Are disturbances in hemostatic biomarkers associated with early Type II endoleak development in patients undergoing EVAR for abdominal aortic aneurysms?
Reduced thrombin generation (lower F1+2) and impaired fibrinolysis (higher PAI-1 activity) may predispose patients to early Type II endoleak formation after EVAR.
Endovascular aneurysm repair (EVAR) is a widely used minimally invasive treatment for abdominal aortic aneurysms. However, postoperative type II endoleak (T2EL) remains a relevant complication associated with a risk of aneurysm rupture and the need for repeated imaging follow-up, resulting in exposure to ionizing radiation. Identification of biological factors predisposing to T2EL may improve risk stratification. This pilot study aimed to investigate whether disturbances in hemostasis are associated with early T2EL development after EVAR. A total of 103 patients treated with EVAR for symptomatic or asymptomatic abdominal aortic aneurysms in a tertiary vascular center were prospectively enrolled. Blood samples were collected preoperatively and one month postoperatively to assess fibrinogen, prothrombin fragment F1+2 (F1+2), thrombin–antithrombin complex (TAT), tissue plasminogen activator antigen (tPA), plasminogen activator inhibitor-1 (PAI-1) activity, and platelet activity. Computed tomography angiography (CTA) during follow-up was used to detect endoleaks and calculate their volume. Patients with T2EL had significantly lower levels of prothrombin fragment F1+2 and higher PAI-1 activity compared with patients without endoleak. No significant association was observed between the analyzed biomarkers and endoleak volume. These findings suggest that reduced thrombin generation and impaired fibrinolysis may contribute to endoleak formation after EVAR and warrant further investigation in larger, confirmatory studies.
Rynio et al. (2026) studied this question.