Bambang Irawan

Circulating soluble CD40 ligand mediates the interaction between neutrophils and platelets in acute coronary syndrome

Following plaque rupture, activated platelet will induce subsequent inflammatory process including neutrophil recruitment. In vitro study demonstrated an interaction between neutrophils and platelets via a mechanism involving CD40-CD40 ligand. However, whether this mechanism exists in the clinical setting remains unknown. Fifty-four patients with acute myocardial infarction (AMI) and 25 with unstable angina of pain onset of ≤24 h were enrolled consecutively. Acute myocardial infarction was diagnosed from three diagnostic criteria, i.e., anginal pain, electrocardiogram ST-T changes, and cardiac enzyme elevation. Unstable angina was diagnosed in patients without elevated cardiac enzymes. Peripheral venous blood was drawn at admission for routine blood count and soluble CD40 ligand (sCD40L) measurement. Neutrophil count was determined by an automated blood cell counter. Circulating sCD40L was measured using a standard enzyme-linked immunosorbent assay. Neutrophil count was significantly higher in AMI as compared with unstable angina (P < 0.001), whereas circulating sCD40L did not significantly differ. Despite marked elevation, no correlation was observed between neutrophil count and circulating sCD40L in AMI. Interestingly, we observed a strong and positive significant correlation between neutrophil count and circulating sCD40L level (r = 0.607, P = 0.002) in unstable angina. Circulating sCD40L is associated with neutrophil count and may mediate interaction between neutrophils and platelets in acute coronary syndrome, particularly in unstable angina.

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.