A canine model to study the significance and hemodynamics of type II endoleaks 1

Abstract

The clinical significance of Type 2 endoleak after endovascular repair of abdominal aortic aneurysms (AAA) remains incompletely delineated. This study describes the development of a novel canine model that allows for continuous monitoring of intraaneurysmal pressure in the setting of Type 2 endoleak. Infrarenal AAA were created in 10 mongrel dogs by implanting a prosthetic aneurysm containing an intraluminal, solid-state, strain gauge pressure transducer which is able to measure pressures in both solid and liquid media. A segment of native aorta with two or more patent side branch vessels was reimplanted into the prosthetic aneurysm using a Carrel patch. Four animals had two lumbar vessels implanted; two had two lumbar vessels and the caudal mesenteric artery implanted, and four control animals had no vessels reimplanted. Retrograde flow in the aneurysmal side branches caused a Type 2 endoleak after the aneurysm was excluded from antegrade flow by deploying a stent graft. Both systemic and intra-sac pressures were measured daily for up to 90 days after endovascular exclusion and indexed to systemic pressure. Endoleak patency and flow were assessed with digital subtraction angiography, duplex ultrasound, and cine-magnetic resonance angiography (MRA). Histological characterization of the intraaneurysmal contents was performed. Before endovascular exclusion, the systolic, mean arterial, and pulse pressure within the aneurysmal sac closely matched that of the systemic circulation (systolic, 0.96 +/- 0.22; mean, 0.94 +/- 0.21; pulse pressure, 0.97 +/- 0.22) (R value, 0.97). Endovascular exclusion in animals with no collateral side branch vessels resulted in no endoleak and significantly reduced intraaneurysmal pressure when compared to systemic pressure, with systolic, mean arterial, and pulse pressure 0.172 +/- 0.05, 0.137 +/- 0.05, and 0.098 +/- 0.02, respectively (P < 0.001). In animals with Type 2 endoleaks, the pressures were lower than systemic pressure, but statistically significant in their difference from the control group. The systolic pressure of those with Type 2 endoleaks was 0.702 +/- 0.048; mean arterial pressure was 0.784 +/- 0.028, and pulse pressure was 0.406 +/- 0.031 when indexed to systemic pressure (P < 0.001). Cine-MRA and Duplex ultrasound documented persistent patency of the Type 2 endoleaks throughout the study period in animals with multiple side branches. Intraaneurysmal pressure in the setting of Type 2 endoleaks may be accurately determined using this canine model. Intraaneurysmal pressure is maintained at a significant level in the context of this retrograde collateral perfusion, suggesting that persistent Type 2 endoleaks are of clinical significance. This model may serve to allow further evaluation and characterization of Type 2 endoleaks.