Artheroscelrosis

1. ATHEROSCLEROSIS.
CORONARY HEART
DISEASE.
ANGINA PECTORIS

2. ATHEROSCLEROSIS
 is a pathological
process leading
to changes in
the arterial
walls due to
accumulation of
lipids,
formation of fibrous tissue and plaques,
constriction of vascular lumen of a vessel.

3.  Atherosclerosi
s is clinically
manifested in
general and /
or local
circulatory
disorders.
Most commonly, atherosclerotic process
develops in the aorta, femoral, popliteal, tibial,
coronary, internal and external carotid arteries
and in the cerebral arteries.

4. Risk factors of development
of atherosclerosis
 А. Modified (can be eliminated).
 1. Dislipidemia (hypercholesterinemia, atherogenous
hyperlipoprotein emia).
 2. Smoking.
 3. Arterial hypertension.
 4. Obesity.
 5. Hypodynamia.
 6. Diabetes.
 7. Frequent psychoemotonal stresses.
 8. Hyperhomocycteinemia.
 B. Nonmodified (ineradicable).
 1. The burdened heredity.
 2. The male, age is older than 60 years.

5. Stages of atherosclerosis
(А. L. Myasnicov, 1965)
 1. Initial (preclinical) period —
formation of atherosclerotic plaques
is observed, lipidemia takes place,
but there are no clinical
manifestations.
 2. The period of clinical
manifestations:

6. Etiopathogenesis.
Atherosclerot
ic changes
occur in the
endarterium
. This
process has
three
stages:
the fatty streak, the fibrous plaque and
the complex disorders.

7. 1. The fatty streak.
 Spots of
yellowish
color of 1-
2mm in blood
vessels are
detectable
from the
moment of
birth.
These spots are deposits of lipids. They merge and
grow over time. Smooth muscle cells and
macrophages appear in the endartelium; macrophages
accumulate lipids and convert into foam cells.

8.  In this way a
fatty streak
emerges
consisting of
smooth
muscle cells
and lipid-
containing
macrophages.
fatty streak

9. 2. The fibrous plaque
 is located in the
endarterium and
grows interiorly to
diminish the
vessel’s lumen
over time. A
fibrous plaque has
a thick capsule.
It is composed of endothelial cells, smooth muscle
cells, T-lymphocytes, foam cells (macrophages),
fibrous tissue, and has a soft core containing esters
and cholesterol crystals. Cholesterol comes from
blood.

10. 3. Complex disorders
 are manifested as
reduced thickness
of a capsule of a
fibrous plaque and
its broken
intactness:
development of
cracks, ulcers,
fractures.

11.  Broken
intactness of
the fibrous
plaque leads
to adhesion
of platelets to
it, their
aggregation
and
thrombosis.
Blood circulation in the affected vessels partially or
completely ceases. Myocardial infarction, ischemic
stroke, etc. develop

12. Clinic.
 Atherosclerotic process is silent and its
clinical signs appear over time. They depend
on localization of the process and an extent
of obstruction of the vascular bed.

13.  External signs of atherosclerotic process:
xanthoma (tuberosity in the joints, in the
Achilles tendons caused by cholesterol
deposits), xanthelasma (cholesterol deposits
in the skin of the eyelids, often tuberous)
xanthoma xanthelasma

14.  senile arc on the cornea (a
strip of yellowish color along
the edge of the cornea).
senile arc

15. Clinical manifestations of atherosclerosis depend
on localization of the pathological process.
 Atherosclerosis of the aorta. Palpation:
amplified pulsation of the aortic arch in
the jugular fossa.
Percussion: expanded
vascular bundle.
Auscultation: diastolic
shock in the 2nd
intercostal space right
of the sternum,
functional systolic
murmur over the aorta.

16.  Elevated systolic
blood pressure. Pulse
becomes high over
the radial artery. On
inspection and
palpation of the
atherosclerotic
lesions of arteries
(radial, brachial,
temporal, etc.)
 their density, tortuosity and unevenly thickened
walls are determined. In some cases, there may
be asymmetric blood pressure and pulse in the
arms.

