Aortic stiffness, pressure and flow pulsatility, and target organ damage

Abstract

Measures of aortic stiffness and pressure and flow pulsatility have emerged as correlates of and potential contributors to cardiovascular disease, dementia, and kidney disease. Higher aortic stiffness and greater pressure and flow pulsatility are associated with excessive pulsatile load on the heart, which increases mass and reduces global longitudinal strain of the left ventricle. Excessive stiffness and pulsatility are also associated with microvascular lesions in high-flow organs, such as the brain and kidney, suggesting that small vessels in these organs are damaged by pulsatility. This brief review will summarize evidence relating aortic stiffness to cardiovascular, brain, and kidney disease.

Keywords: aorta; cardiovascular disease; chronic kidney disease; dementia; hemodynamics; pulsatility index.

Fig. 1.

Proximal aortic “spring” plays a critical role in normal systolic and early diastolic function of the left ventricle (LV). The aortic arch and cardiac apex are relatively fixed during the cardiac cycle (dashed lines). In addition, total heart volume is nearly constant throughout the cardiac cycle (blue containers) because of pericardial constraint (only the left heart is shown for clarity). During systole, LV long axis shortening (global longitudinal strain) pulls the base of the heart (dotted lines) toward the apex (red arrow). This atrioventricular plane displacement ejects blood from the LV (middle; thick, black arrow) but also fills the left atrium (thin, black arrows) and stretches and stores energy in the walls of the proximal aortic spring. During diastole (right), recoil of the aortic spring pulls the base of the heart upward (green arrow), which translocates a volume of blood from the left atrium into the LV (pink disk), because of motion of the atrioventricular plane alone, but also stretches and thins the walls of the LV, creating suction that facilitates early diastolic filling (thick, black arrow). [Reprinted by permission from Springer Nature Current Hypertension Reports (c) 2015 Bell and Mitchell (9).]

Fig. 2.

Impedance matching in the cerebrovasculature. Top: a simple model of the aorta and cerebrovascular circuit. To facilitate calculation of the reflection coefficient, local properties are expressed as the admittance, which is the reciprocal of local characteristic impedance. Aortic admittance (A_Prox) is coupled to a lumped bilateral carotid admittance (A_Car) and distal aortic admittance (A_Dist). The reflection coefficient (RC) at this interface is RC = (A_Prox – A_Car – A_Dist)/(A_Prox + A_Car + A_Dist). Disproportionate stiffening of the proximal aorta reduces proximal admittance (A_Prox) and thereby reduces wave reflection. Bottom: a reduction in local wave reflection is associated with a reciprocal increase in the pulsatility of the flow waveform entering the carotid circulation. [Bottom is modified from Mitchell et al. (67) by permission of Oxford University Press.]

Fig. 3.

Relations among aortic stiffness, renal artery flow pulsatility, and kidney structure and function. In the older Age, Gene/Environment Susceptibility-Reykjavik Study cohort, there was a relation between carotid-femoral pulse-wave velocity (CFPWV) and measured glomerular filtration rate (GFR). The total effect for the relation between CFPWV and GFR was −2.28 ml/min per SD. Mediation analysis demonstrated that most of the effect was attributable to indirect effects mediated through excessive renal artery flow pulsatility index (PI), which damages small vessels, leading to loss of arterial volume in the cortex (AVC; A) or an increase in renal vascular resistance (RVR; B), accounting for 54% and 70% of the total effect, respectively. CI, confidence interval. [Modified from Woodard et al. (100) with permission.]

Fig. 4.

Relations between aortic stiffness and incident cardiovascular disease (CVD). A: relations between carotid femoral pulse-wave velocity (CFPWV) and a first major CVD event. B: the prevalence of CFPWV > 12 m/s, which corresponds to the highest quartile group in A. [Modified from Mitchell et al. (63, 64) with permission of Wolters Kluwer Health, Inc.]