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Inflammation and hemostasis are key processes in the pathogenesis of atherosclerotic cardiovascular disease (1,2). Vascular inflammation in response to lipid depositions causes formation of atherosclerotic plaques (1). In addition, inflammation in existing plaques is the primary process responsible for progression toward a phenotype that is vulnerable to rupture and thereby causing acute events such as acute myocardial infarction and stroke (1,3,4). Plaque rupture can trigger the hemostatic system, which once activated generates intraplaque and intravascular platelet thrombi (2). Small nonocclusive thrombi contribute to

P-Selectin Imaging in Cardiovascular Disease: What You See Is What You Get?