Arteriosclerosis Blood lipids

This is an adequate basis for a therapy, although the biochemical pathogenetic correlations between increased blood lipids and arteriosclerosis or other diseases are largely unknown. In any case a lipid lowering therapy will be useful only if started early and understood as long-term therapy. 

V9 Villanyi, P., Votin, J. and Rahlfs, V. Arteriosclerosis, myocardial infarct and blood lipids their therapeutic modification by magnesium orotate. Wien. Med. Wochenschr., 120, 76-83 (1970) (Germ.)... 

Cardiovascular disease is the primary cause of death, in both the United States and Europe, with arteriosclerosis being the most common form. The process of arteriosclerosis is considered to consist largely of the accumulation of lipids within the artery wall [1]. By surgical therapy new pathways (conduits) are being constructed, connecting the aorta or other major arteries and distal segments of arteries (e.g., coronary arteries) with vessels beyond the stenosis or obstructing lesions. By this means, blood supply to ischemic tissues can be re-established... 

Fig. 2. Proposed process of arteriosclerosis leading to ischemic disease. It is proposed that arteriosclerosis is a process of inflammation within the arterial wall that is initiated by arterial injury (endothelial dysfunction), causing the trapping of lipoproteins (Rll, Zl). These undergo oxidation as proposed in Fig. 1, leading to foam cells saturated with lipid droplets. Continued accumulation of fatty material within the blood vessel wall promotes a fatty streak. Ultimately, there is muscle cell migration and fibrosis leading to a plaque that consists of a fibrous cap with cholesterol crystals and debris within the deep necrotic layer, while inflammatory cells form a dynamic outer edge. It is thought that oxidized lipoproteins can facilitate many of these processes. Mechanical forces predispose the soft outer layer of the plaque to rupture at sites of structural weakness. Rupture of plaques causes thrombosis and incorporation of thrombi into the plaque. Ultimately, a large thrombus appearing in an obstructed vessel can lead to sudden ischemia and unstable coronary syndromes.

Thyroid hormones have long been known to affect lipid metabolism. Thyroxine undoubtedly controls cholesterol metabolism serum cholesterol levels are markedly increased in hypothyroidism and decreased in hyperthyroidism. There are various ways by which thyroxine could cause cholesterol to accumulate in blood direct stimulation of the pathway involved in cholesterol biosynthesis block of cholesterol use for further biosynthesis indirect stimulation of cholesterol synthesis by acceleration of pathways that provide precursors of coenzymes needed for cholesterol synthesis and indirect stimulation of cholesterol synthesis by blocking pathways that use those precursors involved in cholesterol synthesis. The exact mechanism by which thyroxine induces the accumulation of cholesterol in serum needs to be elucidated. The effect of thyroid hormones on blood cholesterol must be understood because hypothyroidism is known to enhance the development of experimental arteriosclerosis in animals. 

Humoral Changes in Arteriosclerosis. Investigation of Lipids, Fatty Acids, Ketone Bodies, P ruvic Acid, Lactic Acid and Glucose in the Blood... 

Christie (2) has discussed various functions of lipids as follows their involvement in disturbances of lipid metabolism associated with specific lipidoses and gangliosidoses accumulation of various neutral, complex, and conjugated lipids in arteriosclerosis and atherosclerosis (coronary blood vessel and heart disease) the role of lipids in nutrition, disease, and human welfare the importance of fats and oils as agricultural products and as major items in international trade the role of fats as a major dietary component and supplier of calories for humans in developed countries the contribution that fats make to the taste and structure of foods. 

E. Bohle, and R. Biegler Humoral changes in arteriosclerosis. Investigation on lipids, fatty acids, ketone bodies, pyruvic acid, lactic acid, and glucose in the blood. Lancet 1960/11, 1409. 

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