thromboplastin and Mitral-Valve-Stenosis

The mechanism underlying thrombosis in atrial fibrillation (AF) is not yet clearly understood. Oncostatin M (OSM), as a member of IL-6 family, is involved in atherosclerosis-mediated thrombosis. The present study hypothesizes that OSM and its downstream factors play a role in thrombogenesis in AF.The specimens of left atrial appendages collected from patients with rheumatic mitral stenosis who underwent valve replacement were divided into 3 groups: sinus rhythm, AF(+)/thrombus(-), and AF(+)/thrombus(+) group. The macrophage infiltration in atrial tissue was assessed by immunohistochemistry, and the amount of OSM, tissue factor (TF), and tissue factor pathway inhibitors (TFPIs) was detected by Western blot.The infiltration of the M1 macrophages was significantly increased in the AF with thrombus group compared with the sinus rhythm group (P = .03). Moreover, the expression of OSM and TF was much higher in the AF with thrombus group compared with the sinus rhythm group (P = .02, .009, respectively) while the TFPI was decreased in the AF with thrombus group (P = .04).OSM might be correlated with thrombosis in patients with AF mediated by TF and TFPI.

Topics: Atrial Fibrillation; Blotting, Western; Heart Atria; Heart Valve Prosthesis Implantation; Humans; Immunohistochemistry; Lipoproteins; Macrophages; Mitral Valve Stenosis; Oncostatin M; Rheumatic Heart Disease; Thromboplastin; Thrombosis

While rheumatic valvular disease (RVD) is known to develop subsequent to rheumatic carditis, we examined whether in addition to the inflammatory and repair process, thromboplastic and fibrinolytic activities of the valvular tissue play a contributory role in the pathogenesis of RVD. Both activities were higher in resected valves from RVD cases than in the controls. Tissue thromboplastin was localized in the valvular endothelium and the subendothelial connective tissue. Tissue fibrinolytic activity was prevalent in the small blood vessels of RVD valves, while it was lower on the surface of RVD valves than in the controls. High thromboplastic and low fibrinolytic activity in the surface layer of RVD valves may accelerate the deposition of thrombi, thereby inducing valvular thickening.

Topics: Blood Coagulation; Fibrinolysis; Humans; In Vitro Techniques; Mitral Valve; Mitral Valve Insufficiency; Mitral Valve Stenosis; Rheumatic Heart Disease; Thromboplastin