Salvioni A, Giraldi F, Assanelli E, Lauri G, Grazi M, Pardea S, Marenzi G
Istituto di Cardiologia, Università degli Studi, Centro di Studio per le Ricerche Cardiovascolari del CNR, IRCCS, Milano.
Cardiologia. 1998 Aug;43(8):825-32.
Myocardial infarction and thrombolysis are proven to be associated with platelet activation. However, the time relationship of platelet activation with the onset of symptoms and with thrombolysis, and the response to aspirin are not well defined. In this study we measured platelet activity in the early phase of myocardial infarction treated with either streptokinase or recombinant tissue-type plasminogen activator (rt-PA) and evaluated whether and to what extent it may be counteracted by aspirin. Fourty-one patients (mean age 57 +/- 6 years) received thrombolytic therapy after coronary occlusion: 1.5 million units of streptokinase (Group 1; 21 patients) or 100 mg of rt-PA (Group 2; 20 patients). Ten randomly selected patients in either group were given 500 mg aspirin i.v. prior to infusion of the thrombolytic compound and, then, 325 mg/die of aspirin orally. Beta-thromboglobulin (BTG), a marker of platelet activity, was determined at admission, after thrombolysis and in the subsequent 48 hours. At admission, BTG plasma levels averaged 125 +/- 31 IU/ml in Group 1 and 134 +/- 35 IU/ml in Group 2 (NS). Thrombolysis produced a similar increase in platelet activity in both groups, and maximal values were reached at the third hour (196 +/- 43 IU/ml in Group 1 and 192 +/- 39 in Group 2, p < 0.001 vs baseline and NS between groups). Levels of BTG were higher in streptokinase-treated group starting from 24 hours (p < 0.05). Differences in BTG levels between aspirin-treated and aspirin-untreated patients became significant at 48 hours after thrombolysis in both groups. An inverse correlation was found between time elapsed from onset of symptoms and BTG value on admission (r = -0.86, p < 0.001); in patients admitted within 2 hours after the beginning of symptoms, and having the higher BTG levels, thrombolysis did not induce a significant increase in platelet activity; this, on the contrary, was observed in patients admitted later. Platelet activation is greater early after myocardial infarction and is differently influenced by thrombolytic treatment, depending on the delay of the patient's admission. Streptokinase and rt-PA induce a similar increase in platelet activity which is more persistent after streptokinase; cycloxygenase inhibition with aspirin seems to influence platelet activity only starting from the second day.
心肌梗死和溶栓治疗已被证实与血小板激活有关。然而，血小板激活与症状发作及溶栓治疗之间的时间关系，以及对阿司匹林的反应尚不清楚。在本研究中，我们测量了用链激酶或重组组织型纤溶酶原激活剂（rt-PA）治疗的心肌梗死早期患者的血小板活性，并评估了阿司匹林是否以及在何种程度上可以抵消血小板活性。41例患者（平均年龄57±6岁）在冠状动脉闭塞后接受了溶栓治疗：150万单位链激酶（第1组；21例患者）或100mg rt-PA（第2组；20例患者）。每组随机选择10例患者在输注溶栓药物前静脉注射500mg阿司匹林，然后口服325mg/d的阿司匹林。在入院时、溶栓后及随后48小时测定血小板活性标志物β-血小板球蛋白（BTG）。入院时，第1组BTG血浆水平平均为125±31IU/ml，第2组为134±35IU/ml（无显著性差异）。两组溶栓后血小板活性均有相似程度的升高，且在第3小时达到最大值（第1组为196±43IU/ml，第2组为192±39IU/ml，与基线相比p<0.001，两组间无显著性差异）。从24小时起，链激酶治疗组的BTG水平较高（p<0.05）。两组溶栓后48小时，阿司匹林治疗组和未治疗组的BTG水平差异均有统计学意义。症状发作至入院时间与入院时BTG值呈负相关（r=-0.86，p<0.001）；症状开始后2小时内入院且BTG水平较高的患者，溶栓后血小板活性无显著升高；相反，在较晚入院的患者中观察到血小板活性升高。心肌梗死后早期血小板激活更明显，且溶栓治疗对其影响不同，这取决于患者入院的延迟时间。链激酶和rt-PA诱导的血小板活性升高相似，但链激酶诱导的升高更持久；阿司匹林抑制环氧化酶似乎仅从第二天起影响血小板活性。
