Influence of type II endoleak volume on aneurysm wall pressure and distribution in an experimental model.

OBJECTIVE(S): We have previously shown that type II endoleak size is a predictor of aneurysm growth after aortic endografting. To better understand this observation, we investigated the influence of endoleak size on pressure transmitted to the aneurysm wall and its distribution within the aneurysm sac. METHODS: In an ex vivo model, an artificial aneurysm sac was incorporated within a mock circulation comprised of rubber tubing and a pulsatile pump. Three strain-gauge pressure transducers were placed in the aneurysm wall at different locations, including the site of maximum aneurysm diameter. The aneurysm was filled with either human aneurysm thrombus or dough that mimicked thrombus and simulated type II endoleaks of varying volumes (1 to 10 mL) were created. Aneurysm wall pressure (AWP) measurements were recorded at mean arterial pressures (MAPs) of 60, 80, and 100 mm Hg. Correlation coefficients ( r ) and analysis of variance were used to assess the relationship between endoleak volume and AWP. RESULTS: Increasing endoleak volume '3 cm 3 resulted in proportionally increased AWP at all levels of MAP and at all sites, with highest pressures recorded at the site of the maximum aneurysm diameter (r = 0.83 when MAP = 100 mm Hg; r = 0.85 when MAP = 80 mm Hg; r = 0.88 when MAP = 60 mm Hg; P < .001). AWP plateaued when the endoleak volume was >3 cm 3 . Pressure distribution within the sac was not uniform. Although the difference was within +/-10%, statistically significant higher AWPs were observed at the site of maximum aneurysm diameter (P <.001). AWP also correlated with MAP. CONCLUSIONS: Increasing type II endoleak volume results in proportionally higher AWP, which is greatest at the site of maximum aneurysm diameter. This study confirms the clinical observation that type II endoleak volume and MAP may be important predictors of aneurysm expansion. CLINICAL RELEVANCE: Our experimental model of a type II endoleak revealed that endoleak size is a significant factor that influences the magnitude of pressure transmission into the aneurysm wall. Increasing volume of the endoleak nidus was associated with proportionally higher aneurysm sac pressures. This mechanism may, in fact, account for the increased risk of aneurysm expansion observed in our clinical experience, thereby suggesting the need for more aggressive surveillance and possibly earlier intervention for patients with larger endoleaks.

Predicting aneurysm enlargement in patients with persistent type II endoleaks.

OBJECTIVE: The clinical significance of type II endoleaks is not well understood. Some evidence, however, indicates that some type II endoleaks might result in aneurysm enlargement and rupture. To identify factors that might contribute to aneurysm expansion, we analyzed the influence of several variables on aneurysm growth in patients with persistent type II endoleaks after endovascular aortic aneurysm repair (EVAR). METHODS: In a series of 348 EVARs performed during a 10-year period, 32 patients (9.2%) developed type II endoleaks that persisted for more than 6 months. Variables analyzed included those defined by the reporting standards for EVAR (SVS/AAVS) as well as other endoleak characteristics. Univariate, receiver operating characteristic curve, and Cox regression analyses were used to determine the association between variables and aneurysm enlargement. RESULTS: The median follow-up period was 26.5 months (range, 6-88 months). Thirteen patients (41%) had aneurysm enlargement by 5 mm or more (median increase in diameter, 10 mm), whereas 19 (59%) had stable or shrinking aneurysm diameter. Univariate and Cox regression analyses identified the maximum diameter of the endoleak cavity, ie, the size of the nidus as defined on contrast computed tomography scan, as a significant predictor for aneurysm enlargement (relative risk, 1.12; 95% confidence interval, 1.04-1.19; P =.001). The median size of the nidus was 23 mm (range, 13-40 mm) in patients with aneurysm enlargement and 8 mm (range, 5-25 mm) in those without expansion (Mann-Whitney U test, P <.001). Moreover, receiver operating characteristic curve and Cox regression analyses showed that a maximum nidus diameter greater than 15 mm was particularly associated with an increased risk of aneurysm enlargement (relative risk, 11.1; 95% confidence interval, 1.4-85.8; P =.02). Other risk factors including gender, smoking history, hypertension, need of anticoagulation, aneurysm diameter, type of endograft used, and number or type of collateral vessels were not significant predictors of aneurysm enlargement. CONCLUSIONS: In patients with persistent type II endoleaks after EVAR, the maximum diameter of the endoleak cavity or nidus is an important predictor of aneurysm growth and might indicate the need for more aggressive surveillance as well as earlier treatment.