scholarly journals Effect of simulated obstructive hypopnea and apnea on thoracic aortic wall transmural pressures

2013 ◽  
Vol 115 (5) ◽  
pp. 613-617 ◽  
Author(s):  
Christian F. Clarenbach ◽  
Giovanni Camen ◽  
Noriane A. Sievi ◽  
Christophe Wyss ◽  
John R. Stradling ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Esophageal Pressure ◽  
Preliminary Evidence ◽  
Aortic Aneurysms ◽  
Aortic Dilatation ◽  
Central Apnea ◽  
Obstructive Apnea ◽  
Obstructive Sleep ◽  
Mueller Maneuver ◽  
The Difference

Preliminary evidence supports an association between obstructive sleep apnea (OSA) and thoracic aortic dilatation, although potential causative mechanisms are incompletely understood; these may include an increase in aortic wall transmural pressures, induced by obstructive apneas and hypopneas. In patients undergoing cardiac catheterization, mean blood pressure (MBP) in the thoracic aorta and esophageal pressure was simultaneously recorded by an indwelling aortic pigtail catheter and a balloon-tipped esophageal catheter in randomized order during: normal breathing, simulated obstructive hypopnea (inspiration through a threshold load), simulated obstructive apnea (Mueller maneuver), and end-expiratory central apnea. Aortic transmural pressure (aortic MBP minus esophageal pressure) was calculated. Ten patients with a median age (range) of 64 (46–75) yr were studied. Inspiration through a threshold load, Mueller maneuver, and end-expiratory central apnea was successfully performed and recorded in 10, 7, and 9 patients, respectively. The difference between aortic MBP and esophageal pressure (and thus the extra aortic dilatory force) was median (quartiles) +9.3 (5.4, 18.6) mmHg, P = 0.02 during inspiration through a threshold load, +16.3 (12.8, 19.4) mmHg, P = 0.02 during the Mueller maneuver, and +0.4 (−4.5, 4.8) mmHg, P = 0.80 during end-expiratory central apnea. Simulated obstructive apnea and hypopnea increase aortic wall dilatory transmural pressures because intra-aortic pressures fall less than esophageal pressures. Thus OSA may mechanically promote thoracic aortic dilatation and should be further investigated as a risk factor for the development or accelerated progression of thoracic aortic aneurysms.

A Critical Dissection of Obstructive Apnea in the Human Infant

PEDIATRICS ◽  
1983 ◽  
Vol 71 (5) ◽  
pp. 721-725
Author(s):  
V. Van Someren ◽  
J. K. Stothers
Keyword(s):  
Esophageal Pressure ◽  
Mouth Breathing ◽  
Human Infant ◽  
Respiratory Pattern ◽  
Central Apnea ◽  
Thoracic Impedance ◽  
Obstructive Apnea ◽  
Closed Glottis ◽  
Respiratory Movements

It is universally accepted that with the cessation of airflow, the infant is technically apneic, but the significance of such respiratory "pauses" remains a matter of discussion. Central apnea is easily recognized, but the absence of airflow with continued "respiratory" movements is commonly interpreted as obstructive apnea. The respiratory pattern of individual normal and abnormal infants was studied in depth. Airflow was monitored using a recently devised facial plate thermistor system; chest movement was recorded by measuring changes in thoracic impedance. On several occasions, esophageal pressure was also recorded as was expired CO2. Using the above systems, it was confirmed that mouth breathing in the infant is confined to periods of crying or yawning, and that many "obstructive" episodes merely represent straining against a closed glottis during movement.

Radial Compressive Properties of an Aortic Stent Graft

2012 ◽  
Author(s):  
Chaid Schwarz ◽  
Madhavan L. Raghavan
Keyword(s):  
Computational Models ◽  
Aortic Wall ◽  
Aortic Aneurysms ◽  
Compressive Properties ◽  
Stent Grafts ◽  
Multiple Factors ◽  
Aortic Stent Graft ◽  
Aortic Neck ◽  
The Difference

The long-term fixation characteristics of stent grafts used to treat aortic aneurysms are likely related to the nature of its apposition to the aortic wall after deployment. But we only have a rudimentary understanding of the mechanisms involved and the factors that determine the nature of deployment of these implants. One factor that has been shown to be of particular relevance is oversizing — the % difference between the size of the graft to that of the aorta in which it is deployed (oversizing implies the former is larger) [1]. Other proposed factors include the angulation in the aortic neck and stent design. Naturally, issues of mechanics are central to this problem. Computational models of the mechanics involved, if developed with rigor, can be useful for gaining insights into the mechanisms involved and for interrogating the interactions among these multiple factors.

