Elastin contributes to 30% of the dry weight of the vascular wall. Elastogenesis begins with the synthesis and secretion of the soluble precursor tropoelastin that becomes cross-linked into insoluble elastin in the presence of the enzyme lysyl oxidase. Under normal conditions cross-linked elastin is the only form of the molecule present in the vessel wall whereas tropoelastin is absent. Conversely, under pathological conditions including atherosclerosis and abdominal aortic aneurysm (AAA), elastogenesis resumes and tropoelastin accumulates in the vessel wall [1-4]. We recently developed a novel tropoelastin-specific MR contrast-agent (TESMA) that may allow in vivo visualization and quantification of pathologic elastin degradation and elastogenesis. In this study, we sought to assess focal changes in the integrity of the aortic vessel wall that occur during the development and rupture of AAA.The merits of new tropoelastin-binding contrast agent (Gd-DOTA)-VVGSPSAQDEASPLS (TESMA) were investigated to assess focal changes in tropoelastin composition during the development of abdominal aortic aneurysms (AAA) in a murine model of angiotensin-II (Ang-II) induced hypertension and vessel wall inflammation. In vitro binding studies using Eu(III) analogues and a DELFIA method were used to screen the binding properties of the tropoelastin binding probes and to choose the best candidate for the in vivo implementation. 8-week-old ApoE-/- mice were implanted with minipumps for continuous subcutaneous infusion of Ang-II at a dose of 1000 ng/kg/min [4]. In vivo MRI of the abdominal aorta was performed before and 7, 14 and 21 days after implantation of the pumps and infusion of Ang-II. A 3T Philips Achieva scanner and a 47mm single loop microscopy surface coil were used for signal reception. Images were acquired for up to 1h after intravenous administration of 0.2 mmol/kg tropoelastin-binding probes. 3D gradient-echo late gadolinium enhancement (LGE)-MRI images were acquired with a FOV=35x35x12mm, matrix=348x348, in-plane resolution=0.1x0.1x1mm, TR/TE=27/8ms, TR between subsequent IR pulses=1000ms, and flip angle=30°. T1 mapping was performed using a modified Look Locker (MOLLI) sequence that employs two non-selective inversion pulses with inversion times ranging from 20ms to 2000ms, followed by eight segmented readouts for eight individual images. The two imaging trains result in a set of 16 images per slice with increasing inversion times. For T1 mapping the acquisition parameters were: FOV=36x22x10mm, matrix=180x102, in-plane resolution=0.2x0.2x0.5mm, TR/TE=9/4.6ms, flip angle=10°. T1 values were computed on a pixel-by-pixel basis using a 2-parameter fit with in-house software (Matlab, Natick, MA). In vitro binding assays showed high selectivity of the compounds towards tropoelastin compared to other proteins and particularly mature elastin. The VVGS probe achieved the best discrimination between tropoelastin and mature elastin (64±7 % vs 1±0%) and was used for the in vivo imaging of AAA in the murine model. In vivo MRI of AAA development at different time-points after infusion of Ang-II is illustrated in Fig. 1. Panel A shows maximum-intensity projection images of the abdominal aorta used to identify the location of the AAA (Fig. 1; arrows). Panel B shows LGE-MRI images of the vessel wall after administration of the tropoelastin-binding contrast agent. There is little to no uptake of TESMA in control animals and at Day 7 post-infusion of Ang-II. Conversely, there is enhancement of the vessel wall at the level of the AAA diseased vessel wall at days 14 and 21 post-infusion of Ang-II (Fig. 1; arrows). At day 21, the AAA forms a pseudo-lumen (Fig. 1; asterisk *). Quantitative analysis of the vessel wall gadolinium concentration using inductively coupled mass spectroscopy (ICP-MS) showed accumulation of gadolinium, which was in agreement with accumulation of tropoelastin molecules in the vessel wall during AAA development (Fig. 2). These data are in agreement with previous studies in our group that showed increased tropoelastin deposition during AAA formation and a significant linear correlation between the immunopositive tropoelastin area and AAA diameter in this murine model (unpublished data).We demonstrate focal changes in elastogenesis that occur during the evolution of AAA using a newly developed gadolinium-based tropoelastin-binding contrast agent. TESMA may allow molecular imaging of impaired elastogenesis that occurs during the development of AAA and may serve as a novel imaging biomarker to non-invasively assess aortic wall integrity and risk of rupture, beyond aneurysmal diameter.