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.