11 research outputs found
A computational model for false lumen thrombosis in type B aortic dissection following thoracic endovascular repair
Thoracic endovascular repair (TEVAR) has recently been established as the preferred treatment option for complicated type B dissection. This procedure involves covering the primary entry tear to stimulate aortic remodelling and promote false lumen thrombosis thereby restoring true lumen flow. However, complications associated with incomplete false lumen thrombosis, such as aortic dilatation and stent graft induced new entry tears, can arise after TEVAR. This study presents the application and validation of a recently developed mathematical model for patient-specific prediction of thrombus formation and growth under physiologically realistic flow conditions. The model predicts thrombosis through the evaluation of shear rates, fluid residence time and platelet distribution, based on convection-diffusion-reaction transport equations. The model was applied to 3 type B aortic dissection patients: two TEVAR cases showing complete and incomplete false lumen thrombosis respectively, and one medically treated dissection with no signs of thrombosis. Predicted thrombus growth over time was validated against follow-up CT scans, showing good agreement with in vivo data in all cases with a maximum difference between predicted and measured false lumen reduction below 8%. Our results demonstrate that TEVAR-induced thrombus formation in type B aortic dissection can be predicted based on patient-specific anatomy and physiologically realistic boundary conditions. Our model can be used to identify anatomical or stent graft related factors that are associated with incomplete false lumen thrombosis following TEVAR, which may help clinicians develop personalised treatment plans for dissection patients in the future
Imaging of the vulnerable carotid plaque: biological targeting of inflammation using ultrasmall superparamagnetic particles of iron oxide (USPIO) and MRI
MRI detection of endothelial cell inflammation using targeted superparamagnetic particles of iron oxide (SPIO).
BACKGROUND: There is currently no clinical imaging technique available to assess the degree of inflammation associated with atherosclerotic plaques. This study aims to develop targeted superparamagnetic particles of iron oxide (SPIO) as a magnetic resonance imaging (MRI) probe for detecting inflamed endothelial cells. METHODS: The in vitro study consists of the characterisation and detection of inflammatory markers on activated endothelial cells by immunocytochemistry and MRI using biotinylated anti-P-selectin and anti-VCAM-1 (vascular cell adhesion molecule 1) antibody and streptavidin conjugated SPIO. RESULTS: Established an in vitro cellular model of endothelial inflammation induced with TNF-α (tumor necrosis factor alpha). Inflammation of endothelial cells was confirmed with both immunocytochemistry and MRI. These results revealed both a temporal and dose dependent expression of the inflammatory markers, P-selectin and VCAM-1, on exposure to TNF-α. CONCLUSION: This study has demonstrated the development of an in vitro model to characterise and detect inflamed endothelial cells by immunocytochemistry and MRI. This will allow the future development of contrast agents and protocols for imaging vascular inflammation in atherosclerosis. This work may form the basis for a translational study to provide clinicians with a novel tool for the in vivo assessment of atherosclerosis
Predicting flow in aortic dissection: Comparison of computational model with PC-MRI velocity measurements
Aortic dissection is a life-threatening process in which the weakened wall develops a tear, causing separation of wall layers. The dissected layers separate the original true aortic lumen and a newly created false lumen. If untreated, the condition can be fatal. Flow rate in the false lumen is a key feature for false lumen patency, which has been regarded as one of the most important predictors of adverse early and later outcomes. Detailed flow analysis in the dissected aorta may assist vascular surgeons in making treatment decisions, but computational models to simulate flow in aortic dissections often involve several assumptions. The purpose of this study is to assess the computational models adopted in previous studies by comparison with in vivo velocity data obtained by means of phase-contrast magnetic resonance imaging (PC-MRI).Aortic dissection geometry was reconstructed from computed tomography (CT) images, while PC-MRI velocity data were used to define inflow conditions and to provide distal velocity components for comparison with the simulation results. The computational fluid dynamics (CFD) simulation incorporated a laminar-turbulent transition model, which is necessary for adequate flow simulation in aortic conditions. Velocity contours from PC-MRI and CFD in the two lumens at the distal plane were compared at four representative time points in the pulse cycle.The computational model successfully captured the complex regions of flow reversal and recirculation qualitatively, although quantitative differences exist. With a rigid wall assumption and exclusion of arch branches, the CFD model over-predicted the false lumen flow rate by 25% at peak systole. Nevertheless, an overall good agreement was achieved, confirming the physiological relevance and validity of the computational model for type B aortic dissection with a relatively stiff dissection flap. © 2014 IPEM
