Knudsen J B, Kjøller E, Skagen K, Gormsen J
Thromb Haemost. 1985 Jun 24;53(3):332-6.
A group of 43 consecutive patients with AMI were randomized to treatment with a novel platelet inhibitor, ticlopidine, or placebo in a double blind study. Treatment was started within 12 hr after onset of precordial pain. Patients who had taken drugs with known platelet inhibitory effect prior to the onset of therapy were excluded. Platelet survival time (PS) was measured 24-36 hr after onset of precordial pain and after 3 months of treatment in both groups. In the early phase of AMI CK-MB and ASAT were taken twice daily for estimation of infarction size. Platelet function, coagulation factors and fibrinolysis parameters were followed sequentially for 21 days and repeated after 3 months. In the placebo group a significant reduction in PS (5.62 +/- 1.63 S. D. days) was measured in the acute phase of AMI compared to PS 3 months after infarction (8.03 +/- 1.20 S.D. days). In the ticlopidine group PS was normal during the acute phase (8.35 +/- 1.82 S.D. days). After 3 months of treatment PS was normal in both groups. During the first two weeks after AMI significant changes in coagulation parameters and fibrinolysis indicated an increased risk of thrombosis in both groups. These parameters were unaffected by the platelet inhibitory therapy. Estimated by peak CK-MB and ASAT, infarction size was significantly reduced in the ticlopidine group.
在一项双盲研究中,将43例连续的急性心肌梗死(AMI)患者随机分为两组,分别接受新型血小板抑制剂噻氯匹定治疗或安慰剂治疗。在胸前区疼痛发作后12小时内开始治疗。排除在治疗开始前服用过已知具有血小板抑制作用药物的患者。在两组患者胸前区疼痛发作后24 - 36小时以及治疗3个月后测量血小板存活时间(PS)。在AMI早期,每天两次测定肌酸激酶同工酶(CK - MB)和天门冬氨酸氨基转移酶(ASAT)以评估梗死面积。连续21天依次跟踪血小板功能、凝血因子和纤维蛋白溶解参数,并在3个月后重复测量。在安慰剂组中,与梗死后3个月时的PS(8.03±1.20标准差天)相比,AMI急性期的PS显著降低(5.62±1.63标准差天)。在噻氯匹定组中,急性期PS正常(8.35±1.82标准差天)。治疗3个月后,两组的PS均正常。在AMI后的前两周,凝血参数和纤维蛋白溶解的显著变化表明两组的血栓形成风险增加。这些参数不受血小板抑制治疗的影响。通过CK - MB和ASAT峰值估计,噻氯匹定组的梗死面积显著减小。