Does Uncontrolled Platelet Activation Promote Coronary Artery Disease?

SEE PAGE 849 P latelets play a critical role in the development of intracoronary thrombosis. Recent discoveries have documented that platelets augment chronic vascular inflammation and remodeling of the arterial wall resulting in progression of atherosclerosis (1,2). Dual antiplatelet therapy consisting of aspirin and adenosine diphosphate receptor inhibitor has become the cornerstone of preventing thromboischemic events in patients undergoing coronary stenting (3). High on-treatment platelet activity (HPR) after percutaneous coronary intervention is associated with enhanced occurrence of cardiovascular events and death (4–6). Clinical studies have shown that an increase in activation of circulating platelets is associated with the severity of coronary artery disease and progression of atherosclerosis (1,2,7). HPR correlates with coronary plaque burden and calcification as assessed by cardiac computed tomography (8). Further, systemic platelet activation is associated with progression of carotid artery disease in patients with diabetes (9) and cardiac transplant vasculopathy (10) within 1 year. The effect of dual antiplatelet therapy in patients with coronary artery disease is highly variable and dependent on comorbidity (11,12). HPR is influenced by various clinical risk factors including diabetes mellitus, increased body mass index, left ventricular ejection fraction, renal failure, acute coronary syndrome, advanced age, and congestive heart failure (13,14). Previously, a simple clinical risk score, PREDICT (Residual Platelet Aggregation after Deployment of Intracoronary Stent), has been developed