17.  If distinction in
systolic pressure
on both hands
exceeds 10-15
mm Hg, it may
often suggest
disordered
patency in one
of the branches
of the aortic
arch, caused by
presence of an
atherosclerotic
plaque
 at the place of origin of the subclavian artery
or the brachiocephalic trunk.
CT angiogram showing occlusion of
proximal left subclavian artery

18. Atherosclerosis of the abdominal
aorta.
 In atherosclerotic
constriction of unpaired
visceral branches of the
abdominal aorta a
specific clinical picture
of abdominal coronary
disease develops in most
cases.
In these patients, moderate tenderness on abdominal
palpation, especially in its superior sections is
present. Functional systolic murmur in the epigastric
region is heard in most patients.

19. Atherosclerosis of the coronary
arteries (coronary heart disease).
 The physical
examination
is described
in the
relevant
section.

20. Atherosclerosis of cerebral vessels.
 Dyscirculatory
encephalopathy
develops. In its
first stage,
dysarthria,
abnormal axial
reflexes,
decreased step
length, slowed
walk are revealed
on inspection.

21.  In the second
stage,
disorders
associated
with
dysfunction
of the frontal
lobes are
revealed:
loss of memory, impaired attention, thinking,
ability to plan and control actions.

22.  Slightly disordered function of the pelvic organs in the
form of frequent nocturnal urination develop.
Occupational and social adaptation of the patient is
affected; but the patient is still able to take care of
him/herself. The same symptoms are typical for the third
stage, though become are more marked. Dementia,
marked emotional and personality-related disorders, gait
disorders, marked cerebellar disorders, urinary
incontinence develop.

23. Atherosclerosis of peripheral
arteries.
 On inspection of an affected limb, signs of
impaired trophism are revealed: pale and
cold skin, hypotrophy and atrophy of
muscles,
trophic changes (dry
and flaky skin, nail
dystrophy with
frequent fungal
infection, lack of
body hair).

24.  Cyanosis or
bluish-red
color of the
skin of the
fingers and
feet is
specific,
especially, in
an upright or
sitting
position.
 Cyanosis is a sign of arterial blood flow
disorders

25.  Slowly
healing
ulcers
and
necrosis
in the
toes and
feet are
possible.
 On palpation, attenuated pulsation or its
absence determined on the limb arteries.

26. Atherosclerosis of the renal
arteries.
 Increased blood pressure is specific, the disease does not
very well respond to therapy. Over the area of
constricted renal artery, a systolic murmur is auscultated.
In the later stages of the disease, the signs of chronic
renal failure are revealed.

27. Laboratory diagnostic studies in
arteriosclerosis
 involve determination of lipid disorders
(dyslipidemias detection) and total
cholesterol in blood plasma.

28. Variants of hypercholesterolemia
Level Total
cholesterol,
mmol/l
LDL,
mmol/l
Optimal below 5.0 below 3.0
Moderately
elevated
≥ 5.0-5.9 ≥ 3.0-3.9
High ≥ 6.0 ≥ 4.0

29. CORONARY HEART DISEASE
 (CHD) is a
pathological
condition
that develops
when there is
discrepancy
between the demand of the heart in blood
supply and actual blood supply.

30. Nonatherosclerotic causes
of coronary failure
 1. Arteritis (nodous periarteritis, Takaiasu disease,
systemic lupus erythematosus, lues, etc.).
 2. Traumas of coronary arteries.
 3. Spastic stricture of coronary arteries.
 4. Embolism of coronary arteries (contagious
endocarditis, intracardiac thrombuses implanted
valves, etc.).
 5. Congenital anomalies of coronary arteries.
 6. Other causes — aortal heart diseases,
thyrotoxicosis, hypercoagulation, complications of
catheterization of heart.

31. Pathogeny of ischemic heart
disease
The need of myocardium for Oxygen depends
of:
 — Frequencies of cardiac reductions.
 — Myocardial contraction.
 — Strains of the left ventricle during systole.
Supply of the myocardium with Oxygen
depends on the size of coronary blood-flow
which is defined by:
 — The size of resistance of coronary arteries
(diameter, elastance).
 — The size of perfused pressure in the phase of
diastole (the difference between diastolic
pressure in the aorta and diastolic pressure in
the left ventricle).

