Cardiovascular Pathology

AJ

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 Learning tasks
At the end of this session, students are expected to be
able to:
• Explain diseases of the arteries.
• Explain diseases of the veins.
• Explain diseases of the lymphatics.
• Explain diseases of the heart.

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 Overview of Cardiovascular
disorders
• Diseases of the arteries.
• Diseases of the veins. Vascular diseases
• Diseases of the lymphatics.
• Heart diseases.
– Hypertensive Heart Diseases.
– Ischemic Heart Diseases.
– Infections/inflammatory.
– Congenital Heart Diseases.
• Cardiovascular tumors.

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Structure of Blood vessel

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 Vascular diseases
• Vascular disease is responsible for more morbidity
and mortality.
• Most clinically significant lesions involve arteries.
• Venous pathology can also cause clinical disorders.
• Endothelial injury contributes to a host of pathologies
including thrombosis, atherosclerosis and
hypertensive vascular lesions.
– For example, endothelial cells denudation stimulates
clotting.

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 Vascular diseases cont…
• Vascular disease develops through two principal
mechanisms:
1. Narrowing or complete obstruction of vessel lumina,
occurring:
– Acutely (e.g., by thrombosis or embolism).
– Progressively (e.g., by atherosclerosis).
2. Weakening of vessel walls, causing dilation and/or
rupture.

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Emboli- blood clot (thromboemboli), air, fat, amniotic fluid

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 Arteriosclerosis
• Arteriosclerosis literally means “hardening of the
arteries”.
– It is a generic term reflecting arterial wall thickening and
loss of elasticity.
– It affects small arteries and arterioles
• There are (3) distinct types are arteriosclerosis:
a) Arteriolosclerosis.
b) Medial calcific sclerosis (Mönckeberg medial
sclerosis).
c) Atherosclerosis.
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 Arteriosclerosis

Arteriosclerosis
Hardening

Atherosclerosis M edial Calcific Arteriolosclerosis

Large BV Sclerosis Sm all vessel
Intim a M edia Full thickness
Mockenberg’s

Hyaline Hyperplastic
 a. Arteriolosclerosis
Types of Arteriolosclerosis
1. Hyaline arteriolosclerosis.
– Associated with benign hypertension, diabetes mellitus.
– Homogeneous, pink hyaline thickening of arteriolar walls,
loss of underlying structural detail and luminal narrowing.
2. Hyperplastic arteriolosclerosis.
– Hyperplastic arteriolosclerosis is more typical of severe
hypertension.
– Vessels exhibit “onionskin,” concentric, laminated
thickening of arteriolar walls and luminal narrowing.

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• Fibrinoid necrosis takes
place in hyperplastic
arteriolosclerosis.
• It results in the death of
cells in small blood
vessels due to high
blood pressure that
damages the cells in the
blood vessels.

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 b. Medial calcific sclerosis
(Mönckeberg medial sclerosis).
• Calcification of the media of large and medium-sized
muscular arteries, especially of the extremities and of
the genital tract. (in arteries of the thyroid and uterus)
• Affect persons past the age of 50.
– Condition occurs as an age-related degenerative process.
• It is an example of dystrophic calcification.
• Characterized by calcification of the internal elastic
layer of arterial wall but without thickening or
narrowing of the vessel lumen

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• It is a non-obstructive calcification in the internal elastic
lamina or tunica media of muscular arteries

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 c. Atherosclerosis
• A specific form of arteriosclerosis affecting primarily
the intima of large and medium-sized muscular
arteries, characterized by deposition of fibrofatty
plaques (atheromas).
– Chronic inflammatory disorder of intima of large &
medium-sized arteries characterised by formation of
fibrofatty plaques called atheroma.
• The term ‘atherosclerosis’ is derived from:
– athero (meaning porridge) referring to the soft lipid-rich
material in the centre of atheroma.
– sclerosis (hardening/scarring) referring to connective tissue
in the plaques. 17
• It is characterized by thickening of the intima
with plaques that can contain lipid-laden
macrophages (foam cells).
• The plaques contain free lipid (cholesterol)
and are prone to calcification and ulceration

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 Atherosclerosis cont…
• Most commonly affected vessels are the aorta, the
coronary and cerebral arterial systems.
• Therefore, the major clinical syndromes resulting
from ischaemia due to atherosclerosis pertain to
the:
– Heart (angina and myocardial infarcts or heart attacks).
– Brain (transient cerebral ischaemia and cerebral
infarcts or strokes.

