Arterial Calcification Alters Lumen Surface Roughness of Branches of the Circle of Willis

Atherosclerotic lesions within carotid and cerebral vessels are likely to influence hemodynamics and manifest into vascular pathologies, including Alzheimer's Disease and ischemic stroke. Hemodynamics are influenced by changes in luminal diameter of vessels and wall shear stress derived from vortex formation which directly relates to the surface topography of the lumen. In this study, we performed a quantitative assessment of surface metrology of carotid and cerebral arteries in relation to calcification, vessel size and location among individuals. We speculate intracranial vessels will follow suit of extracranial vessels, with increased surface roughness in larger-diameter vessels. Samples of the internal carotid, common carotid, and multiple branches of the Circle of Willis were collected at 18 different sites from 10 human whole body donors. For each vessel, arterial calcification was quantified from image analyses of Alizarin red stained histological sections. The arterial surface metrology of the adjacent parts of the same segments was opened and gently cleaned, and then analyzed using a Sensofar S Neox 3D optical profiler, from which scale-sensitive fractal analyses (SSFA) were analyzed using SensoMap software. ANOVAs testing for the influence of calcification percentage, vessel identity, vessel size, individual differences, age, sex, and the role of cardiovascular disease in the donor's cause of death found no significant differences in SSFA variables for vessel identity, individuals, age, sex, and cause of death. The most significant differences are correlated with vessel calcification percentage, though surface roughness appears also greater in the larger vessels. These findings support ideas that calcification plays a role in alterations of vortex formation and wall shear stresses in intracranial vessels as they do in coronaries. With further research in this field, the pathophysiology of intracranial atherosclerosis and the role of atherosclerosis in neurodegenerative disorders might be understood at another, more granular level.