The behavior of blood coagulation and fibrinolysis-related parameters in patients after PTA treatment with special reference to the soluble fibrin (SF)

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  • ＰＴＡ後の可溶性フィブリン（ｓｏｌｕｂｌｅ　ｆｉｂｒｉｎ，ＳＦ）の動態について：ＳＦが上昇したＰＴＡ施行群の動脈硬化関連因子の検討
  • PTA ゴ ノ カヨウセイ フィブリン soluble fibrin SF ノ ドウタイ ニ ツイテ SF ガ ジョウショウ シタ PTA シコウグン ノ ドウミャク コウカ カンレン インシ ノ ケントウ

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Abstract

The mechanisms involved in thrombus formation at or near the arterio-venous shunt (a-v shunt) prepared for hemodialysis are necessarily rather complicated because blood access is quickly shifted from the high shear stress on the arterial side to medium or low shear stress on the venous side. However, the mechanisms involving shear stress and arterial sclerotic lesions at the a-v shunt in thrombus formation are not yet fully understood. In this study, we analyzed the behavior of blood coagulation and fibrinolysis-related molecular markers in blood samples obtained at the locus of a-v shunt in patients with PTA-treatment and found that SF specifically related to the early stage of thrombus formation was extremely elevated in 4 of 15 patients. The thrombin-antithrombin complex (TAT), an established molecular marker appearing at the early stage of thrombus formation was also elevated, but did not correlate with the level of SF, suggesting that the mechanisms by which these two molecular markers formed were not necessarily interrelated with each other even at the early stage of thrombus formation at or near the a-v shunt. SF is proposed to be a tri-molecular complex composed of 1 molecule of fibrin monomer (formed when a pair of fibrinopeptide A is cleaved from fibrinogen by thrombin) and 2 molecules of native fibrinogen. We previously reported that thrombin further cleaved the paired alpha C domain attached to the central E domain of the fibrin monomer, and exposed the RGD domain present at the alpha(95-97) segment on the molecular surface. Thus, the exposed RGD domain is allowed to interact with α5 β1 integrin that functions as a fibrinogen receptor and αvβ3integrin that functions as vitronectin receptor on the cell surface, and thus promotes cell attachment and extension. In this regards, SF must be considered to contribute to the attachment of platelets to the endothelial cell surface of blood vessels as well as functioning as a molecular marker of accelerated blood coagulation. In 4 patients with elevated SF in the local blood (SF-elevated group), the pulse wave velocity (PWV), a marker of arteriosclerosis, was significantly increased as compared with that in the group without SF elevation. Furthermore, the annual incidence of shunt occlusion was also high in the group with SF elevation compared with that in the group without such elevation. Thus, SF is expected to function as a molecular marker not only for accelerated blood coagulation but also for early recognition of shunt occlusion and its prognosis.

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