Hầu hết các trường hợp của STEMI được gây ra bởi một tắc huyết khối động mạch vành lớn hơn (5). Quá trình sinh lý bệnh cơ bản được bắt đầu bởi huyết khối hình thành bức tranh tường như một phản ứng của một vỡ một mảng xơ vữa xơ vữa động mạch không ổn định hoặc xói mòn nội mô (17). | Most cases of STEMI are caused by a thrombotic occlusion of a larger coronary artery 5 . The underlying pathophysiological process is initiated by mural thrombus formation as a reaction of a rupture of an unstable atherosclerotic plaque or endothelial erosion 17 . It is of interest that the majority of cases are not due to a higher degree of stenosis. Indeed most infarctions develop at plaque sites that are haemodynamically irrelevant 18 . The initial process of mural thrombus formation is adhesion and aggregation of platelets followed by integration of fibrin via the glycoprotein IIb IIIa GP IIb IIIa receptor which finally stabilises the clot. Following this concept the initial causal treatment targets inhibition of both platelet activation and fibrin formation. Antiplatelet treatment Acetylsalicylic acid ASA ASA is the mainstay of antiplatelet therapy inhibiting the COX1 pathway of thromboxane formation Fig 3 . Thus ASA blocks one of the routes to the common final step of activation of the GP IIb IIIa receptor which is necessary for bridging platelets by fibrin and the final formation of a stable thrombus. ASA has been shown to reduce the case fatality rate by 1 4 in the ISIS II trial 19 . Since then ASA has become routine in the treatment of STEMI patients irre- ArachidonicAcid ASA Adhesion X GP llb llla receptor blockers Platelet aggregation Thrombus formation Figure 3 Mechanism of platelet activation This is trial version spective of whether primary PCI or thrombolysis is planned for reperfusion. In addition ASA is standard for life-long secondary prevention after an ischaemic cardiac event 20 . Even if there is no stringent data on time dependency of ASA treatment for STEMI there is a general consensus in all guidelines that an initial loading dose of 160-325 mg as a chewable tablet or . should be given as early as possible provided that the patient does not suffer from a true allergy to ASA. This initial loading dose may also be given to
