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1

Laurent, Stéphane, Pierre Boutouyrie, and Elie Mousseaux. "Aortic Stiffening, Aortic Blood Flow Reversal, and Renal Blood Flow." Hypertension 66, no. 1 (July 2015): 10–12. http://dx.doi.org/10.1161/hypertensionaha.115.05357.

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2

Muchada, Raoul, Dominique Cathignol, Bernard Lavandier, Jean Lamazou, and Dominique Haro. "Aortic Blood Flow Measurement." American Journal of Noninvasive Cardiology 2, no. 1-2 (1988): 24–31. http://dx.doi.org/10.1159/000470655.

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3

Gjurich, Breanne, Parésa Taghavie-Moghadam, Klaus Ley, and Elena Galkina. "L-selectin deficiency decreases aortic B1a and Breg subsets and promotes atherosclerosis." Thrombosis and Haemostasis 112, no. 10 (2014): 803–11. http://dx.doi.org/10.1160/th13-10-0865.

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SummaryThere is a significant recruitment of leucocytes into aortas during atherogenesis. L-selectin regulates leucocyte migration into secondary lymphoid and peripheral tissues and was proposed to play a role in leucocyte homing into aortas. Here, we determine the role of L-selectin in atherosclerosis. L-selectin-deficient Apoe -/- (Sell -/- Apoe -/-) mice had a 74% increase in plaque burden compared to Apoe -/- mice fed a chow diet for 50 weeks. Elevated atherosclerosis was accompanied by increased aortic leucocyte content, but a 50% reduction in aortic B cells despite elevated B cell counts in the blood. Follicular B cells represented 65%, whereas B1a and regulatory B cells (Breg) comprised 5% of aortic B cells. B1a and Breg cell subsets were reduced in Sell -/- Apoe -/- aortas with accompanied two-fold decrease in aortic T15 antibody and 1.2-fold decrease of interleukin-10 (IL-10) levels. L-selectin was required for B1 cell homing to the atherosclerotic aorta, as demonstrated by a 1.5-fold decrease in the migration of Sell -/- Apoe -/- vs Apoe -/- cells. Notably, we found a 1.6-fold increase in CD68hi macrophages in Sell -/- Apoe -/- compared to Apoe -/- aortas, despite comparable blood monocyte numbers and L-selectin-dependent aortic homing. L-selectin had no effect on neutrophil migration into aorta, but led to elevated blood neutrophil numbers, suggesting a potential involvement of neutrophils in atherogenesis of Sell -/- Apoe -/- mice. Thus, L-selectin deficiency increases peripheral blood neutrophil and lymphocyte numbers, decreases aortic B1a and Breg populations, T15 antibody and IL-10 levels, and increases aortic macrophage content of Sell -/- Apoe -/- mice. Altogether, these data provide evidence for an overall atheroprotective role of L-selectin.
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4

R, VINOTH. "TRANSIENT ANALYSIS OF BLOOD FLOW IN FUSIFORM MODELS OF AORTIC ANEURYSMS." International Journal of Psychosocial Rehabilitation 24, no. 04 (February 29, 2020): 1450–62. http://dx.doi.org/10.37200/ijpr/v24i4/pr201114.

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5

Lehmann, E. D., K. D. Hopkins, R. L. Jones, A. G. Rudd, and R. G. Gosling. "Aortic Distensibility in Patients with Cerebrovascular Disease." Clinical Science 89, no. 3 (September 1, 1995): 247–53. http://dx.doi.org/10.1042/cs0890247.

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1. Non-invasive aortic compliance measurements have been used previously to assess the distensibility of the aorta in several pathological conditions associated with increased cardiovascular risk. We set out to establish whether aortic compliance is abnormal in patients with stroke. 2. Pulse wave velocity measurements of thoracoabdominal aortic compliance were made in 20 stroke patients and 25 age- and sex-matched hospitalized, non-stroke control subjects putatively free of cardiovascular disease. Since compliance varies with non-chronic changes in blood pressure, a blood pressure corrected index of aortic distensibility, Cp, was calculated. 3. Aortic compliance was significantly reduced in patients with stroke compared with non-stroke control subjects (0.46 ± 0.27 versus 0.86 ± 0.34%/10 mmHg, P < 0.0002), corresponding with higher values for pulse wave velocity. Stroke patients also had significantly higher systolic and diastolic blood pressures (P < 0.02 and P < 0.002 respectively) and total cholesterol levels (P < 0.004) than the control subjects. Calculation of Cp did not alter the observation of stiffer aortas in the stroke cohort (P < 0.0007). 4. In both stroke patient and control cohorts, as expected, inverse trends were observed between aortic compliance and blood pressure. Also as expected, in the control group Cp values did not show a relationship with blood pressure (r = 0.02, P = 0.092, not significant). However, in the stroke cohort a marked dependence of Cp on blood pressure was observed (r = −0.48, P = 0.03). 5. Transoesophageal echocardiographic studies have recently identified advanced atherosclerosis in the ascending aorta as a possible source of cerebral emboli and an independent risk factor for ischaemic stroke. Our observations of significantly stiffer thoracoabdominal aortas in patients with stroke lead us to hypothesize that a totally non-invasive assessment of aortic compliance may potentially prove a useful surrogate marker of such atherosclerotic risk. 6. Blood pressure-corrected indices of arterial elastic properties based on normotensive models are widely applied in the literature. Our observation that these indices exhibit a considerable blood pressure dependence leads us to urge caution in the use of such corrections, especially in hypertensive patients.
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6

JONES, DAVID R., RICHARD W. BRILL, and DENNIS C. MENSE. "The Influence of Blood Gas Properties on Gas Tensions and pH of Ventral and Dorsal Aortic Blood in Free-Swimming Tuna, Euthynnus Affinis." Journal of Experimental Biology 120, no. 1 (January 1, 1986): 201–13. http://dx.doi.org/10.1242/jeb.120.1.201.

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We have developed a technique for capture, anaesthetization, instrumentation and release of tuna and have made the first determinations of blood gas values in dorsal and ventral aortae of free-swimming tuna. Dorsal aortic Po2 varied from 34.5 to 91.7 mmHg, and Pcoco2 ranged from 3.7 to 7mmHg. Dorsal aortic blood [pHa = 7.77 ± 0.04 (8), mean ± one S.E.M. (N)] was more alkaline than ventral aortic blood [pHv = 7.65 ± 0.02 (7)]. Warming dorsal aortic blood from 25 to 35 °C in a closed system caused Po2 and PCOCO2 to rise and pH to fall. Oxygen-combining curves forwhole blood were sigmoid [mean Hill's number = 1.72 ± 0.05 (11), range 1.57-2.0]and P50 over the pH range found in free-swimming animals was 21 ± 1.75(8) mmHg. The CO2-induced Bohr coefficient (ΔlogP50/Δ pH) was −0.59 ± 0.046(30). Unusual features of CO2-combining curves are attributed to a significant Rooteffect. Although these in vitro properties of tuna whole blood are at variance withother published data on tuna they nevertheless substantiate our determinations madein vivo.
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7

Azam, M. A., and S. A. A. Salam. "Three Dimensional Analysis of the Blood Flow Regime within Abdominal Aortic Aneurysm." International Journal of Engineering and Technology 3, no. 6 (2011): 621–27. http://dx.doi.org/10.7763/ijet.2011.v3.295.

