Computed Tomography of Aortic Wall Calcifications in Aortic Dissection Patients

Jong, Pim A. de; Hellings, Willem E.; Takx, Richard A.P.; Išgum, Ivana; Herwaarden, Joost A. van; Mali, Willem P.Th.M.

doi:10.1371/journal.pone.0102036

Cited by 26 publications

(12 citation statements)

References 29 publications

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“…However, there is no consensus on how best to define vessel wall properties from imaging data alone as yet. This difficulty is exacerbated in the case of AD, which is often accompanied by increased vessel wall stiffness [ 32 ], which may not be evenly distributed throughout the domain. The present simulation uses a simple hyperelastic model extracted from experimental data on an aneurysm, and a uniform wall thickness throughout (except the intimal flap) and as such may not perfectly capture the wall dynamics.…”

Section: Discussionmentioning

confidence: 99%

Aortic dissection simulation models for clinical support: fluid-structure interaction vs. rigid wall models

et al. 2015

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BackgroundThe management and prognosis of aortic dissection (AD) is often challenging and the use of personalised computational models is being explored as a tool to improve clinical outcome. Including vessel wall motion in such simulations can provide more realistic and potentially accurate results, but requires significant additional computational resources, as well as expertise. With clinical translation as the final aim, trade-offs between complexity, speed and accuracy are inevitable. The present study explores whether modelling wall motion is worth the additional expense in the case of AD, by carrying out fluid-structure interaction (FSI) simulations based on a sample patient case.MethodsPatient-specific anatomical details were extracted from computed tomography images to provide the fluid domain, from which the vessel wall was extrapolated. Two-way fluid-structure interaction simulations were performed, with coupled Windkessel boundary conditions and hyperelastic wall properties. The blood was modelled using the Carreau-Yasuda viscosity model and turbulence was accounted for via a shear stress transport model. A simulation without wall motion (rigid wall) was carried out for comparison purposes.ResultsThe displacement of the vessel wall was comparable to reports from imaging studies in terms of intimal flap motion and contraction of the true lumen. Analysis of the haemodynamics around the proximal and distal false lumen in the FSI model showed complex flow structures caused by the expansion and contraction of the vessel wall. These flow patterns led to significantly different predictions of wall shear stress, particularly its oscillatory component, which were not captured by the rigid wall model.ConclusionsThrough comparison with imaging data, the results of the present study indicate that the fluid-structure interaction methodology employed herein is appropriate for simulations of aortic dissection. Regions of high wall shear stress were not significantly altered by the wall motion, however, certain collocated regions of low and oscillatory wall shear stress which may be critical for disease progression were only identified in the FSI simulation. We conclude that, if patient-tailored simulations of aortic dissection are to be used as an interventional planning tool, then the additional complexity, expertise and computational expense required to model wall motion is indeed justified.

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Section: Discussionmentioning

confidence: 99%

Aortic dissection simulation models for clinical support: fluid-structure interaction vs. rigid wall models

et al. 2015

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“…Whereas CAC is mostly intimal, TAC is thought to better represent a generalized atherosclerosis process [4] , [7] . The differentiation of the aortic wall from the lumen would need enhanced CT protocols that are not recommended for our patients [31] . Aortic valve calcium was not measured in this study because the vessel segmentation method was limited to tubular cross-sections starting at the left main coronary artery [8] .…”

Section: Discussionmentioning

confidence: 99%

Calcifications of the Thoracic Aorta on Extended Non-Contrast-Enhanced Cardiac CT

