Search

Fibronectin (FN) may be involved in time- and stage-dependent and inter-related controlled processes of inflammation, coagulation, and wound healing accompanying peripheral arterial disease (PAD). In the present study, FN and FN-containing extra-domain A (EDA-FN), macromolecular FN-fibrin complexes, and FN monomer were analysed in the plasma of 142 PAD patients, including 37 patients with restenosis, for 37 months after revascularisation. FN concentration increased significantly in the plasma of PAD patients within 7 to 12 months after revascularisation, whereas the high concentration of EDA-FN was maintained up to 24 months, significantly higher in the group 7 to 12 months after revascularisation with recurrence of stenosis and lower in the PAD groups 1 to 3 months and 4 to 6 months after revascularisation with comorbid diabetes and ulceration, respectively. The relative amounts of FN-fibrin complexes up to 1600 kDa and FN monomer were significantly higher, within intervals of 4 to 24 months and 4 to 6 months after revascularisation, respectively. Moreover, the relative amounts of 750 to 1600 kDa FN-fibrin complexes within 13 to 24 months after revascularisation were higher in comparison with those in the group without restenosis. In conclusion, high levels of EDA-FN and FN-fibrin complexes could have potential diagnostic value in the management of PAD patients after revascularisation, predicting restenosis risk., (© 2018 Medicalhelplines.com Inc and John Wiley & Sons Ltd.)

Surgical and endovascular revascularization of ischemic legs in patients with peripheral arterial disease (PAD) can damage the arterial wall (endothelial and smooth muscle cells). Hemostatic factors released during endothelial dysfunction can lead to restenosis. 1. Determination of selected endothelial hemostatic factors in PAD patients and a reference group. 2. Prospective observation of new restenosis appearance in PAD patients after endovascular revascularization. 3. Comparison of selected endothelial hemostatic factors between non-restenotic and restenotic PAD patients. 150 PAD patients after endovascular revascularization - 90 men and 60 women, aged 44-88 (mean 65.5) years - were examined. During one-year observation after the revascularization procedures in 38 PAD patients restenosis occurred, when blood samples were also collected. The reference group consisted of 53 healthy persons - 44 men and 9 women, aged 20-56 years. Blood was drawn in the morning into 3.2% sodium citrate at a ratio of 9:1. Tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombomodulin (TM), von Willebrand factor (vWF) and tissue plasminogen activator (t-PA) were measured in plasma with commercial tests using the enzyme immunoassay. In the plasma of PAD patients after revascularization, the concentrations of TF and vWF were significantly higher, TM lower, TFPI and t-PA similar compared to the reference group. Six months after revascularization the level of TF had increased and vWF had significantly decreased. The endothelial hemostatic factors before and after restenosis did not significantly differ except TF, which after restenosis was higher. Increased TF and vWF levels in PAD patients indicate arterial endothelial cell damage, by atherosclerotic and revascularization processes. In PAD patients with restenosis compared to these patients before restenosis the determined endothelial hemostatic factors, except TF level, did not significantly differ. Perhaps TF participates in restenosis formation.

Background: In patients with peripheral artery disease (PAD) a hypercoagulable state and thromboembolic complications occur. Revascularization procedures increase this state, sometimes leading to restenosis. Restenosis following balloon angioplasty (PTA)and stent implantation is ≥ 50% of artery stenosis., Objectives: To determine the concentration of tissue factor (TF), tissue factor pathway inhibitor (TFPI), thrombin-antithrombin (TAT) complexes, fibrinogen and D-dimers in the blood of patients with PAD after peripheral endovascular revascularization of the lower legs and in PAD patients with restenosis., Material and Methods: The study included 150 patients with PAD, 90 men and 60 women, aged 44-88 (mean 65.5) years, after successful peripheral angioplasty (PTA) and/or with stenting. During the 6 months after the revascularization procedures, restenosis occurred in 27 patients. The reference group consisted of 53 healthy persons (44 men and 9 women, aged 20-56 years). Blood was drawn in the morning into 3.2% natrium citrate at a ratio of 9 : 1. The concentration of TF, TFPI, TAT complexes and D-dimers were measured in plasma with commercial tests using an enzyme immunoassay. Fibrinogen was determined with coagulometer., Results: In the plasma of patients with PAD after endovascular revascularization, the concentrations of TF, TAT complexes, fibrinogen and D-dimers were significantly higher compared to the reference group. During the six months of observation, 27 patients developed restenosis. The results of hemostatic factors in patients with restenosis were compared with the same patients before restenosis and the group of 123 PAD patients after endovascular revascularization. TF and fibrinogen levels in the 27 patients with restenosis were significantly higher than in the group of PAD patients before restenosis., Conclusions: Statistically significantly higher levels of tissue factor (TF) and fibrinogen in PAD patients with new restenosis, compared to those without restenosis after endovascular revascularization, indicate they can participate in the formation of restenosis.

Background: Tissue factor (TF), tissue factor pathway inhibitor (TFPI) and vascular endothelial growth factor A (VEGF-A) present in vascular structures take part in blood coagulation and in organ revascularisation. The concentration of thrombin-antithrombin complexes (TAT) in blood of patients with abdominal aortic aneurysms (AAA) reflects thrombin-generation., Aim: To determine the concentration of TF, TFPI, VEGF-A and TAT complexes in blood of patients with AAA and to consider if these factors after clot formation can play a role in the pathogenesis of abdominal aortic aneurysms., Methods: Forty eight patients (43 men and 5 women) in the age of 59-80 (mean 72) years with AAA were examined. The blood was drawn in the morning to 3.2% natrium citrate in proportion 9:1. The concentration of TF, TFPI, VEGF-A and TAT complexes were measured in plasma with commercial kits using enzyme immunoassay., Results: In plasma of patients with AAA the mean concentration of TF was elevated almost twice and TAT complexes were three times higher compared with controls. But the mean levels of TFPI and VEGF-A were similar as in control group., Conclusions: Increased concentrations of TF and TAT complexes indicate on high thrombin-generation, hypercoagulability and formation in abdominal aortic aneurysm of intraluminal thrombus, which can induce proteolytic processes in aortic wall.

The aim of the work was to study the influence of extracorporal circulation (ECC) on the vascular endothelial markers: von Willebrand factor (vWf), tissue plasminogen activator (t-PA) and trombomodulin (TM) in patients with coronary heart disease (CHD) undergoing coronary artery bypass graft (CABG). Examined group consisted of 30 patients (22 men, 8 women) at mean age 58.0 +/- 8.0 years, among them 19--were operated with ECC, 11--without ECC. Before and during operation blood was drawn 6 times. Control group consisted of 23. healthy volunteers at similar age. In the plasma vWf, t-PA and TM were determined with immunoenzymatic methods. Before operation the examined parameters were significantly higher compared to controls. The concentration of vWf during ECC was higher than in operation without ECC, but not significant. Differences statistically significant in the blood collected during ECC and without it appeared in t-PA only on the 3. and in TM on the 1. and 3. day after operation. It seems that ECC does not damage vascular endothelium direct, only indirect trough proinflammatory factors released from activated during ECC granulocytes and platelets.