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 Risk factors of Atherosclerosis
Major Minor(modifiable)
Constitutional(non 1. Environmental
modifiable) influences.
1. Age. 2. Obesity.
2. Sex. 3. Hormones-OCs,
Oestrogen deficiency.
3. Genetic factors. 4. Physical inactivity.
4. Familial & racial factors. 5. Stress.
Modifiable: 6. Infections
5. Hyperlipidemia (LDL). ([Link],
6. Hypertension. herpesvirus, CMV)
7. Homocystenuria.
7. Diabetes mellitus.
8. Alcohol. 21
8. Smoking.
 Pathogenesis of Atherosclerosis
• According response-to-injury hypothesis
atherosclerosis results from the following events:
i. Endothelial injury and resultant endothelial
dysfunction.
– Increased permeability, leukocyte adhesion, thrombosis.
ii. Accumulation of lipoproteins (mainly oxidized LDL
and cholesterol crystals) in the vessel wall.
iii. Platelet adhesion.
iv. Monocyte adhesion to the endothelium, migration
into the intima and differentiation into macrophages
and foam cells. 22
 Pathogenesis of Atherosclerosis
cont…
v. Lipid accumulation within macrophages, which
release inflammatory cytokines.
vi. Smooth muscle cell recruitment due to factors
released from activated platelets, macrophages, and
vascular wall cells.
vii. Smooth muscle cell proliferation and ECM
production.

Refer to Handout 26.1 for additional information on

Atherosclerosis.
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Complications of atherosclerosis
Local Distant/systemic
1. Luminal narrowing/ 1. Embolism.
obstruction. 2. Hemorrhage/shock.
2. Thrombosis, 3. Ischaemia/infarction-end
thromboembolism. organ failure.
3. Fibrosis and calcification. – Stroke, myocardial
4. Necrosis. Infarctions, renal
5. Aneurysm infarction, mesenteric
6. Rupture causing vein thrombosis,
hemorrhage. intermittent claudication,
gangrene +/-
amputations etc.
4. Sudden death.
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Pathogenesis of Aneurysms
and Dissections

AJ

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 Aneurysm
• An aneurysm is defined as a permanent abnormal
dilatation of a blood vessel occurring due to
congenital or acquired weakening or destruction of
the vessel wall.
• Most commonly aneurysms involve large elastic
arteries especially the aorta and its major branches.
• Aneurysms can cause various complications such as:
1. Thrombosis and thromboembolism causing ischemia.
2. Alteration in the flow of blood (stasis).
3. Rupture of the vessel.
4. Compression of neighbouring structures.
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 Causes of Aneurysm
• Conditions that weaken vessel walls and lead to
aneurysms include:
i. Trauma.
ii. Vasculitis.
iii. Congenital defects. (berry aneurysm)
iv. Infections (mycotic aneurysms, syphilis)
v. Atherosclerosis.
vi. Hypertension.

NOTE: Atherosclerotic aneurysms occur most frequently in the

abdominal aorta, but the common iliac arteries, aortic arch, and
descending thoracic aorta can also be involved.
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 Classification of Aneurysms
1. Depending upon the composition of the wall:
i. True aneurysm.
ii. False aneurysm.
2. Depending upon the shape:
i. Saccular.
ii. Fusiform.
iii. Cylindrical.
iv. Serpentine.
v. Racemose.

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Classification of Aneurysms cont…

3. Based on pathogenetic mechanisms:

i. Atherosclerotic (arteriosclerotic) aneurysms
ii. Syphilitic (luetic) aneurysms
iii. Mycotic aneurysms
iv. Berry aneurysms
v. Dissecting aneurysms

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 Arterial dissection
• Occurs when blood splays apart laminar planes of the
tunica media to form a blood-filled channel within the
arterial wall.
• The most common site is the aorta.
• Pressurized blood gains entry to arterial wall through
a surface defect and then pushes apart underlying
layers.
• Arterial dissections are important causes of stasis and
subsequent thrombosis.
• Arterial dissections also have a propensity to rupture
often with catastrophic results.
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Veins and lymphatics

