Late aortic rupture: the Achilles' heel of endovascular abdominal aortic aneurysm repair.

Endovascular aneurysm repair (EVAR) of abdominal aortic aneurysms (AAA) was introduced 20 years ago as a minimally invasive prophylactic procedure to prevent aneurysm rupture. However, rupture after EVAR has been reported and is associated with a high mortality. Rupture after successful EVAR is usually preceded by endograft-related complications, such as type I endoleak and stentgraft migration detected by optimal imaging surveillance. In this issue of JEVT, Venermo et al. attempt to calculate the risk of AAA rupture after EVAR with persistent type Ia endoleak compared to the risk in a cohort of patients with untreated AAA of a similar size. The conventional wisdom is that type I endoleak increases aneurysm rupture risk after EVAR equal to that of a non-operated AAA and therefore needs endovascular reintervention or open conversion. Therefore, the findings that the rupture rate and aneurysm-related death are lower in patients with type I endoleaks compared to the untreated AAA group are interesting and challenge the commonly held notion that type I endoleak following EVAR is evidence of inadequate treatment. This observation suggests that EVAR is beneficial to the patient even if the deployment is not technically successful, which may be of importance in the high-risk patient with multiple comorbidities, a large AAA, and anatomy hostile to stent-graft repair. The authors report that the aneurysmrelated mortality was significantly reduced in the endoleak group compared to the untreated AAA cohort at all time points up to 3 years. The surveillance imaging protocol was good in that the investigators used both duplex ultrasound and contrast-enhanced computed tomography at each follow-up interval with independent classification of endoleak type by both a radiologist and vascular surgeon, although no misclassification rate is given. The length of follow-up is, however, relatively short; ruptures occur at all times during follow-up, with the mean interval from EVAR to rupture recently reported at 4.8 years. The importance of long-term 10year follow-up has been recently highlighted, and the patients in this study require further surveillance before we can draw robust conclusions. As the authors acknowledge, the potential mechanism of protection from rupture despite a persistent type I endoleak is unknown. It may involve prevention or limitation of AAA enlargement by endograft placement. Good stent position, despite an imperfect sealing zone, may allow only a small amount of blood to flow into an already depressurized aneurysm sac, limiting AAA enlargement. The cohort from this study was a ‘‘controlled’’ group of endoleak patients, whereby prompt secondary endovascular intervention was undertaken to try and seal proximal sites that gave rise to type Ia endoleaks. Hence, the