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A comparative review of the hemodynamics and pathogenesis of cerebral and abdominal aortic aneurysms: lessons to learn from each other.

Tanweer O, Wilson TA, Metaxa E, Riina HA, Meng H - J Cerebrovasc Endovasc Neurosurg (2014)

Bottom Line: Current concepts on pathogenesis and hemodynamics were collected and compared.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, New York University School of Medicine, 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.

No MeSH data available.


Related in: MedlinePlus

A representation of laminar flow adjacent to an arterial wall during a systole-diastole phase resulting in retrograde flow.
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Figure 2: A representation of laminar flow adjacent to an arterial wall during a systole-diastole phase resulting in retrograde flow.

Mentions: There is marked variation in the hemodynamic conditions along the length of the aorta, and this is thought to contribute to the predilection of aneurysms to form in the distal aorta.25) One of the most significant differences is between the resting aortic WSS in the suprarenal and infrarenal segments of the aorta.25) In the suprarenal aorta, flow is anterograde and laminar throughout the entire cardiac cycle, providing continuous, directed WSS. In the infrarenal aorta, flow is anterograde at the beginning of the cardiac cycle, however, toward the end of systole and throughout diastole, there is reverse, recirculating flow and low, oscillating WSS.25) (Fig. 2)


A comparative review of the hemodynamics and pathogenesis of cerebral and abdominal aortic aneurysms: lessons to learn from each other.

Tanweer O, Wilson TA, Metaxa E, Riina HA, Meng H - J Cerebrovasc Endovasc Neurosurg (2014)

A representation of laminar flow adjacent to an arterial wall during a systole-diastole phase resulting in retrograde flow.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4296046&req=5

Figure 2: A representation of laminar flow adjacent to an arterial wall during a systole-diastole phase resulting in retrograde flow.
Mentions: There is marked variation in the hemodynamic conditions along the length of the aorta, and this is thought to contribute to the predilection of aneurysms to form in the distal aorta.25) One of the most significant differences is between the resting aortic WSS in the suprarenal and infrarenal segments of the aorta.25) In the suprarenal aorta, flow is anterograde and laminar throughout the entire cardiac cycle, providing continuous, directed WSS. In the infrarenal aorta, flow is anterograde at the beginning of the cardiac cycle, however, toward the end of systole and throughout diastole, there is reverse, recirculating flow and low, oscillating WSS.25) (Fig. 2)

Bottom Line: Current concepts on pathogenesis and hemodynamics were collected and compared.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurosurgery, New York University School of Medicine, 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.

No MeSH data available.


Related in: MedlinePlus