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人体心室中超速串刺激的总和与抑制

Summation and inhibition by ultrarapid train pacing in the human ventricle.

作者信息

Swerdlow C D, Liem L B, Franz M R

机构信息

Cardiac Arrhythmia Unit, Stanford University Medical Center 94305.

出版信息

Circulation. 1987 Nov;76(5):1101-9. doi: 10.1161/01.cir.76.5.1101.

DOI:10.1161/01.cir.76.5.1101
PMID:3664995
Abstract

Trains of ultrarapid stimuli that begin late in the refractory period have been reported both to produce early single captures to terminate tachyarrhythmias and to inhibit the response to subsequent threshold stimuli. To determine which characteristics of trains facilitate capture and which enhance inhibition, we compared the right ventricular strength interval relationship for single extrastimuli (S2) with that for 100 Hz trains with a duration of 100 msec in 29 patients. Pulse frequency was varied in 12 patients (50, 100, and 200 Hz) and train duration (50, 100, and 150 msec) was varied in 11 patients; the effect of procainamide (10.1 +/- 2.3 micrograms/ml) was assessed in 10 patients. Relative to S2, 100 Hz trains with a duration of 100 msec prolonged the effective refractory period (ERP) at low current strength (inhibition), but shortened the ERP at high-current strength (summation): at 0.5 mA, the train ERP was 47 +/- 6 (SEM) msec longer than the S2 ERP (p less than .001); at 16 mA it was 12 +/- 1 msec shorter (p less than .001). Trains prolonged the functional refractory period (FRP) slightly at low currents (13 +/- 3 msec, p = .001 at .05 mA), but did not shorten FRP significantly at high currents (2 +/- 2 msec, p = NS at 16 mA) because of increased stimulus-response latency. Inhibition increased with increasing pulse frequency (p less than .001), increasing train duration (p less than .001), and procainamide (p less than .01). Summation increased with increasing pulse frequency (p less than .001), but not increasing train duration or procainamide, suggesting that inhibition and summation depend on different electrophysiologic mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

据报道,在不应期晚期开始的超速刺激串既能产生早期单次夺获以终止快速性心律失常,又能抑制对后续阈刺激的反应。为了确定刺激串的哪些特征有助于夺获,哪些特征增强抑制作用,我们比较了29例患者单次额外刺激(S2)与持续时间为100毫秒的100赫兹刺激串的右心室强度-间期关系。12例患者的脉冲频率有所变化(50、100和200赫兹),11例患者的刺激串持续时间(50、100和150毫秒)有所变化;对10例患者评估了普鲁卡因酰胺(10.1±2.3微克/毫升)的作用。相对于S2,持续时间为100毫秒的100赫兹刺激串在低电流强度时延长有效不应期(ERP)(抑制),但在高电流强度时缩短ERP(总和):在0.5毫安时,刺激串ERP比S2 ERP长47±6(SEM)毫秒(p<0.001);在16毫安时,它短12±1毫秒(p<0.001)。刺激串在低电流时轻度延长功能不应期(FRP)(在0.05毫安时为13±3毫秒,p = 0.001),但在高电流时未显著缩短FRP(在16毫安时为2±2毫秒,p = 无显著性差异),因为刺激-反应潜伏期增加。抑制作用随脉冲频率增加(p<0.001)、刺激串持续时间增加(p<0.001)和使用普鲁卡因酰胺(p<0.01)而增强。总和作用随脉冲频率增加(p<0.001)而增强,但不随刺激串持续时间增加或使用普鲁卡因酰胺而增强,这表明抑制和总和作用依赖于不同的电生理机制。(摘要截断于250字)

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