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8

Bulpitt, Christopher J., C. Rajkumar, and James D. Cameron. "Central aortic blood pressure measurements." Journal of Human Hypertension 14, no. 8 (August 2000): 531. http://dx.doi.org/10.1038/sj.jhh.1001066.

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9

Bukoski, R. D., and D. A. McCarron. "Altered aortic reactivity and lowered blood pressure associated with high calcium intake." American Journal of Physiology-Heart and Circulatory Physiology 251, no. 5 (November 1, 1986): H976—H983. http://dx.doi.org/10.1152/ajpheart.1986.251.5.h976.

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The hypothesis that dietary calcium (dCa) alters functional properties of aortic smooth muscle in the spontaneously hypertensive rat (SHR) was tested. At 6 wk of age, Wistar Kyoto (WKY) and (SHR) rats were placed on a control diet containing 1% Ca. The experimental SHR group received a 2%-calcium diet. After an average of either 8 or 15 wk on the diets (WOD), aortic rings were prepared for measurement of passive elastic properties and isometric force development. Differences in blood pressure (BP) were not apparent until after 8 WOD when the BP of SHRs on 2% dCa were 10-15 mmHg lower than SHRs on 1% dCa (P less than 0.05). After 8 WOD, when the BP effect first emerged, no significant differences in aortic properties were observed between the SHR groups. However, after 15 WOD, aortas of SHRs on 2% dCa were more compliant than those of SHRs on 1% dCa and between 8 and 15 WOD the sensitivity to KCl decreased in aortas from the WKY group and the SHRs on 2% dCa, but not the SHR-1% dCa group (mean effective dose went from 14.4 +/- 0.4 to 18.5 +/- 0.9 mM for WKY and from 13.6 +/- 0.6 to 17.1 +/- 1.2 mM for SHRs on 2% dCa, P less than 0.05). In addition, between 8 and 15 WOD, a significant decrease in response to a calcium (Ca2+) challenge after removal of K+ and Ca2+ occurred in aortas of the SHRs on 2% dCa, but not in the control diet groups, indicating that a decrease in aortic reactivity was present in the Ca2+-supplemented SHR.(ABSTRACT TRUNCATED AT 250 WORDS)
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10

Zindovic, Igor, Gustaf Edgren, Shahab Nozohoor, and Ammar Majeed. "ABO blood group and the risk of aortic disease: a nationwide cohort study." BMJ Open 10, no. 10 (October 2020): e036040. http://dx.doi.org/10.1136/bmjopen-2019-036040.

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ObjectivesTo analyse the association between ABO blood group and aortic disease using data on blood donors and transfused patients from Sweden.DesignThis was a retrospective study using data from the Swedish portion of the Scandinavian Donations and Transfusions Database. The association between ABO blood group and aortic disease was analysed using log-linear Poisson regression models and presented as incidence rate ratios (IRRs).SettingSwedish population-based study.ParticipantsThe study cohort consisted of 1 164 561 Swedish blood donors and 961 637 transfused patients with a combined follow-up time of 29 390 649 person-years.Primary and secondary outcome measuresIRRs of aortic events (ie, aortic aneurysms and/or aortic dissections) in relation to patient blood group.ResultsA total of 20 684 aortic events occurred during the study period. Non-O donors and patients had similar incidence of aortic events when compared with blood group O donors and patients with an IRR of 0.98 (95% CI, 0.93–1.04) and 1.00 (95% CI, 0.97–1.03), respectively. There were no differences between non-O and blood group O individuals when aortic dissections and aortic aneurysms were analysed separately. Blood group B conferred a lower risk of aortic aneurysms in the patient cohort when compared with blood group O (IRR, 0.90; 95% CI, 0.85–0.96).ConclusionsIn the present study, there were no statistically significant associations between ABO blood group and the risk of aortic disease. A possible protective effect of blood group B was observed in the patient cohort but this finding requires further investigation.
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11

Dziuba, O. S. "Blood coagulation and aortic wall integrity in rats with obesity-induced insulin resistance." Ukrainian Biochemical Journal 90, no. 2 (April 10, 2018): 14–23. http://dx.doi.org/10.15407/ubj90.02.014.

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12

Bogren, Hugo, Michael Buonocore, and David Follette. "Four-Dimensional Aortic Blood Flow Patterns in Thoracic Aortic Grafts." Journal of Cardiovascular Magnetic Resonance 2, no. 3 (2000): 201–8. http://dx.doi.org/10.3109/10976640009146568.

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13

Ye, Dien, Congqing Wu, Hui Chen, Ching-Ling Liang, Deborah A. Howatt, Michael K. Franklin, Jessica J. Moorleghen, et al. "Fludrocortisone Induces Aortic Pathologies in Mice." Biomolecules 12, no. 6 (June 13, 2022): 825. http://dx.doi.org/10.3390/biom12060825.

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Background and Objective: In an experiment designed to explore the mechanisms of fludrocortisone-induced high blood pressure, we serendipitously observed aortic aneurysms in mice infused with fludrocortisone. The purpose of this study was to investigate whether fludrocortisone induces aortic pathologies in both normocholesterolemic and hypercholesterolemic mice. Methods and Results: Male adult C57BL/6J mice were infused with either vehicle (85% polyethylene glycol 400 (PEG-400) and 15% dimethyl sulfoxide (DMSO); n = 5) or fludrocortisone (12 mg/kg/day dissolved in 85% PEG-400 and 15% DMSO; n = 15) for 28 days. Fludrocortisone-infused mice had higher systolic blood pressure, compared to mice infused with vehicle. Fludrocortisone induced aortic pathologies in 4 of 15 mice with 3 having pathologies in the ascending and aortic arch regions and 1 having pathology in both the ascending and descending thoracic aorta. No pathologies were noted in abdominal aortas. Subsequently, we infused either vehicle (n = 5/group) or fludrocortisone (n = 15/group) into male ApoE −/− mice fed a normal laboratory diet or LDL receptor −/− mice fed either normal or Western diet. Fludrocortisone increased systolic blood pressure, irrespective of mouse strain or diet. In ApoE −/− mice infused with fludrocortisone, 2 of 15 mice had ascending aortic pathologies, but no mice had abdominal aortic pathologies. In LDL receptor −/− mice fed normal diet, 5 had ascending/arch pathologies and 1 had pathologies in the ascending, arch, and suprarenal aortic regions. In LDL receptor −/− mice fed Western diet, 2 died of aortic rupture in either the descending thoracic or abdominal region, and 2 of the 13 survived mice had ascending/arch aortic pathologies. Aortic pathologies included hemorrhage, wall thickening or thinning, or dilation. Only ascending aortic diameter in LDLR −/− mice fed Western diet reached statistical significance, compared to their vehicle. Conclusion: Fludrocortisone induces aortic pathologies independent of hypercholesterolemia. As indicated by the findings in mouse studies, people who are taking or have taken fludrocortisone might have an increased risk of aortic pathologies.
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14

Palmier, Mickael, Quentin Cohen, Benjamin Bottet, and Didier Plissonnier. "Competition between Conflicting Aortic Blood Flows." Journal of Vascular and Interventional Radiology 32, no. 8 (August 2021): 1239. http://dx.doi.org/10.1016/j.jvir.2021.03.547.

