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Atherosclerosis

Atherosclerosis is a disease affecting arterial blood vessel. It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple plaques within the arteries. Pathologically, the atheromatous plaque is divided into three distinct components: more...

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The atheroma ("lump of porridge", from Athera, porridge in Greek,) is the nodular accumulation of a soft, flaky, yellowish material at the center of large plaques, composed of macrophages nearest the lumen of the artery, sometimes with underlying areas of cholesterol crystals and possibly also calcification at the base of older/more advanced lesions.

Arteriosclerosis ("hardening of the artery") results from a deposition of tough, rigid collagen inside the vessel wall and around the atheroma. This increases the stiffness, decreases the elasticity of the artery wall. Arteriolosclerosis (hardening of small arteries, the arterioles) is the result of collagen deposition, but also muscle wall thickening and deposition of hyaline cartilage.

Calcification, sometimes even ossification (formation of complete bone tissue) occurs in the thickest parts of sclerosed vessel wall.

Some sources draw a distinction between "Arteriosclerosis", "Atherosclerosis," and "Arteriolosclerosis". In these contexts, "Atherosclerosis" is used when referring to larger arteries, and "Arteriolosclerosis" is used when referring to arterioles, with "Arteriosclerosis" used as a parent of both terms. Atherosclerosis causes two main problems. First, the atheromatous plaques causes stenosis (narrowing) of the artery and, therefore, an insufficient blood supply to the organ it feeds. This complication is chronic, slowly progressing. A common scenario is claudication from insufficient blood supply to the legs. Second, the soft plaque may suddenly rupture (see vulnerable plaque), causing the formation of a blood clot (thrombus) that will rapidly stop blood flow, leading to death of the tissues fed by the artery. This catastrophic event is called an infarction. The most common scenario is a thrombosis of a coronary artery causing myocardial infarction (a heart attack).

Symptoms

Atherosclerosis typically begins in later childhood, is usually found in most major arteries, yet is asymptomatic and not detected by most diagnostic methods during life. It most commonly becomes seriously symptomatic when interfering with the coronary circulation supplying the heart or cerebral circulation supplying the brain, and is considered the most important underlying cause of strokes, heart attacks, various heart diseases including congestive heart failure and most cardiovascular diseases in general. Atheroma in arm or more often leg arteries and producing decreased blood flow is called Peripheral artery occlusive disease (PAOD).

According to United States data for the year 2004, for about 65% of men and 47% of women, the first symptom of atherosclerotic cardiovascular disease is heart attack or sudden cardiac death (death within one hour of symptom onset).

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B-vitamins reverse carotid atherosclerosis
From Townsend Letter for Doctors and Patients, 12/1/05 by Alan R. Gaby

Fifty patients (mean age, 60 years) with carotid intimamedia thickness (IMT) [greater than or equal to] 1 mm, which is associated with an increased risk of cerebral ischemia, were randomly assigned to receive daily, in double-blind fashion, either 1) 2.5 mg of folic acid, 25 mg of vitamin B6, and 0.5 mg of vitamin B12, or 2) placebo for 1 year. In the active-treatment group, the mean plasma homocysteine concentration decreased from 10.50 to 6.56 micromol/L (p < 0.0001), but remained unchanged in the placebo group (10.76 vs. 10.45 micromol/L). Mean IMT in the active-treatment group decreased from 1.50 to 1.42 mm (p = 0.034), a change suggestive of a regression of atherosclerosis. In contrast, mean IMT increased from 1.47 to 1.54 mm in the placebo group (< 0.02 for the difference in the change between groups).

Comment: In this study, supplementation with folic acid, vitamin B6, and vitamin B12 significantly reduced carotid intimamedia thickness in patients at risk of cerebral ischemia. While some of this improvement may have been due to a reduction in homocysteine levels, the effect appeared to be at least partly independent of both baseline plasma homocysteine concentrations and the change in homocysteine levels during treatment. Vitamin B6, in particular, has actions unrelated to homocysteine metabolism that might be expected to improve vascular health, such as enhancement of endothelial-tissue integrity and inhibition of platelet aggregation.

Till U, et al. Decrease of carotid intima-media thickness in patients at risk to cerebral ischemia after supplementation with folic acid, vitamins B6 and B12. Atherosclerosis 2005;181:131-135.

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group

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