Høst N B, Stoltenberg M B, Jensen L T, Larsen O G, Aurup P
Department of Medicine, Hvidovre Hospital, Copenhagen, Denmark.
Eur J Clin Invest. 1995 Jan;25(1):15-8. doi: 10.1111/j.1365-2362.1995.tb01519.x.
This paper assesses alterations in collagen metabolism following thrombolytic therapy of acute myocardial infarction with tissue-plasminogen activator. Sequential serum measurements of the amino-terminal propeptide of type III procollagen (S-PIIINP) and the carboxyterminal propeptide of type I collagen (S-PICP) in patients suspected of acute myocardial infarction randomized to tissue-plasminogen activator or placebo were used. S-PIIINP increased at 3 h in patients with acute myocardial infarction treated with tissue-plasminogen activator (P < 0.05). S-PIIINP was higher in patients treated with tissue-plasminogen activator compared with placebo-treated patients at 3 and 6 h (P < 0.05). S-PICP decreased independently of therapy and diagnosis. Tissue-plasminogen activator, therefore, induces breakdown of collagen, some of which is located in the wall of atheromatous arteries. Vascular patency following thrombolytic therapy may partly be mediated by breakdown of thrombogenic collagen in the vessel wall. The findings may suggest a role for S-PIIINP as a non-invasive indicator of the risk of reocclusion.
本文评估了使用组织型纤溶酶原激活剂对急性心肌梗死进行溶栓治疗后胶原代谢的变化。对疑似急性心肌梗死的患者进行随机分组，分别给予组织型纤溶酶原激活剂或安慰剂，并对其血清中III型前胶原氨基端前肽（S-PIIINP）和I型胶原羧基端前肽（S-PICP）进行连续测定。接受组织型纤溶酶原激活剂治疗的急性心肌梗死患者在3小时时S-PIIINP升高（P<0.05）。在3小时和6小时时，接受组织型纤溶酶原激活剂治疗的患者的S-PIIINP高于接受安慰剂治疗的患者（P<0.05）。S-PICP的降低与治疗和诊断无关。因此，组织型纤溶酶原激活剂可诱导胶原分解，其中一些胶原位于动脉粥样硬化动脉壁中。溶栓治疗后的血管通畅可能部分是由血管壁中促血栓形成的胶原分解介导的。这些发现可能提示S-PIIINP作为再闭塞风险的非侵入性指标具有一定作用。
