Introduction
Aortic valve disease affects more than 26% of adult patients over 65 years of age1; the main indication for AVR is aortic stenosis (AS), an active biological process with similarities atherosclerosis2. It begins with a lesion in the valvular endothelium that promotes the accumulation of lipoproteins and infiltration by macrophages and T lymphocytes. These cells secrete tumor growth factor (TGF-α), interleukin 1-β (IL-1β)3, and other cytokines that generate the synthesis of matrix metalloproteinases (MMPs) and promote local remodeling4.
In parallel, osteogenesis occurs when resident interstitial aortic valve cells (AVICs) are activated to fibroblasts by tumor necrosis factor-alpha (TNF-α) and IL-1β, cells differentiate to fibrotic tissue and osteoblast-like cells. This process is promoted by the action of IL-6 and IL-45, as well as by other promoter factors such as Osteopontin (OPN)6, the osteoprotegerin axis (OPG), the receptor activator of nuclear factor κB (RANK), and its ligand (RANKL)7. These processes perpetuate valvular calcification, progressive reduction of the aortic valve area (AVA)8.
The treatment for severe AS is AVR; however, the inflammatory state will persist in half of the patients in the short term9. Among them are prosthetic material (titanium)10, the hemodynamic flow profile11, the biological prosthetic valve tissue (porcine or equine)12, or mechanical factors13. Long-term surgical success can be improved with pre- and postoperative therapeutic measures.
This study’s objective was to evaluate the function and long-term inflammatory response in post-operated patients with AVR using bioprostheses or mechanical prostheses.