Atherosclerosis, the process by which plaque forms in the arteries, has been described much like a plumbing problem. Cholesterol, which is a solid fat, gradually builds up on the walls of the arteries, eventually forming plaques that cause problems with blood flow, which causes the heart or brain to be starved of oxygen causing a heart attack or stroke. While there is no doubt that cholesterol levels are a major contributing factor to heart and blood vessel diseases, research has firmly established that inflammation plays a key role in heart disease.

Inflammation is the process by which our bodies fight infection and repair tissue damage, both positive roles. When involved in atherosclerosis and autoimmune diseases, inflammation proves harmful. The role of inflammation may help to explain why many heart attacks occur without warning and why preventative measures often fail to prevent heart attacks or strokes.

Low density lipoprotein (LDL), known as LDL, is produced to move cholesterol from the liver, where cholesterol is made, and the intestine, where it is absorbed, to organs where cholesterol is used to make new cells and hormones. Trouble begins when excess LDL in the blood begins to accumulate in the cells lining the walls of arteries, known as the intima. At normal levels in the blood, LDL can pass in and out of the intima with no problem. In excess, LDL accumulates in the intima matrix. As LDL accumulates it begins to oxidize, which triggers an inflammatory response. Chemicals are released that attract immune system cells to scavenge the LDL. This process causes a fibrous cap to form over the plaque. Autopsies have shown that only about 15% of heart attacks are caused by large plaques that block arteries; most heart attacks occur after a plaque's fibrous cap ruptures causing a blood clot to form over the break. This description helps to explain why many heart attacks occur without warning. Plaques that rupture may not protrude very far into the blood vessel so do not restrict blood flow. This process may also explain why bypass surgeries, angioplasty and stents often fail to prevent heart attack. As a matter of fact, these procedures may actually increase inflammation.

Other risk factors may contribute to the role inflammation plays in a heart attack. Smoking, for example, accelerates oxidation, which can cause inflammation in people even with normal LDL levels.

The role inflammation plays in heart attack and stroke is now a focus of research. Research is aimed at identifying vulnerable plaques and genetic markers that indicate risk of developing atherosclerosis and chronic inflammation. Scientists strive for a deeper understanding of the intricate that drive the inflammatory process in the arteries.

Reference: http://www.dentalcare.com/soap/products/pdfs/owbh_03.pdf

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