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J Vasc Surg. 2016 Apr;63(4):895-901. doi: 10.1016/j.jvs.2015.10.088. Epub 2016 Jan 12.

Risk factors and consequences of persistent type II endoleaks.

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Division of Vascular and Endovascular Surgery, Beth Israel Deaconess Medical Center, Boston, Mass.
Division of Vascular and Endovascular Surgery, Massachusetts General Hospital, Boston, Mass.
Section of Vascular Surgery, Dartmouth-Hitchcock Medical Center, Lebanon, NH.
Division of Vascular and Endovascular Surgery, Beth Israel Deaconess Medical Center, Boston, Mass. Electronic address:



Type II endoleaks are common after endovascular aneurysm repair (EVAR), but their clinical significance remains undefined and their management controversial. We determined risk factors for type II endoleaks and associations with adverse outcomes.


We identified all EVAR patients in the Vascular Study Group of New England abdominal aortic aneurysm database. Patients were subdivided into two groups: (1) those with no endoleak or transient type II endoleak and (2) persistent type II endoleak or new type II endoleak (no endoleak at completion of case). Patients with other endoleak types and follow-up shorter than 6 months were excluded. Multivariable analysis was used to evaluate predictors of persistent or new type II endoleaks. Kaplan-Meier and Cox regression analysis were used to evaluate predictors of reintervention and survival.


Two thousand three hundred sixty-seven EVAR patients had information on endoleaks: 1977 (84%) were in group 1, of which 79% had no endoleaks at all, and 21% had transient endoleaks that resolved at follow-up. The other 390 (16%) were in group 2, of which 31% had a persistent leak, and 69% had a new leak at follow-up that was not seen at the time of surgery. Group 2 was older (mean age, 75 vs 73 years; P < .001) and less likely to have chronic obstructive pulmonary disease (COPD; 24% vs 34%; P < .001) or elevated creatinine levels (2.6% vs 5.3%; P = .027). Coil embolization of one or both hypogastric arteries was associated with a higher rate of persistent type II endoleaks (12 vs 8%; P = .024), as was distal graft extension (12% vs 8%; P = .008). In multivariable analysis, COPD (odds ratio [OR], 0.7; 95% confidence interval [CI], 0.5-0.9; P = .017) was protective against persistent type II endoleak, while hypogastric artery coil embolization (OR, 1.5; 95% CI, 1.0-2.2; P = .044), distal graft extension (OR, 1.6; 95% CI, 1.1-2.3; P = .025), and age ≥ 80 (OR, 2.7; 95% CI, 1.4-5.3; P = .004) were predictive. Graft type was also associated with endoleak development. Persistent type II endoleaks were predictive of postdischarge reintervention (OR, 15.3; 95% CI, 9.7-24.3; P < .001); however, they were not predictive of long-term survival (OR, 1.1; 95% CI, 0.9-1.6; P = .477).


Persistent type II endoleak is associated with hypogastric artery coil embolization, distal graft extension, older age, the absence of COPD, and graft type, but not with aneurysm size. Persistent type II endoleaks are associated with an increased risk of reinterventions, but not rupture or survival. This reinforces the need for continued surveillance of patients with persistent type II endoleaks and the importance of follow-up to detect new type II endoleaks over time.

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