Biomedical Engineering Reference
In-Depth Information
In some cases, the arterial wall can remodel 5 itself by increasing its external
diameter to accommodate a plaque without narrowing the lumen, producing angio-
graphic silent plaques detectable only by intravascular ultrasound. In the majority
of cases where this does not occur, the resulting stenosis reduces blood flow to
some degree. Due to a pathological remodelling of the arteries, a relationship exists
between localization of atherosclerotic lesions and haemodynamics.
The preferred surgical intervention for atherosclerosis is balloon angioplasty,
which is quick and involves minimal risk. It involves a small catheter with an inflat-
able balloon inserted into the femoral artery and guided to the stenosis by angiogra-
phy. Inflation of the balloon then crushes the stenosis. Healing entails proliferation
of smooth muscle cells followed by the deposition of new collagen (Davies 1996)
thus thickening the cap and reducing the risk of thrombus formation, as well as
pushing the plaque into the wall thereby increasing blood flow.
2.3.2
Calcification of Lesions in Plaque
Atherosclerosis constitutes a high number of deaths related to cardiovascular dis-
eases in developed countries. It is a chronic systemic disease, frequently leading to
vascular morbidity and premature mortality. Atherosclerosis causes the thickening
and hardening of arteries by lining the arterial wall with fatty deposits, which results
in plaque build-up or atheroma. Three main components (the atheroma, cholesterol,
and calcification) form an atheromatous plaque.
Although atherosclerosis is systemic, plaque rupture is local and leads to acute
cardiac syndromes such as ischemia and myocardial infarction or cerebrovascular
events. Plaque material and structural characteristics are important factors in the
natural progression of the disease and may have important clinical predictive value.
Atherosclerotic stenoses are the main cause of stable angina. Plaque rupture can
lead to the formation of a thrombus that blocks blood flow to the heart leading to
unstable angina or myocardial infarction. Plaques with large atheromatous cores,
thin fibromuscular caps and inflamed caps are particularly vulnerable regardless
of the degree of stenosis. There is some speculation that wall shear stress leads to
luminal thinning and promotes plaque rupture although there are also questions
about whether high haemodynamic shear alone would disrupt a stenotic plaque as
haemodynamic stresses are usually much smaller than mechanical stresses imposed
by blood and pulse pressures.
Calcified lesions most likely represent atherosclerosis at later stages of remodel-
ling and may reflect more stable lesions (O'Rourke et al. 2000). However, early
stages of atherosclerosis that do not contain calcium deposits may be more prone to
rupture with subsequent occurrence of acute events (Schuijf et al. 2007).
Non- or less-invasive imaging can identify flow-limiting coronary stenosis (Meij-
boom et al. 2008), detect plaque components, measure atherosclerotic plaque burden
5 Artery remodelling is a permanent change in the walls in response to long-term inflammation or
obstruction in the vessel walls.
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