Transcript Cardio-vascular system diseases

Cardio-vascular system diseases
Associate professor Golovata T.
Cardiovascular disease is a class of diseases
that involve the heart or blood vessels (arteries,
capillaries and veins) and is leading cause of death
in Europe and North America.
In the UK in 2009, around one third of all
deaths in the UK were due to cardiovascular
disease. Of these, over 82,000 deaths were caused
by coronary heart disease, and about 49,000 were
caused by stroke.
Types
Cardiovascular disease includes:
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coronary heart disease (heart attacks)
cerebrovascular disease (stroke)
raised blood pressure (hypertension)
peripheral artery disease
rheumatic heart disease
congenital heart disease and heart failure
valvular heart disease
cardiomyopathy - diseases of cardiac muscle
inflammatory heart disease
Risk factors

Almost all cardiovascular disease in a population
can be explained in terms of a limited number of
risk factors: age, gender, high blood pressure,
high serum cholesterol levels, tobacco smoking,
excessive alcohol consumption, family history,
obesity, lack of physical activity, psychosocial
factors, diabetes mellitus, air pollution.
Epidemiology
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The most studied mortality from cardiovascular diseases as a
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manifestation of generalized atherosclerosis. In the Russian
Federation in 2000, deaths from cardiovascular diseases was
800.9 per 100 000 population.
For comparison:
France - 182.8 (the lowest in Europe);
Japan - 187.4.
It is shown that reducing the risk of cardiovascular disease
in these countries is concerned not so much with the quality
of medical care as a way of life and eating habits.
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Atheroma (Atherosclerosis)
According to the WHO definition atherosclerosis - a
"diverse mix changes the inner lining of the
arteries, which manifest as focal deposits of
lipids, complex carbohydrates compounds, and
elements of blood circulating in the matter, the
formation of connective tissue and calcium
adjournment."
Deposits formed atheromatous plaques. The next expansion in their
connective tissue (sclerosis) and calcification of the vessel wall
leading to deformity and lumen narrowing up to their obliteration
(obstruction).
Etiology.
Causes of atheroma is not known.
There are several theories of atheroma
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Theory lipoprotein infiltration - initial accumulation of
lipoproteins in the vascular wall;
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Theory of endothelial dysfunction - primary violation of
protective properties of the endothelium and its mediators;
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Autoimmune - primary dysfunction of macrophages and
leucocytes infiltration of their vascular wall;
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Monoclonal - initial clone of abnormal smooth muscle cells;
Pathogenesis of atherosclerosis
Pathogenetic essence of atherosclerosis is the focal
putting off in the intima of the arteries so-called
atherogenic lipoproteins. Lipoproteins are spherical
particles consisting of a core and outer shell. In the
nucleus consists of triglycerides and cholesterol esters,
the composition of the outer shell - proteins,
phospholipids and cholesterol.
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Pathogenesis of atherosclerosis
Atherosclerosis is a multifactorial disease that usually
develops many years before any clinical symptoms are
manifest.
 Clinical events include ischemic heart disease (coronary
arteries), arterial occlusive disease (peripheral arteries),
stroke (cerebral arteries), kidney failure (renal arteries),
and aortic aneurism (aorta)
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Morphogenesis of atherosclerosis
Macroscopically distinguish the following
stages:
Yellow spots or bands;
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fibrous plaque
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Stage complicated changes (ulceration,
calcification, thrombosis)
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Morphogenesis of atherosclerosis
Microscopic manifestations
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The
first
stage
of
atherosclerosis is endothelial
damage
and
dysfunction,
which
stimulates
the
accumulation and oxidation of
LDL-C in the vessel wall.
Monocytes migrate from the
blood into the subendothelial
intima and transform into
macrophages,
which
accumulate lipids (foam cells)
to form the lipid core of the
atherosclerotic plaque.
Morphogenesis of atherosclerosis
Liposclerosis
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Production of inflammatory
mediators and cytokines
stimulate migration and
proliferation of smooth
muscle cells of the vascular
intima, and deposition of
extracellular matrix
molecules such as elastin
and collagen, which leads to
plaque expansion and the
formation of the fibrous cap.
