Calcific (degenerative) aortic valve disease is the most common etiology of acquired aortic valve stenosis. Historically, it was seen as a degenerative, "senile-like" process, resulting from aging--"wearing and tearing"--of the aortic valve. However, several lines of evidence suggest that calcific valve disease is not simply due to age-related degeneration but, rather, it is an active disease process with identifiable initiating factors, clinical and genetic risk factors, and cellular and molecular pathways that mediate disease progression. Histopathologically, the early lesions of aortic valve sclerosis resemble arterial atherosclerotic plaques. Furthermore, atherosclerotic risk factors and clinical atherosclerotic cardiovascular disease are independently associated with aortic sclerosis suggesting that it represents an atherosclerosis-like process involving the aortic valve. Until now, the only established treatment for symptomatic aortic valve stenosis has been valve replacement. Newer therapies that may modify or reduce the likelihood of developing aortic valve disease are highly desirable and are currently under investigation. In this article we tried to review the available data on calcific aortic valve disease, starting from histological and pathogenic aspects and finishing with therapeutic implications, in order to characterize its relationship with the atherosclerotic process.