Abdominal aortic hemodynamic conditions in healthy subjects aged 50–70 at rest and during lower limb exercise: in vivo quantification using MRI

Abstract

The prevalence of atherosclerosis in the abdominal aorta increases with age and is hypothesized to be related to adverse hemodynamic conditions including flow recirculation and low wall shear stress. Exercise has been shown to modulate these adverse conditions observed in the infrarenal aorta of healthy young subjects at rest. A custom magnetic resonance (MR)-compatible stationary cycle, an open MRI, and custom image processing software were used to quantify hemodynamic conditions in the abdominal aorta at rest and during cycling exercise in healthy subjects aged 50–70 years. The subjects increased their heart rate from 63±8 bpm at rest to 95±12 bpm during cycling exercise. Supraceliac blood flow increased from 2.3±0.4 to 6.0±1.4 l/min (P<0.001) and infrarenal flow increased from 0.9±0.3 to 4.9±1.7 l/min (P<0.001) from rest to exercise. Wall shear stress increased from 2.0±0.7 to 7.3±2.4 dynes/cm² at the supraceliac level (P<0.001) and 1.4±0.8 to 16.5±5.1 dynes/cm² at the infrarenal level (P<0.001) from rest to exercise. Flow and shear oscillations present at rest were eliminated during exercise. At rest, these older subjects experienced lower mean wall shear stress at the supraceliac level of the aorta and greater oscillations in wall shear stress as compared to a group of younger subjects (23.6±2.2 years). Compared to the younger subjects, the older subjects also experienced greater increases in mean wall shear stress and greater decreases in wall shear stress oscillations from rest to exercise.

Introduction

It is well known that the incidence and severity of vascular disease increases with age. For example, approximately 80% of Americans who die from coronary artery disease are of the age 65 or older [1]. Cases of stroke, congestive heart failure, and peripheral atherosclerosis are more frequent as age increases [2]. It has been hypothesized that the correlation of chronic inflammatory disease and accumulation of plaque with old age is related to changes in the biology of arterial tissue, vascular anatomy and physiology, and local hemodynamic conditions.

Biologic, anatomic and physiologic changes due to age have been observed in the vascular system. Arteries become thicker, stiffer, and hence less distensible with age [3], [4], [5], [6], [7], [8]. Aside from arterial stiffening caused directly by atherosclerosis, arterial elastin fibers degrade while the collagen fibers, which are less distensible than elastin, support an increasingly greater proportion of load [3]. This loss of load-bearing from the elastin fibers also causes vessel dilation [7], [8]. In terms of arterial wall physiology, endothelium-derived nitric oxide, which has been hypothesized to be an atheroprotective agent which prevents vasoconstriction and platelet activation, has been shown to be released more slowly and in lower concentration in the aortas of old rats as compared to young rats [5].

Variations in hemodynamic conditions due to age have also been studied in the vasculature. In the aorta, age negatively correlated with peak velocity and peak acceleration of blood flow, measured by Doppler ultrasound, for both rest and lower limb exercise states [7]. Since peak velocities are correlated with blood flow rate and arterial wall shear stress, and flow rate and shear stress have been shown to affect the localization of atherosclerosis [9], [10], [11], [12], hemodynamic differences between young and older populations may be important. In particular, it has been hypothesized that flow recirculation, low mean wall shear stress, and oscillations in shear stress can cause localization of atherosclerotic lesions in regions of complex flow sites in the carotid bifurcation, coronary arteries, and abdominal aorta [9], [10], [11], [12].

In contrast to the effects of low blood flow and wall shear stress, elevated flow and shear stress induce direct cellular structural changes including cell elongation in the direction of maximum stress and results in inhibition of atherosclerosis [13]. We have shown that light to moderate lower limb exercise (150% of rest heart rate) increases mean blood flow and wall shear stress in the infrarenal aorta of healthy, young subjects (aged 23.6±2.2 years) by approximately six- and four-fold, respectively [14]. Furthermore, oscillations in flow and wall shear stress present at rest are eliminated during lower limb exercise for young, healthy subjects [14]. It is hypothesized that due to biologic changes that occur in the arteries initiated by increased fluid mechanical forces, even short bouts of exercise may influence vascular health after the cessation of physical activity [13], [15], [16], [17].

Although peak blood flow velocities have been compared in the aortas of young and older subjects, direct measurements of volume flow and wall shear stress have not been performed. In this study we focus on the hemodynamic environment of the abdominal aorta, which is a more disease-prone location as compared to the thoracic aorta [18], [19]. With cine phase-contrast magnetic resonance imaging (cine PC-MRI) techniques [20] in a 0.5 T open MRI (GE Signa SP, GE Medical Systems, Milwaukee, WI), in combination with a custom MR-compatible stationary cycle, we have measured, in vivo, the spatial distribution of axial blood flow velocities in the abdominal aortas of healthy human subjects aged 50–70 at rest and during cycling exercise conditions. With these data, we compute volume flow, wall shear stress, and lumen cross-sectional area at the supraceliac and infrarenal levels of the aorta, and compare these quantities with those measured in young, healthy subjects at rest and during exercise conditions.