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Abbas Orabi
Atherogenic Particles
Apolipoprotein B
MEASUREMENTS:
Non-HDL-C
Foam cells
Growth factors
VSMC fibroblast
Atheromateous plaque
Inflammatory cells
Proteolytic enzymes
Plaque Rupture
Platelets aggregation
Thrombus
Glagov’s Coronary Remodeling
Hypothesis
Progression
Due to :
VLDL overproduction ( Insulin)
VLDL & chylomicrons impaired clearance ( LPL)
well controlled
Nearly, normal lipids profile
Lipoprotein abnormalities in type 2 diabetes :
Low HDL-cholesterol
Elevated Triglyceride
HYPERTRIGLYCERIDEMIA
CETP
Hepatic lipases
Large
VLDL-1
VLDL
Small
VLDL-2
small
LDL Pattern
LDL Large B
LDL
Large
HDL-2
HDL Small
HDL-3
LDL density :
PLTP
PLTP
Nascent HDL2
HDL density :
The plasma triglyceride concentration is
negatively correlated with that of large HDL2
and positively correlated with the level of
small HDL3.
„ASTEROID“
20
Change in Atheroma
15
Volume mm3
10
5
0
-5 50% LDL-C reduction
-10
n=502
-15
-80 -70 -60 -50 -40 -30 -20 -10 0 10 20
% Change in LDL Cholesterol
To reduce atheroma
Both treatment
volume: 53%groups
LDL
reduction in ASTEROID
80 mg Atorvastatin or 40 mg
PATIENTSPravastatin
NEED A 50% LDL-C REDUCTION TO HALT THE
PROGRESSION OF ATHEROSCLEROSIS – “REVERSAL”
:To Reach Levels Below 70 mg/dl
Cholesterol
Reduction
51% mg 80
Atorvastatin
53% mg 40
Rosuvastatin
51% Ezetimibe +
Standard dose
statin