Biomedical Engineering Reference
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event triggering myocardial infarctions and acute coronary syndromes. The fail-
ure of the cap exposes collagen and lipid to the blood stream, which subse-
quently causes thrombus formation [48], often resulting in partial or complete
blockage of the vessel. The exact mechanisms responsible for plaque rupture
are unknown.
Finite element analyses of idealized plaque geometries have suggested that,
for eccentric plaques, maximum stress levels occur at the shoulder area of the
cap where the fibrous cap meets the healthy intima [49, 50]. Finite element anal-
yses using model geometries based on atherosclerotic lesions indicate that the
areas of high stress in and near the plaque correlate with the locations of plaque
rupture. Fifty-eight per cent of in vivo plaque ruptures have been found to occur
in the areas of maximum stress, while 83% of failures occurred in high stress
areas [51]. FE studies have suggested that decreased cap thickness causes an in-
crease in the peak shoulder stress when fully developed lipid layers are present.
Similarly, increasing the lipid layer size increases the shoulder stress. [52-54].
Reliable predictions of stress and strain in physiologically loaded plaques
in vivo would provide insight into plaque mechanics. Direct measurement of
stress during loading of a coronary artery is currently not possible in vivo or ex
vivo . However, the measurement of strain within the plaque and the wall of the
coronary artery can provide an insight into the stress distribution.
Intravascular ultrasound (IVUS) yields detailed images of atherosclerotic
plaques and the vessel wall. IVUS uses a catheter-mounted ultrasound transducer
to acquire cross-sectional images of an artery with a spatial resolution of 80-100
µ m radially and 150-200 µ m circumferentially [55, 56]. Current IVUS catheters
are as small as 0.9 mm and can interrogate most areas of the coronary tree,
including coronary arteries in the range of 1.5-5.0 mm in diameter. IVUS provides
a high resolution means to quantify lesion geometry [55, 56]. Our long-term
goal is to use Hyperelastic Warping to determine the strain distributions within
coronary plaque both ex vivo and in vitro during physiological loading as well
as the loading associated with interventional techniques such as angioplasty
and stent placement. The strain distributions can be correlated with the plaque
histology to determine which plaque cap components are associated with the
largest strain during loading. Hyperelastic Warping has been validated for use
with IVUS and the details may be found in our previous publication [39].
Hyperelastic Warping was used to estimate the strain distributions in two
unfixed left anterior descending (LAD) human coronary arteries. These arteries
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