The Heart - Biofluidmechanics: An Introduction to Fluid Mechanics Macrocirculation and Microcirculation - page 120

beds and that the heart requires a large quantity of blood at all times, any cholesterol
deposition within the coronary blood vessels is potentially a major problem for the
patient.
After cholesterol deposition occurs, there are a few processes that proceed in parallel.
The first process that can happen is that cholesterol molecules can coalesce to form larger
deposits. As this is occurring, macrophages can invade the sub-endothelial space to ingest
the cholesterol deposits. Macrophages that ingest a large quantity of cholesterol transform
into foam cells that are basically cells full of fat/cholesterol. Generally, foam cells are large
in size and they cannot migrate out of the sub-endothelial space. Along with these two
processes, fibrous tissue and smooth muscle cells (that both naturally surround the blood
vessels) begin to proliferate and sometimes can become calcified. The net result of these
three processes (cholesterol coalesce, foam cell production, and cell proliferation) is that a
plaque forms that extends into the blood vessel lumen. A blockage in the vessel lumen
decreases blood flow, because the resistance to flow increases. If the blood vessel becomes
calcified, it becomes less pliant, hence more brittle, and if it is severe enough, the vessel
potentially cannot withstand the normal pressure forces exerted by the fluid. This can lead
to the vessel bursting.
Atherosclerosis development is very common in the first few centimeters of the coro-
nary arteries. This is most likely caused by the three-dimensional structure of the coronary
arteries ( Figure 4.14 ). Immediately after branching from the aorta, there is a high degree of
tortuosity (twists/bends) and tapering within the coronary vessels. Because the blood flow
in these vessels is very fast, these rapid geometric changes induce turbulence with the
blood vessel. Regions of turbulence are characterized by flow separation, stagnation
points, and recirculation zones, in which the flow rate is reduced, allowing cholesterol
enough time to migrate into the sub-endothelial space.
Reduced blood flow throughout the coronary vessels is devastating to the muscle mass
of the heart (see Section 4.6.2 ). However, if the blockage is not severe enough or if it pro-
gresses slowly enough, the coronary arterioles can protect the heart tissue for some time.
At the time of a blockage, the dilation of the downstream coronary arterioles can counter-
balance the flow restriction for approximately 24 to 48 hours. For a long-term solution, the
coronary collateral circulation will need to adapt and supply the under-nourished tissue
with blood. The collateral circulation of the coronary vessels allows for a large redundancy
of flow to one particular region of cardiac muscle, meaning that at a minimum two large
arterioles supply the same capillary bed with blood. If one of these arterioles is blocked,
the second arteriole (and potentially others in the vicinity) will remodel so that the blood
flow to that region returns to 100% of the normal value. In most cases, atherosclerotic
lesions progress slowly enough to allow for a dilation of downstream arterioles and a
remodeling of collateral vessels to occur. These two processes potentially allow a patient
with a coronary lesion to survive for years after the onset of the disease.
4.6.2 Myocardial Infarction
One of the immediate effects of a blocked coronary artery is decreased blood flow into
the region downstream of the blockage. If the muscle that is being supplied by the blocked