Atherosclerosis
Athogenesis (sequences of events)

Endothelial injury
® adherence of blood macrophage or moncytes which imbibe LDL and actively enter the intima and become (foam cells).
Active macrophages release free radical that oxidize the LDL, the oxidized LDL is toxic to endothelium causing endothelial loss and exposure of the subendothelial C.T.
® platelets aggregation.
Platelets will release mitogenic factors
® migration of smooth muscles into the intima and its proliferation.
Also activated macrophage secretes cytokines e.g. plat growth factors, T.N.F, fibroblast growth. F and ILI.
The smooth mus cell & macropohags accumulate LDL from the plasma this is enhanced by
­ LDL in blood.

Pathologic feature of atherosclerosis
A- The fatty streak
Thin, flat, yellow streaks in the intima they consists of macrophages and smooth muscles cells whose cytoplasm distended with lipids (foam cells).
They are present very early in life, they
­­ in number until about 20 yrs and then remain static or ¯¯

N.B.
There is controversy about whether some fatty streaks progress into fibrous atheromatous plaque or whether they are independent of atherosclerosis.

B- Fibrous atheromatous plaque
It consists of fibrous cap under the endothelium & lipid zone consists of lipid laden macrophages.
C- Complicated plaque

Ulceration of plaque + calcification will lead to thrombosis.

N.B.
Risk factors of atherosclerosis & C.Hr.D.

LDL : HDL > 5: 1 liable to atherosclerosis.

­­
Level of HDL seem to be protective.
HDL may allow elution of cholesterol out of coronary Vs.
Other risk factors see before in coronary heart disease.


Source: Internal Medicine Book of Dr.Osama Mahmoud (Ain Shams University)