Severe structural damage of the seemingly non-diseased infrarenal aortic aneurysm neck

Diehm, Nicolas; Santo, Stefano Di; Schaffner, Thomas; Schmidli, Juerg; Völzmann, Jan; Jüni, Peter; Baumgartner, Iris

doi:10.1016/j.jvs.2008.03.001

Cited by 31 publications

(33 citation statements)

References 50 publications

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“…For example, noting that plasmin is a key activator of proMMP-9, plasminogen -/-mice had reduced macrophage migration through the extracellular matrix that was rescued with administration of active MMP-9 [67]. Nevertheless, increased MMP-9 activity in the wall significantly exceeded the increase in MMP-9 expression [66], consistent with diffusion/convection from the ILT and/or increased release and activation of stored MMPs.…”

Section: Medial and Abluminal Layersmentioning

confidence: 97%

“…Indeed, the aneurysmal wall has shown 100-fold higher tPA activity than the ILT [63], and MMP-9 activity has been localized to the inner wall of AAA [64] as has elastase activity [52] and plasmin [65], consistent with an ILT-mediated degradation of the wall. Yet, remnant SMCs, infiltrating macrophages, and endothelial cells from the vasa vasorum may also produce MMP-9 [66], which may relate to the ability of these cells to migrate toward and neovascularize the injured aortic wall. For example, noting that plasmin is a key activator of proMMP-9, plasminogen -/-mice had reduced macrophage migration through the extracellular matrix that was rescued with administration of active MMP-9 [67].…”

Section: Medial and Abluminal Layersmentioning

confidence: 99%

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Biochemomechanics of Intraluminal Thrombus in Abdominal Aortic Aneurysms

Wilson

Virag

Achille

et al. 2013

Journal of Biomechanical Engineering

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Most computational models of abdominal aortic aneurysms address either the hemodynamics within the lesion or the mechanics of the wall. More recently, however, some models have appropriately begun to account for the evolving mechanics of the wall in response to the changing hemodynamic loads. Collectively, this large body of work has provided tremendous insight into this life-threatening condition and has provided important guidance for current research. Nevertheless, there has yet to be a comprehensive model that addresses the mechanobiology, biochemistry, and biomechanics of thrombus-laden abdominal aortic aneurysms. That is, there is a pressing need to include effects of the hemodynamics on both the development of the nearly ubiquitous intraluminal thrombus and the evolving mechanics of the wall, which depends in part on biochemical effects of the adjacent thrombus. Indeed, there is increasing evidence that intraluminal thrombus in abdominal aortic aneurysms is biologically active and should not be treated as homogeneous inert material. In this review paper, we bring together diverse findings from the literature to encourage next generation models that account for the biochemomechanics of growth and remodeling in patient-specific, thrombus-laden abdominal aortic aneurysms.

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Section: Medial and Abluminal Layersmentioning

confidence: 97%

Section: Medial and Abluminal Layersmentioning

confidence: 99%

Biochemomechanics of Intraluminal Thrombus in Abdominal Aortic Aneurysms

Wilson

Virag

Achille

et al. 2013

Journal of Biomechanical Engineering

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“…14,15 Moreover, aneurysmal disease shows a continuous circumferential destruction of the media, with inflammation first occurring in the adventitial and medial space, whereas classic atherosclerosis is characterized by a scattered distribution of plaques in the subendothelial space. 16 Hereditary elements, elastin, and collagen degradation may correlate with genetically unstable proteins or locally increased protease production in aneurysmal lesions. Of note, approximately 25% of cases occur in patients with firstdegree relatives who have AAA.…”

mentioning

confidence: 99%

Determinants of Aneurysmal Aortic Disease

Diehm

Baumgartner

2009

Circulation

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“…Inflammatory cell invasion occurs in all arterial layers and is accompanied by elastin fragmentation, resulting in large, fragile vessel walls at risk for rupture and hemorrhage (7). Inflammatory cells that invade the vessel include macrophages, CD8+ cytotoxic T lymphocytes (CTL), and CD4+ T helper cells (5,8) as well as neutrophils, fibroblasts, and mast cells (5,6).…”

mentioning

confidence: 99%

“…Apoptosis of VSMCs reduces secreted elastin and collagen in the arterial wall with reduced tensile strength of the vessel wall (5,9). Apoptosis of endothelial cells, macrophage, or T lymphocytes induces release of clotting factors and cytokines and produces pro-thrombotic and pro-inflammatory states (2,7,8). Apoptosis in VSMCs is closely associated with aneurysm formation; however, the contribution of apoptotic inflammatory cells to aneurysm progression is less well defined.…”

mentioning

confidence: 99%

Viral Anti-Inflammatory Proteins Target Diverging Immune Pathways with Converging Effects on Arterial Dilatation, Plaque and Apoptosis

et al. 2014

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Abdominal aortic aneurysms are often fatal due to atherosclerosis, thromboembolism, rupture, and hemorrhage, however, treatment is limited to expectant monitoring and surgical intervention. Inflammation is detected in aneurysms and in plaque with associated increased apoptosis, chemokines, cytokines, hemorrhage, and thrombosis. We compared treatment with three different myxomavirusderived anti-inflammatory proteins targeting apoptosis, thrombosis, and chemokine pathways. The effect of each protein on aortic dilatation and plaque growth was assessed after angioplasty in Apolipoprotein Enull mice. Four myxomavirus-derived proteins were studied; Serp-l a serine protease inhibitor (serpin) targeting thrombotic and thrombolytic proteases, Serp-2 a cross-class serpin inhibiting granzyme Band caspases land 8, M-T7 a broad spectrum C, CC, and CXC chemokine inhibitor, and Rl7lE, an inactive M-T7 mutant. Cell invasion, elastin breaks, plaque progression, and aortic dilatation were significantly reduced by Serp-l, Serp-2, or M-T7 protein treatment, but not by Rl7lE. PCR array analysis detected altered expression of a group of shared 40 apoptotic genes in monocytes after treatment with each active protein, but not Rl71E. Interference with inflammatory cell responses, through highly divergent inflammatory response pathways, produces similar reductions in monocyte invasion, arterial dilatation, and plaque growth potentially through modified expression of apoptotic genes.Although the risk associated with atherosclerotic cardiovascular disease is now markedly improved, the incidence ofabdominal aortic aneurysms (AAAs) is increasing (1-7). AAA is a localized dilatation of the aorta with diameter greater than 3 em (or more than 50% increase) with loss of medial elastin and associated cell death (apoptosis). There is often a marked increase in local atherosclerotic plaque and thrombosis at sites of aneurysmal dilatation. Undiagnosed AAAs affect 5% of men over 65 years of age, often causing sudden death (1-3). Nearly 2 million Americans are at risk for AAAs, with 4-8.9% prevalence worldwide, increasing as the population ages (1). Sudden rupture of the destabilized aneurysmal vessel has 50% to 80% associated mortality (1-3). While control of atherosclerotic

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Severe structural damage of the seemingly non-diseased infrarenal aortic aneurysm neck

Abstract: The seemingly non-diseased infrarenal AAA neck in patients with AAA undergoing surgical repair shows histological signs of destruction and upregulation of potential drug targets.

Cited by 31 publications

References 50 publications

Biochemomechanics of Intraluminal Thrombus in Abdominal Aortic Aneurysms

Biochemomechanics of Intraluminal Thrombus in Abdominal Aortic Aneurysms

Determinants of Aneurysmal Aortic Disease

Viral Anti-Inflammatory Proteins Target Diverging Immune Pathways with Converging Effects on Arterial Dilatation, Plaque and Apoptosis

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