Hemostatic Markers of Endothelial Dysfunction in Patients with Atherosclerotic Peripheral Arterial Disease before and after Endovascular Treatment


  • #ES 02-EP-8
  • Endovascular Surgery. E-POSTER (ORAL) SESSION-2
  • E-Poster (oral)

Hemostatic Markers of Endothelial Dysfunction in Patients with Atherosclerotic Peripheral Arterial Disease before and after Endovascular Treatment

Igor A. Suchkov, Roman E. Kalinin, Nina D. Mzhavanadze, Emma A. Klimentova, Olga N. Zhurina, Aleksandr S. Pshennikov

Ryazan State Medical University, Ryazan, Russia

Date, time and location: 2018.05.26 13:30, Exhibition area, 1st Floor. Zone – A

Abstract

Objective: assessment of hemostatic markers of endothelial dysfunction in patients with atherosclerotic peripheral arterial disease (PAD) before and after endovascular treatment.

Material and methods: the study included 40 patients (30 men and 10 women) with PAD. The median age of patients was 63.9 ± 7.93 years. All patients had severe claudication. Patients underwent physical examination,ankle-brachial index measurement, duplex ultrasound and/or digital substraction angiography before and at 3 months after endovascular treatment. Peripheral venous blood samples were collected to assess the activity of von Willebrand factor (VWF), plasminogen activator inhibitor type 1 (PAI-I), soluble endothelial protein C receptor (sEPCR), and metabolites of nitric oxide II (NO) at the same time points.

Results: primary patency of the reconstruction area was 79% at 6 months after intervention. Limb salvage rate was 97%. Restenosis, which required secondary endovascular intervention, was registered in 6 (15.7%) patients. Thrombosis of the area of intervention occurred in 2 (5%) patients. The average activity of VWF was to 621.5±438.2 and 595±358%, PAI-I 76.1±39.16 and 90.15±39.97 ng/ml, sEPCR 62.7±23.5 and 65.4±25.4 ng/ml, NO metabolites 71.1±24.6 and 56.78±20.9 µmol/l before and at 3 months after endovascular surgery, respectively. Statistically significant differences were obtained for PAI-I (p=0.032) and NO metabolites (p=0.008) levels. There was a correlation between PAI-I and sEPCR values (r=+0.354) before and at 3 months after invervention, between the level of NO metabolites and VWF activity (r=-0.402) only at 3 months. Thus, at 3 months after endovascular treatment the activity of VWF, levels PAI-I and sEPCR increased, while levels of NO metabolites decreased.

Conclusion: increased activity of VWF, levels of PAI-I and sEPCR prior to endovascular treatment reflect protrombogenic state of the hemostatic system in patients with PAD. Endovascular treatment provides a further shift towards a hypercoagulable state and impaired functional activity of endothelium.


To top