Lindgren A, Lindoff C, Norrving B, Astedt B, Johansson B B
Department of Neurology, University Hospital, Lund, Sweden.
Stroke. 1996 Jun;27(6):1066-71. doi: 10.1161/01.str.27.6.1066.
Abnormal endogenous fibrinolytic activity may be a risk factor for stroke. Since the possible variation of tissue-type plasminogen activator (TPA) antigen and plasminogen activator inhibitor-1 (PAI-1) antigen concentrations over time after stroke has been rarely studied, it was examined in plasma from stroke patients in the acute and convalescent phases of the disease and in a control group.
Plasma concentrations of TPA and PAI-1 were determined in 135 stroke patients and in 77 control subjects. All but 4 patients were examined within 7 days after stroke onset, and 32 patients and 18 control subjects were reexamined 2 to 4 years later.
In the acute phase, stroke patients had significantly higher TPA (median, 10 micrograms/L) and PAI-1 (median, 14 micrograms/L) antigen concentrations, compared with control subjects (median values, 6 micrograms/L [P = .0001] and 8 micrograms/L [P < .01], respectively); TPA levels were higher in both the cerebral infarction (n = 122) and cerebral hemorrhage (n = 12) subgroups, whereas PAI-1 levels were higher in the cerebral infarction subgroup only. Stepwise logistic regression analysis (with correction for age, sex, history of hypertension, diabetes mellitus, and heart disease) showed TPA antigen level to be an independent discriminator between the cerebral infarction subgroup and control subjects (P = .0001), whereas the corresponding difference for PAI-1 antigen levels just failed to reach significance (P = .05). TPA antigen levels were correlated with concentrations of serum cholesterol (Spearman's rho = 0.15; P < .05), serum triglyceride (rho = 0.33; P = .0001), and plasma homocysteine (rho = 0.19; P < .01). PAI-1 antigen levels were correlated with serum triglyceride levels only (rho = 0.41; P = .0001). At reexamination after 2 to 4 years, neither TPA nor PAI-1 levels had changed significantly from the baseline values.
In stroke patients, high TPA antigen concentrations may indicate an activation of the fibrinolytic system or may be due to a delayed clearance of TPA complexed with inhibitors. High PAI-1 antigen concentrations in patients with cerebral infarction represent increased fibrinolytic inhibition. The findings in this longitudinal study suggest that TPA and PAI-1 antigen concentrations both differ little between the acute and convalescent phases after stroke.
内源性纤溶活性异常可能是卒中的危险因素。由于卒中后组织型纤溶酶原激活物（TPA）抗原和纤溶酶原激活物抑制剂-1（PAI-1）抗原浓度随时间的可能变化鲜有研究，因此对卒中患者急性期和恢复期血浆以及对照组血浆进行了检测。
测定了135例卒中患者和77例对照者的血浆TPA和PAI-1浓度。除4例患者外，所有患者均在卒中发病后7天内接受检测，32例患者和18例对照者在2至4年后再次接受检测。
急性期时，卒中患者的TPA（中位数为10微克/升）和PAI-1（中位数为14微克/升）抗原浓度显著高于对照者（中位数分别为6微克/升[P = 0.0001]和8微克/升[P < 0.01]）；在脑梗死（n = 122）和脑出血（n = 12）亚组中TPA水平均较高，而仅在脑梗死亚组中PAI-1水平较高。逐步逻辑回归分析（校正年龄、性别、高血压病史、糖尿病史和心脏病史）显示，TPA抗原水平是脑梗死亚组与对照者之间的独立鉴别指标（P = 0.0001），而PAI-1抗原水平的相应差异刚未达到显著性（P = 0.05）。TPA抗原水平与血清胆固醇浓度（Spearman秩相关系数rho = 0.15；P < 0.05）、血清甘油三酯（rho = 0.33；P = 0.0001）和血浆同型半胱氨酸（rho = 0.19；P < 0.01）相关。PAI-1抗原水平仅与血清甘油三酯水平相关（rho = 0.41；P = 0.0001）。在2至4年后的复查中，TPA和PAI-1水平与基线值相比均无显著变化。
在卒中患者中，高TPA抗原浓度可能表明纤溶系统激活，或可能是由于与抑制剂结合的TPA清除延迟所致。脑梗死患者中高PAI-1抗原浓度代表纤溶抑制增强。这项纵向研究的结果表明，卒中后急性期和恢复期TPA和PAI-1抗原浓度差异均不大。
