Lidón R M
Servei de Cardiologia, Hospital Vall d'Hebron, Barcelona.
Rev Esp Cardiol. 1999;52 Suppl 1:90-6.
Coronary artery thrombosis, due to a rupture of the vulnerable plaque, plays an important role in acute coronary syndromes. The interaction between platelets and thrombin with ruptured vulnerable plaque trigger a complex mechanism. The clinical manifestations depend on the extent and duration of thrombus formation. In the acute phase, aspirin, heparin and the new drugs reduce ischemic clinical outcomes. However, clinical rebound after withdrawal antithrombotic therapy has been observed and, follow-up studies have also documented a high risk of recurrence in the following months. A hypercoagulable state, thrombin generation and activation and haematological rebound is shown in acute coronary syndrome patients. Thus, the goal of treatment could be to control thrombotic response in the acute phase and to allow the healing and stabilization of the culprit lesion to avoid clinical ischemic events in the long-term.
由于易损斑块破裂导致的冠状动脉血栓形成在急性冠状动脉综合征中起重要作用。血小板与凝血酶和破裂的易损斑块之间的相互作用触发了复杂的机制。临床表现取决于血栓形成的程度和持续时间。在急性期，阿司匹林、肝素和新药可降低缺血性临床结局。然而，已观察到停用抗血栓治疗后的临床反跳现象，并且随访研究也记录了接下来几个月内复发的高风险。急性冠状动脉综合征患者表现出高凝状态、凝血酶生成和激活以及血液学反跳。因此，治疗目标可能是在急性期控制血栓形成反应，并使罪犯病变愈合和稳定，以避免长期临床缺血事件的发生。