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15

Narayan, Om, Joshua Casan, Martin Szarski, Anthony M. Dart, Ian T. Meredith, and James D. Cameron. "Estimation of central aortic blood pressure." Journal of Hypertension 32, no. 9 (September 2014): 1727–40. http://dx.doi.org/10.1097/hjh.0000000000000249.

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16

Orliaguet, Gilles A., and Pierre Y. Gueugniaud. "Non-invasive aortic blood flow measurement." Current Opinion in Anaesthesiology 13, no. 3 (June 2000): 307–12. http://dx.doi.org/10.1097/00001503-200006000-00013.

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17

Takagi, Hisato. "Blood group and abdominal aortic aneurysm." European Journal of Preventive Cardiology 27, no. 19 (September 12, 2019): 2195–99. http://dx.doi.org/10.1177/2047487319876044.

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18

Mitchell, G. F. "Aortic Stiffness and Cerebral Blood Flow." American Journal of Hypertension 24, no. 10 (October 1, 2011): 1056. http://dx.doi.org/10.1038/ajh.2011.112.

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19

Heffernan, Kevin S., James E. Sharman, Eun Sun Yoon, Eui Jin Kim, Su Jin Jung, and Sae Young Jae. "Effect of increased preload on the synthesized aortic blood pressure waveform." Journal of Applied Physiology 109, no. 2 (August 2010): 484–90. http://dx.doi.org/10.1152/japplphysiol.00196.2010.

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In the present study, we examined the influence of preload augmentation via passive leg elevation (PLE) on synthesized aortic blood pressure, aortic augmentation index (AIx), and aortic capacitance (a reflection of aortic reservoir function). Central and peripheral hemodynamics were measured via tonometry with a generalized transfer function in 14 young, healthy men (age = 24 yr). Aortic blood flow was calculated from the left ventricular outflow tract (LVOT) velocity-time integral (VTI) using standard two-dimensional echocardiographic-Doppler techniques. Measures were made in the supine position at rest (Pre), during PLE, and during recovery (Post). There was a significant increase in LVOT-VTI, synthesized aortic systolic blood pressure (BP) and AIx from Pre to PLE, with values returning to baseline Post ( P < 0.05). There was a reduction in aortic capacitance from Pre to PLE, with values returning to baseline Post ( P < 0.05). There was no change in heart rate, systemic arterial compliance, aortic elastance, aortic wave travel timing, or vascular resistance ( P > 0.05). Change in AIx from Pre to PLE was associated with change in LVOT-VTI ( r = 0.66, P < 0.05) and inversely associated with change in aortic capacitance ( r = −0.73, P < 0.05). These data suggest that in a setting of isolated augmented preload with minimal changes in other potential confounders, the morphology of the synthesized aortic BP waveform and AIx may be related to changes in aortic reservoir function.
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20

Lam, Chen-Fuh, Timothy E. Peterson, Darcy M. Richardson, Anthony J. Croatt, Livius V. d'Uscio, Karl A. Nath, and Zvonimir S. Katusic. "Increased blood flow causes coordinated upregulation of arterial eNOS and biosynthesis of tetrahydrobiopterin." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (February 2006): H786—H793. http://dx.doi.org/10.1152/ajpheart.00759.2005.

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Shear stress, imposed on the vascular endothelium by circulating blood, critically sustains vascular synthesis of nitric oxide (NO). Endothelial NO synthase (eNOS) activity is determined by heat shock protein 90 (HSP90), caveolin-1, and the cofactor tetrahydrobiopterin (BH4). To determine whether increased blood flow concomitantly upregulates eNOS and GTP cyclohydrolase I (GTPCH I, the rate-limiting enzyme in BH4 biosynthesis), an aortocaval fistula model in the rat was employed wherein aortic blood flow is enhanced proximal but decreased distal to the fistula. Eight weeks after the creation of the aortocaval fistula, the proximal and distal aortic segments were harvested; sham-operated rats served as controls. Vasomotor function was assessed by isometric force recording. Expression of eNOS, HSP90, caveolin-1, Akt, phosphorylated eNOS (eNOS-Ser1177), and GTPCH I were determined by Western blot analysis. Biosynthesis of BH4 and GTPCH-I activity was examined by HPLC. In the aortic segments exposed to increased flow, contractions to KCl and phenylephrine were reduced, whereas endothelium-dependent relaxations were not affected compared with sham-operated or aortic segments with reduced blood flow. Expression of eNOS, caveolin-1, phosphorylated Akt, and eNOS-Ser1177 was enhanced in aortas exposed to increased blood flow. High flow augmented levels of cGMP and BH4 and increased expression of GTPCH I. In aggregate, these findings provide the first demonstration in vivo that coordinated vascular upregulation of eNOS, and GTPCH I accompanies increased blood flow. This induction of GTPCH I increases BH4 production, thereby optimizing the generation of NO by eNOS and thus the adaptive, vasorelaxant response required in sustaining increased blood flow.
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21

Sherrah, Andrew, Fraser Callaghan, Rajesh Puranik, Richmond Jeremy, Paul Bannon, Michael Vallely, and Stuart Grieve. "Multi-Velocity Encoding Four-Dimensional Flow Magnetic Resonance Imaging in the Assessment of Chronic Aortic Dissection." AORTA 05, no. 03 (June 2017): 80–90. http://dx.doi.org/10.12945/j.aorta.2017.16.046.

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Background: Chronic descending thoracic aortic dissection (CDTAD) following surgical repair of ascending aortic dissection requires long-term imaging surveillance. We investigated four-dimensional (4D)-flow magnetic resonance imaging (MRI) with a novel multi-velocity encoding (multi-VENC) technique as an emerging clinical method enabling the dynamic quantification of blood volume and velocity throughout the cardiac cycle. Methods: Patients with CDTAD (n = 10; mean age, 55.1 years; standard deviation (SD) 10.8) and healthy volunteers (n = 9; mean age, 37.1 years; SD 11.4; p < 0.01) underwent 3T MRI, and standard views and 4D-flow data were obtained. Flow measurements were made in selected regions of interest within the ascending and descending thoracic aorta. Results: The overall flow profile at peak systole was reduced in the false lumen (FL) compared with the true lumen (TL) and normal aortas (p < 0.05 for velocity < 0.4 m/s). Peak systolic flow rate per aortic lumen area (mL/s/cm2) was lower in the FL than in the TL (p < 0.05), and both rates were lower than that of control aortas (p < 0.05). Blood flow reversal was higher in the FL than in the TL throughout the descending aorta in CDTAD patients (p < 0.05). A derived pulsatility index was elevated in the TL compared with that in the FL in CDTAD patients. Generated pathline images demonstrated flow patterns in detail, including sites of communication between the true and FL. Conclusions: 4D-flow MRI revealed FL blood flow and reduced blood flow velocity and flow rate in the TL of CDTAD patients compared with normal aortas of healthy participants. Thus, multi-VENC 4D-flow MRI could serve as an adjunct in the long-term assessment of CDTAD following surgical repair of ascending aortic dissection.
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Middeke, Martin. "Zentraler aortaler Blutdruck: Bedeutender Parameter für Diagnostik und Therapie." DMW - Deutsche Medizinische Wochenschrift 142, no. 19 (September 2017): 1430–36. http://dx.doi.org/10.1055/s-0043-113212.

