An expanding body of evidence continues to build on the central role of inflammation in the progression and clinical manifestations of atherosclerosis. Platelets, long thought to play only a reactionary role at the time of endothelial disruption, are now recognized as important mediators of the inflammatory process. Platelet activation, which is modulated by both inflammatory and hemostatic factors, can lead to the release of hundreds of proteins--many with known proinflammatory functions. Although compelling evidence is lacking that antiplatelet therapies directly lower markers of inflammation, there are intriguing, although preliminary, data suggesting that markers of inflammation predict the clinical benefit of antiplatelet therapies.