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阿司匹林赖氨酸盐对不稳定型心绞痛患者凝血酶生成的影响。

Effects of aspirin DL-lysine on thrombin generation in unstable angina pectoris.

作者信息

Yasu T, Oshima S, Imanishi M, Nonogi H, Haze K, Kuramochi M, Omae T, Hayashi Y, Yamamoto S

机构信息

Department of Medicine, National Cardiovascular Center, Osaka, Japan.

出版信息

Am J Cardiol. 1993 May 15;71(13):1164-8. doi: 10.1016/0002-9149(93)90640-x.

Abstract

To evaluate the effects of aspirin on thrombin generation in patients with unstable angina, plasma levels of thrombin-antithrombin III complex (TAT) as a new marker of thrombin generation and of 11-dehydro-thromboxane B2 (11-dehydro-TXB2) as an indicator of platelet activation were measured in 18 patients with unstable angina, including 8 patients with prolonged rest angina (> 15 minutes). Aspirin DL-lysine (900 mg) was administered intravenously to 9 of the 18 patients (aspirin group); the other 9 were not given aspirin during the first 24 hours of hospitalization (non-aspirin group). Clinical characteristics, angiographic features and medications other than aspirin were similar between the 2 groups. Levels of plasma TAT and 11-dehydro-TXB2 were significantly higher (p < 0.05) in patients with prolonged rest angina than in those without the condition (n = 10). In 5 patients with prolonged rest angina who received aspirin, plasma TAT levels (ng/ml) were significantly decreased (4.52 +/- 1.18 at baseline, 2.50 +/- 0.65 at 1 hour and 2.16 +/- 0.42 at 24 hours after aspirin administration, p < 0.01) with a significant decrease in plasma 11-dehydro-TXB2 levels. However, the reduction in TAT after aspirin administration was slight in patients without prolonged rest angina (n = 4). In contrast, levels of plasma TAT and 11-dehydro-TXB2 in the non-aspirin group remained unchanged during the study period. These results suggest that aspirin rapidly reduces thrombin generation through inhibition of platelet activity in patients with unstable angina with prolonged rest angina.

摘要

为评估阿司匹林对不稳定型心绞痛患者凝血酶生成的影响,我们检测了18例不稳定型心绞痛患者血浆中作为凝血酶生成新标志物的凝血酶 - 抗凝血酶III复合物(TAT)水平以及作为血小板活化指标的11 - 去氢血栓烷B2(11 - dehydro - TXB2)水平,其中包括8例静息性心绞痛持续时间较长(>15分钟)的患者。对18例患者中的9例静脉注射阿司匹林赖氨酸盐(900毫克)(阿司匹林组);另外9例在住院的最初24小时内未给予阿司匹林(非阿司匹林组)。两组患者的临床特征、血管造影特征以及除阿司匹林外的用药情况相似。静息性心绞痛持续时间较长的患者血浆TAT和11 - dehydro - TXB2水平显著高于无此情况的患者(n = 10,p < 0.05)。在5例接受阿司匹林治疗的静息性心绞痛持续时间较长的患者中,血浆TAT水平(ng/ml)显著降低(给药前基线水平为4.52±1.18,给药后1小时为2.50±0.65,24小时为2.16±0.42,p < 0.01),同时血浆11 - dehydro - TXB2水平也显著降低。然而,在无静息性心绞痛持续时间较长情况的患者(n = 4)中,阿司匹林给药后TAT的降低幅度较小。相比之下,非阿司匹林组患者血浆TAT和11 - dehydro - TXB2水平在研究期间保持不变。这些结果表明,阿司匹林可通过抑制静息性心绞痛持续时间较长的不稳定型心绞痛患者的血小板活性,迅速降低凝血酶生成。

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