Effect of antiplatelet therapy on aneurysmal sac expansion associated with type II endoleaks after endovascular aneurysm repair

J Vasc Surg . 2017 Aug;66(2):396-403. doi: 10.1016/j.jvs.2016.11.032. Epub 2017 Feb 9.

Fecha de la publicación: 09/02/2017

Autor: Francisco Álvarez Marcos (1), José Manuel Llaneza Coto (2), Francisco José Franco Meijide (3), Ahmad Amer Zanabili Al-Sibbai (2), Jorge Vilariño Rico (3), Manuel Alonso Pérez (2), Santiago Caeiro Quinteiro (3)



1Vascular Surgery Department, A Coruña University Healthcare Complex (CHUAC), A Coruña, Spain. Electronic address: alvarezmarcos@seacv.es.

2Vascular Surgery Department, Asturias University Central Hospital (HUCA), Oviedo, Spain.

3Vascular Surgery Department, A Coruña University Healthcare Complex (CHUAC), A Coruña, Spain.


Objective: Endovascular aneurysm repair (EVAR) of abdominal aortic aneurysms (AAAs) has gained widespread use through a solid reputation of safety and effectiveness. However, some issues, such as endoleaks and sac growth over time, still arise as important concerns. Antiplatelet therapy, mandatory as secondary prevention of cardiovascular disease, may play a role in both phenomena by interfering with blood clotting properties and the inflammatory process associated with AAA. We analyzed whether different antiplatelet therapies were independent risk factors for type II endoleak (T2E) persistence and midterm sac growth after EVAR.

Methods: All patients with T2E detected in the first post-EVAR control were included, except those without at least 1 year of complete follow-up. Data for demographics, clinical comorbidities, EVAR devices, and antiplatelet therapies were recorded. All patients underwent routine follow-up with contrast-enhanced tomography at 1 month, 6 months, 12 months, and annually thereafter. A three-dimensional rendering of each endoleak was performed for detailed volumetry. Main outcomes were endoleak persistence at 6 months and sac growth >5 mm at end of follow-up.

Results: During a 9-year period, 87 patients with initial T2E were monitored for a mean of 41.5 months. On discharge, salicylates were prescribed to 50, clopidogrel to 16, and multiagent therapy or anticoagulation to 9; no therapy was given to 12. No significant differences in comorbidities or baseline AAA characteristics were found between groups. At 6 months thereafter, 59% (n = 51) of the initial T2Es persisted. At end of follow-up, 32 patients had sac growth >5 mm (37%). Sac growth was significantly less frequent in the group treated with salicylates (26% vs 60%; P = .004). Cox proportional hazards model reinforced the role of salicylates as protectors for sac growth over time (hazard ratio, 0.34; 95% confidence interval, 0.13-0.87; P = .024), whereas T2E nidus volume and endoleak complexity behaved like independent risk factors.

Conclusions: Antiplatelet therapy with salicylates appears to be linked to a decreased risk of sac growth >5 mm over time in patients with T2Es detected right after EVAR. Population-based cohort studies are mandatory to confirm this finding and to guide a potential recommendation.