘要

在有意识的完全性房室传导阻滞犬中,室性自主心律的超速起搏通常会导致超速抑制(OS)。然而,我们经常观察到对超速起搏的另一种反应,即QRS波群或偶联间期意外缩短的QRS波群,随后是正常的OS。我们将这种QRS波群命名为“过早逸搏”(PEB)。基于PEB对电刺激的反应,我们推测PEB基于延迟后去极化引起的触发活动。在82项实验中通过以下方式对该假设进行了检验:1)在对照条件下刺激,并与2)20 - 50微克/千克的亚中毒和中毒量的哇巴因、3)3毫克/千克的利多卡因以及4)16 - 24毫克/平方米的阿霉素联合使用。刺激方案随机重复5至10次,包括使用200、400、600和800毫秒的刺激间期进行10次和50次刺激。该方案不仅在自发室性自主心律期间进行,也在刺激间期为800毫秒的连续起搏心律期间进行。结果发现:1)使用短驱动或快驱动或两者兼用会增加诱发一个或多个PEB的机会,2)其首次起搏后间期显著缩短。哇巴因显著且呈剂量依赖性地增加:1)诱发PEB的能力,2)每个刺激序列中PEB的数量,并且还缩短了其首次起搏后间期。利多卡因、阿霉素和连续起搏后则出现相反的效果:1)PEB的发生率较低,2)其首次起搏后间期延长。这些结果支持了我们的假设,即PEB基于延迟后去极化引起的触发活动。

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