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Inflammatory changes in the aneurysm wall: a review
  1. Riikka Tulamo1,2,
  2. Juhana Frösen1,3,
  3. Juha Hernesniemi1,3,
  4. Mika Niemelä1,3
  1. 1Neurosurgery Research Group, Biomedicum Helsinki, Finland
  2. 2Department of Bacteriology and Immunology, Haartman Institute, University of Helsinki, Finland
  3. 3Department of Neurosurgery, Helsinki University Central Hospital, Helsinki, Finland
  1. Correspondence to Riikka Tulamo, Neurosurgery Research Group, Room B408a2, Biomedicum Helsinki 1, PO Box 700, Huch FI-00029, Finland; riikka.tulamo{at}hus.fi

Abstract

Rupture of a saccular intracranial artery aneurysm (IA) causes subarachnoid hemorrhage, a significant cause of stroke and death. The current treatment options, endovascular coiling and clipping, are invasive and somewhat risky. Since only some IAs rupture, those IAs at risk for rupture should be identified. However, to improve the imaging of rupture-prone IAs and improve IA treatment, IA wall pathobiology requires more thorough knowledge. Chronic inflammation has become understood as an important phenomenon in IA wall pathobiology, featuring inflammatory cell infiltration as well as proliferative and fibrotic remodulatory responses. We review the literature on what is known about inflammation in the IA wall and also review the probable mechanisms of how inflammation would result in the degenerative changes that ultimately lead to IA wall rupture. We also discuss current options in imaging inflammation and how knowledge of inflammation in IA walls may improve IA treatment.

  • Aneurysm
  • inflammation
  • intracranial aneurysm
  • bFGF
  • Basic fibroblast growth factor
  • CRP
  • C reactive protein
  • ECM
  • Extracellular matrix
  • IA
  • Intracranial aneurysm
  • IEL Internal elastic lamina
  • IFN
  • interferon
  • IgG
  • Immunoglobulin G
  • IgM
  • Immunoglobulin M
  • IL
  • Interleukin
  • MAPK
  • Mitogen-activated protein kinase
  • MCP
  • Monocyte chemotactic protein
  • MMP
  • matrix metalloprotein
  • NFκB
  • Nuclear factor kappa B
  • NO
  • Nitric oxide
  • oxLDL
  • Oxidatively modified low density lipoprotein
  • ROS
  • Reactive oxygen species
  • SAH
  • Subarachnoid hemorrhage
  • SMC
  • Smooth muscle cell
  • TIMP
  • tissue inhibitors of metalloproteinases
  • TGF
  • Transforming growth factor
  • TNF
  • Tumor necrosis factor
  • VCAM
  • Vascular cell adhesion molecule; VEGF, vascular endothelial growth factor vascular endothelial growth factor

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Footnotes

  • Funding This work was supported by Helsinki University Central Hospital (HUCH) EVO grant TYH 2009303.

  • Competing interests None.

  • Ethics approval This study was conducted with the approval of the HUCH Ethics Committee.

  • Provenance and peer review Commissioned; not externally peer reviewed.

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