Ex vivo model for bioprosthetic valve calcification via stem cell differentiation to bone

Abstract

Calcific aortic stenosis is the most common indication for surgical valve replacement in the United States and Europe [1]. Currently, mechanical versus bioprosthetic heart valves are the two options for valve replacement. The choice of valve depends on patient characteristics at the time of surgery [2]. Bioprosthetic heart valves have decreased risk of thrombosis, therefore decreasing the need for anticoagulation. It is estimated that 20-30 % of implanted bioprosthetic heart valves will have some degree of hemodynamic dysfunction at 10 years. For years, the mechanisms of valve degeneration were thought to be due to a passive process in which calcium sticks to the valve directly from the circulation. However, recent studies have demonstrated risk factors for bioprosthetic valve calcification that are similar to vascular atherosclerosis [3, 4]. Furthermore, recent pathologic studies [5] have clearly shown that an inflammatory reaction develops in these calcifying bioprosthesis, which including lipid deposits, inflammatory cell infiltration, and bone matrix proteins expression.