الفهرس 
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Abstract
ACS is a major cause of morbidity and mortality worldwide. ACS is typically arising from atherosclerotic plaque rupture with subsequent coronary thrombosis and/or spasm. The resulting coronary artery occlusion gives rise to intense myocardial ischemia or even necrosis. In the pathophysiology of CAD, platelet activation is important. The a-granule is a crucial component of platelet secretion and has a role in both membrane-bound proteins that are produced on the surface of the platelet and soluble proteins that are released into the extracellular environment. sTLT-1 is one of the several membranebound and soluble proteins that the a-granules release. By sticking to endothelial cells and leaving chemotactic mediators on their surface, platelets have an impact on atherogenesis. As a result, it is possible that sTLT-1, which acts as a chemotactic mediator after being released, plays a role in the process of atherothrombosis. This mediator helps to connect organized thrombi to the vascular endothelium as well as stimulate additional platelets. The pathogenic processes causing ACS include platelet aggregation and thrombus development following plaque rupture. This study was conducted on 80 individuals divided into: 60 patients with ACS selected from cardiology department, Faculty of Medicine, Tanta university hospitals and 20 apparently healthy subjects used as reference group. In this study we assessed sTLT-1 as a biomarker for ACS. Plasma sTLT-1 was measured by enzyme-linked immunosorbent assay in patients with ACS and control subjects. In this work, sTLT-1 level was significantly increased in patients with ACS than control group ( P value <0.001). In conclusion, this study revealed that ACS is associated with increased level of sTLT-1. It suggests a means of how sTLT-1 participates in the pathophysiology of plaque generation and/or atherothrombosis.