3. 8
More than million people die from
CHD, every year worldwide, more than
cancer, infectious diseases or any other
causes.
In the U.S. alone, the prevalence of CHD is
around 15 millions ( 5%) 650’000 die
annually of CHD.
In Egypt, the WHO estimate for CHD is 3.5
Million. it is estimated that around 150’000
die from CHD in Egypt annually.
6. Positive family history of premature
vascular ds.
Advancing age
Male Gender or post-menopause in
females
Dyslipidemia ( LDL-C or HDL-C)
DM II
Smoking
Hypertension
Obesity
Sedentary life
8. Positive family history of premature
vascular ds.
Advancing age
Male Gender or post-menopause in
females
Dyslipidemia ( LDL-C or HDL-C)
DM II
Smoking
Hypertension
Obesity
Sedentary life
9. DM II predisposes to both premature onset
& severity of atherosclerosis in coronary
arteries CHD.
CHD is the commonest cause of morbidity &
mortality in DM II.
10. Five of the treatable and
preventable risk factors for CHD are
obesity, sedentary life, hypertension,
smoking & dyslipidemia.
11. Management of dyslipidemia is
primarily carried out through
lifestyle modifications then drug
therapy.
In recent years, more emphasis has
cholester
been focused on the management of
cholesterol. ol.
12.
13.
14. FUNCTIONS OF CHOLESTEROL
Structure of cell membrane
Precursor of Steroid Hormones
Precursor of Bile Acids
16. Diameter Density Protein Total lipid % of Lipid Fraction
(nm) (g/ml) (%) (%) TG PL FC CE
90 - 1000 < 0.95 1-2 98 - 99 88 8 1 3
30 - 90 0.95 - 1.006 7 - 10 90 - 93 56 20 8 15
25 - 30 1.006 - 1.019 11 89 29 26 9 34
20 - 25 1.019 - 1.063 21 79 13 28 10 48
10 - 20 1.063 - 1.125 33 - 57 67 - 43 16 43 10 31
Lipoproteins have different sizes, different
densities, different content, different apoproteins,
different receptor sites, different pathways &
different effects.
17.
18. Go lgi
Lipoprotein Lipase
Transported by
Glucose synthesis serum albumin
Glycerol free fatty a
in the liver
= Chylomicron
Cholesterol ester Triacylglycerol
Hydrophilic layer: phospholipids, FC, Apoproteins Fig 1-A
19.
20. There are two major ways in which dyslipidemias are
classified:
1. Etiological i.e. the cause of the condition genetic (familial), or secondary
(non familial).
This classification can be problematic, because most conditions involve the
intersection of genetics and lifestyle issues.
2. Phenotype i.e. the presentation in the body type of lipoprotein & the
This classification points to the problem, the(the specific type of lipid
increased).
specific blood lipid increased as well as the treatment of choice for that
specific error.
Fredrickson
Classification:
Phenotype I IIa IIb III IV V
Type of
Chylomicro LDL LDL & VLDL IDL (VLDL) VLDL &
Lipoprote
ns Triglycerid chylomicrons
in
es
Elevated
Both Cholesterol Triglycerid
es
21.
22. Lipoprotein Lipase
Transported by
Glucose synthesis serum albumin
Glycerol free fatty a
in the liver
= Chylomicron
Cholesterol ester Triacylglycerol
Hydrophilic layer: phospholipids, FC, Apoproteins Fig 1-A
23.
24. 1. Lipinorm is indicated for the
1. LDL-cholesterol 4. Familial hypercholesterolemia
treatment of :
2. total-cholesterol 5. Combined hyperlipidemia
3. ApoB lipoproteinemia 6. Familial Dysbetalipoproteinemia
25. 1. Lipinorm is indicated for the
1. LDL-cholesterol 4. Familial hypercholesterolemia
treatment of :
2. total-cholesterol 5. Combined hyperlipidemia
3. ApoB lipoproteinemia 6. Familial Dysbetalipoproteinemia
2. Lipinorm is indicated for the
Prevention of :Disease in High Risk
Coronary Heart i.e. with multiple risk
factors.
•patients: the risk of angina
Reduces
• Reduces the risk of myocardial
infarction
• Reduces the risk of stroke
26. Positive family history of premature
vascular ds.
Advancing age
Treatmen Male Gender or post-menopause in
HDL-
t females
C with retinopathy, albuminuria or
Dyslipidemia ( LDL-C or HDL-C)
macroangiopathy.
DM II
1- Prevention of Cardiovascular Disease in
Smoking risk adults:
Hypertension •• Reduces the risk of angina.
Reduces the risk of myocardial infarction.
Obesity • Reduces the risk of stroke.
2- Treatment of Dyslipidemia:
Sedentary lifeLDL-cholesterol
total-cholesterol
ApoB lipoproteinemia Familial
hypercholesterolemia
34. A significant proportion of patients switching from atorvastatin
to simvastatin received a low dose in terms of efficacy -lower than
that which can achieve the therapeutic goal- which may have an
adverse impact on patients' healthcare quality and probability of
vascular morbidities and mortality.
Switching from more expensive brand name drugs to generic
equivalents may reduce aggregate prescription costs.
Therapeutic benefit may not be compromised if the patient is
Reference: Gregory Hess, Therapeutic Dose Assessment of Patient Switchingprofile.
switched to a generic with an equivalent therapeutic from Atorvastatin to
Simvastatin (Am J Manag Care. Jun 2007; suppl 3; vol 13:S80-S85)
35. By the end of the first 16-week period, when patients in both
groups were on the 10 mg/day dose, 10 of the 15 patients on
atorvastatin (66%) presented a LDL-C level <130 mg/dl, while only 4
of the 15 patients on simvastatin (27%) achieved this goal.
Atorvastatin in equipotent doses to simvastatin appeared to be
more effective than the latter in reducing triglyceride and plasma
fibrinogen in patients with hypercholesterolaemia, and also in
those with Frederickson's phenotype IIb.
Regarding HDL-C, it was increased by simvastatin only with the
20mg dose: 7% vs. baseline vs. atorvastatin; 4% at the 10mg dose and
5% at the 20mg dose vs. baseline.
Reference: Atorvastatin vs. Simvastatin on Lipid Profile
from Clinical Drug Investigation [TM] 2002.