32. The pathogenetic factors promoting to the
development of ischemia of the myocardium
 1. Organic narrowing of the lumen of the coronary artery by
atherosclerotic process (plaques, units of thrombocytes,
thrombuses).
 2. The spastic stricture of coronary arteries on the background
of atherosclerosis which alters the reactivity of arteries and
makes their hypersensitive to the influence of neurogenic
stimulants and environmental factors.
 3. Drop of ability of coronary arteries to extend adequately
under the influence of the metabolites arising in conditions of
rising of need of myocardium in Oxygen (adenosine, lactic
acid, Inosinum, hypoxanthine).
 4. The dysfunction of endothelium caused by atherosclerosis,
characterized by predominance of coagulator and
vasoconstrictive factors.

33. Clinical classification of
coronary heart disease.
• 1. Sudden cardiac death (primary cardiac arrest).
• 2. Angina.
• 2.1. Stable angina (four functional classes).
• 2.2. Unstable angina:
• 2.2.1. Primary angina.
• 2.2.2. Progressive angina.
• 2.2.3. Early post-infarction or post-operative angina.
• 2.3. Spontaneous (vasospastic, variant, Prinzmetal's) angina.
• 3. Painless myocardial ischemia.
• 4. Microvascular angina ("Syndrome X").
• 5. Myocardial infarction.
• 5.1. Myocardial infarction with Q-wave (macrofocal, transmural).
• 5.2. Myocardial infarction without Q-wave (microfocal).
• 6. Postinfarction cardiosclerosis.
• 7. Heart failure (with indicated form and stage).
• 8. Disordered cardiac rhythm and conductivity (with indicated form).

34.  Primary circulatory arrest is a sudden
death associated with electrical instability
of the myocardium. It is most often
associated with development of
ventricular fibrillation.

35.  Stable angina (angina of effort) is
characterized by transient episodes of pain
caused by exertion or other factors leading
to increased
demand of the
myocardium in
oxygen (psycho-
emotional stress,
high blood
pressure).

36.  The pain disappears at
rest or after sublingual
intake of nitroglycerine.

37. Exertional angina is divided into four functional
classes (FC) based on the extent of physical
exertion (FE), which causes pain.
 FC 1: normal, everyday physical exertion
(walking, stair climbing) does not cause
attacks. They appear only against the patient
extreme or intense exertion.

38.  FC 2: Slightly restricted usual physical
activity. Attacks occur in normal patient
exertion (walking on a flat ground
covering a distance of more than 200m or
climbing stairs of more than one floor).

39.  FC 3: markedly
restricted physical
activity. Attacks
occur on performing
insignificant
physical exertion
(walking at a normal
pace on flat ground
at a distance of 100-
200 m or climbing
the stairs of less than
one floor).

40.  FC 4: inability to tolerate slightest
physical exertion without discomfort. Pain
may also arise at rest.

41. Unstable angina is subdivided into
three forms:
 1. Primary angina: duration of
the disease is less than 1 month.
It may be a
precursor or a first
manifestation of
myocardial
infarction; it may
transit into a stable
angina or disappear.

42.  Progressive angina: increased frequency,
severity and duration of attacks of
retrosternal pain in response to normal
exertion.
Onset of angina
attacks in response to
less than normal
effort. Pain becomes
more frequent, more
intense and
prolonged. Patients
have to increase
intake of
nitroglycerin, with its
effect reduced.

43.  Spontaneous Prinzmetal’s angina is
characterized by retrosternal pain
attacks occurring irrespective of
physical exertion.
The pain is usually
more intense and
prolonged. It can
be hardly relieved
by nitroglycerin
intake.

44. Clinical picture.
 Angina of effort is characterized by a
squeezing, pressing, non-intensive
retrosternal pain.
To describe its
localization the patient
often puts the fist or
the palm upon the
sternum ("clenched
fist" sign).