Two-vessel branched stent graft for severely angulated aortic arch aneurysm in a Jehovah's Witness
Aneurysmal disease involving the origins of supra aortic vessels often requires complex open and/or endovascular repair that is not only associated with significant risk of mortality and morbidity but also often with perioperative blood loss requiring transfusion. We report a successful repair of a large thoracic aortic aneurysm (TAA) involving the aortic arch with a custom-made Bolton Relay 2-vessel branched thoracic aortic endograft in a 42-year-old Jehovah’s Witness who would otherwise be very unlikely to survive an open repair. Branched thoracic aortic endografting offers a potentially safe, minimally invasive, and effective alternative for TAA disease involving the supra-aortic arteries, especially in patients who are at high risk of open surgery
Early outcomes of patients transferred with ruptured suprarenal aneurysm or dissection
Objective Despite centralisation of the provision of vascular care, not all areas in England and Wales are able to offer emergency treatment for patients with acute conditions affecting the aorta proximal to the renal arteries. While cardiothoracic centres have made network arrangements to coordinate care for the repair of type A dissections, a similar plan for vascular care is lacking. This study investigates early outcomes in patients with ruptured suprarenal aortic aneurysm or dissection (rSRAD) transferred to a specialist centre. Methods Retrospective observational study over a five-year period (2009–2014) assessing outcomes of patients with ruptured sRAD diagnosed at their local hospital and then transferred to a tertiary centre capable of offering such treatment. Results Fifty-two patients (median age 73 years, 32 male) with rSRAD were transferred and a further four died during transit. The mean distance of patient transfer was 35 miles (range 4–211 miles). One patient did not undergo intervention due to frailty and two died before reaching the operating theatre. A total of 23 patients underwent endovascular repair, 9 hybrid repair and 17 open surgery. Median follow-up was 12 months (range 1–43 months). Complications included paraplegia (n = 3), stroke (n = 2), type IA endoleak (n = 4); 30-day and in-hospital mortality were 16% and 27%. For patients discharged alive from hospital, one-year survival was 67%. Conclusions Although the number of patients with rSRAD is low and those who are transferred alive are a self-selecting group, this study suggests that transfer of such patients to a specialist vascular centre is associated with acceptable mortality rates following emergency complex aortic repair. </jats:sec
Imaging vulnerable plaques by targeting inflammation in atherosclerosis using fluorescent-labeled dual-ligand microparticles of iron oxide and magnetic resonance imaging
OBJECTIVE: Identification of patients with high-risk asymptomatic carotid plaques remains an elusive but essential step in stroke prevention. Inflammation is a key process in plaque destabilization and a prelude to clinical sequelae. There are currently no clinical imaging tools to assess the inflammatory activity within plaques. This study characterized inflammation in atherosclerosis using dual-targeted microparticles of iron oxide (DT-MPIO) as a magnetic resonance imaging (MRI) probe. METHODS: DT-MPIO were used to detect and characterize inflammatory markers, vascular cell adhesion molecule 1 (VCAM-1). and P-selectin on (1) tumor necrosis factor-α-treated cells by immunocytochemistry and (2) aortic root plaques of apolipoprotein-E deficient mice by in vivo MRI. Furthermore, apolipoprotein E-deficient mice with focal carotid plaques of different phenotypes were developed by means of periarterial cuff placement to allow in vivo molecular MRI using these probes. The association between biomarkers and the magnetic resonance signal in different contrast groups was assessed longitudinally in these models. RESULTS: Immunocytochemistry confirmed specificity and efficacy of DT-MPIO to VCAM-1 and P-selectin. Using this in vivo molecular MRI strategy, we demonstrated (1) the DT-MPIO-induced magnetic resonance signal tracked with VCAM-1 (r = 0.69; P = .014), P-selectin (r = 0.65; P = .022), and macrophage content (r = 0.59; P = .045) within aortic root plaques and (2) high-risk inflamed plaques were distinguished from noninflamed plaques in the murine carotid artery within a practical clinical imaging time frame. CONCLUSIONS: These molecular MRI probes constitute a novel imaging tool for in vivo characterization of plaque vulnerability and inflammatory activity in atherosclerosis. Further development and translation into the clinical arena will facilitate more accurate risk stratification in carotid atherosclerotic disease in the future
A null model for Pearson co-expression networks
<p>Presented at the Fondazione Edmund Mach</p
