Aortic valve stenosis (AoS) is the most common acquired valvular disorder found in developed countries, being present in 2% to 7% of adults over the age of 65 [ 1 Stewart B.F. Siscovick D. Lind B.K. et al. Clinical factors associated with calcific aortic valve disease: Cardiovascular Health Study. J Am Coll Cardiol. 1997; 29: 630-634 Abstract Full Text Full Text PDF PubMed Scopus (1575) Google Scholar , 2 Otto C.M. Lind B.K. Kitzman D.W. Gersh B.J. Siscovick D.S. Association of aortic-valve sclerosis with cardiovascular mortality and morbidity in the elderly. N Engl J Med. 1999; 341: 142-147 Crossref PubMed Scopus (1051) Google Scholar , 3 Iung B. Baron G. Butchart E.G. et al. A prospective survey of patients with valvular heart disease in Europe: The Euro Heart Survey on Valvular Heart Disease. Eur Heart J. 2003; 24: 1231-1243 Crossref PubMed Scopus (2584) Google Scholar ]. Calcified AoS is a chronic progressive disease. The pathomechanisms leading to valve degeneration remain unknown. Valve disease shares many features with atherosclerosis. Platelet activation is an important constituent of the atherosclerotic process [ 4 Gear A.R. Camerini D. Platelet chemokines and chemokine receptors: linking hemostasis, inflammation, and host defense. Microcirculation. 2003; 10: 335-350 Crossref PubMed Google Scholar , 5 Wagner D.D. Burger P.C. Platelets in inflammation and thrombosis. Arterioscler Thromb Vasc Biol. 2003; 23: 2131-2137 Crossref PubMed Scopus (438) Google Scholar ]. The study focused on two platelet-derived chemokines, which bridge three important components of atherogenesis: platelet activation, inflammation, and generation of atheroma.