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AbstractIn recent years great emphasis has been placed on the role of central aortic blood pressure as measured non invasively using pulse wave analysis in pathophysiology of cardiovascular diseases and clinical aspects of hypertension. The difference of blood pressure between the central aorta and the brachial artery (amplification) is not constant but varies according to physiological, pathological and pharmacological mechanisms. Central aortic blood pressure is more strongly related to cardiovascular organ damages than does brachial pressure. Several antihypertensive drugs have different effects on aortic blood pressure as compared with brachial pressure. Central aortic blood pressure emerges superior to brachial pressure as target blood pressure in antihypertensive treatment.
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23

Yvernogeau, Laurent, Anna Klaus, Joris Maas, Ismaël Morin-Poulard, Bart Weijts, Stefan Schulte-Merker, Eugene Berezikov, Jan Philipp Junker, and Catherine Robin. "Multispecies RNA tomography reveals regulators of hematopoietic stem cell birth in the embryonic aorta." Blood 136, no. 7 (August 13, 2020): 831–44. http://dx.doi.org/10.1182/blood.2019004446.

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Abstract The defined location of a stem cell within a niche regulates its fate, behavior, and molecular identity via a complex extrinsic regulation that is far from being fully elucidated. To explore the molecular characteristics and key components of the aortic microenvironment, where the first hematopoietic stem cells are generated during development, we performed genome-wide RNA tomography sequencing on zebrafish, chicken, mouse, and human embryos. The resulting anterior-posterior and dorsal-ventral transcriptional maps provided a powerful resource for exploring genes and regulatory pathways active in the aortic microenvironment. By performing interspecies comparative RNA sequencing analyses and functional assays, we explored the complexity of the aortic microenvironment landscape and the fine-tuning of various factors interacting to control hematopoietic stem cell generation, both in time and space in vivo, including the ligand-receptor couple ADM-RAMP2 and SVEP1. Understanding the regulatory function of the local environment will pave the way for improved stem cell production in vitro and clinical cell therapy.
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Fatahillah, Arif, Azza Liarista Anggraini, and Susi Setiawani. "Numerical analysis of blood flow in abdominal aortic aneurysm using finite volume method." Desimal: Jurnal Matematika 5, no. 2 (August 30, 2022): 131–42. http://dx.doi.org/10.24042/djm.v5i2.9928.

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There is a deadly cardiovascular disease that can cause swelling of the Abdominal Aorta. This disease is known as Abdominal Aortic Aneurysm (AAA). AAA is believed to be a degenerative process caused by genetic factors, gender, body weight, and age. Changes in collagen and elastin in the aortic wall are the cause of the degeneration process. Therefore, it will cause dilatation of the aortic wall. Swelling of the aortic blood vessels will affect the blood flow velocity in the aortic blood vessels. This research aims to analyze the velocity of blood flow in the Abdominal Aortic Aneurysm based on swelling diameter, proximal neck length, and aneurysm channel length using Computational Fluids Dynamics (CFD). The blood flow velocity was modeled using mathematical language based on mass continuity equations and momentum equations. Then the finite volume method was one method to solve the mathematical model. MATLAB and ANSYS FLUENT software were used to simulate the velocity of blood flow analysis. The results of the research were shown that the larger the diameter and swelling channel length, the smaller the velocity of blood flow produced. Then, the greater the length of the proximal neck, the faster the resulting blood flow will be.
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Castrejón-Téllez, Vicente, María Esther Rubio-Ruiz, Agustina Cano-Martínez, Israel Pérez-Torres, Leonardo Del Valle-Mondragón, Elizabeth Carreón-Torres, and Verónica Guarner-Lans. "High Sucrose Ingestion during a Critical Period of Vessel Development Promotes the Synthetic Phenotype of Vascular Smooth Muscle Cells and Modifies Vascular Contractility Leading to Hypertension in Adult Rats." International Journal of Hypertension 2022 (June 21, 2022): 1–12. http://dx.doi.org/10.1155/2022/2298329.

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Cardiometabolic diseases, including hypertension, may result from exposure to high sugar diets during critical periods of development. Here, we studied the effect of sucrose ingestion during a critical period (CP) between postnatal days 12 and 28 of the rat on blood pressure, aortic histology, vascular smooth muscle phenotype, expression of metalloproteinases 2 and 9, and vascular contractility in adult rats and compared it with those of adult rats that received sucrose for 6 months and developed metabolic syndrome (MS). Blood pressure increased to a similar level in CP and MS rats. The diameter of lumen, media, and adventitia of aortas from CP rats was decreased. Muscle fibers were discontinuous. There was a decrease in the expression of alpha-actin in CP and MS rat aortas, suggesting a change to the secretory phenotype in vascular smooth muscle. Metalloproteinases 2 and 9 were decreased in CP and MS rats, suggesting that phenotype remains in an altered steady stationary state with little interchange of the vessel matrix. Aortic contraction to norepinephrine did not change, but aortic relaxation was diminished in CP and MS aortas. In conclusion, high sugar diets during the CP increase predisposition to hypertension in adults.
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FUJI, Motoaki, Haruhisa HURUMOTO, Tsutomu TAJIKAWA, and Kenkichi OHBA. "0225 Influence of blood flow and blood pressure at aortic valve on pathogeny of aortic valve sclerosis." Proceedings of the Bioengineering Conference Annual Meeting of BED/JSME 2009.22 (2010): 209. http://dx.doi.org/10.1299/jsmebio.2009.22.209.

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27

Gonzalez-Urquijo, Mauricio, Raul Garza de Zamacona, Ana Karen Martinez Mendoza, Miranda Zamora Iribarren, Erika Garza Ibarra, Marcos David Moya Bencomo, and Mario Alejandro Fabiani. "3D Modeling of Blood Flow in Simulated Abdominal Aortic Aneurysm." Vascular and Endovascular Surgery 55, no. 7 (April 27, 2021): 677–83. http://dx.doi.org/10.1177/15385744211012926.

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Background: Besides biological factors, abdominal aortic aneurysm rupture is also caused by mechanical parameters, which are constantly affecting the wall’s tissue due to their abnormal values. The ability to evaluate these parameters could vastly improve the clinical treatment of patients with abdominal aortic aneurysms. The objective of this study was to develop and demonstrate a methodology to analyze the fluid dynamics that cause the wall stress distribution in abdominal aortic aneurysms, using accurate 3D geometry and a realistic, nonlinear, elastic biomechanical model using a computer-aided software. Methods: The geometry of the abdominal aortic aneurysm; was constructed on a 3D scale using computer-aided software SolidWorks (Dassault Systems SolidWorksCorp., Waltham MA). Due to the complex nature of the abdominal aortic aneurysm geometry, the physiological forces and constraints acting on the abdominal aortic aneurysm wall were measured by using a simulation setup using boundary conditions and initial conditions for different studies such as finite element analysis or computational fluid dynamics. Results: The flow pattern showed an increase velocity at the angular neck, followed by a stagnated flow inside the aneurysm sack. Furthermore, the wall shear stress analysis showed to focalized points of higher stress, the top and bottom of the aneurysm sack, where the flow collides against the wall. An increase of the viscosity showed no significant velocity changed but results in a slight increase in overall pressure and wall shear stress. Conclusions: Conducting computational fluid dynamics modeling of the abdominal aortic aneurysm using computer-aided software SolidWorks (Dassault Systems SolidWorksCorp., Waltham MA) proves to be an insightful approach for the clinical setting. The careful consideration of the biomechanics of the abdominal aortic aneurysm may lead to an improved, case-specific prediction of the abdominal aortic aneurysm rupture potential, which could significantly improve the clinical management of these patients.
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Ben Driss, A., J. Benessiano, P. Poitevin, B. I. Levy, and J. B. Michel. "Arterial expansive remodeling induced by high flow rates." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 2 (February 1, 1997): H851—H858. http://dx.doi.org/10.1152/ajpheart.1997.272.2.h851.