scholarly journals Tissue microRNA expression in aortic aneurysm dissection

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Goliopoulou ◽  
E Oikonomou ◽  
M Gazouli ◽  
N Koumalos ◽  
D Lymperiadis ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Rna Extraction ◽  
Tissue Expression ◽  
Microrna Expression ◽  
Aortic Aneurysms ◽  
Control Group ◽  
Aortic Dilatation ◽  
Elisa Method ◽  
Significant Difference

Abstract Background Dissection and other complications of ascending aortic aneurysms are potentially life-threatening. Several factors may be implicated in aneurysm progression and dissection. The role of tissue microRNAs may be of interest. Purpose To examine how serum biomarkers and tissue expression of microRNAs are associated with thoracic aortic aneurysms and dissection. Methods We compared three groups of patients; 21 patients with aneurysm of the aortic root, ascending aorta or aortic arch undergoing scheduled repair, 11 patients with acute Stanford type A aortic dissection who underwent emergency surgery and 18 patients with normal aortic diameter undergoing other cardiac surgery (control group). Prior to surgery, peripheral blood samples were obtained from patients, to assess osteoprotegerin and adiponectin levels with the ELISA method. Tissue samples from ascending aortic wall were obtained from patients during surgery. Following appropriate storage and homogenization, tissue Matrix Metalloproteinases (MMPs) 2 and 9 were measured with the ELISA method, while tissue microRNAs 29 and 195 were measured using qrtPCR, after RNA extraction. Results There was no significant difference among control, aneurysm and dissection groups in terms of age (62±10 years vs 66±12 years vs 59±12 years, p=0.052), gender distribution (77.8% male vs 81% male vs 90% male, p=0.28) or BMI (28.51±2.92 kg/m2 vs 25.72±3.09 kg/m2 vs 27.02±3.2 kg/m2, p=0.76). There was also no difference among control, aneurysm and dissection groups regarding hypertension (72% vs 62% vs 73%, p=0.73), diabetes mellitus (22% vs 19% vs 36%, p=0.54), smoking (44% vs 29% vs 46%, p=0.09) or dyslipidemia (78% vs 43% vs 55%, p=0.08). The groups of control subjects, aneurysms and dissections did not differ in osteoprotegerin [44 (28, 52) pmol/l vs 31 (28, 37) pmol/l vs 45 (24, 71) pmol/l, p=0.17], adiponectin [6,65 (2,39, 9,79) μg/ml vs 5,28 (2,34, 6,98) μg/ml vs 4,13 (2,49, 7,52) μg/ml, p=0.43], tissue MMP2 [0.97 (0.42, 27.66) ng/ml vs 9.12 (1.72, 61.49) ng/ml vs 2.51 (0.22, 235.72) ng/ml, p=0.34] and tissue MMP9 levels [0.96 (0.29, 8.56) ng/ml vs 10.31 (1.18, 25.58) ng/ml vs 2.76 (0.63, 54.83) ng/ml, p=0.09] (Figure 1). Importantly, tissue expression of mir29 was 2.11-fold higher in the dissection group (p=0.001) and 2.99-fold higher in the aneurysm group (p<0.001) compared to the control group. Tissue expression of mir195 was 2.72-fold higher in the dissection group (p<0.001) and 2.00-fold lower in the aneurysm group (p=0.08) compared to the control group (Figure 2). Conclusions These findings highlight the role of epigenetic modifications through altered microRNA tissue expression in aortic wall synthesis, extracellular matrix degradation and progress of aneurysm formation and dissection. The exact role of microRNA expression in aortic dilatation and dissection, as well as their role as potential biomarkers, merit further validation. FUNDunding Acknowledgement Type of funding sources: None. Figure 1 Figure 2

Glutathione system participation in thoracic aneurysms from patients with Marfan syndrome

VASA ◽  
2017 ◽  
Vol 46 (3) ◽  
pp. 177-186 ◽  
Author(s):  
Alejandra María Zúñiga-Muñoz ◽  
Israel Pérez-Torres ◽  
Verónica Guarner-Lans ◽  
Elías Núñez-Garrido ◽  
Rodrigo Velázquez Espejel ◽  
...  
Keyword(s):  
Aortic Aneurysm ◽  
Marfan Syndrome ◽  
Aortic Aneurysms ◽  
Aortic Dilatation ◽  
Glutathione S Transferase ◽  
Reduced And Oxidized Glutathione ◽  
Total Antioxidant ◽  
Elevated Activity ◽  
Acute Dissection ◽  
Thoracic Aneurysms

