An 8-year experience with type II endoleaks: natural history suggests selective intervention is a safe approach.

摘要

OBJECTIVE: The treatment of type II endoleaks remains controversial because little is known about their long-term natural history and impact on changes in aneurysm morphology. This study reviews type II endoleaks occurring in patients after endovascular abdominal aortic aneurysm repair (EVAR) at a single-institution over an 8-year period. METHODS: All patients undergoing EVAR who had type II endoleaks documented on follow-up imaging studies at our institution between January 1997 and March 2005 were reviewed. Data regarding patient demographics in addition to aneurysm size, device type, operative complications, and secondary interventions were reviewed. Outcomes evaluated included the rate of spontaneous sealing, freedom from secondary intervention, and aneurysm enlargement, rupture, or conversion. RESULTS: Type II endoleaks were present in 154 of 965 patients (16.0%) undergoing EVAR. Mean follow-up time was 22.0 months (range, 1 to 72 months). Fifty-five patients (35.7%) with type II endoleaks sealed spontaneously in a mean time of 14.5 months. According to Kaplan-Meier analysis, approximately 75% of type II endoleaks sealed spontaneously within a 5-year period. Nineteen patients (12.3%) with type II endoleaks were treated at a mean time of 19.9 months at the operating surgeon's discretion, including 13 with sac enlargement >5 mm. Kaplan-Meier analysis estimated that approximately 65% of the patients remained free of intervention after a period of 4 years. Thirteen patients (8.4%) experienced aneurysm sac enlargement >5 mm. Kaplan-Meier analysis estimated that approximately 80% of patients with type II endoleaks remained free of sac enlargement >5 mm over a 4-year period. No patients with type II endoleaks experienced rupture or required conversion to open repair during their follow-up. Cox regression analysis showed that cancer, coronary artery disease, and chronic obstructive pulmonary disease were associated with earlier spontaneous closure of the type II endoleaks (P < .05). CONCLUSIONS: We observed that type II endoleaks have a relatively benign course, and in the absence of sac expansion, can be followed for a prolonged course of time without the need for intervention. The rate of spontaneous seal continues to increase with time and, therefore, close follow-up of patients with type II endoleaks who show no signs of aneurysm expansion is a safe approach. For patients in whom the exact etiology of their endoleak is in question, dynamic imaging should be used to exclude the presence of a type I endoleak.