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The effects of chronic increase in aortic blood flow on arterial wall remodeling were investigated in vivo with the use of an aortocaval fistula (ACF) model in rats. Phasic hemodynamics and aortic wall structure upstream and downstream in 30 male Wistar rats with ACF and 30 sham-operated rats were compared immediately and 2 mo after the ACF was opened in anesthetized rats. Opening the ACF upstream acutely decreased aortic pressure (-30%, P < 0.001) and increased aortic blood velocity (x12, P < 0.001), blood flow (x9, P < 0.001), wall shear stress (x10, P < 0.001) and guanosine 3',5'-cyclic monophosphate (cGMP) wall content (+50%, P < 0.01). After 2 mo, aortic pressure decreased (-22%, P < 0.001) and aortic blood velocity, diameter, and blood flow increased (+114%, P < 0.001; +60%, P < 0.001; and +250%, P < 0.001; respectively) compared with the control group. Aortic wall shear stress and cGMP wall content dropped over time and tended to recover control values; aortic wall tensile stress was higher than in the control group (P < 0.05). Medial cross-sectional area and elastin and collagen contents increased (+38%, P < 0.01; +50%, P < 0.01; and +30%, P < 0.05, respectively) and were associated with smooth muscle cell hypertrophy) (+23%, P < 0.05), despite a decrease in arterial wall thickness (-13%, P < 0.01). Opening the ACF downstream acutely decreased aortic pressure (-30%, P < 0.001) without any change in aortic blood velocity, diameter, blood flow, shear stress, and cGMP wall content. After 2 mo, pressure, blood velocity, shear stress, and cGMP wall content decreased (-22%, P < 0.001; -31%, P < 0.01; -46%, P < 0.02; and -50%, P < 0.05; respectively) and diameter and blood flow were unchanged; smooth muscle cell hypertrophy and hypoplasia were the only observed changes in the aortic wall structure. These results suggest that both shear and tensile stresses are involved in the aortic wall remodeling. Increase in shear stress likely induces expansive remodeling in relation to flow-dependent vasodilation, whereas increase in tensile stress is responsible for medial hypertrophy and fibrosis.
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29

Ghorbani, Niky, Vivek Muthurangu, Abbas Khushnood, Leonid Goubergrits, Sarah Nordmeyer, Joao Filipe Fernandes, Chong-Bin Lee, et al. "Impact of valve morphology, hypertension and age on aortic wall properties in patients with coarctation: a two-centre cross-sectional study." BMJ Open 10, no. 3 (March 2020): e034853. http://dx.doi.org/10.1136/bmjopen-2019-034853.

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ObjectiveWe aimed to investigate the combined effects of arterial hypertension, bicuspid aortic valve disease (BAVD) and age on the distensibility of the ascending and descending aortas in patients with aortic coarctation.DesignCross-sectional study.SettingThe study was conducted at two university medical centres, located in Berlin and London.ParticipantsA total of 121 patients with aortic coarctation (ages 1–71 years) underwent cardiac MRI, echocardiography and blood pressure measurements.Outcome measuresCross-sectional diameters of the ascending and descending aortas were assessed to compute aortic area distensibility. Findings were compared with age-specific reference values. The study complied with the Strengthening the Reporting of Observational Studies in Epidemiology statement and reporting guidelines.ResultsImpaired distensibility (below fifth percentile) was seen in 37% of all patients with coarctation in the ascending aorta and in 43% in the descending aorta. BAVD (43%) and arterial hypertension (72%) were present across all ages. In patients >10 years distensibility impairment of the ascending aorta was predominantly associated with BAVD (OR 3.1, 95% CI 1.33 to 7.22, p=0.009). Distensibility impairment of the descending aorta was predominantly associated with arterial hypertension (OR 2.8, 95% CI 1.08 to 7.2, p=0.033) and was most pronounced in patients with uncontrolled hypertension despite antihypertensive treatment.ConclusionFrom early adolescence on, both arterial hypertension and BAVD have a major impact on aortic distensibility. Their specific effects differ in strength and localisation (descending vs ascending aorta). Moreover, adequate blood pressure control is associated with improved distensibility. These findings could contribute to the understanding of cardiovascular complications and the management of patients with aortic coarctation.
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Tian, Wen, Zhijun Mei, Jian Zhou, Qingsheng Lu, and Zaiping Jing. "A neglected event in endovascular repair of aortic dissection: acute blood pressure variability during aortic angiography." International Journal for Innovation Education and Research 6, no. 8 (August 31, 2018): 235–40. http://dx.doi.org/10.31686/ijier.vol6.iss8.1139.

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[Purpose]To investigate acute blood pressure change during aortic angiography in aortic dissection endovascular repair, and analyse the potential risk of this incident.[Method]24 patients with aortic dissection underwent endovascular repair in department of vascular surgery of Changhai hospital between May 2016 and July 2016 were enrolled in this research. Patients were divided into two groups: patients underwent general anesthesia and patients underwent lumbar anesthesia. Blood pressure was monitored by intro-artery catheter. Blood pressure readings were recorded every 10 seconds during the procedure of angiography. Outcome of these patients were observed in hospital. [Result] All patients received endovascular aortic repair, with 19 underwent lumbar anesthesia and 5 underwent general anesthesia. Patients underwent lumbar anesthesia presented temporary blood pressure decrease with average of -11.2±13.4mmHg, while patients underwent general anesthesia presented temporary blood pressure elevation with average of 4.2±6.3mmHg. The Maximum time interval were 26.7±12.7s vs25.8±15.8s, and difference in blood pressure between pre- and post-angiography were 1.53±4.4mmHg vs. 4.6±3.4mmHg, both without significance (P>0.05).[Conclusion] Angiography is an effective factor influencing blood pressure during TEVAR, it’s a potential “trigger” of intra-operative cardiovascular events. Blood pressure should be kept on proper level to avoid cardiovascular events induced by blood pressure variability with angiography. Angiography with General anesthesia has less influence on blood pressure than with lumbar anesthesia.
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31

Skibitskiy, V. V., A. A. Kiselev, and A. V. Fendrikova. "Effectiveness of Chrono-Pharmacotherapy Depending on the Salt Sensitivity of Patients with Arterial Hypertension and Diabetes Mellitus Type 2." Rational Pharmacotherapy in Cardiology 14, no. 6 (January 5, 2019): 846–51. http://dx.doi.org/10.20996/1819-6446-2018-14-6-846-851.

