Atherogenesis coronary heart disease

Corona.iy Hea.rt Disea.se, A theory for atherogenesis (120) has been developed whereby oxidation of low density Hpoprotein (LDL) within the arterial wall is the critical first step. It has been hypothesized that sufficient intake of antioxidants would prevent oxidation of LDL and reduce development of coronary heart disease (122). Interest in determining the role of antioxidants in blocking LDL oxidation has led to the development of in vitro test systems. 

Hyperlipidemia is a major cause of atherosclerosis and atherosclerosis-associated conditions, such as coronary heart disease (CHD), ischemic cerebrovascular disease, and peripheral vascular disease. These conditions account for most morbidity and mortality among middle-aged and older adults. DysUpidemias, including hyperhpidemia (hypercholesterolemia) and low levels of high-density-hpoprotein cholesterol (HDL-C), are major causes of increased atherogenesis both genetic disorders and lifestyle (sedentary behavior and diets high in calories, saturated fat, and cholesterol) contribute to the dysUpidemias seen in developed countries. 

The distribution of plasma cholesterol between HDL, on one hand, and VLDL/ IDL/LDL on the other, is strongly related to the prevalence of coronary heart disease. LTP are able to catalyse cholesterylester transport in either direction. Therefore, elucidation of the mechanism of action and regulation of lipid transfer processes should contribute to our understanding of atherogenesis. 

The nutritional value of nut and seed products is closely associated with the fatty acid content of the oil. High Unoleic acid content decreases shelf-life. Increasing the oleic/linoleic acid ratio produces a more stable oil with a longer shelf-life. Nutritionally, a high linoleic acid content is desirable, because this acid is an essential fatty acid and produces a hypocholenic effect. Of more than 100 fatty acids, three are essential, linoleic, linolenic and arachidonic. The consensus is that polyunsaturated fat (fatty acids) lowers total blood cholesterol and low-density lipoprotein levels. Lx)w levels of these substances are associated with reduced risk of coronary heart disease and atherogenesis. Mono-unsaturated fatty acids may be beneficial in lower blood cholesterol (Sheppard and Rudolf, 1991). 

Elevation of plasma cholesterol, particularly low-density lipoprotein cholesterol (LDL-C), is positively correlated with coronary heart disease (CHD), a major vascular disease predominantly causing by atherosclerosis (1,2). Recent studies have indicated that LDL oxidation, endothelial dysfunction, and inflammation play important roles in the molecular pathogenesis of atherosclerosis (3). Oxidized LDL (OxLDL) appears in the circulation and tends to infiltrate into the aortic endothelium (4). Antioxidants, which inhibit LDL oxidative modification, may reduce early atherogenesis and slow down the disease progression to an advanced stage (5). 

Recently, one investigator in particular has emphasized the positive correlation between sucrose intake and incidence rates for coronary heart disease (15). He has invoked for sucrose a major, primary, and specific role in atherogenesis. This issue has been reviewed at length elsewhere, and its detailed examination is beyond the scope of this presentation (14,16,17). Suffice it... 

One of the most important research advances since World War II is the delineation of the chief mechanism of the etiologic effect of dietary lipid on atherogenesis. This has been the demonstration - as illustrated in the last three figures - that populations differing in habitual intake of saturated fat and cholesterol also differ markedly in serum cholesterol levels, i.e., interpopulation levels of these two sets of variables are highly correlated. So also are dietary saturated fat-cholesterol intake and coronary heart rates, and serum cholesterol level and coronary heart disease rates. 

Coronary artery disease remains the main killer. The mortality from coronary artery disease has decreased by 28% in the last 20 years. A first acute myocardial infarction had mortality of 28% in 1963 and today it is about 7%. The price of life has become more and more valuable. We are only on the threshold of understanding the pathogenic and biological principles of the generation of atheroma, but once established, obstructive lesions need coronary artery dilatation, coronary artery bypass or arterial replacement. The saphenous vein is an excellent bypass conduit but its life expectancy is 3 to 10 years only until it thromboses, or becomes atheromatous and is blocked or obliterated by cholesterol filled intima or clot. The internal mammary artery is ideal but flow is too small to sustain adequate flow to the entire heart. Here too, there is the need for new non-thrombogenic materials to reconstruct artificial arteries, substances which are durable, non-thrombotic and do not promote atherogenesis. There is also the need for simple, non-invasive techniques to measure coronary blood flow and the anatomy of the coronary arteries to plan subsequent surgical procedures. 

---