Risk factors for cardiovascular diseases are of two kinds: variable and fixed.

Fixed factors are: 1) age, 2) gender, 3) family predisposition.
Variable factors are: 1) lipids*, 2) cholesterol*, 3) triglycerides*, 4) LDL*, 5) HDL*, 6) Lp(a), 7) arterial pressure*, 8) diabetes mellitus*, 9) Smoking, 10) obesity*.
(those marked with a * may be modified by the diet)

During the formation and development of arteriosclerosis there can be isolated numerous phases: the initial lesion (1st type), occurs when monocytes migrate into blood to adhere to intima (reasons why they do this are various: one of them is that the amount of cholesterol in their membrane increases and their wall became more rigid; another is that oxidize LDL, which deposits into intima, form some substances that attract monocytes towards endothelium.

Those substances are:

1. VCAM or Vascular Cell Adhesion Molecole
2. ICAM or Intercellular Adhesion molecole
3. MCSF Macrophage Colony Stimulating Factor
4. MCP-1 Monocyte Chemotactict Protein)

Monocytes have a special receptor, the scavenger receptor, with which they inglobate oxidate or modified LDL; furthermore they cannot metabolize cholesterol and so inglobating it they becam foam cells, full of fats. Monocytes and smooth muscolar cells have HDL receptors, that, in addiction to apoprotein A, actuate the trasport of cholesterol to the liver. Deposit of lipids in the monocytes occurs when this transport in insufficient. Monocytes saturated with fats are a very source for all free radicals.
The lesion (2nd type) is visible from the fat stripes that appear since childhood, even in neonates of women with high cholesterol rate, they are formed of accumulations of monocytes saturaded with fats, of smooth muscolar cells and lymphocytes T.
The "Bogalusa Heart Study", in 1986, clearly demonstrated the existence of a direct relation between rates of cholesterol LDL, and of total cholesterol, and of fat stipes in the aorta.
The lesion of 3rd type is characterized from the accumulation of fats, other than inside cells, even in the extra cellullar space.
The lesion of the 4 th type is characterized from the appearing of smooth muscolar cells and the formation of a fat nucleus.
The lesion of the 5th type shows a formation of connective tissue, enveloping lipidic nucleum, and forming a fibrous hood over the plate.
The lesion of the 6th type is characterized by the formation of trombines where plates are ulcerated.
In the esperimental arteriosclerosis on rabbits, pigs, mice, primates, and in the human arteriosclerisis those lesions are always a secondary istance after an increasing of the blood cholesterol rate.
For example, in rabbit, to induce arteriosclerosis, is administrated a diet enriched of 2% of cholesterol and of 4- 10% of vegetal oils.
There are also fibrous plates, made of collagene and smooth muscolar cells poor of fats that are resistent to ulcer.