Inflammation and circulating endothelial progenitor cells in patients with coronary artery disease and residual platelet reactivity

Atherosclerotic plaque development and progression areassociated with vascular inflammation, endothelial dysfunc-tion, and platelet activation (1). Inflammatory mediators,such as C-reactive protein (CRP) and oxidized low-densitylipoprotein (oxLDL), can trigger platelet activation andsubsequent thrombus formation (2). In turn, activatedplatelets secrete cytokines, recruit monocytes, and releasesoluble CD40 ligand (sCD40L), which mediate vascularinflammation (3). An important determinant of endothelialdysfunction in patients with coronary artery disease (CAD)is the reduced number of endothelial progenitor cells (EPCs)(4). Interestingly, EPCs can inhibit platelet activation, whileactivated platelets modulate EPC proliferation (5).Aspirin is widely used in the prevention of complicationsrelated to CAD. However, the mechanisms that promotehigh residual platelet reactivity (RPR) in aspirin-treatedpatients are still under debate (6,7). Because inflammationand endothelial dysfunction may possibly contribute toplatelet activation and RPR, we sought to compareinflammatory markers and EPC levels between stableCAD patients treated with aspirin with and without RPR.