Abstract

Introduction Peripheral arterial disease is one aspect of atherosclerosis, a disease associated with both inflammation and hypercoagulability. Many recent studies have focused on the diversity of mechanisms by which inflammation can promote blood clotting. However, the relationship between plasma concentrations of inflammatory and hemostatic markers and the severity of atherosclerosis is not yet well studied. We want to determine the relations among selected D-dimer, C-reactive protein, fibrinogen, prothrombin time and serum amyloid A, and the ankle brachial index in patients with and without peripheral arterial disease. Materials and methods In a prospective cohort study, 45 consecutive patients with peripheral arterial disease of ankle brachial index < 0.90, and 44 patients without peripheral arterial disease of ankle brachial index 0.90 to 1.50 were included. D-dimer, fibrinogen, C-reactive protein, serum amyloid A, and prothrombin time were measured at the recruitment. Results Median values of serum amyloid A, D-dimer, and C-reactive protein were significantly higher in the peripheral arterial disease group than in those without peripheral arterial disease group ( p < 0.001). The patients with PAD had moderately higher fibrinogen levels than without PAD ( p < 0.01). Prothrombin time levels were normal in both groups. In multivariable regression analyses adjusting for all blood factors as well as potential confounders, patients with peripheral arterial disease, levels of serum amyloid A, and C-reactive protein showed a highly significant, inverse association with the ankle brachial index. D-dimer and fibrinogen level increase were also found to be related to lower ankle brachial index, while no association was observed between prothrombin time levels. Conclusions Higher C-reactive protein, serum amyloid A, and D-dimer levels are showing positive association with the presence of peripheral arterial disease. C-reactive protein and serum amyloid A levels are direct relations between the ankle brachial index and the extent of vascular inflammation.

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