The pathogenesis of intracranial aneurysms remains complex and multifactorial. While vascular, genetic, and epidemiological factors play a role, nascent aneurysm formation is believed to be induced by hemodynamic forces. Hemodynamic stresses and vascular insults lead to additional aneurysm and vessel remodeling. Advanced imaging techniques allow us to better define the roles of aneurysm and vessel morphology and hemodynamic parameters, such as wall shear stress, oscillatory shear index, and patterns of flow on aneurysm formation, growth, and rupture. While a complete understanding of the interplay between these hemodynamic variables remains elusive, the authors review the efforts that have been made over the past several decades in an attempt to elucidate the physical and biological interactions that govern aneurysm pathophysiology. Furthermore, the current clinical utility of hemodynamics in predicting aneurysm rupture is discussed.
Keywords: AR = aspect ratio; BA = basilar artery; CFD = computational fluid dynamics; ECM = extracellular matrix; IA = intracranial aneurysm; IEL = internal elastic lamina; IL = interleukin; IgG = immunoglobulin G; IgM = immunoglobulin M; MCP = monocyte chemoattractant protein; MMP = matrix metalloproteinase; MRA = MR angiography; MWSS = maximum WSS; NO = nitric oxide; OSI = oscillatory shear index; SMC = smooth-muscle cell; SR = size ratio; TNF = tumor necrosis factor; VCAM = vascular cell adhesion molecule; VSMC = vascular SMC; WSS = wall shear stress; WSSG = WSS gradient; cerebral aneurysm; computational fluid dynamics; hemodynamics; vascular remodeling; wall shear stress.