OBJECTIVE: To assess aortic valve probes for valvar C reactive protein (CRP) presence, the relation between valvar and serum CRP, and a possible modification of CRP by statin medication. SETTING: Tertiary referral centre. PATIENTS AND DESIGN: End stage, degenerative valve tissue was taken from 81 patients, 57 with non-rheumatic aortic valve stenosis (AS) and 24 with degenerative aortic valve bioprosthesis (BP). Five non-stenosed valves served as controls. Tissue from four non-implanted bioprostheses was also examined. The presence and location of CRP was analysed by use of immunostaining and morphometry. Serum CRP concentrations were measured preoperatively. RESULTS: The majority of AS and BP valves exhibited CRP labelled cells, predominantly localised to the valvar fibrosa. The expression of CRP was much higher in BP than in AS (by a factor of 3.7, p = 0.03). Notably, non-stenosed aortic valves and non-implanted bioprostheses did not have CRP signalling. Serum CRP was also increased with BP (by a factor of 2.5, p = 0.02) and was significantly correlated with valvar CRP expression (r = 0.54, p < 0.001). The main finding in patients with (n = 26) and without statin treatment (n = 55) was that both valvar CRP expression (p = 0.02) and serum CRP concentrations (p = 0.04) were lower in the statin treated group. CONCLUSIONS: CRP was found in a large series of degenerative aortic valves, more often in bioprostheses than in native cusps. Serum CRP concentrations may reflect inflammatory processes within the aortic valve. The association of statin treatment with decreases in both valvar and serum CRP concentrations may explain known pleiotropic effects of statins in patients with aortic stenosis.
OBJECTIVE: To assess aortic valve probes for valvar C reactive protein (CRP) presence, the relation between valvar and serum CRP, and a possible modification of CRP by statin medication. SETTING: Tertiary referral centre. PATIENTS AND DESIGN: End stage, degenerative valve tissue was taken from 81 patients, 57 with non-rheumatic aortic valve stenosis (AS) and 24 with degenerative aortic valve bioprosthesis (BP). Five non-stenosed valves served as controls. Tissue from four non-implanted bioprostheses was also examined. The presence and location of CRP was analysed by use of immunostaining and morphometry. Serum CRP concentrations were measured preoperatively. RESULTS: The majority of AS and BP valves exhibited CRP labelled cells, predominantly localised to the valvar fibrosa. The expression of CRP was much higher in BP than in AS (by a factor of 3.7, p = 0.03). Notably, non-stenosed aortic valves and non-implanted bioprostheses did not have CRP signalling. Serum CRP was also increased with BP (by a factor of 2.5, p = 0.02) and was significantly correlated with valvar CRP expression (r = 0.54, p < 0.001). The main finding in patients with (n = 26) and without statin treatment (n = 55) was that both valvar CRP expression (p = 0.02) and serum CRP concentrations (p = 0.04) were lower in the statin treated group. CONCLUSIONS:CRP was found in a large series of degenerative aortic valves, more often in bioprostheses than in native cusps. Serum CRP concentrations may reflect inflammatory processes within the aortic valve. The association of statin treatment with decreases in both valvar and serum CRP concentrations may explain known pleiotropic effects of statins in patients with aortic stenosis.
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