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The most common cause of death and disability in the United States is atherosclerosis, popularly known as "hardening of the arteries."
Every year atherosclerosis causes about 500,000 deaths nationally, most of these due to heart attack or stroke. There are about 15 million people in the United States suffering from atherosclerosis, and another 60 million are at risk. The factors that put individuals at risk of atherosclerosis include high blood levels of cholesterol and sugar, high blood pressure, and tobacco use. Another important risk factor is a family history of premature atherosclerosis (e.g., a close relative who has had a heart attack or stroke under the age of sixty). In addition to these risk factors, there is accumulating evidence that elevated plasma levels of lipoprotein (a), C-reactive peptide, asymmetric dimethylarginine, and homocysteine also accelerate atherosclerosis, as do obesity, type A personality, and sedentary lifestyle.
Atherosclerosis is thought to be initiated by a "response to injury" of the endothelium (the lining of the blood vessel). Elevated blood levels of cholesterol or glucose, as well as high blood pressure and smoking, cause changes in the endothelium (normally the "teflon" coating of the vessel), which then becomes sticky. It begins to express on its surface "adhesion molecules," which are a bit like cellular velcro. It also expresses "chemokines" which are proteins that attract white blood cells into the vessel. White blood cells (specifically monocytes and T-lymphocytes) begin to stick to the lining of the vessel, and to infiltrate the vessel.
The monocytes migrate into the vessel wall, where they begin to accumulate cholesterol. They become engorged by cholesterol in the vessel wall and become foam cells. As foam cells accumulate in the vessel they distort the overlying endothelium (forming a "fatty streak" in the vessel), and they eventually may even rupture through the endothelial surface. In these areas of endothelial ulceration, platelets adhere to the vessel wall, releasing molecules that stimulate smooth-muscle migration and proliferation. Vascular smooth-muscle cells in the vessel wall proliferate and migrate into the area above the foam cells. The smooth-muscle cells may also become engorged with lipid to form foam cells, and atherosclerotic plaque begins to take form. The plaque grows with the recruitment of more cells, and with the accumulation of matrix made by the cells and cholesterol from the bloodstream. The progression of atherosclerotic plaque is also related to the growth
Author Info: JOHN P. COOKE, The Gale Group Inc., Macmillan Reference USA, New York, Gale Encyclopedia of Public Health, 2002
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