Abstract. Background: Aortic dilatation in Marfan syndrome (MFS) is progressive. It is associated with oxidative stress and endothelial dysfunction that contribute to the early acute dissection of the vessel and can result in rupture of the aorta and sudden death. We evaluated the participation of the glutathione (GSH) system, which could be involved in the mechanisms that promote the formation and progression of the aortic aneurysms in MFS patients. Patients and methods: Aortic aneurysm tissue was obtained during chest surgery from eight control subjects and 14 MFS patients. Spectrophotometrical determination of activity of glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), lipid peroxidation (LPO) index, carbonylation, total antioxidant capacity (TAC), and concentration of reduced and oxidized glutathione (GSH and GSSG respectively), was performed in the homogenate from aortic aneurysm tissue. Results: LPO index, carbonylation, TGF-β1, and GR activity were increased in MFS patients (p < 0.04), while TAC, GSH/GSSG ratio, GPx, and GST activity were significantly decreased (p < 0.04). Conclusions: The depletion of GSH, in spite of the elevated activity of GR, not only diminished the activity of GSH-depend GST and GPx, but increased LPO, carbonylation and decreased TAC. These changes could promote the structural and functional alterations in the thoracic aorta of MFS patients.

scholarly journals WALL STRESS IN ASCENDING AORTA ANEURYSMS AS A PREDICTIVE FACTOR OF BREAKAGE

2021 ◽  
Vol 108 (Supplement_3) ◽  
Author(s):  
R J Burgos Lázaro ◽  
N Burgos Frías ◽  
S Serrano-Fiz García ◽  
V Ospina Mosquera ◽  
F Rojo Pérez ◽  
...  
Keyword(s):  
Aortic Wall ◽  
Wall Stress ◽  
Middle Layer ◽  
Ascending Aorta ◽  
Aortic Aneurysms ◽  
Maximum Diameter ◽  
Resistance Factors ◽  
Risk Of Rupture ◽  
Traction Test

Abstract INTRODUCTION The surgical indication for ascending aortic aneurysms (AAA) is established when the maximum diameter &gt; 50 mm; It responds to Laplace's Law (T wall = P × r / 2e). The aim of the study is to define wall stress in AAA. MATERIAL AND METHODS 218 ascending aortic walls have been studied: 96 from organ donors, and 122 from AAA: Marfán 58 (47.5%), bicuspid aortic valve 26 (21.4%), and atherosclerosis 38 (31.1%). The samples were studied "in vitro", according to the model Young's (relationship between stress and deformed area), by means of the mechanical traction test (Tension = Force / Area). The analysis was performed with the stress-elongation curve (d Tension / d Elongation). RESULTS The stress of the aortic wall, classified from highest to lowest according to pathology and age was: cystic necrosis of the middle layer, arteriosclerosis, age &gt; 60 years, between 35 and 59, and &lt; 34 years. The stress of “control aortas” wall increased directly in relation to the age of the donors. CONCLUSIONS The maximum diameter of the ascending aorta, the patient's type of pathology and age are factors that affect the maximum tension of the aortic wall and resistance, factors that allow differentiation and prediction of the risk of rupture of the AAA. The validation of the results obtained through numerical simulation was significant and the uniaxial analysis has modeled the response of the vessels to their internal pressure.

scholarly journals Quantitative not qualitative histology differentiates aneurysmal from nondilated ascending aortas and reveals a net gain of medial components

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Sameh Yousef ◽  
Nana Matsumoto ◽  
Issam Dabe ◽  
Makoto Mori ◽  
Alden B. Landry ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Quantitative Assessment ◽  
Cell Number ◽  
Aortic Aneurysms ◽  
Aortic Dilatation ◽  
Adaptive Responses ◽  
Cross Sectional ◽  
Thoracic Aortic Aneurysms ◽  
Medial Degeneration ◽  
The Media

AbstractMedial degeneration is a common histopathological finding in aortopathy and is considered a mechanism for dilatation. We investigated if medial degeneration is specific for sporadic thoracic aortic aneurysms versus nondilated aortas. Specimens were graded by pathologists, blinded to the clinical diagnosis, according to consensus histopathological criteria. The extent of medial degeneration by qualitative (semi-quantitative) assessment was not specific for aneurysmal compared to nondilated aortas. In contrast, blinded quantitative assessment of elastin amount and medial cell number distinguished aortic aneurysms and referent specimens, albeit with marked overlap in results. Specifically, the medial fraction of elastin decreased from dilution rather than loss of protein as cross-sectional amount was maintained while the cross-sectional number, though not density, of smooth muscle cells increased in proportion to expansion of the media. Furthermore, elastic lamellae did not thin and interlamellar distance did not diminish as expected for lumen dilatation, implying a net gain of lamellar elastin and intralamellar cells or extracellular matrix during aneurysmal wall remodeling. These findings support the concepts that: (1) medial degeneration need not induce aortic aneurysms, (2) adaptive responses to altered mechanical stresses increase medial tissue, and (3) greater turnover, not loss, of mural cells and extracellular matrix associates with aortic dilatation.

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