Foam cells heart disease

It is unlikely that the damaging effects of ox-LDL are relevant only to the walls of blood vessels and there is no reason to suppose they are confined to one disease. The initial histopathologjcal sign of coronary heart disease is the appearance of the fetty streak on the luminal surfece of arteries. Fatty streaks are composed of aggregated macrophages that have taken up ox-LDL via the scavenger receptor. Recently, we have detected such foam cells in the rheumatoid synovium (Section 5.5). 

In atherosclerosis, ox-LDL is taken up ultimately by macrophages and smooth muscle cells in the arterial intima. Once loaded with lipid, these cells have a foamy appearance when examined histologically. The accumulation of these so-called foam cells in the artery wall leads to the formation of fatty streaks , which can lead to atheromatous plaque formation and consequent coronary heart disease. 

Cardiovascular heart diseases (CHD) are considered as the clinical expression of advanced atherosclerosis. One of the initial steps in atherogenesis is the oxidative modification of LDL and the uptake of the modified lipoprotein particles by macrophages, which in turn become lipid laden cholesterol-rich cells, so-called foam cells [159]. An accumulation of foam cells in the arterial wall is the first visible sign of atherosclerosis and is termed fatty streak, the precursor to the development of the occlusive plaque [160]. It is well known that oxidation of LDL can be initiated in vitro by incubating isolated LDL particles with cells (macrophages, lymphocytes, smooth muscle cells, or endothelial cells), metal ions (copper or iron), enzymes, oxygen radicals, or UV-light. However less is known about the mechanisms by which... 

Our most common lethal disease is atherosclerosis, which causes constriction and blockage of arteries of the heart, brain, and other organs. In the United States, Europe, and Japan half of all deaths can be attributed to this ailment.a,b There seems to be a variety of causes. However, there is agreement that the disease begins with injury to the endothelial cells that form the inner lining of the arteries.3/C/d This is followed by the aggregation of blood platelets at the sites of injury and infiltration of smooth muscle cells, which may be attracted by 12-hydrox-yeicosotetraenoic acid and other chemoattractants formed by activated platelets.c "Foam cells" laden with cholesterol and other lipids appear, and the lesions enlarge to become the characteristic plaques (atheromas). 

Atherosclerosis in humans can have severe clinical sequelae, including heart attack, stroke, and peripheral vascular disease. In developed countries, atherosclerosis is responsible for more morbidity and mortality than any other single degenerative disease. Research over the past few decades has led to a new consensus on the sequence of events that initiate atherosclerotic lesions. Many of these events, including the accumulation of cholesterol in macrophages ( foam cells ), are accelerated by low-density lipoprotein (LDL) that has undergone oxidative modification. The accumulation of lipoprotein cholesterol is clearly central to the initiation of the fatty streak — the first anatomically defined lesion in atherosclerosis. 

Figure 2 The role of oxidized LDL (OxLDL) in formation of foam cells. Reproduced with permission from Ashwell M (1993) Diet and Heart Disease - A Round Tabie of Factors. London British Nutrition Foundation.

---