Acute coronary processes, main cause of non-traumatic death rate in developed countries, impredictably result from instability of a plaque associated with complex cell and molecular net interactions that begins with endothelial dysfunction and follows with plaque disruption, leukocyte and platelet adhesion to endothelial surface, and fibrin and eritrocyte deposition originating an intra-coronary thrombus. Platelets and P-selectin, an adhesion molecule, are key factors in this process. P-selectin is not only involved in the development of early lesions but also in leukocyte rolling over endothelial surface, mainly after ischaemia and reperfusion. P-selectin plasma levels could allow us a better comprehension about the pathophysiology of acute coronary syndromes. By this manner, treatment and disease control could be greatly improved.