Type II endoleak in porcine model of abdominal aortic aneurysm

The purpose of this study was to develop a reliable in vivo porcine model of type II endoleak resulting from endovascular aortic aneurysm repair (EVAR), for the study and treatment of type II endoleak. Eight pigs underwent creation of an infrarenal aortic aneurysm, with a Dacron patch with preservation of lumbar branches. An indwelling pressure transducer was placed in the aneurysm sac. After 1 week the animals underwent EVAR with a custom-made Talent endograft. After another week the animals underwent laparoscopic lumbar artery ligation. Abdominal and pelvic computed tomography was performed after each procedure. Aneurysm sac pressure was measured in sedated and awake animals. All eight animals underwent successful creation of an aortic aneurysm and EVAR resulting in exclusion of the aneurysm sac. After creation of the aneurysm the sac mean arterial pressure (MAP) was 72.5 ± 6.1 mm Hg and the sac pulse pressure was 44.8 ± 8.7 mm Hg. Postoperative computed tomography scans demonstrated a type II endoleak from the lumbar branches in all animals. While aneurysm sac MAP (56.5 ± 7.9 mm Hg; P < .01) and pulse pressure (13.6 ± 4.1 mm Hg; P < .01) decreased after EVAR, sac pulse pressure remained, with type II endoleak. All animals underwent laparoscopic lumbar artery ligation, which resulted in further reduction in the sac MAP (38.3 ± 4.6 mm Hg; P < .02) and immediate absence of sac pulse pressure (0 mm Hg; P < .01). Necropsy confirmed the absence of collateral flow in the aneurysm sac, with fresh thrombus formation in all animals. We present a reliable and clinically relevant in vivo large animal model of type II endoleak. We set out to show that aortic aneurysm sac pressurization caused by lumbar arterial flow in the setting of type II endoleak can be reproduced in an in vivo porcine model of endovascular aortic aneurysm repair. Indeed, in this model the aneurysm sac pulse pressure was a sensitive indicator of type II endoleak, correlating well with findings at computed tomography, and lumbar artery ligation eliminated the endoleak, as demonstrated on computed tomography scans and sac pressure measurement. Therefore we believe this in vivo large animal model can be instrumental in the study of many aspects of the physiologic features of type II endoleak.