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* References: 1. Kuwahara M et al. Arterioscler Thromb Vasc Biol 2002; 22: 329–34. 2. Libby P, Simon DI. Circulation 2001; 103: 1718–20. Platelet shape Flowing disk-shaped platelets become ball-shaped on interaction with von Willebrand factor via the glycoprotein Ib receptor. This interaction starts the platelet rolling, releasing ‘inside out’ signals, promoting change to a hemispherical shape. This increases the surface area of the platelet in contact with the vessel surface and helps the platelet to resist rapid blood flow which could dislodge it from the surface. At this point, platelets do stop on the vessel surface, but adhesion is still reversible. Further activation via ‘outside-in’ signaling leads to irreversible platelet adhesion and extensive spreading, generating a greater thrombogenic base to capture further platelets to aggregate on the surface.1 Platelet aggregation Platelets themselves are now recognized as a source of inflammatory mediators rather than just responders to thrombotic stimuli. Inflammation can give rise to local thrombosis which can amplify inflammation. Anti-inflammatory therapies (such as ASA) may therefore limit thrombosis and antithrombotic therapies may reduce vascular inflammation, thereby breaking the vicious cycle of acute coronary syndromes.2 * To explain usefulness of 2Strategy manegement, It is useful to propose the Virchows triad. Dr. Virchow proposed three factors in thrombogenesis this way. It is easier for us to explain the 2 Strategy Management by using this triad. * The hemostatic process to form a thrombus is not uniform – size and composition of the blood clot varies with the site of injury. The result of plaque rupture and consequent thrombus formation can therefore be an acute event (such as myocardial infarction), or contribute to the long-term underlying progression of vascular disease. A large fissure typically results in the formation of a large thrombus that completely occludes the vessel resulting