Calcific aortic stenosis: lessons learned from experimental and clinical studies

Abstract

Calcific aortic stenosis is the most common indication for surgical valve replacement in the United States. For years this disease has been described as a passive degenerative process during which serum calcium attaches to the valve surface and binds to the leaflet to form nodules. Therefore, surgical treatment of this disease has been the approach toward relieving outflow obstruction in these patients. Recent studies demonstrate an association between atherosclerosis and its risk factors for aortic valve disease. In 2008, there are increasing number of epidemiology and experimental studies to provide evidence that this disease process is not a passive phenomena. There is an active cellular process that develops within the valve leaflet and causes a regulated bone formation to develop. If the atherosclerotic hypothesis is important in the initiation of aortic stenosis, then treatments used in slowing the progression of atherosclerosis may be effective in patients with aortic valve disease. This review will discuss the pathogenesis and the potential for medical therapy in the management of patients with calcific aortic stenosis by examining the lessons provided from the experimental research.

Figure 1. Cellular, Molecular and Genetic Mechanisms of Calific Aortic Stenosis

Model Implicating Lipids in the Development of Calcific Aortic Stenosis and the potential for Future Medical Therapies Targeting this disease at the cellular level in the Aortic Valve.

Figure 2

Three Factors Responsible for the Development of Calcific Aortic Stenosis: Cardiovascular Risk Factors, Genetic Factors and Osteoblast Regulatory Pathways.