Karlberg K E, Chen J, Hagerman I, Bergström K, Wallin R, Saldeen T, Sylvén C
Department of Medicine, Karolinska Institute, Huddinge University Hospital, Sweden.
J Intern Med. 1993 Nov;234(5):513-9. doi: 10.1111/j.1365-2796.1993.tb00786.x.
To investigate if tissue plasminogen activator (tPA) and streptokinase given during acute myocardial infarction (AMI) have different effects on platelet aggregation which could contribute to the higher reocclusion rate observed after tPA.
Open labelled on consecutive patients.
Coronary care unit.
Twenty patients with chest pain and ST elevations on an electrocardiogram suggestive of AMI.
Ten patients were treated with tPA (100 mg 3 h-1), 10 patients with streptokinase (1.5 x 10(6) IU 1 h-1).
Before, immediately after and 24 h after fibrinolytic therapy, platelet aggregation was estimated with filtragometry and whole blood aggregometry. Fibrinogen, beta-thromboglobulin, elastase and the fibrinogen-derived peptide B beta 30-43 were also measured.
The groups were comparable at baseline. Directly after treatment, streptokinase prolonged aggregation time in filtragometry with 112 +/- 140 s (P < 0.03) and reduced conductance in whole blood aggregometry by 6.2 +/- 6.1 omega (P < 0.03), both tests indicating inhibited platelet function. Fibrinogen decreased 2.5 +/- 1.0 g l-1 (P < 0.02). In the tPA-treated group corresponding changes were 68 +/- 225 s (NS) and 2.5 +/- 7 omega (NS) with no significant reduction in fibrinogen. After 24 h, at which time every patient was on acetylsalicylic acid, aggregation was inhibited in both groups as measured by aggregometry. Directly after fibrinolytic treatment, neutrophils were similarly activated in both groups with increments of elastase and B beta 30-43 by 26 +/- 46 micrograms l-1 (P < 0.03) and 280 +/- 381 pmol l-1 (P < 0.03) respectively (streptokinase) and by 12 +/- 6 micrograms l-1 (P < 0.02) and 919 +/- 856 pmol l-1 (P < 0.02) respectively (tPA).
Despite similar degrees of platelet and leucocyte activation, streptokinase but not tPA treatment appears to inhibit platelet aggregation. One possible reason could be a streptokinase-induced pronounced decrease of fibrinogen and increase of fibrinogen split products. Therefore, further development of adjuvant antiplatelet therapy could be of clinical importance.
研究急性心肌梗死（AMI）期间给予组织型纤溶酶原激活剂（tPA）和链激酶是否对血小板聚集有不同影响，这可能是tPA治疗后再闭塞率较高的原因。
对连续患者进行开放标签研究。
冠心病监护病房。
20例胸痛且心电图ST段抬高提示AMI的患者。
10例患者接受tPA治疗（100mg 3小时-1），10例患者接受链激酶治疗（1.5×10⁶IU 1小时-1）。
在溶栓治疗前、治疗后即刻及治疗后24小时，采用过滤法和全血凝集法评估血小板聚集情况。同时测定纤维蛋白原、β-血小板球蛋白、弹性蛋白酶和纤维蛋白原衍生肽Bβ30-43。
两组在基线时具有可比性。治疗后即刻，链激酶使过滤法中的聚集时间延长112±140秒（P<0.03），全血凝集法中的电导率降低6.2±6.1Ω（P<0.03），两项检测均表明血小板功能受到抑制。纤维蛋白原降低2.5±1.0g/L（P<0.02）。在tPA治疗组中，相应变化为68±225秒（无统计学意义）和2.5±7Ω（无统计学意义），纤维蛋白原无显著降低。24小时后，此时每位患者均服用阿司匹林，通过凝集法检测两组的聚集均受到抑制。溶栓治疗后即刻，两组中性粒细胞均被类似激活，链激酶组弹性蛋白酶和Bβ30-43分别增加26±46μg/L（P<0.03）和280±381pmol/L（P<0.03），tPA组分别增加12±6μg/L（P<0.02）和919±856pmol/L（P<0.02）。
尽管血小板和白细胞激活程度相似，但链激酶治疗而非tPA治疗似乎能抑制血小板聚集。一个可能的原因可能是链激酶诱导纤维蛋白原显著降低和纤维蛋白原裂解产物增加。因此，辅助抗血小板治疗的进一步研发可能具有临床重要性。