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 Diseases of veins
• Varicosities are abnormally dilated and tortuous
veins.
• The veins of lower extremities are involved most
frequently called varicose veins.
• The veins of other parts of the body which are
affected are:
– Lower oesophagus (oesophageal varices).
– Anal region (haemorrhoids).
– Periumbilical veins of the abdominal wall (forming a caput
medusae).
– Spermatic cord (varicocele).
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 Varicose veins
• These are permanently dilated and tortuous
superficial veins of the lower extremities.
– Long saphenous vein and its tributaries.
– Produced by chronically increased intraluminal pressures
and weakened vessel wall support.
• Occurs at 4th and 5th decades of life.
• Females are affected more commonly than the males.
• Obesity increases the risk.
• Pregnancy also a risk factor.
• Familial tendency toward premature varicosities.
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 Varicose veins cont…
• Clinical features:
1. Lower extremity stasis.
2. Congestion.
3. Edema.
4. Pain.
5. Thrombosis.
• Complications include: Persistent edema in the
extremity and secondary ischemic skin changes
(stasis dermatitis and ulcerations).
– Ulcerations can become chronic varicose ulcers as a
consequence of poor wound healing and superimposed
infections. 44
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 Thrombophlebitis
(Phlebothrombosis)
• ‘Phlebothrombosis’ and ‘thrombophlebitis’ are used
synonymously.
• Thrombophlebitis is a condition that causes blood
clot to form and block one or more veins, often in the
legs.
 Superficial thrombophlebitis: the vein is near the
surface of the skin
 Deep vein thrombosis: the vein is deep within the
muscle
• Thrombosis of deep leg veins accounts for more than
90% of cases. 46
• Other locations for thrombophlebitis are:
– Periprostatic venous plexus in males.
– Pelvic veins in the females.
– Near the foci of infection in the abdominal cavity such as
acute appendicitis, peritonitis, acute salpingitis and pelvic
abscesses.

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 Etiopathogenesis of Thrombophlebitis
(Phlebothrombosis)
• Venous thrombosis precedes thrombophlebitis.
– It is initiated by triad of changes: endothelial damage,
alteration in the composition of blood and venous
stasis.
• Factors that predispose to those changes are:
– Cardiac failure.
– Malignancy.
– Use of oestrogen-containing compounds.
– Postoperative state.
– Immobility due to various reasons.

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 Clinical effects of Thrombophlebitis
(Phlebothrombosis)
Local Systemic
• Oedema distal to Due to embolic phenomena
occlusion (Swelling). • Pulmonary
• Heat. thromboembolism (most
• Pain and tenderness. common and most
• Redness. important).
• Others: bacteremia and
septic embolisation to
brain, meninges, liver etc.

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Deep vein thrombosis

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Causes of deep vein thrombosis
• Congestive cardiac failure
• Neoplasia
• Pregnancy
• Obesity
• Postoperative state
• Immobilization
• Polycythemia vera
• Genetic hypercoagubility
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 Diseases of Lymphatics
Lymphangitis and Lymphedema
• Primary disorders of lymphatic vessels are extremely
uncommon.
• Much more commonly, lymphatic vessels are
involved by:
– Inflammatory.
– Infectious.
– Malignant processes secondarily.

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 Lymphangitis
• Acute inflammatory process caused by bacterial
seeding of the lymphatic vessels.
• Clinically, the inflamed lymphatics appear as red,
painful subcutaneous streaks.
• Usually associated with tender enlargement of
draining lymph nodes (acute lymphadenitis).
• If bacteria are not contained within the lymph
nodes, they can pass into the venous circulation
and cause bacteremia or sepsis.

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 Lymphedema
• Can be primary or secondary.
• Primary lymphedema can occur as:
– Isolated congenital defect (simple congenital
lymphedema).
– Familial Milroy disease (heredofamilial congenital
lymphedema) resulting from agenesis or hypoplasia of
lymphatics.

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 Lymphedema cont…
Secondary or obstructive lymphedema.
• Accumulation of interstitial fluid behind an
obstructed previously normal lymphatic.
• Obstruction can result from various disorders/
conditions:
1. Tumors involving either the lymphatic channels or the
regional lymph nodes.
2. Surgical procedures that sever lymphatic connections
(e.g., axillary lymph nodes in radical mastectomy).
3. Postradiation fibrosis.
4. Filariasis.
5. Postinflammatory thrombosis and scarring.
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 Lymphedema cont…
• Lymphedema increases the hydrostatic pressure in the
lymphatics distal to obstruction and causes edema.
– Chronic edema in turn may lead to deposition of ECM and
fibrosis, producing brawny induration or a peau d’orange
appearance of the overlying skin.
• Eventually, inadequate tissue perfusion can lead to skin
ulceration.
• Rupture of dilated lymphatics, typically following
obstruction by an infiltrating tumor mass.
– Lead to milky accumulations of lymph in various spaces:
• Chylous ascites (abdomen)
• Chylothorax (pleura)
• Chylopericardium. 61
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Pathology of HHD