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Aim. To study the effect of two regimens of combined antihypertensive therapy during the day on daily monitoring of arterial pressure, central aortic pressure, and arterial stiffness, depending on the salt sensitivity of hypertensive patients with diabetes mellitus type 2. Material and methods. 130 hypertensive patients with type 2 diabetes mellitus were included into the study. They were divided into 2 subgroups: salt-sensitive (group 1) and salt-resistant (group 2), and then randomized to subgroups A and B of ongoing therapy: in the morning ramipril and indapamide retard, bedtime – amlodipine (subgroup 1A and 2A); or in the morning amlodipine and indapamide retard, bedtime – ramipril (subgroup 1B and 2B). Initially and after 24 weeks of antihypertensive therapy, 24-hour blood pressure monitoring was performed, the indices of central aortic pressure and arterial stiffness were determined. Results. After 24 weeks, in all subgroups, there was a significant positive dynamics of the parameters of 24-hour blood pressure monitoring, central aortic pressure and arterial stiffness indices. In the subgroup 1В, it was registered a significant improvement in the majority of parameters of 24-hour blood pressure monitoring (decrease in 24-hours systolic BP by 24.4%, 24-hours diastolic BP by 22.1%; p<0.05), central aortic pressure (decrease in aortal systolic BP by 15.9%, aortal diastolic BP by 20.8%; p<0.05) and vascular wall stiffness parameters (decrease in pulse wave velocity by 13.8%; p<0.05) in comparison with group 1A (decrease in 24-hours systolic BP by 17.5%, 24-hours diastolic BP by 14.6%, aortal systolic BP by 12.7%, aortal diastolic BP by 9.7%, pulse wave velocity by 9.2%; p<0.05 in comparison with the group 1B). In the case of salt-resistant patients, there were comparable positive changes in the parameters of 24-hour blood pressure monitoring, central aortic pressure and arterial stiffness indices against the background of both dosing regimens during the day. Conclusion. In the study, it was demonstrated the more pronounced antihypertensive and vasoprotective efficacy of the combination of thiazide-like diuretic with calcium channel blocker in the morning and ACE inhibitor in bedtime compared to the alternative regimen of prescribed pharmacotherapy in salt-sensitive patients, and comparable efficacy of both regimens in salt-resistant hypertensive patients with diabetes mellitus type 2.
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32

Williams, Bryan, Ewan McFarlane, Dawid Jedrzejewski, and Peter S. Lacy. "Identifying and treating high blood pressure in men under 55 years with grade 1 hypertension: the TREAT CASP study and RCT." Efficacy and Mechanism Evaluation 6, no. 13 (December 2019): 1–90. http://dx.doi.org/10.3310/eme06130.

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Background There is uncertainty regarding whether or not younger (i.e. aged < 55 years), low-risk patients with grade 1 hypertension (i.e. a clinic blood pressure of 140–159/90–99 mmHg) should be treated with blood pressure-lowering medication. This is a heterogeneous group of patients because of variation in systolic/pulse pressure amplification from the central aorta to the brachial artery. It is hypothesised that within grade 1 hypertension, patients can be divided into those with high central aortic systolic pressure and those with low central aortic systolic pressure. Objectives The aims of this study were to (1) evaluate whether or not non-invasive central aortic systolic pressure measurement can better identify younger patients with grade 1 hypertension, who are more likely to have an increased left ventricular mass index; and (2) determine whether or not blood pressure lowering regresses early cardiac structural change in patients with high central aortic systolic pressure. Setting A university hospital with satellite primary care recruitment sites. Participants A total of 726 men (aged 18 to < 55 years) were screened to identify 162 men with grade 1 hypertension and low or high central aortic systolic pressure. Blood pressure status was classified according to seated clinic blood pressure, central aortic systolic pressure and 24-hour ambulatory blood pressure. Design (1) Evaluating the strength of the correlation between central aortic systolic pressure, clinic blood pressure and 24-hour ambulatory blood pressure with left ventricular mass index in 162 patients; (2) a 12-month randomised controlled trial in patients with grade 1 hypertension and high central aortic systolic pressure (i.e. a central aortic systolic pressure of ≥ 125 mmHg) (n = 105), using a prospective, open, blinded, end-point design; and (3) a 12-month observational study in 57 patients with grade 1 hypertension and low central aortic systolic pressure (i.e. a central aortic systolic pressure of < 125 mmHg). Interventions Randomised controlled trial – patients with high central aortic systolic pressure randomised to blood pressure lowering medication (50–100 mg of losartan ± 5–10 mg of amlodipine once daily) versus usual care (no treatment) for 12 months. Main outcomes Randomised controlled trial primary end point – change in left ventricular mass index as measured by cardiac magnetic resonance imaging, comparing treatment with no treatment. Results (1) At baseline, left ventricular mass index was higher in men with high central aortic systolic pressure than in those with low central aortic systolic pressure (mean ± standard deviation 67.9 ± 8.8 g/m2 vs. 64.0 ± 8.5 g/m2; difference 4.0 g/m2, 95% confidence interval 1.1 to 6.9 g/m2; p < 0.01). Central aortic systolic pressure was not superior to clinic blood pressure as a determinant of left ventricular mass index. Univariate analysis, regression coefficients and slopes for left ventricular mass index were similar for clinic systolic blood pressure, ambulatory systolic blood pressure and central aortic systolic pressure. (2) In the randomised controlled trial, blood pressure-lowering treatment reduced central aortic systolic pressure (–21.1 mmHg, 95% confidence interval – 24.4 to –17.9 mmHg; p < 0.001) and clinic systolic blood pressure (–20.0 mmHg, 95% confidence interval – 23.3 to –16.6 mmHg; p < 0.001) versus no treatment. Treatment was well tolerated and associated with a greater change (i.e. from baseline to study closeout) in left ventricular mass index versus no treatment [–3.3 g/m2 (95% confidence interval –4.5 to –2.2 g/m2) vs. –0.9 g/m2 (95% confidence interval –1.7 to –0.2 g/m2); p < 0.01], with a medium-to-large effect size (Cohen’s d statistic –0.74). (3) Patients with low central aortic systolic pressure had no significant change in left ventricular mass index after 12 months (mean change –0.5 g/m2, 95% confidence interval –1.2 to 0.2 g/m2; p = 0.18). Conclusions Men with grade 1 hypertension and high central aortic systolic pressure tended to have higher clinic blood pressure and more hypertension-mediated cardiac structural change than those with low central aortic systolic pressure. Central aortic systolic pressure was not superior to clinic blood pressure or ambulatory blood pressure at stratifying risk of increased left ventricular mass index. Blood pressure-lowering treatment led to a regression of left ventricular mass index in men with grade 1 hypertension and high central aortic systolic pressure compared with no treatment. Limitations The study was limited to a moderate sample of men and there was a low prevalence of very high amplification. Future work Evaluating effects of blood pressure lowering on cardiac function. Trial registration Current Controlled Trials ISRCTN09502665. Funding This project was funded by the Efficacy and Mechanism Evaluation programme, a Medical Research Council and National Institute for Health Research (NIHR) partnership and will be published in full in Efficacy and Mechanism Evaluation; Vol. 6, No. 13. See the NIHR Journals Library website for further project information.
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33

Axelsson, M., C. Franklin, R. Fritsche, G. Grigg, and S. Nilsson. "The sub-pulmonary conus and the arterial anastomosis as important sites of cardiovascular regulation in the crocodile Crocodylus porosus." Journal of Experimental Biology 200, no. 4 (February 1, 1997): 807–14. http://dx.doi.org/10.1242/jeb.200.4.807.

