Salvioni A, Marenzi G C, Agostoni P, Grazi S, Guazzi M D
Istituto di Cardiologia dell'Università degli Studi, Centro di Studio per le Ricerche Cardiovascolari del Consiglio Nazionale delle Ricerche, Fondazione I. Monzino, IRCCS, Milano, Italy.
Eur Heart J. 1994 May;15(5):654-9. doi: 10.1093/oxfordjournals.eurheartj.a060563.
The purpose of this study was to investigate whether, to what extent, and through which mechanisms intravenous heparin, administered before and after streptokinase, affects the plasma levels of D-dimer and fibrinogen in myocardial infarction. Data concerning mortality and incidence of coronary recanalization in patients receiving heparin and thrombolytic therapy after acute myocardial infarction are controversial; furthermore, the mechanisms through which heparin acts in combination with thrombolytic therapy are unclear. Thirty-eight patients with acute myocardial infarction treated with streptokinase were considered. Nineteen of them received, immediately before the beginning of thrombolytic treatment, a bolus of heparin (100 U.kg-1 intravenously) and, 2 h later, intravenous heparin in doses raising the partial thromboplastin time to 2-2.5 times the normal value (Group 1); the remaining 19 did not receive anticoagulant treatment (Group 2). Multiple determinations of plasma D-dimer and fibrinogen levels were obtained in all patients before, and in the seven days following thrombolytic treatment. Six hours after streptokinase, fibrinogen decreased from 304 +/- 34 to 61 +/- 34 mg.dl-1 in Group 1 and from 312 +/- 29 to 38 +/- 21 mg.dl-1 in Group 2 (P < 0.02 versus Group 1). The same difference between groups persisted at the 12th and at the 18th hour. D-dimer values, from 0.5 +/- 0.1 microgram.dl-1 in Group 1 and 0.4 +/- 0.1 microgram.dl-1 in Group 2, increased at the 1st hour to 37.2 +/- 36.5 micrograms.dl-1 and 52.2 +/- 39.8 micrograms.dl-1, respectively. A peak value was reached in both groups at the 6th hour, which was followed by a slow decrease.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究的目的是调查在链激酶治疗前后静脉注射肝素是否会影响、在何种程度上影响以及通过何种机制影响心肌梗死患者血浆D - 二聚体和纤维蛋白原水平。关于急性心肌梗死后接受肝素和溶栓治疗患者的死亡率及冠状动脉再通发生率的数据存在争议;此外,肝素与溶栓治疗联合作用的机制尚不清楚。研究纳入了38例接受链激酶治疗的急性心肌梗死患者。其中19例在溶栓治疗开始前即刻静脉注射一剂肝素(100 U·kg⁻¹),并在2小时后静脉注射肝素使部分凝血活酶时间延长至正常值的2 - 2.5倍(第1组);其余19例未接受抗凝治疗(第2组)。在所有患者溶栓治疗前及治疗后的7天内多次测定血浆D - 二聚体和纤维蛋白原水平。链激酶治疗6小时后,第1组纤维蛋白原从304±34降至61±34 mg·dl⁻¹,第2组从312±29降至38±21 mg·dl⁻¹(与第1组相比,P < 0.02)。两组间的这种差异在第12小时和第18小时持续存在。第1组D - 二聚体值从0.5±0.1 μg·dl⁻¹,第2组从0.4±0.1 μg·dl⁻¹在第1小时分别增至37.2±36.5 μg·dl⁻¹和52.2±39.8 μg·dl⁻¹。两组均在第6小时达到峰值,随后缓慢下降。(摘要截选至250词)