Evaluation of the Link Between Carotid Arterial Wall Viscosity and Major Neurocognitive Disorders

The mechanical behavior of conductance arteries is viscoelastic. While the elastic component has been extensively studied, the viscous component has often been neglected for methodological reasons and also because it was considered weak. Unlike a purely elastic solid, which exhibits instantaneous deformation/relaxation upon application/discontinuation of a force, a viscoelastic solid is characterized, from a mechanical point of view, by a delay between the application or discontinuation of the force and deformation. Thus, at the arterial level, the elasticity of the arterial wall allows the internal diameter to increase proportionally to the blood pressure during systole. The viscous component will induce a delay in diameter restoration, resulting in a larger diameter at each pressure level during the diastolic phase compared to the systolic phase. This results in a shift between the systolic and diastolic curves of the pressure-diameter relationship, creating a hysteresis loop. From a thermodynamic point of view, while a purely elastic material fully restores the energy stored during the loading phase, viscoelastic arteries will incompletely restore this energy. Thus, the surface of the hysteresis loop reflects the energy dissipated during each cardiac cycle (WV), and the area under the loading phase curve represents the energy stored by the arterial wall (WE) during the latter. Thus, arterial wall viscosity (APV) can be expressed either as the absolute value of WV or as a function of the stored energy (WV/WE). Physiologically, this energy loss is low. Its increase could be accompanied by excessive energy dissipation, leading to increased cardiac work and cardio-circulatory decoupling. Conversely, low parietal viscosity could lead to damage to peripheral organs by excessive transmission of pulsatile energy to the periphery due to lack of damping.

Preliminary work in the laboratories has highlighted the role of vaso-relaxing endothelial factors and smooth muscle tone in the regulation of the Arterial Pulse Rate (APR) of the radial artery in the basal and stimulated state and the alteration of this stimulated regulation during Arterial Hypertension (AH). Furthermore, a decrease in relative carotid APR in middle-aged subjects compared to young subjects, and an increase in carotid APR in diabetic patients has been found in unpublished results. The link between aortic arterial stiffness and the existence of vascular dementia but also Alzheimer's is strongly suggested. Indeed, the increase in arterial stiffness could be responsible for an increase in pulsatility transmitted to the brain, participating in the accumulation of beta amyloid proteins. A probable inflammatory and oxidative stress component could also have an added deleterious role through the production of free radicals. Thus, previous studies have shown the existence of a link between arterial stiffness and the presence of leukoaraiosis, lacunae, microbleeds but also with brain volume and the progression of cerebral atrophy. These repercussions on the cerebral parenchyma are visible on MRI. A link has also been suggested between increased arterial stiffness and impaired cognitive function (as demonstrated by neurocognitive tests) or the presence of markers of small vessel damage in neuroimaging (microbleeds, lacunae, leukoaraiosis). One hypothesis to explain this link is that arterial stiffness promotes impaired hippocampal microcirculation. Other studies have shown that carotid-femoral pressure wave velocity (CFV), a marker of large arterial stiffness, was higher in populations with Alzheimer's disease and vascular dementia than in older populations without cognitive impairment or with minor neurocognitive impairment. However, no studies have evaluated the link between baseline VPA and vascular dementia or Alzheimer's disease. Our study suggests that carotid VPA is associated with increased cerebrovascular injury, impaired cognitive testing, and the diagnosis of vascular dementia.