45.  A pain radiating into the left arm,
shoulder, blade and neck is specific. The
more severe angina, the broader an area
of ​​pain irradiation.

46.  Pain arises on physical or psycho-
emotional stress, cold, after heavy meal,
lasts up to 15-20 minutes, disappears at rest
and after nitroglycerin intake.

47. Diagnostics.
 The main supplementary technique for diagnostics
of coronary artery is the ECG study. In-between the
attacks, the ECG changes may be absent in
patients. During an angina attack, depending on
localization of myocardial ischemia, negative or
high peaked ("coronary") T-waves are registered in
ECG.

high peaked and negative ("coronary") T-waves

48.  Simultaneously, especially in long-standing
ischemia, myocardial ischemic lesion develops. It
is manifested in shifted ST-segment upwards or
downwards the isoline . The emerging changes on
the ECG are reversible; they disappear after the
blood flow in the myocardium is restored.
Before attack After attack

49. Loading electrocardiography-Tests
1. Tests provoking ischemia of myocardium by
rising oxygen consumption:
 — veloergometria;
 — tredmil-test;
 — transesophageal atrial pacing;
2. Tests provoking ischemia of myocardium by
drop of Oxygen delivery:
 — test with dipiridamolum;
 — test with adenosine.

50.  Veloergometry. It
allows to determine
cardiac exertion
tolerance and to
identify latent
coronary insufficiency.
This test is carried out
in patients with no
visible changes on the
ECG. Exertion
enhances cardiac
performance and,
therefore, increases
myocardial demand in
oxygen.
 In patients with affected coronary arteries, exertion
induces changes on the ECG - depressed or elevated ST-
segment by more than 1 mm from the isoelectric line, or
appearance of a negative T-wave

51. Other tool methods of ischemic
heart disease diagnostics
 1. Holter’s monitoring — prolonged registration of
electrocardiography (ECG) in conditions of free
(habitual) for a tested activity with the subsequent
analysis of the received findings on the decoder.
 2. Coronary angiography — «the gold standard» of
coronary artery lesion and atherosclerosis
diagnostics. It is carried out with the help of the
angiograph by introduction into of coronary artery
ostium of a contrast agent through a catheter with
the subsequent roentgenography.

52. Laboratory tests.
 Activity of cardiac specific
enzymes (aspartic
aminotransferase, lactate
dehydrogenase, creatine
phosphokinase) in angina is
not different from that in
normal condition. Only in a
severe course of the disease
against long-standing
myocardial ischemia,
necrosis of some
cardiomyocytes may occur.
In these cases, a slightly
increased activity of these
enzymes is noted.
 The most specific and sensitive laboratory test for
diagnosing cardiomyocyte necrosis a test for
determining the level of troponins in blood serum.

53.  Echocardiography in patients with angina
reveals signs of local myocardial contractility.

54. Coronary angiography
 It allows to specify
the location, extent
and nature of
lesion in the
coronary vessels.
These findings are
necessary to make
a decision on the
expediency of
surgical
intervention.
 Coronary angiography of a
critical sub-occlusion of the
common trunk of the left
coronary artery and the
circumflex artery.

55. Samples of diagnosis formulations:
1. Coronary heart disease. Angina of
effort. FC III. Chronic heart failure,
stage I.
 2. Coronary heart disease.
Progressive angina. Chronic heart
failure, stage I.

56. Treatment.
 The main objectives:
to reduce the risk of
myocardial infarction
and of a sudden
death; to reduce of
the aftereffects of an
acute ischemia of the
left ventricular
myocardium
 (disturbances in the cardiac rhythm and
conduction, and others).

57. The following medications and non-
medication measures are used for this
purpose:
 • antianginal medications: β-blockers, nitrates, slow
calcium channel blockers;
 • antithrombin preparations: heparins (unfractionated
and low-molecular), direct thrombin inhibitors;
 • antiplatelet agents, aspirin, adenosine diphosphate
receptor antagonists (thienopyridines), blockers of
glycoprotein IIb / IIIa platelet receptors;

58. Thank you for
attention!