Relationship between stenosis severity and distensibility.

<p>(a) Distensibility_MLA and (b) Distensibility_Ref.</p

FFR_CFD in ART_rigid and ART_distensible models for 26 coronary arteries.

<p>Blue triangles represent the coronary arteries with FFR < 0.8 when modeled as rigid vessels and had FFR > 0.8 when modeled as distensible vessels.</p

Effect of vessel rigidity on FFR_CFD.

<p>FFR_CFD for representative arteries with percentage diameter stenosis of (a) 40, (b) 50.5, (c) 62.5, and (d) 73 are shown.</p

Representative comparison of two coronary arteries with similar lesion characteristics but different distensibility.

<p>(a) vessel with high distensibility, (b) vessel with low distensibility.</p

CFD model.

<p>(a) Coronary angiogram of LAD artery with initial definition of lesion, and non-stenotic segments proximal and distal to the lesion, (b) Two-dimensional representation of vessel lumen, (c) Three-dimensional reconstruction of vessel lumen showing lesion length (L) and percentage cross sectional area stenosis (CS). Yellow cross defines lesion site, cross denoted by “P” defines proximal site and cross denoted by “D” defines distal site, (d) Defined inlet and outlet with the corresponding boundary condition, (e) contours of CFD-based FFR.</p

Baseline clinical and lesion characteristics.

<p>Baseline clinical and lesion characteristics.</p

Scatterplots showing relationship between FFR and distensibility.

<p>(a) Distensibility_MLA and (b) Distensibility_Ref.</p

Bland-Altman analysis of the comparison between IVUS and 3D-QCA derived distensibility.

<p>Bland-Altman analysis of the comparison between IVUS and 3D-QCA derived distensibility.</p

Relationship between FFR, percentage diameter stenosis and distensibility.

<p>(a) Distensibility_MLA and (b) Distensibility_Ref.</p

Evaluation of synthetic vascular grafts in a mouse carotid grafting model

<div><p>Current animal models for the evaluation of synthetic grafts are lacking many of the molecular tools and transgenic studies available to other branches of biology. A mouse model of vascular grafting would allow for the study of molecular mechanisms of graft failure, including in the context of clinically relevant disease states. In this study, we comprehensively characterise a sutureless grafting model which facilitates the evaluation of synthetic grafts in the mouse carotid artery. Using conduits electrospun from polycaprolactone (PCL) we show the gradual development of a significant neointima within 28 days, found to be greatest at the anastomoses. Histological analysis showed temporal increases in smooth muscle cell and collagen content within the neointima, demonstrating its maturation. Endothelialisation of the PCL grafts, assessed by scanning electron microscopy (SEM) analysis and CD31 staining, was near complete within 28 days, together replicating two critical aspects of graft performance. To further demonstrate the potential of this mouse model, we used longitudinal non-invasive tracking of bone-marrow mononuclear cells from a transgenic mouse strain with a dual reporter construct encoding both luciferase and green fluorescent protein (GFP). This enabled characterisation of mononuclear cell homing and engraftment to PCL using bioluminescence imaging and histological staining over time (7, 14 and 28 days). We observed peak luminescence at 7 days post-graft implantation that persisted until sacrifice at 28 days. Collectively, we have established and characterised a high-throughput model of grafting that allows for the evaluation of key clinical drivers of graft performance.</p></div