Atherogenic coefficient (A.N. Klimov)
AC= total cholesterol – HDL cholesterol HDL cholesterol
N 5,0
It has now been proven that different degrees of atherogenicity in violation of lipid metabolism depends not only on the level hypercholesterolemia, but also from qualitative changes in circulating lipids. This is mainly due to what glycoproteins are associated with lipids (called apoproteins).
Classification of hyperlipoproteinemia (Fredrickson D.S. et al. 1967):
phenot |
Content of |
Incraesed levels |
|
atheroge |
ype |
major |
|
|
nicity |
|
apoproteins |
lipoprotein |
lipids |
|
I |
A-I, A-II, B |
Chylomicrons |
ТG |
- |
II-A |
B |
LDL |
HS |
++ |
II-B B, C III |
LDL+ VLDL |
ТG + HS + |
III |
CBE |
LDPP |
TG + HS |
++ |
IV |
C III |
VLDL |
ТG |
+- |
V |
C III E |
Chylomicrons+ |
ТG+ HS |
- |
|
|
VLDL |
|
|
Stages of atherogenesis:
Atherosclerotic changes occur in the inner shell arteries.This process takes place in three stages:
-fatty streak,
-fibrous plaque and
-Complex violations.
1.Fat streaks can be found in anyone over the age of
10.The yellow color of these spots is associated with the deposition of lipids in the cells of the intima, as well as in the extracellular space.
2.Fibrous plaques are usually considered as cell damage, characteristic of the advanced form of atherosclerosis. They consist of smooth muscle cells, lipids, collagen, elastic fibers and glycosaminoglycans.
3.Complicated lesions. Complicated lesions include fibrous plaques, which are modified due to increased cell necrosis, calcification and sloughing of the endothelium covering the plaque with the formation of a parietal thrombus or wall rupture with hemorrhage.