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驱动链刺激强度对人体心室不应期的影响。

Effects of drive train stimulus intensity on ventricular refractoriness in humans.

作者信息

Langberg J J, Calkins H, Sousa J, el-Atassi R, Morady F

机构信息

Department of Internal Medicine, University of Michigan Medical Center, Ann Arbor, 48109-0022.

出版信息

Circulation. 1991 Jul;84(1):181-7. doi: 10.1161/01.cir.84.1.181.

Abstract

BACKGROUND

The strength-interval relation between the intensity of premature stimulus and the ventricular effective refractory period (VERP) has been well characterized. The effects of variation in the intensity of the basic drive train stimuli (S1) on VERP are not as well defined. This relation was studied in 44 patients undergoing clinically indicated electrophysiological study.

METHODS AND RESULTS

The outputs of two stimulus isolation units were connected in parallel, allowing the intensity of S1 to be varied independently of intensity of the extrastimulus (S2). To prevent confounding effects from cycle length change, continuous overdrive pacing was performed for 3 minutes before each measurement of VERP. The effect of S1 intensity on VERP was assessed in 24 patients with S2 intensity kept constant at twice threshold. VERP shortened from 232 +/- 19 msec at an S1 intensity of 1.5 times threshold to 219 +/- 20 msec at 5 mA and 211 +/- 19 msec at 10 mA (p less than 0.0001 for baseline versus 5 mA and for 5 mA versus 10 mA). Autonomic blockade with atropine and propranolol blunted but did not completely eliminate this effect. To assess whether the effect of S1 intensity on VERP was independent of S2 intensity, S2 strength-interval curves were generated in 10 patients at low (1.5 times threshold) and high (10 mA) S1 intensities. All portions of the strength-interval curve were shifted to the left by an increase in S1 intensity. The time course of change in VERP after an abrupt increase in S1 intensity was assessed in an additional 10 patients. VERP changed slowly, requiring 18 +/- 28 seconds to shorten by 2 msec and 64 +/- 46 seconds to decrease by 10 msec after a change in S1 intensity from 1.5 times threshold to 10 mA. In a final group of 10 patients, VERP was measured using an eight-beat drive train and a 4-second intertrain interval. With this more conventional protocol, VERP shortened by 14 +/- 8 msec with an increase in S1 intensity from 1.5 times threshold to 10 mA.

CONCLUSIONS

Increasing S1 intensity results in clinically significant, progressive shortening of VERP in man. This effect is independent of S2 intensity. The prolonged time course of the change in VERP after an increase in S1 intensity and the attenuation of this effect by autonomic blockade are consistent with stimulation of sympathetic nerve terminals and catecholamine release as a result of intense stimulation.

摘要

背景

过早刺激强度与心室有效不应期(VERP)之间的强度-间期关系已得到充分表征。基础驱动序列刺激(S1)强度变化对VERP的影响尚不明确。在44例接受临床指征性电生理研究的患者中对这种关系进行了研究。

方法与结果

将两个刺激隔离单元的输出并联,使S1强度能够独立于额外刺激(S2)的强度进行变化。为防止周期长度变化产生混淆效应,在每次测量VERP前进行3分钟的连续超速起搏。在24例患者中,将S2强度保持在阈值的两倍不变,评估S1强度对VERP的影响。VERP在S1强度为阈值1.5倍时为232±19毫秒,在5毫安时缩短至219±20毫秒,在10毫安时缩短至211±19毫秒(基线与5毫安以及5毫安与10毫安相比,p均小于0.0001)。使用阿托品和普萘洛尔进行自主神经阻滞可减弱但不能完全消除这种效应。为评估S1强度对VERP的影响是否独立于S2强度,在10例患者中,分别在低(阈值1.5倍)和高(10毫安)S1强度下生成S2强度-间期曲线。随着S1强度增加,强度-间期曲线的所有部分均向左移位。另外10例患者评估了S1强度突然增加后VERP变化的时间进程。VERP变化缓慢,S1强度从阈值1.5倍增加到10毫安后,VERP缩短2毫秒需要18±28秒,缩短10毫秒需要64±46秒。在最后一组10例患者中,使用八次搏动的驱动序列和4秒的序列间期测量VERP。采用这种更传统的方案,随着S1强度从阈值1.5倍增加到10毫安,VERP缩短了14±8毫秒。

结论

增加S1强度会导致人体VERP出现具有临床意义的渐进性缩短。这种效应独立于S2强度。S1强度增加后VERP变化的时间进程延长以及自主神经阻滞对这种效应的减弱,与强烈刺激导致交感神经末梢受刺激和儿茶酚胺释放一致。

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