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We present evidence to support the hypothesis that the arterial anastomosis and the cogteeth-like valves located in the sub-pulmonary conus in the right ventricle are important sites of cardiovascular regulation in the crocodile Crocodylus porosus. The influence of the arterial anastomosis on the development of the 'foramen spike' in the left aortic pressure trace, which occurs at the onset of diastole when the pressures in the right and left aortas become equal, and on gastrointestinal blood flow was examined in unanaesthetised C. porosus using blood vessel occluders. Measurements of blood flow in the arterial anastomosis showed that, during non-shunting conditions, there was a substantial systolic blood flow from the right aorta into the coeliac artery. The total coeliac artery blood flow was the sum of the anastomosis flow from the right aorta plus the left aortic flow originating from the right aorta via the foramen of Panizza during diastole. During mechanically induced pulmonary-to-systemic shunting, the anastomosis blood flow was reversed, with blood flowing from the left to the right aorta. The magnitude of the 'foramen spike' was directly related to the vascular resistance in the anastomosis. When vascular resistance in the anastomosis was high, such as during mechanical occlusion, there was an increase in the right aortic to left aortic pressure gradient during systole which resulted in an increase the foramen spike amplitude. Recordings of right intraventricular pressure in unanaesthetised C. porosus showed spontaneous changes in right intracardiac systolic pressure. The pressure recordings were biphasic, with the second contraction (isometric) being highly variable in size, indicating the control of pulmonary outflow resistance, possibly via the 'cogteeth valves' located in the sub-pulmonary conus in the right ventricle.
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34

Petuchova, Aleksandra, and Algirdas Maknickas. "Computational analysis of aortic haemodynamics in the presence of ascending aortic aneurysm." Technology and Health Care 30, no. 1 (December 29, 2021): 187–200. http://dx.doi.org/10.3233/thc-219002.

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BACKGROUND: The usefulness of numerical modelling of a patient’s cardiovascular system is growing in clinical treatment. Understanding blood flow mechanics can be crucial in identifying connections between haemodynamic factors and aortic wall pathologies. OBJECTIVE: This work investigates the haemodynamic parameters of an ascending aorta and ascending aortic aneurysm in humans. METHODS: Two aortic models were constructed from medical images using the SimVascular software. FEM blood flow modelling of cardiac cycle was performed using CFD and CMM-FSI at different vascular wall parameters. RESULTS: The results showed that highest blood velocity was 1.18 m/s in aorta with the aneurysm and 1.9 m/s in healthy aorta model. The largest displacements ware in the aorta with the aneurysm (0.73 mm). In the aorta with the aneurysm, time averaged WSS values throughout the artery range from 0 Pa to 1 Pa. In the healthy aorta, distribution of WSS values changes from 0.3 Pa to 0.6 Pa. CONCLUSIONS: In the case of an ascending aortic aneurysm, the maximum blood velocity was found to be 1.6 times lower than in the healthy aorta. The aneurysm-based model demonstrates a 45% greater wall displacement, while the oscillatory shear index decreased by 30% compared to healthy aortic results.
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35

Song, Chao, Guanyu Yu, Xiang Feng, Rui Feng, Junmin Bao, Zhiqing Zhao, Yifei Pei, Zaiping Jing, and Qingsheng Lu. "Impact of high blood pressure variability on the occurrence of acute type B aortic dissection." Vascular 28, no. 4 (March 26, 2020): 413–20. http://dx.doi.org/10.1177/1708538120902630.

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Background Acute type B aortic dissection is a life-threatening medical emergency, and hypertension is believed to be an important predictor of aortic dissection; the impact of blood pressure variability on the onset and development of aortic dissection has attracted increasing attention. Methods A total of 120 acute type B aortic dissection patients and 57 hypertensive patients without aortic dissection were consecutively enrolled and retrospectively reviewed between January 2013 and November 2015. There were 60 acute type B aortic dissection patients in both high and low blood pressure variability groups. Results Blood pressure variability showed higher diagnostic value than hypertension in aortic dissection, and the best threshold of blood pressure variability is 5.71 mmHg. By performing multivariable logistic regression, we found that the history of hypertension was likely to be a risk factor of blood pressure variability (95% CI: 1.155–6.422, P = 0.022). Nine patients from high blood pressure variability group and two from low blood pressure variability group ( χ2 = 4.90, P = 0.027) received emergency surgery within 24 hours after admission. The presence of multiple tears (>2, 55.0% vs. 45.0%, P = 0.001), configuration of the false lumen (spiral false lumen) (50.0% vs. 21.7%, P = 0.001), the diameter of the false lumen (49.6 ± 15.0 mm vs. 37.6 ± 10.8 mm, P < 0.001), the false/true lumen ratio (1.53 ± 1.02 vs. 0.929 ± 0.733, P < 0.001), and the number of visceral arteries involved (1.75 ± 0.942 vs. 0.800 ± 0.927, P < 0.001) showed significant differences between high and low blood pressure variability groups. Nine (30%) patients from the high blood pressure variability group showed a maximum diameter of false lumen over 60 mm, while none was found in the low blood pressure variability group. Conclusions High blood pressure variability, the presence of multiple tears (>2), the configuration of false lumen, the diameter of the false lumen, false/true lumen ratio, and the number of visceral arteries involved were independent risk factors for acute type B aortic dissection.
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36

Arai, Tatsuya, Kichang Lee, Robert P. Marini, and Richard J. Cohen. "Estimation of changes in instantaneous aortic blood flow by the analysis of arterial blood pressure." Journal of Applied Physiology 112, no. 11 (June 1, 2012): 1832–38. http://dx.doi.org/10.1152/japplphysiol.01565.2011.

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The purpose of this study was to introduce and validate a new algorithm to estimate instantaneous aortic blood flow (ABF) by mathematical analysis of arterial blood pressure (ABP) waveforms. The algorithm is based on an autoregressive with exogenous input (ARX) model. We applied this algorithm to diastolic ABP waveforms to estimate the autoregressive model coefficients by requiring the estimated diastolic flow to be zero. The algorithm incorporating the coefficients was then applied to the entire ABP signal to estimate ABF. The algorithm was applied to six Yorkshire swine data sets over a wide range of physiological conditions for validation. Quantitative measures of waveform shape (standard deviation, skewness, and kurtosis), as well as stroke volume and cardiac output from the estimated ABF, were computed. Values of these measures were compared with those obtained from ABF waveforms recorded using a Transonic aortic flow probe placed around the aortic root. The estimation errors were compared with those obtained using a windkessel model. The ARX model algorithm achieved significantly lower errors in the waveform measures, stroke volume, and cardiac output than those obtained using the windkessel model ( P < 0.05).
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37

Ma, Ben, Elaina Melton, Robert Wiener, Ning Zhou, Wenqian Wu, Lo Lai, Charles Wang, Kevin D. Costa, and Hongyu Qiu. "Age and Blood Pressure Contribute to Aortic Cell and Tissue Stiffness Through Distinct Mechanisms." Hypertension 79, no. 8 (August 2022): 1777–88. http://dx.doi.org/10.1161/hypertensionaha.121.18950.