Morphogenesis of atherosclerosis
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The cholesterol clefts of
lipid, along with a few
scattered foam cells and a
couple of lymphocytes,
are
seen
at
high
magnification in this
atheromatous plaque.
Morphogenesis of atherosclerosis
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Atheromatous plaques may
undergo a series of changes
resulting
in
complicated
plaques.
These
include
calcification,
ulceration,
overlying thrombus formation,
haemorrhage (as seen in this
case)
and
aneurysmal
dilatation of the vessel. It is
these changes that usually
account for the serious clinical
consequences of this disease.
Atherosclerosis of the aorta-macroscopic
pathology
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It shows multiple variable
sized atheromatous plaques
which become confluent in
the abdominal aorta. These
plaques
are
well
circumscribed,
slightly
raised and yellow/white in
colour. Some of the larger
plaques are complicated by
superficial
ulceration
with adherent thrombus
and focal dystrophic
calcification.
Complication
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Rupture of aortic aneurysm
Atherosclerosis is the most
frequent cause of aortic aneurysms.
Aneurysms is a focal stretching or
ballooning of the aorta.
Usually occur in the abdominal
aorta
When they reach a diameter of
over five centimeters (about two
inches), the risk of fatal rupture
increases. A rupturing aneurysm
may cause symptoms of abdominal
pain or rigidity, rapid heart rate,
nausea and anxiety. A rapid loss of
blood pressure (shock) may follow.
Sudden rupture is associated with a
high death rate.
Atherosclerosis of cerebral arteries
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Defined
as
cerebrovascular disease.
Manifestations
are
ischemic (usually) or
hemorrhagic stroke
Atherosclerosis of lower extremities
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Blood flow to the
extremities
may
be
reduced because of this
narrowing, and may not
adequately provide for the
need of oxygen for the
tissues.
Many patients
experience
leg
pain,
referred to as "intermittent
claudication".
complete occlusion causes
gangrene
Atherosclerosis of the renal arteries
Atrophy secondary to
renal
artery
atherosclerosis:
Gross, natural color,
both kidneys one very
atrophic
and
wrinkled. The large
left kidney weighed
220 grams and the
small left one 90 gram
HYPERTENSION (High Blood Pressure)
Hypertension is the commonest cause of cardiac
failure in many societies and a major risk factor for
atherosclerosis. Furthermore, it is a major risk factor
for cerebral haemorrhage, another leading cause of
death worldwide. There is no universally agreed
definition of hypertension, but most authorities would
accept that a sustained resting blood pressure of more
than 160/95 mmHg is definite hypertension
Aetiological classification
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Essential (primary) hypertension: Genetic
susceptibility. Excessive sympathetic nervous
system activity. Abnormalities of Na/K membrane
transport. High salt intake. Abnormalities in
renin-angiotensin-aldosterone system.
Aetiological classification
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Secondary hypertension: Chronic renal failure.
Renal artery stenosis. Glomerulonephritis.
Endocrine causes. Adrenal tumours (cortical or
medullary). Cushing's syndrome. Coarctation of
aorta.
Pathological classification
Hypertension is classified also according to the
clinicopathological consequences of the blood
pressure elevation. Benign or essential hypertension
is often asymptomatic and discovered only during a
routine
medical
examination.
Malignant
hypertension is a serious condition necessitating
prompt treatment to minimise organ damage or the
risk of sudden death from cerebral haemorrhage
Vascular lesions in hypertension
Aorta-elastofibrosis
Arteries-hyperelastosis.
Arteriolar- hyalinosis
Myocardial changes-left ventricular
hypertrophy
Hypertension
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The
characteristic
histological lesion of
malignant hypertension is
fibrinoid necrosis of small
arteries and arterioles
Changes in kidneys - Primary-wrinkled
kidney
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The underlying sclerosis and hyalinosis of arterioles
renal glomeruli (1.2). Kidney wrinkled, its fine-grained
surface.
