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止血对接受择期经皮腔内冠状动脉成形术的临床稳定患者再狭窄的相关性。

Relevance of hemostasis on restenosis in clinically stable patients undergoing elective PTCA.

作者信息

Schoebel F C, Peters A J, Kreis I, Gradaus F, Heins M, Jax T W

机构信息

Heinrich Heine Universität Düsseldorf, Medizinische Klinik und Poliklinik B, Klinik für Kardiologie, Pneumologie und Angiologie, Moorenstrasse 5, 40225 Düsseldorf, Germany.

出版信息

Thromb Res. 2008;122(2):229-36. doi: 10.1016/j.thromres.2007.10.007. Epub 2007 Dec 3.

DOI:10.1016/j.thromres.2007.10.007
PMID:18054069
Abstract

BACKGROUND

Secondary coronary thrombus formation is considered to be co-factor in the pathogenesis of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Therefore systemic factors indicating a hypercoagulable disease state may be relevant for the process of coronary renarrowing. Even though experimental data suggest that in particular thrombin may be of major relevance for restenosis induced by mechanical injury, only little clinical data has been presented so far.

METHODS AND RESULTS

In 60 consecutive patients, who had been clinical stable for at least 2 months, and who underwent elective and primarily successful PTCA, follow-up films were evaluated by means of quantitative coronary angiography in respect to a categorical and a continuous definition of restenosis, luminal narrowing >50% and late luminal loss respectively. Of the chosen laboratory variables prothrombin fragment 1+2 (1.3+/-0.5 vs. 0.9+/-0.4 mmol/l, p<0.001) red blood cell aggregation at low shear stress (13.5+/-2.9 vs. 11.6+/-2.8 units, p<0.05), and plasminogen-activator inhibitor (3.7+/-1.8 vs. 5.3+/-3.2 U/ml p<0.05) differentiated between patients with (n=18) and without restenosis (n=42). Late luminal loss correlated positively with prothrombin fragment 1+2 (r=0.41, p<0.001), plasminogen-activator inhibitor (r= -0.28, p<0.05) and plasmin-alpha2-antiplasmin complex (r=0.39, p<0.01).

CONCLUSIONS

A hypercoagulable disease state and in particular thrombin generation characterize a high-risk group prone for restenosis in clinically stable coronary artery disease.

摘要

背景

继发性冠状动脉血栓形成被认为是经皮腔内冠状动脉成形术(PTCA)后再狭窄发病机制中的一个辅助因素。因此,提示高凝疾病状态的全身因素可能与冠状动脉再狭窄过程相关。尽管实验数据表明,尤其是凝血酶可能与机械损伤诱导的再狭窄密切相关,但迄今为止仅有少量临床数据。

方法与结果

对60例连续患者进行研究,这些患者临床稳定至少2个月,接受了择期且初次成功的PTCA,通过定量冠状动脉造影对随访影像进行评估,采用再狭窄的分类和连续定义,即管腔狭窄>50%和晚期管腔丢失。在所选择的实验室变量中,凝血酶原片段1+2(1.3±0.5 vs. 0.9±0.4 mmol/l,p<0.001)、低切应力下红细胞聚集(13.5±2.9 vs. 11.6±2.8单位,p<0.05)以及纤溶酶原激活物抑制剂(3.7±1.8 vs. 5.3±3.2 U/ml,p<0.05)在有再狭窄(n=18)和无再狭窄(n=42)的患者之间存在差异。晚期管腔丢失与凝血酶原片段1+2(r=0.41,p<0.001)、纤溶酶原激活物抑制剂(r=-0.28,p<0.05)和纤溶酶-α2-抗纤溶酶复合物(r=0.39,p<0.01)呈正相关。

结论

高凝疾病状态,尤其是凝血酶生成,是临床稳定的冠状动脉疾病中易于发生再狭窄的高危人群的特征。

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