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Background: Aortic stiffening is strongly associated with both aging and hypertension, but the underlying mechanisms remain unclear. We hypothesized that aging-induced aortic stiffness is mediated by a mechanism differing from hypertension. Methods: We conducted comprehensive in vivo and in vitro experiments using multiple rat models to dissect the different mechanisms of aortic stiffening mediated by aging and hypertension. Results: A time-course study in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) normotensive rats showed more pronounced aging-associated aortic stiffening in SHR versus WKY. Angiotensin II–induced hypertension was associated with more significant aortic stiffening in older versus young WKY rats. Hypertension aggravated aging effects on aortic wall thickness and extracellular matrix content, indicating combinational effects of aging and hypertension on aortic stiffening. Intrinsic stiffness of isolated aortic vascular smooth muscle cells (VSMCs) increased with age in WKY rats, although no significant difference between older SHR and older WKY VSMCs was observed in 2-dimensional culture, reconstituted 3-dimensional tissues were stiffer for older SHR versus older WKY. A selective inhibitor that reduced hypertension-mediated aortic stiffening did not decrease age-related stiffening in aortic VSMCs and aortic wall. Integrin β1 and SM22 (smooth muscle–specific SM22 protein) expression were negligibly changed in WKY VSMCs during aging but were markedly increased by hypertension in older versus young WKY VSMCs. A notable shift of filamin isoforms from B to A was detected in older WKY VSMCs. Conclusions: Our results indicate distinct mechanisms mediating aging-associated aortic VSMC and vessel stiffness, providing new insights into aortic stiffening and the pathogenesis of hypertension in the elderly.
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38

Schnell, Susanne, Danielle A. Smith, Alex J. Barker, Pegah Entezari, Amir R. Honarmand, Maria L. Carr, S. Chris Malaisrie, et al. "Altered aortic shape in bicuspid aortic valve relatives influences blood flow patterns." European Heart Journal – Cardiovascular Imaging 17, no. 11 (July 26, 2016): 1239–47. http://dx.doi.org/10.1093/ehjci/jew149.

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39

Farag, Emile S., Luca Peroni, Lukas M. Gottwald, Jeroen Vendrik, S. Matthijs Boekholdt, Aart J. Nederveen, Pim van Ooij, Bas AJM de Mol, and Jolanda Kluin. "Bileaflet Mechanical Aortic Valve Prosthesis Orientation Influences Ascending Aortic Blood Flow Patterns." Structural Heart 3, sup1 (April 9, 2019): 12. http://dx.doi.org/10.1080/24748706.2019.1587948.

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40

Hartley, C. J., L. H. Michael, and M. L. Entman. "Noninvasive measurement of ascending aortic blood velocity in mice." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 1 (January 1, 1995): H499—H505. http://dx.doi.org/10.1152/ajpheart.1995.268.1.h499.

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Mice are useful models in numerous research protocols, but monitoring cardiovascular parameters in small animals is difficult. Therefore we evaluated the use of 20-MHz pulsed Doppler ultrasound to measure ascending aortic blood velocity in intact anesthetized mice. Using a 0.5-mm-diameter 20-MHz transducer applied to the right sternal border, we recorded audio Doppler signals from the ascending aorta of 31 mice [24.4 +/- 1.5 (SD) g body wt]. The signals were played back at speed into a fast Fourier transform analyzer from which we measured heart rate (453 +/- 96 beats/min), ejection time (38 +/- 3%), peak velocity (90 +/- 11 cm/s), mean velocity (23 +/- 4 cm/s), rise time (7.3 +/- 2 ms), stroke distance (29 +/- 7 mm), and acceleration (163 +/- 63 m/s2) from the spectral envelopes. We determined aortic diameter (1.2 +/- 0.2 mm) and Doppler angle (0–20 degrees) in six mice by molding the aortic root and major systemic vessels with casting resin infused at 100 mmHg pressure. For an aortic diameter of 1.2 mm, cardiac output was estimated to be 14.8 ml/min and stroke volume to be 33 microliters. To verify the origin of the signals and to test responsiveness to known stimuli, we measured velocity signals from the aorta and other nearby vessels and varied heart rate and aortic velocity by warming or by infusion of isoproterenol in three open-chest animals. For the noninvasive applications, acoustic coupling was adequate through the moistened fur, and aortic velocity signals were obtained in all animals.(ABSTRACT TRUNCATED AT 250 WORDS)
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41

MINAMOTO, Yukiko, Masaki WAKAMATSU, and Fukuichiro OKUMURA. "Autologous blood transfusion during abdominal aortic reconstruction." JOURNAL OF JAPAN SOCIETY FOR CLINICAL ANESTHESIA 10, no. 2 (1990): 180–85. http://dx.doi.org/10.2199/jjsca.10.180.

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42

Schoenhagen, Paul. "IMH aortic arch with mediastinal blood products." ASVIDE 5 (March 2018): 251. http://dx.doi.org/10.21037/asvide.2018.251.

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43

Colson, Pascal, Jacques Séguin, Bernard Roquefeuil, and Vaul-André Chaptal. "Transesophageal Doppler to Evaluate Aortic Blood Flow." Chest 96, no. 4 (October 1989): 962. http://dx.doi.org/10.1378/chest.96.4.962-a.

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44

Hashimoto, Junichiro, and Sadayoshi Ito. "Aortic Blood Flow Reversal Determines Renal Function." Hypertension 66, no. 1 (July 2015): 61–67. http://dx.doi.org/10.1161/hypertensionaha.115.05236.

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45

Viklander, Gertrud, Jonas Wallinder, and Anders E. Henriksson. "ABO blood groups and abdominal aortic aneurysm." Transfusion and Apheresis Science 47, no. 3 (December 2012): 351–53. http://dx.doi.org/10.1016/j.transci.2012.07.016.

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46

Witteman, JacquelineC M., DiederickE Grobbee, and Albert Hofman. "Relation between aortic atherosclerosis and blood pressure." Lancet 343, no. 8913 (June 1994): 1649. http://dx.doi.org/10.1016/s0140-6736(94)93108-9.

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47

DeGroff, Curt, Michael Silberbach, David J. Sahn, and Paul Droukas. "Giant blood cyst of the aortic valve." Journal of the American Society of Echocardiography 8, no. 4 (July 1995): 543–45. http://dx.doi.org/10.1016/s0894-7317(05)80343-8.

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48

Swiers, Gemma, Nancy A. Speck, and Marella F. T. R. de Bruijn. "Visualizing Blood Cell Emergence from Aortic Endothelium." Cell Stem Cell 6, no. 4 (April 2010): 289–90. http://dx.doi.org/10.1016/j.stem.2010.03.007.

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49

Narayan, Om, Kim H. Parker, Justin E. Davies, Alun D. Hughes, Ian T. Meredith, and James D. Cameron. "Reservoir pressure analysis of aortic blood pressure." Journal of Hypertension 35, no. 10 (October 2017): 2025–33. http://dx.doi.org/10.1097/hjh.0000000000001424.

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50

Lehmann, Ed, K. D. Hopkins, R. G. Gosling, J. M. Cruickshank, Margaret Mac Mahon, Noirin Sheahan, J. F. Malone, and Davis Coakley. "Relation between aortic atherosclerosis and blood pressure." Lancet 343, no. 8905 (April 1994): 1106–7. http://dx.doi.org/10.1016/s0140-6736(94)90222-4.

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