Histological and ultrastructural study of intracranial saccular aneurysmal wall

Scanarini, M.; Mingrino, S; Giordano, R; Baroni, A.

doi:10.1007/bf01587953

Cited by 60 publications

(24 citation statements)

References 8 publications

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“…As mentioned, there is a striking loss or fragmentation of the internal IEL. Other histopathological features include irregularity of the luminal surface within the aneurysm sac, intimal hyperplasia, loss of cellular components, and disorganization of muscle fiber structure (Abruzzo et al, 1998;Draghia et al, 2008;Kataoka et al, 1999;Santiago-Sim and Kim, 2011;Scanarini et al, 1978;Schlote and Gaus, 1994). As a consequence of vascular remodeling, other changes in composition of the vessel wall have been noted including collagen content and extracellular matrix components.…”

Section: Changes In Constituents Of the Cerebral Blood Vessel Wall Inmentioning

confidence: 99%

Biology of Intracranial Aneurysms: Role of Inflammation

Chalouhi

Ali

Jabbour

et al. 2012

J Cereb Blood Flow Metab

444

418

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Intracranial aneurysms (IAs) linger as a potentially devastating clinical problem. Despite intense investigation, our understanding of the mechanisms leading to aneurysm development, progression and rupture remain incompletely defined. An accumulating body of evidence implicates inflammation as a critical contributor to aneurysm pathogenesis. Intracranial aneurysm formation and progression appear to result from endothelial dysfunction, a mounting inflammatory response, and vascular smooth muscle cell phenotypic modulation producing a pro-inflammatory phenotype. A later final common pathway appears to involve apoptosis of cellular constituents of the vessel wall. These changes result in degradation of the integrity of the vascular wall leading to aneurysmal dilation, progression and eventual rupture in certain aneurysms. Various aspects of the inflammatory response have been investigated as contributors to IA pathogenesis including leukocytes, complement, immunoglobulins, cytokines, and other humoral mediators. Furthermore, gene expression profiling of IA compared with control arteries has prominently featured differential expression of genes involved with immune response/inflammation. Preliminary data suggest that therapies targeting the inflammatory response may have efficacy in the future treatment of IA. Further investigation, however, is necessary to elucidate the precise role of inflammation in IA pathogenesis, which can be exploited to improve the prognosis of patients harboring IA.

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Section: Changes In Constituents Of the Cerebral Blood Vessel Wall Inmentioning

confidence: 99%

Biology of Intracranial Aneurysms: Role of Inflammation

Chalouhi

Ali

Jabbour

et al. 2012

J Cereb Blood Flow Metab

444

418

View full text Add to dashboard Cite

show abstract

“…In either case, these layers do not seem to contribute significantly to the structural integrity of the aneurysmal wall. Thus, the wall of saccular cerebral aneurysms can roughly be described as a development of the adventitia of the original healthy artery (Abruzzo et al, 1998;Scanarini et al, 1978;Schievink, 1997). In the media of a healthy cerebral artery, the smooth muscle and collagen components are almost perfectly aligned in the circumferential direction of the artery (Finlay et al, 1995;Walmsley et al, 1983), whereas the collagen of the adventitia (which dominates the mechanical behaviour of this layer) shows a dispersion from the circumferential to the longitudinal orientation (Finlay et al, 1995;Smith et al, 1981).…”

Section: Introductionmentioning

confidence: 99%

A theoretical model for fibroblast-controlled growth of saccular cerebral aneurysms

Kroon

Holzapfel

2009

Journal of Theoretical Biology

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A new theoretical model for the growth of saccular cerebral aneurysms is proposed by extending the recent constitutive framework of Kroon and Holzapfel (J. Theor. Biol., 247:775-787, 2007). The continuous turnover of collagen is taken to be the driving mechanism in aneurysmal growth. The collagen production rate depends on the magnitude of the cyclic deformation of fibroblasts, caused by the pulsating blood pressure during the cardiac cycle. The volume density of fibroblasts in the aneurysmal tissue is taken to be constant throughout the growth process. The growth model is assessed by considering the inflation of an axisymmetric membranous piece of aneurysmal tissue, with material characteristics representative of a cerebral aneurysm. The diastolic and systolic states of the aneurysm are computed, together with its load-free state. It turns out that the value of collagen pre-stretch, that determines growth speed and stability of the aneurysm, is of pivotal importance. The model is able to predict aneurysms with typical berry-like shapes observed clinically, and the predicted wall stresses correlate well with the experimentally obtained ultimate stresses of this type of tissue. The model predicts that aneurysms should fail when reaching a size of about 1.2-3.6 mm, which is smaller than what has been clinically observed. With some refinements, the model may, however, be used to predict future growth of diagnosed aneurysms.

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“…Various degenerative changes of the vessel wall have been observed including mechanical fatigue, occlusion of the vasa vasorum (20) , existence of media gaps (21) , apoptosis of medial smooth muscle cells (SMCs) (22) , reduced production of collagen (23) - (25) , and enzymatic digestion (26) . These degenerative changes may lead to the focal weakening of the arterial wall and are supposed to be responsible for the initiation of intracranial aneurysms (23), (27) .…”

Section: Discussionmentioning

confidence: 99%

Growth of Intracranial Aneurysms Arised from Curved Vessels under the Influence of Elevated Wall Shear Stress-A Computer Simulation Study

Feng

Wada

Tsubota

et al. 2004

JSME Int. J., Ser. C

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Recent studies have suggested that long standing elevated wall shear stress might degenerate the arterial wall and be involved in the pathogenesis of intracranial aneurysm formation and development. The present study focuses on the interplay between the hemodynamic stresses, arterial wall degeneration and deformation. By constructing a computational model and examining the hypotheses that govern the rules to grow an intracranial aneurysm, we simulate the formation and development of intracranial aneurysms. The high wall shear stress is found to propagate towards the proximal and distal end of the formed aneurysm, which becomes the key factor for the expansion of wall degeneration and aneurysm progression. The development of aneurysm is influenced by the wall shear stress threshold, the Reynolds number and the rate of wall degeneration. Our preliminary results indicate that computer simulation can be used in the study of aneurysm mechanics and yields new insight into the mechanism of aneurysm pathophysiology.

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Histological and ultrastructural study of intracranial saccular aneurysmal wall

Cited by 60 publications

References 8 publications

Biology of Intracranial Aneurysms: Role of Inflammation

Biology of Intracranial Aneurysms: Role of Inflammation

A theoretical model for fibroblast-controlled growth of saccular cerebral aneurysms

Growth of Intracranial Aneurysms Arised from Curved Vessels under the Influence of Elevated Wall Shear Stress-A Computer Simulation Study

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