There is no effect of TAFI inhibition of the growth of an established AAA in the Angiotensin II model.

<p>AAA were induced in hyperlipidaemic mice by infusion of Ang II 750 ng/kg/min. After 1 week, mice were treated with a single injection of either MA-TCK26D6 or NaCl control. AAA progression in both groups was evaluated at 2 weeks post injection using Vevo2100 pre-clinical ultrasound scanning, and 3D reconstructions of the aortic segment at risk of AAA formation were created. Panel A Aortic diameter, Panel B Aortic volume, Panel C The process of creating the 3D aortic reconstruction. Panel D Example 3D reconstruction showing AAA progression over time (0, 1 and 3 weeks post Angiotensin II infusion). Data is shown as mean±standard deviation.</p

AAA formation is altered in the presence of a TAFI-inhibitor.

<p>Mice were treated with saline control, NaCl 0.9%, (n = 23), Ang II (n = 35), Ang II and MA-TCK26D6 (n = 12) or Ang II and UK-396082 (n = 12) for 28 days. Panel A Incidence of AAA in each group. Panel B AAA size. Data is shown as mean±standard deviation. * p<0.05 compared to Angiotensin II alone by Chi-Squared testing.</p

The effect of TAFI inhibition on mortality in the Angiotensin II model of AAA.

<p>Panel A and B Blood pressure (BP) and heart rate (HR) measurements taken in all groups of mice in the second week of the experimental period using the CODA non-invasive BP device. Panel C and D Mortality of mice treated with Ang II, compared with NaCl 0.9% or Ang II plus MA-TCK26D6 or UK-396082. Data is shown as mean±standard deviation. Mortality in this model of AAA typically occurred early (Days 3–8 post initiation of Ang II infusion). * p<0.05 compared to Angiotensin II alone by Chi-Squared testing.</p

Aortic distensibility decreases with AAA formation, but is not affected by TAFI-inhibition, in the Angiotensin II model of AAA.

<p>The aorta was imaged in longitudinal section using the Vevo2100 scanner, and the distensibility measured using ECG-gated images and VevoVasc software. Panel A shows aortic wall distensibility in all mice with AAA (MA-TCK26D6 treated and sham treated). One week following initiation of Ang II infusion, mice received either MA-TCK26D6 or control (NaCl 0.9%) as an IV injection via the femoral vein. Panel B and C There was no difference in the change of distensibility by week 3 in mice receiving treatment with MA-TCK26D6 at 1 week compared with controls (data shown is change in distensibility between week 1 and week 3). Data is shown as mean±standard deviation, *** p = 0.001 compared to baseline by student t-test.</p