Experimental evidence for the role of atherosclerosis in calcific aortic valve disease

Abstract

Calcific aortic stenosis is the most common indication for surgical valve replacement in the United States (www.sts.com). Currently, in 2012 surgical valve replacement is the number one indication for the treatment of this disease process (Bonow et al. 1998). For years, this disease has been described as a passive phenomena during which serum calcium attaches to the valve surface and binds to the leaflet to form nodules. Over decades, as aortic stenosis progressed, it will cause progressive left ventricular hypertrophy, left ventricular diastolic and systolic dysfunction, congestive heart failure, angina, arrhythmias, and syncope. Recent studies demonstrate an association between atherosclerotic risk factors and aortic valve disease. Although a unifying hypothesis for the role of atherosclerotic risk factors towards the mechanism of vascular and aortic valve disease is emerging, progress in studying the cell biology of this disease has been defining turning point in understanding the overall mechanisms.