et al. 2014

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BackgroundThe presence of calcified atherosclerosis in different vascular beds has been associated with a higher risk of mortality. Thoracic aorta calcium (TAC) can be assessed from computed tomography (CT) scans, originally aimed at coronary artery calcium (CAC) assessment. CAC screening improves cardiovascular risk prediction, beyond standard risk assessment, whereas TAC performance remains controversial. However, the curvilinear portion of the thoracic aorta (TA), that includes the aortic arch, is systematically excluded from TAC analysis. We investigated the prevalence and spatial distribution of TAC all along the TA, to see how those segments that remain invisible in standard TA evaluation were affected.Methods and ResultsA total of 970 patients (77% men) underwent extended non-contrast cardiac CT scans including the aortic arch. An automated algorithm was designed to extract the vessel centerline and to estimate the vessel diameter in perpendicular planes. Then, calcifications were quantified using the Agatston score and associated with the corresponding thoracic aorta segment. The aortic arch and the proximal descending aorta, “invisible” in routine CAC screening, appeared as two vulnerable sites concentrating 60% of almost 11000 calcifications. The aortic arch was the most affected segment per cm length. Using the extended measurement method, TAC prevalence doubled from 31% to 64%, meaning that 52% of patients would escape detection with a standard scan. In a stratified analysis for CAC and/or TAC assessment, 111 subjects (46% women) were exclusively identified with the enlarged scan.ConclusionsCalcium screening in the TA revealed that the aortic arch and the proximal descending aorta, hidden in standard TA evaluations, concentrated most of the calcifications. Middle-aged women were more prone to have calcifications in those hidden portions and became candidates for reclassification.

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“…A discrete and temporary intracellular Ca increase, due to Na/K pump inhibition or blocking a natural Ca antagonist like Mg, may alter cell contraction and transcription and cause cell death [20]. This pathophysiological effect may evolve, at endothelial level, in pro-inflammatory mechanisms characteristic of AAD, including the release of pro-inflammatory mediators, pro-coagulant and endothelial factors from damaged vascular cells [1, 21, 22].…”

Section: Introductionmentioning

confidence: 99%

A pilot observational study on magnesium and calcium imbalance in elderly patients with acute aortic dissection

et al. 2017

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BackgroundMagnesium (Mg) and calcium (Ca) are the principal essential elements involved in endothelial cell homeostasis. Extracellular changes in the levels of either alter endothelial contraction and dilatation. Consequently Mg and Ca imbalance is associated with a high risk of endothelial dysfunction, the main process observed during acute aortic dissection (AAD); in this clinical condition, which mainly affects elderly men, smooth muscle cell alterations lead to intimal tears, creating a false new lumen in the media of the aorta. AAD patients have a high risk of mortality as a result of late diagnosis because often it is not distinguished from other cardiovascular diseases.We investigated Mg and Ca total circulating levels and the associated pro-inflammatory mediators in elderly AAD patients, to gain further information on the pathophysiology of this disorder, with a view to suggesting newer and earlier potential biomarkers of AAD.ResultsTotal circulating Mg and Ca levels were both lower in AAD patients than controls (p < 0.0001). Using Ca as cut-off, 90% of AAD patients with low Ca (<8.4 mg/dL) came into the type A classification of AAD. Stratifying AAD according to this cut-off, Mg was lower in patients with lower total Ca.Compared to controls, both type A and B AAD patients had higher levels of all the pro-coagulant and pro-inflammatory mediators analyzed, including sP-sel, D-dimer, TNF-α, IL-6, and CRP (p < 0.05). Dividing types A and B using the Stanford classification, no significant differences were found (p > 0.05) The levels of both ICAM-1 and EN-1 were lower in AAD than in a control group (p < 0.0001 and p < 0.05 respectively).ConclusionsThese findings suggest that low Mg and Ca in AAD elderly patients may contribute to altering normal endothelial physiology and also concur in changing the normal concentrations of different mediators involved in vasodilatation and constriction, associated with AAD onset and severity.

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Computed Tomography of Aortic Wall Calcifications in Aortic Dissection Patients

Cited by 26 publications

References 29 publications

Aortic dissection simulation models for clinical support: fluid-structure interaction vs. rigid wall models

Aortic dissection simulation models for clinical support: fluid-structure interaction vs. rigid wall models

Calcifications of the Thoracic Aorta on Extended Non-Contrast-Enhanced Cardiac CT

A pilot observational study on magnesium and calcium imbalance in elderly patients with acute aortic dissection

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