Purpose: Most clinical end points after endovascular aneurysm repair (EVAR) are endograft-specific, but type II endoleaks have been assumed to be an unavoidable consequence of the repair method and independent of the type of endograft used. Some recent data have suggested that the rate of type II endoleaks may also be graft-dependent. We reviewed a large clinical experience with six endografts to determine the behavior of type II endoleaks and whether they are graft-specific.

Methods: All elective EVAR cases from five university institutions from 1996 to 2003 were retrospectively analyzed. Endografts used in <50 patients were excluded. Endoleaks were diagnosed and classified from contrast-enhanced computed tomography (CT) scans by the treating surgeons. Results of angiography and interventions for endoleaks were tracked. The rate of type II endoleaks was compared among endografts at 1, 6, and 12 months, and yearly thereafter. Statistical significance was defined as P < .05.

Results: During the study period, 1909 patients underwent elective EVAR and had an adequate imaging follow-up at one of the specified time points. At 1 month, the overall rate of type II endoleak was 14.0% (range, 9.8% to 25.2%.) The Excluder had a significantly higher incidence of type II endoleaks at 1 month but was similar to most other grafts during longer follow-up. At 6 months, the overall rate of type II endoleak was 16.3% (range, 8.3% to 16.8%). The Talent and Lifepath had an apparent lower initial rate of type II leaks, but this was only significant for the Talent at 6 months compared with Excluder, Zenith, and Ancure, and at 1 year compared with Excluder and Zenith. No graft had a long-term statistically significant difference in the rate of type II endoleak formation. Intervention rates varied by institution and graft type but in general were quite low. Of 25 successful interventions (Ancure, 12; AneuRx, 8; Excluder, 2; Lifepath, 2; Zenith, 1; Talent, 0), 21 were performed during the first year. Interim spontaneous resolution, defined as a negative CT scan after a CT positive for endoleak, was high, especially in the first year. Resolution of type II endoleaks occurred in 54 (33%) of 164 between 1 and 6 months, in 37 (33%) of 112 between 6 and 12 months, in 20 (35%) of 57 from 12 to 24 months, and in 5 (20%) of 25 between 24 and 36 months. The various grafts had a nearly identical pattern, but the rates were highest for the Talent. Late appearing endoleaks, defined as a positive CT after a negative CT, were frequent. At 6 months, 44 (30%) of 147 type II endoleaks were newly diagnosed. The rates were 37 (35%) of 107 at 12 months, 15 (27%) of 56 at 2 years and 5 (25%) of 20 at 3 years. No conversions to open repair for type II endoleaks were noted in the first 4 years. The thrombus burden could not be determined in this analysis.

Conclusions: Type II endoleaks occur in nearly 15% of patients treated by EVAR. The early incidence varies only slightly with graft type. The long-term prevalence and clinical significance are masked by different treatment patterns, spontaneous resolution, newly evident endoleaks, and aneurysm size at initial treatment.

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