CARDIOVASCULAR DISEASES

practical clinic class

for 3nd years students
(medical faculty)
АTHEROSCLEROSIS

is chronic disease affecting primary the

intima of large and medium-sized elastic and
muscular-elastic arteries and is characterized
by deposition and accumulation in it plasma
atherogenous apoprotein-B-containing
lipoproteins with father vegetation of
connective tissue and fibrofatty plaques or
atheromas formation.
CLASSIFICAION OF АTHEROSCLEROSIS (А. L. Myasnikov,
1960)

Localization of the process: 1. Aorta. 2. Coronary

arteries. 3. Cerebral arteries. 4. Renal arteries. 5.
Mesenteric arteries. 6. Inferior limbs arteries.

Clinical aspects:
I period (preclinical): а) vasomotor disturbances; b)
complex of laboratory disturbances.
II period (clinical): stages а) ischemic; b)
trombonecrotic; c) sclerotic.

Fazes of course: 1. Progression of atherosclerosis. 2.

Stabilization of process. 3. Regression of
atherosclerosis.
PATHOGENESIS OF ATHEROSCLEROSIS
Atherosclerosis starts from endothelial injury
causes adherence, aggregation and platelet release
reaction at the site of exposed subendothelial
connective tissue.

Increase of endothe-
lium and endothelian
membrane permeability and
migration of smooth myocytes
and magrophagocytes into
tunica intima. These cells
accumulate lipids and
transform into foam cells.

Proliferation of intimal smooth muscle cells is

stimulated by various mitogens, the most
important of which is platelet-derived growth
factor (PDGF); others are fibroblast growth factor,
epidermal growth factor, and transforming growth
factor-alpha (TGF-α).
 MORPHOGENESIS OF ATHEROSCLEROSIS

Kinds of atherosclerotic changes (macroscopic):

- fatty streaks and dots ,

- fibrous plaques,
- complicated plaques
(plaques with ulceration,
haemorrhages and
thrombosis)
- calcification, or
atherocalcification
MORPHOGENESIS OF ATHEROSCLEROSIS

Kinds of atherosclerotic changes (macroscopic):

- fatty streaks and dots ,

- fibrous plaques,
- complicated plaques (plaques with
ulceration, haemorrhages and
thrombosis)
- calcification, or atherocalcification
 MORPHOGENESIS OF ATHEROSCLEROSIS

Kinds of atherosclerotic changes (macroscopic):

- fatty streaks and dots ,

- fibrous plaques,
- complicated plaques (plaques with
ulceration, haemorrhages and
thrombosis)
- calcification, or atherocalcification
Stages of atherosclerosis morphogenesis (microscopic):

- prelipid,
- lipoidosis,
- liposclerosis,
- atheromatosis,
- ulceration,
- atherocalcification.
MORPHOGENESIS OF ATHEROSCLEROSIS

Foam cells in
atherosclerotic plague

The ulcerated plaque and the areas of

endothelial damage are vulnerable sites for
formation of superimposed thrombi. These
thrombi may get dislodged to become emboli
and lodge elsewhere in the circulation, or may
get organised and incorporated into the arterial
wall as mural thrombi.
ATHEROSCLEROSIS OF AORTA

Aneurysm of aorta – dilation of aorta

wall in the place of it`s damage (more often
ulceration).

There are:
- cylindrical,
- bag like,
- hernia like,
- dissected aneurysms.
 COMPLICATIONS OF ATHEROSCLEROSIS
Resulting from acute ischemia of tissues and organs are:

gangrene,
infarct,
haemorrhages
 HYPERTENSIVE DISEASES

is disease of cardiovascular system resulting from

primary disfunction (neurosis) of regulating nerve
centers and neurohormonal and renal mechanisms,
which is characterized by arterial hypertension,
functional and then structural changes of kidney,
heart, central nerve system.

Symptomatic arterial hypertension — arterial hypertension

caused by diseases or lesions of some organs, which take
part in the regulation of arterial pressure.
HYPERTENSIVE DISEASES

Classification (WHO; М. S. Кushakovsky, 1982)

I. Range of arterial pressure.

II. Classification according to certain organs lesions.

III. Classification according to etiology.

IV. Classification according to course: 1. Benign arterial

hypertension (with slow progression). 2. Malignant АH
(with rapid progression).
 HYPERTENSIVE DISEASES

Classification according to etiology:

1. Essential (primary).

2. Symptomatic (secondary):
а) renal pathology (stenosis of renal arteries,
glomerulonephritis, pyelonephritis, tuberculosis, cysts,
tumors, hydronephrosis);
б) diseases of adrenal glands cortex (primary
hyperaldosteronism, Icenko- Cushing syndrome, and other);
в) diseases of adrenal glands medullar
(pheochromocytoma);
г) aorta coarctation;
д) due to use of hypertensive medicins, oral
contraceptives, glucocorticoid hormons.
HYPERTENSIVE DISEASES

