M. Paassilta , K. Kervinen , K.J. Peuhkurinen , Y.A. Kesäniemi
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引用次数: 3
摘要
Lp(a)可能干扰血栓形成和溶栓。我们跟踪了20名急性心肌梗死患者的Lp(a)水平,这些患者随机接受链激酶(SK,n=10)或组织纤溶酶原激活剂(t-PA,n=10。将结果与五名保守治疗患者的结果进行比较。研究组的基线特征相同。Lp(a)水平在t-PA输注期间显著增加(22.1%)(P<0.005 t-PA vs SK,P<0.005 t-PA vs保守治疗),但在SK输注和保守治疗期间保持不变。在所有三组中,入院3天后,观察到血清Lp(a)水平更显著增加(t-PA、SK和保守治疗组分别为51.8%、24.4%和36.8%),可能反映了急性期反应。尽管这项研究的规模相对较小,但Lp(a)与t-PA溶栓治疗之间的联系可能值得关注,其背后的机制有待阐明。Lp(a)水平的改变可能与溶栓剂、血栓、凝血级联反应和影响溶栓和再闭塞的内皮之间的复杂相互作用有关。
Thrombolysis with tissue plasminogen activator enhances serum lipoprotein(a) levels compared to streptokinase and conservative treatment in patients with acute myocardial infarction
Lp(a) may interfere with thrombosis and thrombolysis. We followed Lp(a) levels in 20 patients with acute myocardial infarction randomized to receive streptokinase (SK, n=10) or tissue-plasminogen activator (t-PA, n=10). The results were compared to those obtained with five patients treated conservatively. Baseline characteristics were equal in the study groups. Lp(a) levels increased significantly, (22.1%) during t-PA infusion (P<0.005 t-PA vs SK, P<0.005 t-PA vs conservative treatment), but they remained unchanged during SK infusion and conservative treatment. In all three groups, a more prominent increase in serum Lp(a) levels, (51.8%, 24.4%, and 36.8% for the t-PA, SK, and conservative treatment groups, respectively), was observed 3 days after the admission to the hospital, probably reflecting an acute phase reaction. Although the size of the study is relatively small, the suggested linkage between Lp(a) and thrombolytic treatment with t-PA may be of interest, and the mechanisms behind it need to be elucidated. The alterations in Lp(a) levels may be involved in the complex interactions between thrombolytic agents, thrombus, clotting cascade, and endothelium affecting thrombolysis and reocclusion.