Persistent type 2 endoleak after endovascular repair of abdominal aortic aneurysm is associated with adverse late outcomes

Abstract

Objective: Type 2 endoleak occurs in up to 20% of patients after endovascular aneurysm repair (EVAR), but its long-term significance is debated. We reviewed our experience to evaluate late outcomes associated with type 2 endoleak.

Methods: During the interval January 1994 to December 2005, 873 patients underwent EVAR. Computed tomography (CT) scan assessment was performed < or =1 month of the operation and at least annually thereafter. Sequential 6-month CT scan follow-up was adopted for those patients with persistent type 2 endoleaks, and reintervention was limited to those with sac enlargement >5 mm. Study end points included overall survival, aneurysm sac growth, reintervention rate, conversion to open repair, and abdominal aortic aneurysm (AAA) rupture. Preoperative variables and anatomic factors potentially associated with these endpoints were assessed using multivariate analysis.

Results: We identified 164 (18.9%) patients with early (at the first follow-up CT scan) type 2 endoleaks. Mean follow-up was 32.6 months. In 131 (79.9%) early type 2 endoleaks, complete and permanent leak resolution occurred < or =6 months. Endoleaks persisted in 33 patients (3.8% of total patients; 20.1% of early type 2 endoleaks) for >6 months. Transient type 2 endoleak (those that resolved < or =6 months of EVAR) was not associated with adverse late outcomes. In contrast, persistent endoleak was associated with several adverse outcomes. AAA-related death was not significantly different between patients with and without a type 2 endoleak (P = .78). When evaluating patients with no early endoleak vs persistent endoleak, freedom from sac expansion at 1, 3, and 5 years was 99.2%, 97.6%, and 94.9% (no leak) vs 88.1%, 48.0%, and 28.0% (persistent) (P < .001). Patients with persistent endoleak were at increased risk for aneurysm sac growth vs patients without endoleak (odds ratio [OR], 25.9; 95% confidence interval [CI] 11.8 to 57.4; P < .001). Patients with a persistent endoleak also had a significantly increased rate of reintervention (OR, 19.0; 95% CI, 8.0 to 44.7); P < .001). Finally, aneurysm rupture occurred in 4 patients with type 2 endoleaks. Freedom from rupture at 1, 3, and 5 years for patients with a persistent type 2 endoleak was 96.8%, 96.8%, and 91.1% vs 99.8%, 98.5%, and 97.4% for patients without a type 2 endoleak. Multivariate analysis demonstrated persistent type 2 endoleak to be a significant predictor of aneurysm rupture (P = .03).

Conclusions: Persistent type 2 endoleak is associated with an increased incidence of adverse outcomes, including aneurysm sac growth, the need for conversion to open repair, reintervention rate, and rupture. These data suggest that patients with persistent type 2 endoleak (>6 months) should be considered for more frequent follow-up or a more aggressive approach to reintervention.