Early Type II Endoleaks Are Associated With Late Type I and III Endoleaks and Rupture After Endovascular Aortic Aneurysm Repair

Abstract

Type II endoleaks (TIIELs) are the most common complication after endovascular aortic aneurysm repair (EVAR) with a reported occurrence rate of 8% to 45%. However, their clinical significance is still a matter of debate. Treatment policies have varied from conservative management to angiographic evaluation and intervention. With most TIIELs managed conservatively, the question remains whether persistent collateral sac reperfusion increases the risk of reintervention, morbidity, or mortality. We sought to assess the effects of the development of early TIIELs on the midterm outcomes after EVAR. We identified all patients who had undergone EVAR from January 2010 to December 2016 in the Vascular Implant Surveillance and Interventional Outcomes Network (VISION). The patients were divided into two groups: those with and without TIIELs at 30 days of follow-up. The 2-year outcomes included freedom from reintervention for type I and III endoleaks, freedom from abdominal aortic aneurysm (AAA)-related reinterventions, freedom from rupture, and all-cause mortality. Total of 12,728 patients had undergone EVAR during the study period, of whom, 1088 (8.5%) had developed an early TIIEL. The patients with a TIIEL were older (mean age, 77 ± 7 years vs 75 ± 7 years; P < .001) and less likely to have a history of smoking (79% vs 82.6%; P < .001). The 2-year freedom from reintervention for a type I/III endoleak estimate was 97% for the TIIEL group compared with 99.2% for the no TIIEL group (P < .001). The TIIEL group had significantly lower rates of freedom from AAA-related reinterventions (92.1% vs 94%, P = .02) and freedom from AAA rupture (95.1% vs 96.2%; P = .05) at 2 years. No difference was found in the freedom from all-cause mortality between the two groups (TIIEL, 95.5% vs no TIIEL, 94.5%; P = .19). After adjustment, the development of early TIIELs was associated with a 3.3-fold increase in reinterventions for type I and III endoleaks (adjusted hazard ratio [aHR], 3.37; 95% confidence interval [CI], 2.13-5.34; P < .001), a 28% increase in AAA-related reinterventions (aHR, 1.28; 95% CI, 1.01-1.6; P = .03), and a 38% increase in AAA rupture (aHR, 1.38; 95% CI, 1.03-1.84). Our findings suggest that TIIELs are not benign and can lead to high-pressure endoleaks and even rupture after EVAR. This is likely the result of sac expansion and the stress placed on the endograft seal zones and areas of modular component overlap. Thus, it is important to identify the modifiable risk factors for TIIEL occurrence and evaluate the effectiveness of prophylactic measures in reducing their incidence.