Nordt T K, Moser M, Kohler B, Ruef J, Peter K, Kübler W, Bode C
Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany.
Thromb Haemost. 1998 Dec;80(6):881-6.
Reocclusion after thrombolysis diminishes the benefits of early reperfusion after acute myocardial infarction (AMI). No clinical or laboratory variables have been identified as predictors for reocclusion yet.
To evaluate hemostatic variables as potential risk determinants platelet aggregation (PA, representing platelet activity), thrombin/antithrombin complexes (TAT, representing thrombin generation), and plasminogen activator inhibitor type 1 (PAI-1, representing endogenous fibrinolysis) were determined in 31 patients with AMI at 0, 1, 2. and 12 h after the start of thrombolysis as well as at hospital discharge. Reocclusion (defined as reinfarction or angiographically confirmed, clinically silent coronary reocclusion) occurred in 5 patients within 5-14 days and in 8 patients within 1 year. TAT plasma concentrations were lower in patients with reocclusion than in those without (9.9+/-5.7 vs. 22.9+/-22.2 ng/ml at 2 h, 6.5+/-3.1 vs. 1 1.2+/-6.4 ng/ml at 12 h, means+/-SD, p <0.05 each). Neither concentration nor activity of PAI-1 in plasma differed between both patient groups. However, both slope and maximum of PA (induced by 2 micromol/l ADP) were augmented in patients with reocclusion (slope: 39.4+/-1.7 vs. 32.5+/-7.4 at 2 h, p <0.001; 42.6+/-2.6 vs. 36.6+/-8.9 at 12 h, p <0.01). Results were independent of the thrombolytic agent used (alteplase or reteplase). A PA slope at 2 h higher than the average slope before thrombolysis (37.2+/-5.7) could be identified as best predictor for early (within 5-14 d, p=0.017, sensitivity 1.00, specificity 0.69) and late reocclusion (within 1 y, p=0.009, 0.88 and 0.74, respectively).
Increased PA following coronary thrombolysis appears to be associated with early and late reocclusion. This marker could be useful in identifying patients who may benefit from more aggressive antiplatelet (such as GP IIb/IIIa receptor antagonists), interventional, or both strategies.
溶栓后再闭塞会降低急性心肌梗死（AMI）早期再灌注的益处。目前尚未确定任何临床或实验室变量可作为再闭塞的预测指标。
为了评估止血变量作为潜在风险决定因素，我们对31例AMI患者在溶栓开始后的0、1、2和12小时以及出院时测定了血小板聚集（PA，代表血小板活性）、凝血酶/抗凝血酶复合物（TAT，代表凝血酶生成）和纤溶酶原激活物抑制剂1型（PAI-1，代表内源性纤维蛋白溶解）。5例患者在5至14天内发生再闭塞（定义为再梗死或血管造影证实的临床无症状冠状动脉再闭塞），8例患者在1年内发生再闭塞。再闭塞患者的TAT血浆浓度低于未发生再闭塞的患者（2小时时分别为9.9±5.7 vs. 22.9±22.2 ng/ml，12小时时分别为6.5±3.1 vs. 11.2±6.4 ng/ml，均值±标准差，每次p<0.05）。两组患者血浆中PAI-1的浓度和活性均无差异。然而，再闭塞患者的PA（由2微摩尔/升ADP诱导）斜率和最大值均增加（斜率：2小时时为39.4±1.7 vs. 32.5±7.4，p<0.001；12小时时为42.6±2.6 vs. 36.6±8.9，p<0.01）。结果与所用溶栓药物（阿替普酶或瑞替普酶）无关。2小时时的PA斜率高于溶栓前的平均斜率（37.2±5.7）可被确定为早期（5至14天内，p = 0.017，敏感性1.00，特异性0.69）和晚期再闭塞（1年内，分别为p = 0.009，敏感性0.88，特异性0.74）的最佳预测指标。
冠状动脉溶栓后PA增加似乎与早期和晚期再闭塞有关。该标志物可能有助于识别那些可能从更积极的抗血小板治疗（如糖蛋白IIb/IIIa受体拮抗剂）、介入治疗或两者结合的策略中获益的患者。
