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J Cerebrovasc Endovasc Neurosurg. 2014 Dec;16(4):335-349. English. Review. https://doi.org/10.7461/jcen.2014.16.4.335
Tanweer O , Wilson TA , Metaxa E , Riina HA , Meng H .
Department of Neurosurgery, New York University School of Medicine, NY, United States.
Foundation for Research and Technology - Hellas Institute of Applied and Computational Mathematics, Crete, Greece.
Toshiba Stroke Research Center, University at Buffalo, NY, United States. huimeng@buffalo.edu
Department of Mechanical and Aerospace Engineering, University at Buffalo, NY, United States.
Department of Neurosurgery, University at Buffalo, NY, United States.
Abstract

OBJECTIVE: Cerebral aneurysms (CAs) and abdominal aortic aneurysms (AAAs) are degenerative vascular pathologies that manifest as abnormal dilations of the arterial wall. They arise with different morphologies in different types of blood vessels under different hemodynamic conditions. Although treated as different pathologies, we examine common pathways in their hemodynamic pathogenesis in order to elucidate mechanisms of formation. MATERIALS AND METHODS: A systematic review of the literature was performed. Current concepts on pathogenesis and hemodynamics were collected and compared. RESULTS: CAs arise as saccular dilations on the cerebral arteries of the circle of Willis under high blood flow, high wall shear stress (WSS), and high wall shear stress gradient (WSSG) conditions. AAAs arise as fusiform dilations on the infrarenal aorta under low blood flow, low, oscillating WSS, and high WSSG conditions. While at opposite ends of the WSS spectrum, they share high WSSG, a critical factor in arterial remodeling. This alone may not be enough to initiate aneurysm formation, but may ignite a cascade of downstream events that leads to aneurysm development. Despite differences in morphology and the structure, CAs and AAAs share many histopathological and biomechanical characteristics. Endothelial cell damage, loss of elastin, and smooth muscle cell loss are universal findings in CAs and AAAs. Increased matrix metalloproteinases and other proteinases, reactive oxygen species, and inflammation also contribute to the pathogenesis of both aneurysms. CONCLUSION: Our review revealed similar pathways in seemingly different pathologies. We also highlight the need for cross-disciplinary studies to aid in finding similarities between pathologies.

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