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      Evaluation of 3D blood flow patterns and wall shear stress in the normal and dilated thoracic aorta using flow-sensitive 4D CMR

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          Abstract

          Background

          The purpose of this study was to investigate 3D flow patterns and vessel wall parameters in patients with dilated ascending aorta, age-matched subjects, and healthy volunteers.

          Methods

          Thoracic time-resolved 3D phase contrast CMR with 3-directional velocity encoding was applied to 33 patients with dilated ascending aorta (diameter ≥40 mm, age=60±16 years), 15 age-matched normal controls (diameter ≤37 mm, age=68±7.5 years) and 15 young healthy volunteers (diameter ≤30 mm, age=23±2 years). 3D blood flow was visualized and flow patterns were graded regarding presence of supra-physiologic-helix and vortex flow using a semi-quantitative 3-point grading scale. Blood flow velocities, regional wall shear stress (WSS), and oscillatory shear index (OSI) were quantified.

          Results

          Incidence and strength of supra-physiologic-helix and vortex flow in the ascending aorta (AAo) was significantly higher in patients with dilated AAo (16/33 and 31/33, grade 0.9±1.0 and 1.5±0.6) than in controls (2/15 and 7/15, grade 0.2 ± 0.6 and 0.6 ± 0.7, P<.05) or healthy volunteers (1/15 and 0/15, grade 0.1 ± 0.3 P<.05). Greater strength of the ascending aortic helix and vortex flow were associated with significant differences in AAo diameters ( P<.05). Peak systolic WSS in the ascending aorta and aortic arch was significantly lower in patients with dilated AAo ( P<.0157-.0488). AAo diameter positively correlated to time to peak systolic velocities (r=0.30-0.53, P<.04), OSI (r=0.33-0.49, P<0.02) and inversely correlated to peak systolic WSS (r=0.32-0.40, P<.03). Peak systolic WSS was significantly lower in AAo aneurysms at the right and outer curvature within the AAo and proximal arch ( P<.01-.05).

          Conclusions

          Increase in AAo diameter is significantly correlated with the presence and strength of supra-physiologic-helix and vortex formation in the AAo, as well with decrease in systolic WSS and increase in OSI.

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          Most cited references28

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          Thoracic and abdominal aortic aneurysms.

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            Thoracic aortic aneurysm clinically pertinent controversies and uncertainties.

            This paper addresses clinical controversies and uncertainties regarding thoracic aortic aneurysm and its treatment. 1) Estimating true aortic size is confounded by obliquity, asymmetry, and noncorresponding sites: both echocardiography and computed tomography/magnetic resonance imaging are necessary for complete assessment. 2) Epidemiology of thoracic aortic aneurysm. There has been a bona fide increase in incidence of aortic aneurysm making aneurysm disease the 18th most common cause of death. 3) Aortic growth rate. Although a virulent disease, thoracic aortic aneurysm is an indolent process. The thoracic aorta grows slowly-0.1 cm/year. 4) Evidence-based intervention criteria. It is imperative to extirpate the thoracic aorta before rupture or dissection occurs; surgery at 5.0- to 5.5-cm diameter will prevent most adverse natural events. Symptomatic (painful) aneurysms must be resected regardless of size. 5) Development of nonsize criteria. Mechanical properties of the aorta deteriorate at the same 6 cm at which dissection occurs; elastic properties of the aorta may soon become useful intervention criteria. 6) Medical treatment of aortic aneurysm. Medical treatment is of unproven value, even beta-blockers and angiotensin-receptor blockers. 7) A genetic disease. Even non-Marfan aneurysms have a strong genetic basis. 8) Need for biomarkers. Virulent but silent, TAA cries out for a biomarker that can predict the onset of adverse events. Pathophysiologic understanding has led to identification of promising biomarkers, especially metalloproteinases. 9) Endovascular therapy for aneurysms. Endovascular therapy has burgeoned, despite the fact that the EVAR-2, DREAM, and INSTEAD trials showed no benefit at mid-term over medical or conventional surgical therapy. We must avoid "irrational exuberance." 10) Inciting events for acute aortic dissection. Recent evidence shows that dissections are preceded by a specific severe exertional or emotional event. 11) "Silver lining" of aortic disease. Proximal aortic root disease seems to protect against arteriosclerosis. Copyright 2010 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
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              Complex hemodynamics at the apex of an arterial bifurcation induces vascular remodeling resembling cerebral aneurysm initiation.

              Arterial bifurcation apices are common sites for cerebral aneurysms, raising the possibility that the unique hemodynamic conditions associated with flow dividers predispose the apical vessel wall to aneurysm formation. This study sought to identify the specific hemodynamic insults that lead to maladaptive vascular remodeling associated with aneurysm development and to identify early remodeling events at the tissue and cellular levels. We surgically created new branch points in the carotid vasculature of 6 female adult dogs. In vivo angiographic imaging and computational fluid dynamics simulations revealed the detailed hemodynamic microenvironment for each bifurcation, which were then spatially correlated with histologic features showing specific tissue responses. We observed 2 distinct patterns of vessel wall remodeling: (1) hyperplasia that formed an intimal pad at the bifurcation apex and (2) destructive remodeling in the adjacent region of flow acceleration that resembled the initiation of an intracranial aneurysm, characterized by disruption of the internal elastic lamina, loss of medial smooth muscle cells, reduced proliferation of smooth muscle cells, and loss of fibronectin. Strong localization of aneurysm-type remodeling to the region of accelerating flow suggests that a combination of high wall shear stress and a high gradient in wall shear stress represents a "dangerous" hemodynamic condition that predisposes the apical vessel wall to aneurysm formation.
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                Author and article information

                Journal
                J Cardiovasc Magn Reson
                J Cardiovasc Magn Reson
                Journal of Cardiovascular Magnetic Resonance
                BioMed Central
                1097-6647
                1532-429X
                2012
                13 December 2012
                : 14
                : 1
                : 84
                Affiliations
                [1 ]Department of Diagnostic Radiology, Medical Physics, University Hospital, Freiburg, Germany
                [2 ]Clinic of Radiology and Nuclear Medicine, University Hospital of Schleswig-Holstein, Campus, Lübeck, Germany
                [3 ]Departments of Radiology and Biomedical Engineering, Northwestern University, Chicago, IL, USA
                Article
                1532-429X-14-84
                10.1186/1532-429X-14-84
                3534249
                23237187
                0e46e8d9-47cf-45b5-a115-ba1a8e4da34b
                Copyright ©2012 Bürk et al.; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 8 July 2012
                : 28 November 2012
                Categories
                Research

                Cardiovascular Medicine
                4d flow,flow quantification,aneurysm of the ascending aorta
                Cardiovascular Medicine
                4d flow, flow quantification, aneurysm of the ascending aorta

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