Atherosclerosis is a disease of the arterial wall. Susceptible sites of the artery become
stenosed by lipid retention. This lipid retention causes arthersclerotic lesions that can cause
ischemia which can trigger occlusions of major conduit arteries of the heart, brain, legs and other
vital organs. These lesions begin in the inner lining of the arteries and progress eventually
effecting the entire wall. The rate of plaque formation is the same regardless of race, ethnicity, sex
or geographic area. Yet, several risk factors contribute to the development of atherosclerosis at a
faster rate: hypertension, tobacco smoke, diabetes mellitis, obesity, genetic disposition and high
cholesterol.
Atherosclerosis develops over the course of 50
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Theses first changes occur at the
branch points of the arteries.
Early Fibroatheroma: occurs in persons in their teens and 20's. Numerous macrophage foam cells,
other inflammatory cells, and the natural cells of arteries accumulate. Macrophage are responsible
for the plaque development. Fibrous tissue is added over the lipidrich necrotic cores developing
into the dominant lesions
Advancing atheroma: Thincap fibratheroma and its rupture: this stage occur greater than 55 years
of age. This fibrous cap are considered “vulnerable plaque” due to its risk to rupture causing a life
threatening thrombosis.
Complex Lesion development: many of the above thin fibrous cap that have ruptured go
unnoticed. The rupture heals by forming fibrous tissue matrices of cells, collegian fibers, and
extracellular space. These cyclic changes in the ruptures caps may occur and reoccur up to four
times at a single site in the arterial wall. The result of the healing is multiple layers of healed
tissue. Sixty percent of sudden cardiac deaths is know to be caused at the point of the cyclic healing.
Lipid treatment with statins can reduce ones risk factor by 2040%. Treatment