Mechanisms of aortic valve calcification

The calcified aortic valve lesion develops in the setting of endothelial injury and inflammation and displays hallmarks of atherosclerosis, including lipid accumulation, MMP activation, and interaction with the renin-angiotensin system. In addition to ectopic calcification, bone formation may occur in severely diseased valves. Our understanding of the molecular mechanisms that participate in an aortic valve lesion has lagged behind atherosclerotic disease of arteries. Further understanding of atherosclerotic disease will assuredly yield new insights into valvular heart disease. Current evidence indicates that modification of atherosclerotic risk factors will slow progression of aortic valve calcification, and valve risk factors should be addressed in all patients who have aortic valve calcification. Prospective trials are needed to evaluate therapeutic approaches to prevent progression of aortic valve disease.