Plaque, Platelets, and Plug – The Pathogenesis of Acute Coronary Syndrome

Acute coronary syndrome is a clinical condition of partial or total obstruction of blood flow in the coronary artery due to acute thrombus formation. Culprit vessel, coronary artery segment within which the site of origin of thrombus formation lies, is occupied by eroded or ruptured atherosclerotic plaque. Direct contact between circulating blood constituent and atherosclerotic plaque content owing to loss of endothelial cell barrier orchestrates the haemostasis events, i.e. thrombus formation and coagulation activation. Evolved within years of human life span, atherosclerotic undergoes three main steps: initiation, progression and finally complication (Libby, 2002). Atherosclerotic plaque development involves cellular and molecular interactions as well as blood flow dynamic alterations in the affected area. Although these steps affect all individual, some gather the risk factors to develop progression and complication of coronary atherosclerotic lesion faster and more prominent than others. Given the dynamic nature of these steps, understanding several mechanisms engage in every step will provide insight into therapeutic approach. Here, we review the last two steps of coronary atherosclerotic plaque development, with the focus in the role of platelets, anucleated cells being the target for therapeutic advancement in atherosclerosis and acute coronary syndrome.