Degenerative, nonrheumatic aortic valve stenosis is the most common acquired valve disease. Regardless whether the stenosis develops on a congenitally normal or abnormal (bicuspid) aortic valve, the progressive fibrosis, calcification, fusion and degeneration of the aortic cusps can be regarded as an atherosclerotic disease. Accordingly, it is strongly correlated to the prevalence of coronary artery disease. Stenotic valves show histologic characteristics similar to atherosclerotic lesions and induce a systemic subclinical inflammatory response. Severe symptomatic aortic stenosis is an indication for surgical valve replacement. There is, however, no established medical treatment to delay the progression of aortic valve stenosis in asymptomatic patients. Recent retrospective studies suppose that statin treatment inhibits the accumulation of aortic valve calcification, as assessed by electron beam computed tomography (EBCT), or delay progression of elevated hemodynamic parameters such as systolic pressure gradients or peak aortic jet velocity, as measured by Doppler echocardiography. Mechanisms responsible for the potential benefit of statins for patients with aortic valve stenosis may be mediated by pleiotropic effects besides lipid lowering. These may include anti-inflammation, anti-angiogenesis, inhibition of matrix degrading enzymes, as well as modulation of local lipid oxidation and / or immune responses. Ongoing randomized prospective clinical trials will provide much stronger evidence for or against the recommendation of aggressive treatment with statins to slow the process of aortic valve stenosis.