Dp. Giddens et al., THE ROLE OF FLUID-MECHANICS IN THE LOCALIZATION AND DETECTION OF ATHEROSCLEROSIS, Journal of biomechanical engineering, 115(4), 1993, pp. 588-594
Fluid dynamics research over the past twenty years has contributed imm
ensely to our knowledge of atherosclerosis. The ability to detect loca
lized atherosclerotic plaques using noninvasive ultrasonic methods was
advanced significantly by investigations into the nature and occurren
ce of velocity disturbances created by arterial stenoses, and diagnosi
s of carotid bifurcation disease using a combination of ultrasonic ima
ging and Doppler measurement of blood velocity is now quite routine. S
ince atherosclerotic plaques tend to be localized at sites of branchin
g and artery curvature and since these locations would be expected to
harbor complex flow patterns, investigators postulated that fluid dyna
mics might play an initiating role in atherogenesis. Several fluid dyn
amic variables were proposed as initiating factors. Investigations wer
e undertaken during the 1980s in which fluid dynamic model experiments
with physiologic geometries and flow conditions were employed to simu
late arterial flows and in which morphometric mapping of intimal thick
ness was performed in human arteries. Correlations between fluid dynam
ic variables and intimal thickness revealed that atherosclerotic plaqu
es tended to occur at sites of low and oscillating wall shear stress,
and these observations were reinforced by studies in a monkey model of
atherosclerosis. Concomitantly, it was realized that arteries adapt t
heir diameters so as to maintain wall shear stress in a narrow range o
f values around 15 dynes/cm2, findings which were based both on observ
ations of normal arteries and on animal studies in which flow rates we
re manipulated and arterial diameter adaptation was measured. Currentl
y, a working hypothesis for the role of fluid dynamics in atherogenesi
s is that intimal thickening is a normal response to low wall shear st
ress, and this intimal thickening can develop into an early atheroscle
rotic plaque under certain circumstances such as excessive low density
lipoprotein concentrations in blood.