Atherosclerosis

1. The atherosclerosis

2. The atherosclerosis
is the chronic disease characterized by systemic
lipoid infiltration of the inner tunic of elastic and
mixed type arteries and deposits of salts of calcium,
development in their wall of a connective tissue,
resulting in the narrowing of a lumen in vessels and
disorder of blood flow in organs.
The atherosclerosis affects large and medium-sized
arteries, namely: aorta, coronary arteries, common
carotid ones, vertebral, illiac and femoral arteries.

3. Atherosclerosis
is a disease characterized by irregular
distributed lipid deposits in the intima of
large and medium-sized arteries; such
deposits are associated with fibrosis and
calcification.

4. Epidemiology - in industrially
developed countries atherosclerosis is
one of the causes of reason of 50 %
death. Annually in the USA from various
manifestations of atherosclerosis die
from 500000 up to 1000000 person, and
people who are older than 60 years in
100 % of cases signs of atherosclerosis
are diagnosed. In Ukraine every second
male dies in the age before 60 years.

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6. RISK FACTORS OF CARDIOVASCULAR
DISEASES
AND THEIR COMPLICATIONS
- Age *
- Males*
-Burdened on cardiovascular
diseases heredity *
- Increased systolic BP
- Increased diastolic BP

7. - Smoking
- Increase in the amount of common
cholesterol and cholesterol of low
density lipoproteids
- Decrease the amount of cholesterol of
lipoproteids of high density
- Reduction in cholesterol lipoproteids
of high density

8. - Hypertrophy left ventricle
- Cardiovascular diseases in anamnesis*
- Cerebrovascular diseases in anamnesis *
- Diabetes mellitus
- Disease or secondary affection of
kidneys
- Microalbuminuria
- Adiposity
- Sedentary life
* Not modified risk factors

9. Ethiology
for the first time the term "atherosclerosis"
was offered by German pathoanatomist
F.Marshan in 1904 but as independent illness
it is used in clinical practice only from 1934.
In 1976. M.Brown and D.Goldstein have
opened proteins-receptors with low density
lipoproteins on the cells membranes. They
are located in the liver and purify blood from
LDL on 75 %.

10. Reduction of the amount of these receptors
results in the increase of the level of these
lipoproteins in plasma and in the
development of atherosclerosis and IHD
(ischemic heart disease) Deficiency of these
receptors may be both genetic, and acquired.
D.Goldstein and M.Brown have established,
that genetically determined defect of genes in
loci B and C system of histocompatibility
НLА appears to be a base of atherosclerosis.

11. Major factors of atherosclerosis
1. Not modified:
- Age (males > 45 years, women> 55
years)
- Male
- Genetic predisposition
2. Modified:
- Smoking

12. - Arterial hypertension (AP (artery
pressure) > 140/90)
- Obesity
3. Partially convertible:
- Increased level LDL (> 4,1 mmol/l)
- Decreased level HDL (<0,9 mmol/l)
4. Other factors:
- Low physical activity
- Mental and emotional stress

13. Cholesterol metabolism in the organism
Endogenous
way synthesis
in the liver
60-80%
Cholesterol
Exogenous way
with food
20-40%
GMGKo A-
reductaza
Transport
proteins
Lipoproteins
HDL LDL VLDL

14. HDL CholesterolHDL Cholesterol
 HDL cholesterol has a protective effect for
risk of atherosclerosis and CHD
 The lower the HDL cholesterol level, the
higher the risk for atherosclerosis and
CHD
low level (<40 mg/dL) increases risk
 HDL cholesterol tends to be low when
triglycerides are high
 HDL cholesterol is lowered by smoking,
obesity and physical inactivity

15. LDL CholesterolLDL Cholesterol
 Strongly associated with atherosclerosis
and CHD events
 10% increase results in a 20% increase in
CHD risk
 Modified by other risk factors
 low HDL cholesterol
 smoking
 hypertension
 diabetes

16. Pathogenesis
There are lipoproteins of high, low and very
low density. Atherosclerosis develops when
the amount of LD lipoproteins increases.
Their amount is up to 60-70 % from the
common cholesterol of serum. If LDL and
VLDL level is 3,5-4 times higher than HDL
level atherosclerosis develops in 95-98 % of
cases. Disorders in thrombocytes are also
peculiar for pathogenesis of atherosclerosis.

17. Under the influence of special lipids
(prostapoids) activity of thrombocytes
increases, that results in formation of throbi.
Inflammation in a vascular wall is another
important factor. Disordrs of cytokins are
revealed - YL-1, YL-3, YL MAC-1 level
raises, amount of phospholipasa A2 changes.
Recently a provoking a role of infection -
bacterial and virus: namely a
cytomegalovirus has been studied.

