Effect of a reduced arterial axial pre-stretch ratio during aging on the cardiac output and cerebral blood flow in the healthy elders.

Background And Objective: It is an indisputable physiological phenomenon that the arterial axial pre-stretch ratio (AAPSR) decreases with age, but little attention has been paid to the effect of this reduction on chronic diseases during aging.

Methods: Here we reported an experimental method to simulate arteries aging, developed a fluid-structure interaction model with the effect of AAPSR changes, and compared it with the anatomy data and structural parameters of the human thoracic aorta.

Results: We showed that with the process of aging, the decrease of AAPSR leads to a decline of arterial elasticity, a decrease of arterial elastic strain energy, which weakens the ability to promote blood circulation, the corresponding decrease in cardiac output (CO) and cerebral blood flow (CBF) causes distal organ and body tissue ischemia, which is one of the main causes of increased blood pressure and decreased cerebral perfusion in the elderly.

Quantitative analysis of systemic perfusion and cerebral blood flow in the modeling of aging and orthostatic hypotension.

Orthostatic hypotension (OH) is common among the older population. The mechanism hypothesized by OH as a risk factor for cognitive decline and dementia is repeated transient cerebral blood flow deficiency. However, to our knowledge, quantitative evaluation of cardiac output and cerebral blood flow due to acute blood pressure changes resulting from postural changes is rare.

A fluid-structure interaction model accounting arterial vessels as a key part of the blood-flow engine for the analysis of cardiovascular diseases.

According to the classical Windkessel model, the heart is the only power source for blood flow, while the arterial system is assumed to be an elastic chamber that acts as a channel and buffer for blood circulation. In this paper we show that in addition to the power provided by the heart for blood circulation, strain energy stored in deformed arterial vessels can be transformed into mechanical work to propel blood flow. A quantitative relationship between the strain energy increment and functional (systolic, diastolic, mean and pulse blood pressure) and structural (stiffness, diameter and wall thickness) parameters of the aorta is described.