Høst N B, Hansen S S, Jensen L T, Husum D, Nielsen J D
Division of Rheumatology, Hvidovre Hospital, Copenhagen, Denmark.
Cardiology. 1994;85(5):323-33. doi: 10.1159/000176705.
The objective of the study was to monitor collagen metabolism after thrombolytic therapy. Sequential measurements of serum aminoterminal type-III procollagen propeptide (S-PIIINP) and carboxyterminal type-I procollagen propeptide (S-PICP) were made in 62 patients suspected of acute myocardial infarction and receiving thrombolytic therapy. Regardless of whether acute myocardial infarction was confirmed or not, S-PIIINP increased (94-120%) 4 h after streptokinase therapy (p < or = 0.02), and decreased during the next 20 h with median values at 24 h still above the baseline (p < 0.02). With confirmed acute myocardial infarction, S-PIIINP increased from 24 h towards a plateau reached at day 2-3 (p < 0.01), with values still elevated at 6 months. No similar biphasic pattern was found for S-PICP, but patients with acute myocardial infarction had S-PICP above baseline at 1, 2, and 6 months (p < 0.05). A less pronounced S-PIIINP increase was noted with tissue-plasminogen activator than with streptokinase. Thrombolytic therapy induces collagen breakdown regardless of whether acute myocardial infarction is confirmed or not. With confirmed acute myocardial infarction collagen metabolism is altered for at least 6 months. Furthermore, fibrin-specific and nonspecific thrombolytic agents appear to affect collagen metabolism differently.
该研究的目的是监测溶栓治疗后的胶原代谢情况。对62例疑似急性心肌梗死并接受溶栓治疗的患者，连续测量血清Ⅲ型前胶原氨基端前肽（S-PIIINP）和Ⅰ型前胶原羧基端前肽（S-PICP）。无论急性心肌梗死是否确诊，链激酶治疗4小时后S-PIIINP升高（94-120%）（p≤0.02），并在接下来的20小时内下降，24小时时的中位数仍高于基线（p<0.02）。确诊为急性心肌梗死时，S-PIIINP从24小时开始上升，至第2-3天达到平台期（p<0.01），6个月时仍升高。S-PICP未发现类似的双相模式，但急性心肌梗死患者在1、2和6个月时S-PICP高于基线（p<0.05）。与链激酶相比，组织型纤溶酶原激活剂导致的S-PIIINP升高不太明显。无论急性心肌梗死是否确诊，溶栓治疗均可诱导胶原分解。确诊为急性心肌梗死时，胶原代谢至少在6个月内发生改变。此外，纤维蛋白特异性和非特异性溶栓剂对胶原代谢的影响似乎不同。