18. High level LDL
Low level HDL
Sticking of monocytes together Infiltration of intima LDL
Accumulation of macrophages + Oxidation LDL
Formation of foamy cells
Lipid streak Damage of epithelium
Sticking of thrombocytes
Production of thrombocytes
growth factor
Cells proliferation
Plague

19. CLASSIFICATION OF
HYPERLIPOPROTEINEMIAS /WOHP/
Type common
CHS plasmas
CHS LDL Plasma
triglycirids
Disturbance of
metabolismLP
I increased or
normal
decreased or
normal
increased Excessive amount
of hylomicrones
II A Increased Increased normal Excessive amount
of LDL
II B Increased increased increased Excessive amount
of LDLand VLDL
III Increased increased or
normal
increased Excessive amount
of residuals of
hylomicrons and
LP
IV increased or
normal
Normal increased Excessive amount
of VLDL
V Increased normal increased Excessive amount
of hylomicrons and
VLDL

20. Atherosclerotic plague
Stages of morphogenesis
Lipoidosis: Strips of fat on the vessel
wall are early atherosclerotic damages.
They consist of the macrophages, which
are connected with LDL, called “
foaming cells ” and smooth- musclular
cells.

21. Liposclerosis - is characterised by reactive
growth of connective tissue and formation of
fibrous tegmen. Zone of necrosis -
atheromatosis, crystalls of cholesterol and
calcinosis is formed under it.
Rupture of plague results in a full or partial
thrombosis of the artery, that is manifested
by stenocardia or a myocardial infarction or
thromboembolism.

22. Normal
Fatty streak
Lipid rich plaque
Complex plaque
Thrombus
Lipid core
Fibrous capFoam cells
Development of Atherosclerotic PlaquesDevelopment of Atherosclerotic Plaques

23. Classification of atherosclerosis
(МКБ-10)
170.1 - atherosclerosis of renal
arteries
170.2 - atherosclerosis limb arteries
170.9 - generalized atherosclerosis

24. Clinic
Clinical picture of atherosclerosis
depends on localization of
atherosclerotic plagues and a
degree, of homodynamic disorders
and complications caused by
them (thromboses).

25. Clinical manifestations displays of
atherosclerosis
•IHD (stenocardia, myocardial infarction,
cardiosclerosis, disorder of rhythm and
conductivity, cardiac failure)
•Acute and chronic disorders of cerebral
circulation
•Arterial hypertension
•Thrombosis of mesenteric vessels “ angina
abdominis”
•Aneurysm of aorta

26. Diagnosis of atherosclerosis
• Determining of the level of cholesterol and
lipid a spectrum.
• Angiography (revealing of vascular
stenoses).
• Ultrasonic examination of vessels.
• Impendance plethysmography
• Radiological and ultrasonic revealing of
calcinates in a wall of vessels .
• What normal, boundary and increased
levels of cholesterol, LDL

27. Common cholesterolcholesterol
• Normal: <200 mg of % - <5,2 mmol/l
• Boundary: 200-240 mg of % - 5,2 - 6,2
mmol/l
• Increased:> 240 mg of % - 6,2 mmol/l
•LDL
• Normal: <130 mg of % - <3,4 mmol/l
• Boundary: 130-160 mg of % - 3,4-4,1 mmol/l
• Increased:> 160 mg of % - 4,1 mmol/l

28. Treatment
Diet - the contents of cholesterol in blood is
regulated by mean of a diet with the lower
common caloric content of food at the
expense of animal fats and products saturated
with cholesterol (eggs, meat, creamy fats), It
is necessary to eat: oil of corn, sunflower,
soya, cod-liver oil, nuts, products containing
proteins - meat of poultry and fish, cheese,
milk, vegetables and fruits, beans, and
cereals.

29. Treatment with medicines starts in that
case, when there is no efficiency after 6
months hypocholesterinemia diet.
In accordance with WOHP
recommendations, medicinal therapy
should be started at cholesterol of
plasma level above 250 mg of % - 6,5
mmol/l, and in the presence of IHD - at
the level of 220 mg %- 5,7 mmol/l.

30. Hypolipedemic drugs
- The basic preparations:
•Inhibitors ГМГ-Ko A- reductaze
•Lovastatinum (mevacor) - 20-80 mg 1
time for night
•Simvastinum (Zocor) - 5-40 mg of 1
times for night
•Fluvastinum - 20-40 mg of 1 times for
the night

31. Nicotinic acid
After meal
1 week - 100 mg х 3 times a day
2 week - 200 mg х 3 times a day
3 week - 300 mg х 3 times a day
4 week - 500 mg х 3 times a day
- Secvestrants of bilious acids
Cholesteiraminum (cvestran) - 12-15
mg х 2 times a day
Гуарем - 5 mg х 3 times day

32. Other preparations
- Fibrates
Gemfibrozilum - 600 mg х 2 times
a day
Cirofibratum - 100-200 mg once
a day
Probucol is an antioxidant - 0,5 х 2
times day