Histological features of human abdominal aortic aneurysm are not related to clinical characteristics

Hellenthal, F.A.M.V.I.; Geenen, Irma L.; Teijink, Joep A.W.; Heeneman, Sylvia; Schurink, Geert Willem H.

doi:10.1016/j.carpath.2008.06.014

Cited by 41 publications

(27 citation statements)

References 15 publications

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“…A constant wall thickness was applied to the AAA wall, although it is known that wall thickness may vary within and between patients. 37 This may strongly affect the resulting wall stress, but currently, no noninvasive techniques are available to measure local wall thickness. The presence of calcifications was also neglected.…”

Section: Discussionmentioning

confidence: 99%

The mechanical role of thrombus on the growth rate of an abdominal aortic aneurysm

Speelman

Schurink

Bosboom

et al. 2010

Journal of Vascular Surgery

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145

114

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Section: Discussionmentioning

confidence: 99%

The mechanical role of thrombus on the growth rate of an abdominal aortic aneurysm

Speelman

Schurink

Bosboom

et al. 2010

Journal of Vascular Surgery

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145

114

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“…Histologically, extracellular matrix degeneration is characterized by disruption and degradation of medial elastin and gross medial collagen deposition, whereas inflammation is exemplified by inflammatory cell infiltration of the aortic wall ( Figure 1). 11 Inflammatory cells, such as macrophages, secrete various humoral inflammatory factors and can release active proteases. 12 Additionally, endothelial cells, smooth muscle cells, and fibroblasts can all produce proteases.…”

Section: Introductionmentioning

confidence: 99%

Biomarkers of AAA progression. Part 1: extracellular matrix degeneration

et al. 2009

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Abdominal aortic aneurysm (AAA) is an important health problem. Elective surgical treatment is recommended on the basis of an individual's risk of rupture, which is predicted by AAA diameter. However, the natural history of AAA differs between patients and a reliable and individual predictor of AAA progression (growth and expansion rates) has not been established. Several circulating biomarkers are candidates for an AAA diagnostic tool. However, they have yet to meet the triad of biomarker criteria: biological plausibility, correlation with AAA progression, and prediction of treatment effect on disease outcome. Circulating levels of markers of extracellular matrix degeneration, such as elastin peptides, aminoterminal propeptide of type III procollagen, elastase-alpha1-antitrypsin complexes, matrix metalloproteinase 9, cystatin C, plasmin-antiplasmin complexes and tissue plasminogen activator, have been correlated with AAA progression and have biological plausibility. Although studies of these markers have shown promising results, they have not yet led to a clinically applicable biomarker. In future studies, adjustment for initial AAA size, smoking history and the measurement error for determination of AAA size, among other variables, should be taken into account. A large, prospective, standardized, follow-up study will be needed to investigate multiple circulating biomarkers for their potential role in the prediction of AAA progression, followed by a study to investigate the effect of treatment on the circulating levels of biomarkers.

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“…It is now understood that the pathogenesis of AAA implicates a complex interplay of key mechanisms that include oxidative stress [39][40][41], local production of proinflammatory cytokines [42,43], vascular smooth muscle migration and proliferation [44][45][46], and activation of proteases such as matrix metalloproteinases and cysteine/ serine proteases [6,[47][48][49][50][51]. Substantial experimental evidence implicates early involvement of the monocyte/ macrophage innate immune response, with consequent production of pro-inflammatory cytokines during AAA development [7,[52][53][54]. However, the potential impact of BaP exposure in conjunction with proaneurysmal stimulus has not been investigated extensively.…”

Section: Bap Exposure and Abdominal Aortic Aneurysmsmentioning

confidence: 99%

Benzo[a]pyrene Potentiates the Pathogenesis of Abdominal Aortic Aneurysms in Apolipoprotein E Knockout Mice

Prins

Perati

Kon

et al. 2012

Cell Physiol Biochem

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The objective of this study was to determine the effect of benzo[a]pyrene (BaP), an abundant environmental polycyclic aromatic hydrocarbon compound, on the pathogenesis of abdominal aortic aneurysms (AAA). Earlier studies have shown that BaP promotes vasculopathy, including atherosclerosis, a predisposing factor for AAA development. In two experimental arms, 203 apolipoprotein E knockout (ApoE-/-) mice were evaluated in 4 groups: BaP, angiotensin II (AngII), BaP+AngII and control. Mice in the first arm were exposed to 5mg/kg/week of BaP for 42 days, and in the second arm to 0.71mg/kg daily for 60 days. In arm one, AAA incidence was higher in the BaP+AngII (14/28) versus AngII (8/27) group (p < 0.05), rupture (n=3) was observed only in BaP+AngII treated mice (p < 0.05). In the second arm, AAA incidence did not differ between AngII (17/30) and BaP+AngII (16/29) groups. However, intact AAA diameter was larger in the BaP+AngII (2.3 ± 0.1mm) versus AngII (1.9 ± 0.1mm) group (p < 0.05), but AAA rupture did not differ (p=NS). In both experimental arms, BaP+AngII mice showed increased expression of tumor necrosis factor alpha (TNF-α), cyclophilin A (Cyp A), and matrix metalloproteinase-9 (MMP9) (p < 0.05). No AAA occurred in control or BaP groups. These findings suggest the role of BaP exposure in potentiating AAA pathogenesis, which may have potential public health significance.

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Histological features of human abdominal aortic aneurysm are not related to clinical characteristics

Cited by 41 publications

References 15 publications

The mechanical role of thrombus on the growth rate of an abdominal aortic aneurysm

The mechanical role of thrombus on the growth rate of an abdominal aortic aneurysm

Biomarkers of AAA progression. Part 1: extracellular matrix degeneration

Benzo[a]pyrene Potentiates the Pathogenesis of Abdominal Aortic Aneurysms in Apolipoprotein E Knockout Mice

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