Elevated levels of circulating soluble adhesion molecules in patients with nonrheumatic aortic stenosis

Aortic stenosis (AS) is the most common valvular lesion in the elderly in western societies. Previously this has been thought to be a degenerative condition, but recent data suggest an inflammtory process.1,2 Rheumatic fever and congenital bicuspid valves are known predisposing factors for the development of AS in young and middle-aged subjects, suggesting that postinfectious immune reactions and mechanical trauma may be important etiologic factors. Immunohistochemical studies on nonrheumatic tricuspid stenotic aortic valves obtained from symptomatic subjects undergoing valve replacement and from autopsy specimens with mild macroscopic leaflet thickening have demonstrated activated T lymphocytes in affected valves, suggesting that immune mechanisms may be involved in the pathogenesis.(1,2) The fundamental role of cellular adhesion molecules in immunologic and inflammatory conditions has been elucidated in the past few years. Adhesion molecules are expressed on vascular endothelium and on immune and inflammatory cells. They play a role in the migration of cells to sites of inflammation, transmigration of lymphocytes, and in immune effector functions. The molecules intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and E-selectin are expressed on vascular endothelium and serve as ligands for counterreceptors on circulating inflammatory cells.(3) Soluble adhesion molecules are detectable at low levels in serum of healthy people but are increased in various disorders, particularly in those with inflammatory or vascular etiology. This study examines the serum levels of the adhesion molecules ICAM-1, VCAM-1, and E-selectin in a group of patients with nonrheumatic AS compared with healthy controls.