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 Hypertension
• Hypertension is a common disorder affecting 25% of
the population.
• It is a major risk factor for atherosclerosis, congestive
heart failure, and renal failure.
• There are two (2) types:
– Primary (essential).
– Secondary.
• Essential hypertension represents 95% of cases.
• It is a complex, multifactorial disorder, involving
both environmental influences and genetic factors.
Refer to Handout 26.1 for additional information on64
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 Hypertensive heart disease
(Hypertensive cardiomyopathy)
• It is the disease of the heart resulting from systemic
hypertension of prolonged duration and manifesting
by left ventricular hypertrophy.
• Even mild hypertension of sufficient duration may
induce hypertensive heart disease.
• Second most common form of heart disease.
• Most patients of hypertensive heart disease have
advanced coronary atherosclerosis and may develop
progressive ischemic heart disease.

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 Hypertensive Heart Disease
• Major cardiac complications of hypertension result
from pressure overload and ventricular hypertrophy.
• Myocyte hypertrophy is an adaptive response to
pressure overload.
– There are limits of myocardial adaptive capacity, however,
and persistent hypertension eventually can culminate in
dysfunction, cardiac dilation, CHF, and even sudden death.
• Hypertensive heart disease most commonly affects
the left side of the heart secondary to systemic
hypertension

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 Hypertensive Heart Disease cont…

• The chronic pressure overload of systemic

hypertension causes left ventricular concentric
hypertrophy, often associated with left atrial dilation
due to impaired diastolic filling of the ventricle.
– Persistently elevated pressure overload can cause
ventricular failure with dilation.
• Cor pulmonale results from pulmonary hypertension
due to primary lung parenchymal or vascular
disorders.
– Hypertrophy of both the right ventricle and the right atrium
is characteristic.
– Dilation also may be seen when failure supervenes. 68
 Ischemic Heart Diseases (IHD)
• The manifestations of IHD are a direct consequence of
the insufficient blood supply to the heart.
• The clinical presentation may include one or more of
the following cardiac syndromes:
1. Angina pectoris (literally, “chest pain”).
2. Acute myocardial infarction (MI).
3. Chronic IHD with CHF.
4. Sudden cardiac death (SCD).
Refer to Handout 26.2 for additional information on
Ischemic Heart Diseases.
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List of Congenital heart diseases
1. Ventricular septal 8. Atrioventricular septal
defect. defect.
2. Atrial septal defect. 9. Transposition of great
3. Tetralogy of Fallot. arteries.
4. Coarctation of aorta. 10. Truncus arteriosus.
5. Pulmonary stenosis. 11. Total anomalous
6. Aortic stenosis pulmonary venous
connection.
7. Patent ductus
arteriosus. 12. Tricuspid atresia.

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 Key points
• Atherosclerosis is an intima-based lesion composed
of a fibrous cap and an atheromatous core.
• Aneurysms are congenital or acquired dilations of the
heart or blood vessels that involve the entire wall
thickness.
• Dissections occur when blood enters the wall of a
vessel and separates the various layers.
• Varicosities are abnormally dilated and tortuous
veins.
• Major cardiac complications of hypertension result
from pressure overload and ventricular hypertrophy.
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 Review questions
1. Explain pathophysiology of atherosclerosis.
2. Mention five (5) causes of aneurysms.
3. List three (3) complications of aortic dissection.
4. Mention five (5) risk factors of deep venous
thrombosis.
5. List five (5) causes of secondary lymphedema.

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 References
• Goljan E.;(2007): Rapid Review Pathology (2 th Ed.)
Elsevier Saunders, USA. Pg. 152-194.
• Kumar V. ; Abbas A. K. ; Aster J. C.;(2013): Robbins
and Contran Pathologic Basis of Disease (9th Ed.)
Elsevier Saunders, USA. Pg. 327-356.
• Mohan H.;(2010): Text book of Pathology (6 th Ed.)
Jaypee Brothers Medical Publishers, India. Pg. 390-
423.
• Xiu P.;(2012): Crash Course Pathology (4th Ed.)
Elsevier Saunders, USA. Pg. 55-85.
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