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Review
. 2021 Jul 22;57(8):742.
doi: 10.3390/medicina57080742.

Shedding the Light on the Natural History of Intracranial Aneurysms: An Updated Overview

Affiliations
Review

Shedding the Light on the Natural History of Intracranial Aneurysms: An Updated Overview

Alice Giotta Lucifero et al. Medicina (Kaunas). .

Abstract

The exact molecular pathways underlying the multifactorial natural history of intracranial aneurysms (IAs) are still largely unknown, to the point that their understanding represents an imperative challenge in neurovascular research. Wall shear stress (WSS) promotes the genesis of IAs through an endothelial dysfunction causing an inflammatory cascade, vessel remodeling, phenotypic switching of the smooth muscle cells, and myointimal hyperplasia. Aneurysm growth is supported by endothelial oxidative stress and inflammatory mediators, whereas low and high WSS determine the rupture in sidewall and endwall IAs, respectively. Angioarchitecture, age older than 60 years, female gender, hypertension, cigarette smoking, alcohol abuse, and hypercholesterolemia also contribute to growth and rupture. The improvements of aneurysm wall imaging techniques and the implementation of target therapies targeted against inflammatory cascade may contribute to significantly modify the natural history of IAs. This narrative review strives to summarize the recent advances in the comprehension of the mechanisms underlying the genesis, growth, and rupture of IAs.

Keywords: endothelial disfunction; inflammatory cascade; intra-aneurysmal flow; intracranial aneurysm; subarachnoid hemorrhage; wall shear stress.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Hemodynamic and molecular mechanisms of intracranial aneurysms formation. COX2, cyclooxygenase-2; ECM, extracellular matrix; IL:, interleukin; MCP-1, monocyte chemoattractant protein-1; MMP, matrix metalloproteinase; PGE2, prostaglandin E2; ROS, reactive oxygen species; TNF-α, tumor necrosis factor-α; VCAM-1, vascular cell adhesion molecule-1; VSMC, vascular smooth muscle cell; WS, wall shear stress.
Figure 2
Figure 2
Hemodynamic patterns of intracranial aneurysms growth. eNOS, endothelial nitric oxide synthase; IL, interleukin; iNOS, inducible nitric oxide synthase; MCP-1, monocyte chemoattractant protein-1; MMP, matrix metalloproteinase; NO, nitric oxide; ROS, reactive oxygen species; TNF-α, tumor necrosis factor-α; VCAM-1, vascular cell adhesion molecule-1; WSS, wall shear stress.
Figure 3
Figure 3
Histological subtypes of intracranial aneurysms and risk of rupture. (A) Type A; (B) type B; (C) type C; (D) type D.
Figure 4
Figure 4
Angio-architectural classification of intracranial aneurysms.

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