CORONARY (ISCHEMIC) HEART
DISEASE
Ischemic heart disease (IHD), or myocardial
ischaemia, is a disease characterized by
ischaemia (reduced blood supply) of the
heart muscle, usually due to coronary
artery disease (atherosclerosis of the
coronary arteries).
Classification of IHD
1.
2.
3.
4.
Sudden coronary death.
Angina
Myocardial infarction
Heart failure
The immediate cause of myocardial
infarction
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progressive atherosclerotic stenosis
erosion of an atheromatous plaque with
superimposed thrombosis
rupture of the fibrous cap of a plaque with
haemorrhage into the lesion and thrombosis
prolonged coronary spasm against her
atherosclerotic lesions
Cause of myocardial infarction.
Thrombosis of coronary artery, gross.
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This is thrombosis in a
coronary artery. Such a
thrombus
severely
narrows or occludes the
lumen and can produce a
sudden ischemic event.
"Sudden death" as well as
infarction can occur.
Cause of myocardial infarction.
Thrombosis of coronary artery, microscopic.
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This severely narrowed
coronary artery has the
remaining lumen filled by
thrombus.
Classification myocardial infarction
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Transmural: associated
with
atherosclerosis
involving
a
major
coronary artery. It can
be subclassified into
anterior,
posterior,
inferior, lateral or septal.
Classification myocardial infarction
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Subendocardial:
involving a small area in
the subendocardial wall of
the left ventricle,
ventricular septum, or
papillary muscles.
Myocardial infarction. Morphology
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24 - 72 hours from onset. Total loss of nuclei and striations
along with heavy neutrophilic infiltrate
Myocardial infarction- scarring
Complications
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Arrhythmias
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Extension of infarction, or re-infarction
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Congestive heart failure (pulmonary edema)
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Cardiogenic shock
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Pericarditis
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Mural thrombosis, with possible embolization
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Myocardial wall rupture, with possible tamponade
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Papillary muscle rupture, with possible valvular insufficiency
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Ventricular aneurysm formation
Complications
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When the infarction is 3 to 5
days old, the necrosis and
inflammation are most extensive,
and the myocardium is the
softest, so that transmural
infarctions may be complicated
by rupture. A papillary muscle
may rupture as well to produce
sudden valvular insufficiency.
Rupture through the septum
results in a left-to-right shunt and
right heart failure.
Complications
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A cross section through
the heart reveals a
ventricular aneurysm with
a very thin wall at the
arrow. Note how the
aneurysm bulges out. The
stasis in this aneurysm
allows mural thrombus,
which is present here, to
form within the aneurysm.
Cardiomyopatias
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Cardiomyopathies are diseases of heart muscl.
Cardiomyopathies include a variety of myocardial
disorders that manifest with various structural and
functional phenotypes and are frequently genetic.
Although some have defined cardiomyopathy to include
myocardial disease caused by known cardiovascular
causes (such as hypertension, ischemic heart disease, or
valvular disease), current major society definitions of
cardiomyopathy exclude heart disease secondary to such
cardiovascular disorders.
Cardiomyopatias
-classification
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Dilated cardiomyopathy (DCM)
Hypertrophic cardiomyopathy (HCM)
Restrictive cardiomyopathy (RCM)
Arrhythmogenic right ventricular
cardiomyopathy/dysplasia (ARVC/D)
Unclassified cardiomyopathies
Dilated cardiomyopathy
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Illustration of dilated
cardiomyopathy (right),
showing a dilated left
atrium and left ventricle,
bulging interventricular
septum from left to right,
and thin ventricular walls.
For comparison, a normal
heart is shown on the left.
Hypertrophic cardiomyopathy
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Illustrations of a normal
heart (left) and a heart
with
hypertrophic
cardiomyopathy (HCM).
Note that the heart walls
(muscle)
are
much
thicker (hypertrophied)
in the HCM heart.
Restrictive cardiomyopathy
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Illustration of dilated
cardiomyopathy fibrosis under the
endocardium and in
the the inner third of
the myocardium.
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