Objective-To quantitatively compare aortic curvature and motion with resulting aneurysm location, direction of expansion, and pathophysiological features in experimental abdominal aortic aneurysms (AAAs). Methods and Results-MRI was performed at 4.7 T with the following parameters: (1) 3D acquisition for vessel geometry and (2) 2D cardiac-gated acquisition to quantify luminal motion. Male 24-week-old mice were imaged before and after AAA formation induced by angiotensin II (AngII)-filled osmotic pump implantation or infusion of elastase. AngII-induced AAAs formed near the location of maximum abdominal aortic curvature, and the leftward direction of expansion was correlated with the direction of suprarenal aortic motion. Elastase-induced AAAs formed in a region of low vessel curvature and had no repeatable direction of expansion. AngII significantly increased mean blood pressure (22.7 mm Hg, PϽ0.05), whereas both models showed a significant 2-fold decrease in aortic cyclic strain (PϽ0.05). Differences in patterns of elastin degradation and localization of fluorescent signal from protease-activated probes were also observed. Conclusion-The direction of AngII aneurysm expansion correlated with the direction of motion, medial elastin dissection, and adventitial remodeling. Anterior infrarenal aortic motion correlated with medial elastin degradation in elastaseinduced aneurysms. Results from both models suggest a relationship between aneurysm pathological features and aortic geometry and motion. Key Words: aneurysms Ⅲ angiotensin II Ⅲ magnetic resonance imaging Ⅲ elastase Ⅲ near-infrared fluorescence A bdominal aortic aneurysm (AAA) is a complex disease that leads to significant morbidity and mortality in the United States. 1 AAAs are commonly defined as a 1.5-fold or larger increase in vessel diameter due to a pathological dilation. 2 Diagnosis and monitoring are usually performed using noninvasive ultrasonography, but only surgical options exist to prevent continued vessel growth and reduce the risk of rupture. This "wait-and-see" approach is partially because of a lack of understanding of the mechanisms that lead to AAA development and expansion.As a way to better study disease etiology and progression, murine AAA models have been created that mimic aspects of the human disease. 3,4 In particular, 2 chemically induced murine models have become commonly used. The first model is initiated by subcutaneous systemic delivery of angiotensin II (AngII) into hyperlipidemic apolipoprotein E-deficient (apoE Ϫ/Ϫ ) mice, leading to suprarenal AAAs. 3 The predictable formation of these aneurysms above the renal arteries in this model is of particular interest because most human AAAs are infrarenal. The rationale for the development of the second model, induced by intraluminal infusion of elastase into the murine infrarenal aorta, 4 was based on the disrupted nature of elastin in human AAAs. [5][6][7][8] Although both of these models produce AAAs, there are significant differences. The AngII apoE Ϫ/Ϫ model is associated with ...

Purpose: To develop methods to quantify cyclic strain, motion, and curvature of the murine abdominal aorta in vivo.Materials and Methods: C57BL/6J and apoE À/À mice underwent three-dimensional (3D) time-of-flight MR angiography to position cardiac-gated 2D slices at four locations along the abdominal aorta where circumferential cyclic strain and lumen centroid motion were calculated. From the 3D data, a centerline through the aorta was created to quantify geometric curvature at 0.1-mm intervals. Medial elastin content was quantified with histology postmortem. The location and shape of abdominal aortic aneurysms (AAAs), created from angiotensin II infusion, were evaluated qualitatively.Results: Strain waveforms were similar at all locations and between groups. Centroid motion was significantly larger and more leftward above the renal vessels than below (P < 0.05). Maximum geometric curvature occurred slightly proximal to the right renal artery. Elastin content was similar around the circumference of the vessel. AAAs developed in the same location as the maximum curvature and grew in the same direction as vessel curvature and motion. Conclusion:The methods presented provide temporally and spatially resolved data quantifying murine aortic motion and curvature in vivo. This noninvasive methodology will allow serial quantification of how these parameters influence the location and direction of AAA growth.

Abdominal aortic aneurysm (AAA) disease, defined as a pathological dilation of the vessel wall, is responsible for 15,000 deaths per year in the United States. Human AAA are often asymmetric, typically expanding anteriorly as the posterior region is supported by the vertebral column [1]. Other work has shown that healthy thoracic aortic motion is also asymmetric in pigs and humans [2]. Two commonly used murine models induce AAA growth with either the infusion of angiotensin II (angII) [3] or intra-arterial perfusion of porcine pancreatic elastase (PPE) into the aortic lumen [4]. The purpose of this study was to determine the relationship between vessel motion, circumferential cyclic strain, and aneurysm growth in two different murine models of AAA disease using small animal magnetic resonance imaging (MRI).