Clinicomorphological stages:

1. Preclinical

2. Distributed changes of arteries

3. Changes of organs due to intraorgan blood supply disturbances

HYPERTENSIVE DISEASES

Clinicomorphological forms:

1. Cardiac (base of ischemic heart disease)

2. Cerebral (base of cerebrovascular diseases)

3. Renal (consists of а) acute changes – infarcts of kidney

and arteriolonecrosis, b) chronic changes – hyalinosis,
arteriolosclerosis)
 CEREBROVASCULAR DISEASES
Transitory ischemia of brain is characterized by acute
appearance of local neurological symptoms usually without
general cerebral symptoms (rarely with weak signs) due to
short time local brain ischemia. Local neurological symptoms
continue from some minutes (5-20 min.) to some hours
(rarely to 24) and is completed with restore of disturbed
functions during 24 hours.
Morphologically it is characterized by vascular disturbances
(spasm of arteriols, serum imbibitions of their walls, perivascular
edema and single small haemorrhages) and local changes of brain
tissue (edema, dystrophic changes of neurons).
Sometimes perivascular accumulation of haemosiderin is
revealed at the place of former small haemorrhages.
 CEREBROVASCULAR DISEASES

Stroke - acute (sudden) developed local disturbance of

brain supply which is accompanied with lesion of brain matter
and its functions.

There are:
haemorrhagic stroke (haematoma or
haemorrhagic imbibitions of brain
matter);
ischemic stroke (morphologically is
characterized by infarct development
or gray malacia of brain).
MAIN KINDS OF CEREBRAL ARTERIES LESIONS RESULTING IN
BLOOD SUPPLY DISTURBANCES(ACCORDING TO THEIR ETIOLOGICAL
FACTORS)

1. Occlusive damages (atherosclerotic stenosis and

thrombosis, embolisms, arteriitis of different etiology,
fibromuscular dysplasia and other);
2. Extravascular compressions (compression by osteophyts,
articular processes, muscles, vessels, tumors, scars and
other);
3. Deformation (pathological curves, thrombosis);
4. Abnormalities (hypoplasia, abnormalities of beginning,
localization, topography and other).
CEREBROVASCULAR DISEASES
CEREBROVASCULAR DISEASES
CEREBROVASCULAR DISEASES
CEREBROVASCULAR DISEASES
CEREBROVASCULAR DISEASES
ISCHEMIC HEART DISEASE

Ischemic heart disease – the group of diseases,

resulting from absolute or relative coronary blood supply
insufficiency.

It is cardiac form of atherosclerosis and

hypertensive vascular diseases.
 ISCHEMIC HEART DISEASE
Ischemic heart disease is caused
by an imbalance between the
myocardial blood flow and the
metabolic demand of the
myocardium.

Reduction in
coronary blood flow is
Norm
related to progressive
atherosclerosis with
increasing occlusion of
coronary arteries.
 ISCHEMIC HEART DISEASE
Ischemic heart disease is caused
by an imbalance between the
myocardial blood flow and the
metabolic demand of the
myocardium.

Blood flow can be further

decreased by superimposed events
such as vasospasm, thrombosis, or
circulatory changes leading to
hypoperfusion.
ISCHEMIC HEART DISEASE

Factors reducing coronary blood flow include:

1. Decreased aortic diastolic pressure
2. Increased intraventricular pressure and myocardial
contraction
3. Coronary artery stenosis, which can be further
subdivided into the following etiologies:
- Fixed coronary stenosis
- Acute plaque change (rupture, hemorrhage)
- Coronary artery thrombosis
- Vasoconstriction
4. Aortic valve stenosis and regurgitation
5. Increased right atrial pressure
 ISCHEMIC HEART DISEASE

acute chronic
-
myocardium ischemic - cardiosclerosis (diffuse smallfocal,
dystrophy postinfarction largefocal)
-
myocardium infarction
 ISCHEMIC DYSTROPHY OF MYOCARDIUM, OR ACUTE FOCAL DYSTROPHY OF
MYOCARDIUM

results from short time coronary blood flow disturnbances,

when typical electrocardiogramma changes arise and
myocardium necrosis is absent and there are no changes of
enzymes activity.

Myocardium is soft and pale,

sometime with edema.
Frequently the resent trombus is
revealed in coronary artery.
ISCHEMIC DYSTROPHY OF MYOCARDIUM

Microscopic signs: dilatation of capillaries, stasis and

sludge- phenomena of erythrocytes, edema of interstitial
tissue, perivascular hemorrhages, leukocyte infiltration of
boundary zone.
Muscular fibres loose their striation, glycogen, are
intensively stained by eosin, fuchsin, pyronin and Schiff-
substance (evidences of necrobiotic changes).

