Article Figures & Data
Figures
- Fig 1.
Examples of aneurysm growth (A and B) and rupture (C and D) correlated with high wall shear stress and low WSS. A, In a serial study consisting of a baseline and 4 follow-ups, Acevedo-Bolton et al10 found that the maximal growth region (1) of a giant basilar fusiform intracranial aneurysm consistently had the lowest WSS. B, Sugiyama et al13 reported 2 adjacent growing aneurysms, with different hemodynamic characteristics and growing patterns in 1 patient. The proximal growing aneurysm (2) was subjected to local high flow in the growing lobe, while the distal aneurysm (3) was associated with low and oscillatory WSS in the entire aneurysm sac. C, From multivariate statistical analysis of 119 aneurysms, Xiang et al5 found that intracranial aneurysm rupture could be predicted by low WSS and high oscillatory shear index. D, Castro et al11 found, from analysis of 26 aneurysms, that intracranial aneurysm rupture was correlated with high maximum WSS. Images were adapted with permission from the cited references.
- Fig 2.
How hemodynamics plays into intracranial aneurysm dynamics. A, Three-way relationship of aneurysmal geometry, flow, and pathobiology. Flow exerts mechanical forces on the vessel wall, eliciting cell-mediated biologic pathways. Sustained changes in flow (thus WSS and pressure) lead to remodeling of the wall, resulting in aneurysm geometry change. In turn, geometry determines the flow, which could drive further biologic processes. B, The balance between growth/repair and degradation/destruction results in aneurysm stability. Aberrant hemodynamics disrupts the balance and amplifies degradation and destruction mechanisms, leading to enlargement and rupture of aneurysm.
- Fig 3.
Heterogeneity of saccular aneurysms as a spectrum from type I (A) to type II (D) with various intermediate or combination types in between (B and C). A, A small thin-walled, entirely translucent aneurysm (type I). B, A mostly thin-walled aneurysm with some thicker-walled patches. C, A mostly thick-walled aneurysm with a few thin-walled patches. D, An aneurysm with an entirely thick, atherosclerotic wall (Type II). Images adapted with permission from Kadasi et al 2012.50
- Fig 4.
A unified role of high and low WSS in aneurysm initiation, growth, and rupture.
- Fig 5.
Two hypothesized, independent, hemodynamic-biologic pathways that drive intracranial aneurysm growth and rupture (A) and the proposed relationship between them and the spectrum of intracranial aneurysm phenotypes (B).
Tables
Vascular responses to aberrant WSS conditions reported in literature
Pathobiologic Responses to High WSS and Positive WSS Gradienta Pathobiologic Responses to Low WSS and High OSIb EC damage24,45 Proinflammatory ECs that are “leaky” and “sticky”21,62 EC turnover25,72 Increased ROS62 MMP production by mural cells25 Increased inflammatory cell infiltration70 ECM degradation36 MMP production by macrophages61 Medial thinning36 SMC proliferation and migration63 Mural cell apoptosis25 Thrombus formation23,63
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