Biasucci L M, Liuzzo G, Caligiuri G, Quaranta G, Andreotti F, Sperti G, van de Greef W, Rebuzzi A G, Kluft C, Maseri A
Institute of Cardiology, Catholic University of the Sacred Heart, Rome, Italy.
Circulation. 1996 Jun 15;93(12):2121-7. doi: 10.1161/01.cir.93.12.2121.
Although a major role of coronary thrombosis in the pathogenesis of unstable angina has been demonstrated, the results of a series of studies have suggested that activation of the hemostatic system may not be confined to ischemic episodes. The purpose of this study was to investigate the temporal relation between ischemic episodes and activation of the coagulation system in unstable angina.
Thrombin-antithrombin III (TAT) and prothrombin fragment 1 + 2 (F1 + 2) levels were measured in 13 patients during spontaneous ischemic episodes (time 0, 5, and 15 minutes and 1 hour) to evaluate the time course of the activation of the coagulation system associated with the development of ischemia (protocol A). TAT and F1 + 2 levels were also measured in 28 patients with unstable angina on admission to hospital (every 6 hours for 24 hours and daily for 3 days) to assess their temporal relation with ischemic episodes (protocol B). In protocol A, TAT and F1 + 2 levels were elevated in 10 of 13 patients (77%) in at least 1 sample. The median value of TAT showed a peak at 5 minutes and returned to baseline within 15 minutes (P < .05), consistent with its plasma half-life of 5 minutes, whereas the median value of F1 + 2 showed no significant changes, possibly because of its longer half-life, which tends to dampen sudden bursts of thrombin production. In protocol B, activation of the clotting system was found in 10 of 33 samples (30%) temporally related to ischemia and also in 23 of 150 (15%, P = .07) of those not temporally related to ischemia.
Our study demonstrates that patients with active unstable angina develop frequent bursts of thrombin production not necessarily associated with ischemic episodes and that, conversely, some ischemic episodes are not associated with evidence of thrombin activation.
尽管冠状动脉血栓形成在不稳定型心绞痛发病机制中的主要作用已得到证实，但一系列研究结果表明，止血系统的激活可能并不局限于缺血发作。本研究的目的是探讨不稳定型心绞痛患者缺血发作与凝血系统激活之间的时间关系。
对13例患者在自发性缺血发作期间（0、5、15分钟及1小时）测定凝血酶 - 抗凝血酶III（TAT）和凝血酶原片段1 + 2（F1 + 2）水平，以评估与缺血发展相关的凝血系统激活的时间进程（方案A）。还对28例不稳定型心绞痛患者入院时（24小时内每6小时一次，连续3天每天一次）测定TAT和F1 + 2水平，以评估它们与缺血发作的时间关系（方案B）。在方案A中，13例患者中有10例（77%）至少有1个样本的TAT和F1 + 2水平升高。TAT的中位数在5分钟时达到峰值，并在15分钟内恢复到基线水平（P <.05），与其5分钟的血浆半衰期一致，而F1 + 2的中位数无显著变化，可能是因为其半衰期较长，倾向于抑制凝血酶产生的突然爆发。在方案B中，在与缺血时间相关的33个样本中有10个（30%）发现凝血系统激活，在与缺血时间不相关的150个样本中有23个（15%，P =.07）也发现凝血系统激活。
我们的研究表明，活动性不稳定型心绞痛患者频繁出现凝血酶生成爆发，不一定与缺血发作相关，相反，一些缺血发作与凝血酶激活的证据无关。
