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Biochemistry of atherosclerosis

There are 264 factors of risk of atherosclerosis. The main factors are next:

1) dislipoproteinemias: a) increase of LPVLD in normal value of LPLD; b) increase of LPLD in normal value of LPVLD; c) increase of LPLD and LPVLD;

2) hypertony;

3) smoking;

4) diabetes mellitus;

5) belonging to male (except men in age more 75).

One of factors of risk is a low hard water. One of the suitable theory of pathogenesis of atherosclerosis is the “theory of response to damage”: the big arteries are damaged due to the high pressure of blood stream on them. It occur when the disfunction of big arteries endotheliocytes is observed. The big arteries are naxt: abdominal, coronary, popliteal, femoral, tibialis, breast, carotis and arteries of the brain. There are initial (until lipid) phase, early lipid phase, late and complicated phases of atherogenesis. The initial phase is characterized by disfunction of endothelium of a big arteries. It creates a zones of increased permeability and stickness on the surface of endothelium. The retention of GAG, LPLD and LPVLD in these zones is observed.

The monocytes enter into intima and they are converted into macrophags. Stored LP are oxidated and interact with MDA and become unusual. They are scavengered by macrophags and macrophags are converted to foam cells.

The appearance of foam cells is a feature of transition of initial phase to early lipid phase. The peculiarities of earlu lipid phase are lipid spots and lines. This stage are very often in young men and kids. If the factors of risk continue to act the early phase transmits into late lipid phase which can be complicated. In this stage the atheromas, fibroids, fibroatheromes appear. In the area of atheroma the thrombocytes are activated and thromogenesis beginns to dominate in atheroma. The cells of intima are necrotized.

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