Aortic stenosis is the most common adult heart valve condition seen in the Western world and its incidence continues to rise. No medical treatment has been proven to prevent or delay the disease process in the valve leaflets, and surgical intervention is the only definite treatment. This disease is predominantly due to degenerative calcification. Recent studies have demonstrated that the pathogenesis of calcific aortic stenosis is not merely a result of prolonged “wear and tear” and age associated valve degeneration, but an active, potentially treatable disease process. The histological findings are suggestive of a chronic inflammation, and theoretically, anti-inflammatory and anti-proliferative agents would be anticipated to alter the natural history of the disease. Statins and ACE-inhibitors are two commonly used treatments in cardiovascular disease that exhibit some of these desirable anti-inflammatory and anti-proliferative properties. In large scale studies, statins have yet to show any long-term disease-modifying effects. The use of ACE- inhibitors has until recently been restricted due to concerns about hemodynamic side effects such as hypotension. In recent short-term trials, ACE-inhibitors have proven to be safe regarding medically induced hypotension. Trials evaluating the potentially long-term disease modifying effects of ACE-inhibitors are still awaited.