Hanyang Med Rev.  2006 May;26(2):4-10.

Pathophysiology of Atherosclerosis

• Park JE

Abstract

In humans, early lesions of atherosclerosis, fatty streaks, already begin to be observed from the twenties. In animals grown in nature, atherosclerosis is not known to exist and serum cholesterol levels in the animals are lower than 100mg/dL. Recent clinical trials suggest that if we lower the LDL cholesterol to below 40mg/dL, we can probably halt the progression of atherosclerosis. Atherosclerosis can either progress or regress according to the control of risk factors. If the risk factors are not well controlled, the pressure in the core can be increased and the cap weakens because of the infiltration of macrophages and foam cells instead of healthy smooth muscle cells and the matrix metalloprotenases secreted from these cells weakens the collagen. Acute coronary syndrome results when rupture or erosion occurs in the cap. Recently, atherosclerosis is understood as an inflammatory process, because the infiltrating cells, inflammatory cytokines and T-cells are very much similar to the other inflammatory lesions such as rheumatoid arthritis. Endothelial dysfunction, lipid oxidation and insulin resistance are also the main abnormal findings observed from the early stages of atherosclerosis. HMG Co-A reductase inhibitors can effectively prevent and regress atherosclerosis and is now very widely prescribed for these purposes.

Keyword

Atherosclerosis; Pathogenesis; Inflammation; Plaques; Statins

MeSH Terms

Acute Coronary Syndrome
Animals
Arthritis, Rheumatoid
Atherosclerosis*
Cholesterol
Cholesterol, LDL
Collagen
Cytokines
Foam Cells
Humans
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Inflammation
Insulin Resistance
Macrophages
Myocytes, Smooth Muscle
Oxidoreductases
Risk Factors
Rupture
T-Lymphocytes
Cholesterol
Cholesterol, LDL
Collagen
Cytokines
Oxidoreductases