Calcific aortic stenosis (AS) is a progressive disease that has, until recently, been considered to be a degenerative and unmodifiable process induced by long-lasting mechanical stress. However, histopathologic studies have now demonstrated that the development and progression of calcific AS is based on an active process, sharing a number of similarities with atherosclerosis. Inflammation, lipid infiltration, dystrophic calcification, ossification, platelet deposition and endothelial dysfunction have been observed in both diseases. In addition, several studies have suggested that AS and atherosclerosis share a number of risk factors, such as hypercholesterolemia, elevated lipoprotein (a), smoking, hypertension and diabetes. These findings suggest that statin therapy could be beneficial in AS by its lipid-lowering and/or anti-inflammatory effects, as is the case in atherosclerosis. Although this concept has been supported by experimental work and by four retrospective clinical studies observing significantly slower rates of hemodynamic progression in statin-treated patients, a prospective randomized trial (Scottish Aortic Stenosis and Lipid Lowering Trial, Impact on Regression [SALTIRE]; 80mg of atorvastatin vs placebo) yielded a negative result. In contrast to the retrospective analyses, according to the study protocol, patients with hyperlipidemia had to be excluded in this trial. A recent prospective study (Rosuvastatin Affecting Aortic Valve Endothelium [RAAVE]) treating hypercholesteremic patients with rosuvastatin, found a significantly slower rate of progression in these patients compared with patients with normal cholesterol levels who were left untreated, suggesting that statin therapy may only be beneficial in patients with hyperlipidemia. Lipid-lowering therapy with statins can, therefore, currently only be recommended in this subgroup of patients with AS.