Abdominal Aortic Aneurysm

Desforges, Jane F.; Ernst, Calvin B.

doi:10.1056/nejm199304223281607

Cited by 561 publications

(40 citation statements)

References 80 publications

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“…Patients with increased risk of rupture have no choice but to undergo surgery by means of either open repair with prosthetic graft replacement or endovascular stent graft placement [4]. Clinically, it is usual to measure the aneurysmal diameter periodically in the outpatient clinic until the size reaches 55 mm or exhibits a growth rate of more than 1 cm/year, at which point surgeons recommend that the patient undergoes surgery [4,5,6]. However, a small AAA involves a risk for rupture in some cases [7].…”

Section: Introductionmentioning

confidence: 99%

The Effect of a High-Fat Diet on the Development of Abdominal Aortic Aneurysm in a Vascular Hypoperfusion-Induced Animal Model

Hashimoto

Kugo

Tanaka³

et al. 2018

J Vasc Res

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Abdominal aortic aneurysm (AAA) is a vascular disease characterized by chronic inflammation in the infrarenal aorta. Most cases of AAA remain asymptomatic until rupture, and the mortality rate of patients with AAA rupture is very high. Currently, the relation between dietary habits and AAA development remains unknown. In this study, we evaluated the effects of a high-fat diet on the development of AAA in a vascular hypoperfusion-induced animal model. The risk of AAA rupture and AAA diameter in the high-fat group significantly increased compared with those in the control group. The number and size of adipocytes in the vascular wall in the high-fat group significantly increased as compared with those in the control group. Additionally, the collagen-positive sections in the areas with adipocytes significantly decreased as compared with those without adipocytes. The protein levels of matrix metalloproteinase (MMP)-2, MMP-9, and MMP-12, and macrophage-positive areas in the parts with adipocytes also significantly increased as compared with those without adipocytes. These data suggested that AAA rupture risk increased through accelerating chronic inflammation due to the accumulation of adipocytes in the vascular wall in the high-fat group.

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Section: Introductionmentioning

confidence: 99%

The Effect of a High-Fat Diet on the Development of Abdominal Aortic Aneurysm in a Vascular Hypoperfusion-Induced Animal Model

Hashimoto

Kugo

Tanaka³

et al. 2018

J Vasc Res

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“…Abdominal aortic aneurysm (AAA), defined as a permanent localized aortic dilation with a diameter of 1.5 times the normal aorta diameter, is a silent degenerative disease that can be life-threatening [1]. Although human AAA is histologically characterized by adventitial inflammation, medial attenuation, elastic fiber destruction and subsequent dilation [2], the pathogenesis of AAA is not completely understood.…”

Section: Introductionmentioning

confidence: 99%

Development of a Novel Rabbit Model of Abdominal Aortic Aneurysm via a Combination of Periaortic Calcium Chloride and Elastase Incubation

Zhong

et al. 2013

PLoS ONE

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BackgroundThe purpose of this study was to introduce a novel, simple and effective technique for creating a reliable rabbit model of abdominal aortic aneurysm (AAA) via a combination of periaortic calcium chloride (CaCl2) and elastase incubation.MethodsForty-eight New Zealand white rabbits were divided into four groups. The AAA model was developed via a 20-minute periaortic incubation of CaCl2 (0.5 mol/L) and elastase (1 Unit/µL) in a 1.5-cm aortic segment (Group CE). A single incubation of CaCl2 (Group C) or elastase (Group E) and a sham operation group (Sham Group) were used for the controls. Diameter was measured by serial digital subtraction angiography imaging on days 5, 15 and 30. Animals were sacrificed on day 5 and day 30 for histopathological and immunohistochemical studies.ResultsAll animals in Group CE developed aneurysm, with an average dilation ratio of 65.3%±8.9% on day 5, 86.5%±28.7% on day 15 and 203.6%±39.1% on day 30. No aneurysm was found in Group C, and only one aneurysm was seen on day 5 in Group E. Group CE exhibited less intima-media thickness, endothelial recovery, elastin and smooth muscle cell (SMC) content, but stronger expression of matrix metalloproteinase-2, matrix metalloproteinase-9 and RAM11 compared to the controls.ConclusionsThe novel rabbit model of AAA created by using a combination of periaortic CaCl2 and elastase incubation is simple and effective to perform and is valuable for elucidating AAA mechanisms and therapeutic interventions in experimental studies.

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“…While sometimes aneurysms remain stable in size, frequently the aortic diameter increases in size until rupture occurs. 1 Previous studies have demonstrated that aneurysmal dilatation is an active process that involves infiltration of the adventitia and tunica media with inflammatory cells, 2,3 loss of the smooth muscle cells, thinning of the tunica media 4,5 and degradation of the extracellular matrix. 3,6,7 …”

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confidence: 99%

Overexpression of Catalase in Vascular Smooth Muscle Cells Prevents the Formation of Abdominal Aortic Aneurysms

Parastatidis

Weiss

Joseph

et al. 2013

ATVB

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Objective Elevated levels of oxidative stress have been reported in abdominal aortic aneurysms (AAA), but which reactive oxygen species (ROS) promotes the development of AAA remains unclear. Here we investigate the effect of the hydrogen peroxide (H2O2) degrading enzyme catalase on the formation of AAA. Approach and Results AAA were induced with the application of calcium chloride (CaCl2) on mouse infrarenal aortas. The administration of PEG-catalase, but not saline, attenuated the loss of tunica media and protected against AAA formation (0.91±0.1 mm vs. 0.76±0.09 mm). Similarly, in a transgenic mouse model, catalase over-expression in the vascular smooth muscle cells (VSMC) preserved the thickness of tunica media and inhibited aortic dilatation by 50% (0.85±0.14 mm vs. 0.57±0.08 mm). Further studies showed that injury with CaCl2 decreased catalase expression and activity in the aortic wall. Pharmacologic administration or genetic over-expression of catalase restored catalase activity and subsequently decreased matrix metalloproteinase activity. In addition, a profound reduction in inflammatory markers and VSMC apoptosis was evident in aortas of catalase over-expressing mice. Interestingly, as opposed to infusion of PEG-catalase, chronic over-expression of catalase in VSMC did not alter the total aortic H2O2 levels. Conclusions The data suggest that a reduction in aortic wall catalase activity can predispose to AAA formation. Restoration of catalase activity in the vascular wall enhances aortic VSMC survival and prevents AAA formation primarily through modulation of matrix metalloproteinase activity.

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Abdominal Aortic Aneurysm

Cited by 561 publications

References 80 publications

The Effect of a High-Fat Diet on the Development of Abdominal Aortic Aneurysm in a Vascular Hypoperfusion-Induced Animal Model

The Effect of a High-Fat Diet on the Development of Abdominal Aortic Aneurysm in a Vascular Hypoperfusion-Induced Animal Model

Development of a Novel Rabbit Model of Abdominal Aortic Aneurysm via a Combination of Periaortic Calcium Chloride and Elastase Incubation

Overexpression of Catalase in Vascular Smooth Muscle Cells Prevents the Formation of Abdominal Aortic Aneurysms

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