Staining with orange acrydin provide green color of

muscular fibres in luminescent microscopy (normal fibres
are orange).
Complications - acute heart failure.

Direct cause of death - acute heart failure.

 MYOCARDIAL INFARCTION (MI)

Myocardial infarction – is ischemic necrosis of myocardium.

Usually it is pale (white)

infarction with haemorrhagic
crown.
The pathogenesis can include:
- occlusive intracoronary
thrombus - a thrombus overlying
an ulcerated or fissured stenotic plaque causes 90% of transmural
acute myocardial infarctions.
- vasospasm - with or without coronary atherosclerosis and
possible association with platelet aggregation.
- emboli - from left sided mural thrombosis, vegetative
endocarditis, or paradoxic emboli from the right side of heart through
a patent foramen ovale.
MYOCARDIAL INFARCTION
Myocardial infarction is classified according:

- time of it's appearance;

- localization in different parts of
heart and myocardium;
- spreading;
- duration.

Primary (acute) MI continues 4 weeks from the onset of

myocardium ischemia.
Secondary MI - develops in 4 weeks after primary one.
Recurrent MI – arises during 4 weeks after appearance of primary
one.
 MYOCARDIAL INFARCTION
The gross morphologic appearance of a myocardial infarction can vary. Patterns include:

-
subendocardial infarct
(multifocal areas of necrosis
confined to the inner 1/3-1/2 of
the left ventricular wall. These do
not show the same evolution of
changes seen in a transmural MI);
MI)
- subepicardial infarct;
-
intramural infarct (in middle part
of myocardium).

Subepicardial and transmural infarcts are complicated with

inflamation of heart external coat – fibrinous pericarditis.
 MYOCARDIAL INFARCTION

According to spreading of necrotic changes in the

myocardium there are:

- small focal;
- large focal;
- transmural infarction (involving
the entire thickness of the left
ventricular wall from endocardium
to epicardium, usually the anterior
free wall and posterior free wall
and septum with extension into
the RV wall in 15-30%. Isolated
infarcts of RV and right atrium are
extremely rare).
MYOCARDIAL INFARCTION
Gross morphologic changes evolve over time as follows:

Time from Onset Gross Morphologic Finding

18 - 24 Hours Pallor of myocardium

24 - 72 Hours Pallor with some hyperrhemia
3 - 7 Days Hyperrhemic border with central
yellowing
10 - 21 Days Maximally yellow and soft with vascular
margins
7 weeks White fibrosis
 MYOCARDIAL INFARCTION

Microscopic morphologic changes evolve over time as follows:

Time from Microscopic Morphologic Finding
Onset
1 - 3 Hours Wavy myocardial fibers
2 - 3 Hours Staining defect with tetrazolium or basic fuchsin
dye
4 - 12 Hours Coagulation necrosis with loss of cross
striations, contraction bands, oedema,
hemorrhage, and early neutrophilic infiltrate
18 - 24 Hours Continuing coagulation necrosis, pyknosis of
nuclei, and marginal contraction bands
24 - 72 Hours Total loss of nuclei and striations along with
heavy neutrophilic infiltrate
3 - 7 Days Macrophage and mononuclear infiltration begin,
MYOCARDIAL INFARCTION
There are 2 stages of myocardium infarction course:
- necrotic;
- stage of scaring.
Necrotic stage microscopically is characterized:
- perivascular small foci of normal
cardiomyocytes мелкие участки;
-
necrosis zone is bordered by
demarcation zone (with
hyperrhemia and leucocytes
infiltration.
-
outside necrosis irregular
blood fullness, hemorrhages,
disappearance of glycogen from
cardiomyocytes and appearance
in them lipids, destruction of
mitochondria and sarcoplasmatic
network, necrosis of single
muscular fibres.
 MYOCARDIAL INFARCTION
Scaring stage (organization) continues 7–8 weeks.
Organization of infarction
origins as from demarcation
zone as from the “islands” of
kept tissue in the necrotic
zone.
Macrophagocytes resolve
necrotic masses, in their
cytoplasm lipids and products
of cells degradation appear.

Fibroblasts take part in

fibrillogenesis.
Slides
№27 Atherosclerosis of artery(st. hematoxylin and eosin)
№13а Hyalinosis
(st. hematoxylin and eosin)
 №50 Normal myocardium

№50 Hypertrophy of myocardium

(st. hematoxylin and

eosin)
№98 Haemorrhage in the pia
mater
(st. hematoxylin and eosin)
№107 Large focal cardiosclerosis
(st. hematoxylin and eosin)
№109 Myocardium infarction(st.
hematoxylin and eosin)