the Vascular System
Numerous modeling and experimental studies have been proposed to
investigate the fluid mechanical factors contributing to atherosclerosis.
Car0 et a]. (1971)
were earlier investigators to identify
atherogenesis as regions
reduced wall shear stress and suggested that
the transport of lipoprotein within the arterial wall and across the
major factor in atherosclerosis.
atherosclerotic sites have been illustrated by DeBakey
al. (1985) as
shown in Fig. 5.2.8.
Numerical simulation to predict some
branching sites has been carried in a two-dimensional simulation (Lei et
al., 1995). Friedman (1989) used a model to explain the thickening
arterial intima under shear. Thurbrikar and Robicsec (1995) suggested
the importance of pressure-induced arterial wall stress as an important
factor in atherosclerosis.
Stenosis, or the narrowing
the blood vessel,
associated with a
serious hemodynamic consequence
that develops across
the stenosis. The pressure
is primarily dependent on the flow rate
and the geometry of the stenosis, since the fluid properties of density
and apparent viscosity are relatively constant.
equation for a pressure-drop was first introduced by means
in-vitro steady flow tests utilizing constrictions in the
form of blunt-ended hollow plugs (Seely and Young, 1976).
Arteries with severe stenoses caused by atherosclerotic plague growth
may collapse under physiological conditions (Aorki and Ku, 1993).
Artery collapse is a process where an artery buckles under certain
pressure and stress conditions.
The compression resulting from this
collapse may lead to accelerated fatigue and rupture of the fibrous cap,
which contains the plague. The plague rupture can lead directly to heart
and stroke if occurring in coronary
respectively. It is known that local stenosis formed by an atherosclerotic
lesion may cause mechanical conditions favorable for artery collapse.
Plague fatigue and distal embolization are also important considerations.
Blood flow must accelerate to high velocities in the narrowed
stenosis. The high velocities in turn create a low or negative transmural
pressure, which can result in collapse
high velocities at the stenosis also generate high shear stresses, which
may be related to plague cap rupture and platelet activation (Tang et a].,