| Vitamin E and the Risk of Coronary Artery Disease Reprinted from Medical Sciences Bulletin , published by Pharmaceutical Information Associates, Ltd. Atherosclerosis is characterized by the progressive build-up of fatty plaques in blood vessels, beginning with the appearance of the fatty streak. Composed of fat-rich cells in the arterial intima, the fatty streak evolves over the years into atherosclerotic plaque as vessel walls are damaged by inflammation, cholesterol deposition, and smooth muscle cell proliferation. One major component of the atherosclerotic plaque is foam cells. These cells are macrophages that enter the arterial wall in response to various stimuli, where they absorb fats and then release their fatty load at death, thus damaging surrounding cells, attracting other macrophages, and continuing the cycle of inflammation and proliferation that leads to plaque. Low-density lipoprotein (LDL) cholesterol may be involved in the conversion of macrophages to foam cells. According to Steinberg et al., LDL that has undergone oxidative damage is considerably more atherogenic than native LDL. "A key point is that oxidized LDL particles (and certain other modified forms of LDL) are ligands for the 'scavenger' receptors on macrophages." Antioxidants such as vitamin C, vitamin E, and carotenoids are thought to be protective by preventing the oxidative modification of LDL. |
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