Session 26 Cardiovascular Pathology

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Lecture Notes

Session 26: Cardiovascular Pathology

Alex Simon (MD)

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.

Overview of Cardiovascular disorders

Diseases of the arteries.

Diseases of the veins.

Diseases of the lymphatics.

Heart diseases.

Hypertensive Heart Diseases.

Ischemic Heart Diseases.

Infections/inflammatory.

Congenital Heart Diseases.

Cardiovascular tumors.

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.

Vascular diseases cont…

Vascular disease develops through two principal mechanisms

Narrowing or complete obstruction of vessel lumina, occurring

Acutely (e.g., by thrombosis or embolism).

Progressively (e.g., by atherosclerosis).

Weakening of vessel walls, causing dilation and/or rupture.

Arteriosclerosis

Arteriosclerosis literally means “hardening of the arteries”.

It is a generic term reflecting arterial wall thickening and loss of elasticity.

There are (3) distinct types are arteriosclerosis

Arteriolosclerosis.

Medial calcific sclerosis (Mönckeberg medial sclerosis).

Atherosclerosis.

Mockenberg’s

Types of arteriolosclerosis

Hyaline arteriolosclerosis.

Associated with benign hypertension, diabetes mellitus.

Homogeneous, pink hyaline thickening of arteriolar walls, loss of underlying structural detail and luminal narrowing.

Hyperplastic arteriolosclerosis.

Hyperplastic arteriolosclerosis is more typical of severe hypertension.

Vessels exhibit “onionskin,” concentric, laminated thickening of arteriolar walls and luminal narrowing.

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.

Affect persons past the age of 50.

Condition occurs as an age-related degenerative process.

It is an example of dystrophic calcification.

Has little or no clinical significance.

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.

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.

Risk factors of Atherosclerosis

Major

Constitutional

Age.

Sex.

Genetic factors.

Familial & racial factors.

Modifiable

Hyperlipidemia (LDL).

Hypertension.

Diabetes mellitus.

Smoking.

Minor

Environmental influences.

Obesity.

Hormones-OCs, Oestrogen deficiency.

Physical inactivity.

Stress.

Infections (C.pneumoniae, herpesvirus, CMV)

Homocystinuria.

Alcohol.

Pathogenesis of Atherosclerosis

According response-to-injury hypothesis atherosclerosis results from the following events

Endothelial injury and resultant endothelial dysfunction.

Increased permeability, leukocyte adhesion, thrombosis.

Accumulation of lipoproteins (mainly oxidized LDL and cholesterol crystals) in the vessel wall.

Platelet adhesion.

Monocyte adhesion to the endothelium, migration into the intima and differentiation into macrophages and foam cells.

Pathogenesis of Atherosclerosis cont…

Lipid accumulation within macrophages, which release inflammatory cytokines.

Smooth muscle cell recruitment due to factors released from activated platelets, macrophages, and vascular wall cells.

Smooth muscle cell proliferation and ECM production.

Refer to Handout 26.1 for additional information on Atherosclerosis.

Complications of atherosclerosis

Local

Luminal narrowing/ obstruction.

Thrombosis, thromboembolism.

Fibrosis and calcification.

Necrosis.

Aneurysm

Rupture causing hemorrhage.

Distant/systemic

Embolism.

Hemorrhage/shock.

Ischaemia/infarction-end organ failure.

Stroke, myocardial Infarctions, renal infarction, mesenteric vein thrombosis, intermittent claudication, gangrene +/- amputations etc.

Sudden death.

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

Thrombosis and thromboembolism causing ischemia.

Alteration in the flow of blood (stasis).

Rupture of the vessel.

Compression of neighbouring structures.

Causes of Aneurysm

Conditions that weaken vessel walls and lead to aneurysms include

Trauma.

Vasculitis.

Congenital defects.

Infections.

Atherosclerosis.

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.

Classification of Aneurysms

Depending upon the composition of the wall

True aneurysm.

False aneurysm.

Depending upon the shape

Saccular.

Fusiform.

Cylindrical.

Serpentine.

Racemose.

Classification of Aneurysms cont…

Based on pathogenetic mechanisms

Atherosclerotic (arteriosclerotic) aneurysms

Syphilitic (luetic) aneurysms

Mycotic aneurysms

Berry aneurysms

Dissecting aneurysms

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.

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).

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.

Varicose veins cont…

Clinical features

Lower extremity stasis.

Congestion.

Edema.

Pain.

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.

Thrombophlebitis (Phlebothrombosis)

‘Phlebothrombosis’ and ‘thrombophlebitis’ are used synonymously.

Thrombosis of deep leg veins accounts for more than 90% of cases.

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.

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.

Clinical effects of Thrombophlebitis (Phlebothrombosis)

Local

Oedema distal to occlusion (Swelling).

Heat.

Pain and tenderness.

Redness.

Systemic

Due to embolic phenomena

Pulmonary thromboembolism (most common and most important).

Others: bacteremia and septic embolisation to brain, meninges, liver etc.

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.

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.

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.

Lymphedema cont…

Secondary or obstructive lymphedema.

Accumulation of interstitial fluid behind an obstructed previously normal lymphatic.

Obstruction can result from various disorders/ conditions

Tumors involving either the lymphatic channels or the regional lymph nodes.

Surgical procedures that sever lymphatic connections (e.g., axillary lymph nodes in radical mastectomy).

Postradiation fibrosis.

Filariasis.

Postinflammatory thrombosis and scarring.

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.

Hypertension

Hypertension is a common disorder affecting 25%.

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 on Hypertension.

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.

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 to 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

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.

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:

Angina pectoris (literally, “chest pain”).

Acute myocardial infarction (MI).

Chronic IHD with CHF.

Sudden cardiac death (SCD).

Refer to Handout 26.2 for additional information on Ischemic Heart Diseases.

List of Congenital heart diseases

Ventricular septal defect.

Atrial septal defect.

Tetralogy of Fallot.

Coarctation of aorta.

Pulmonary stenosis.

Aortic stenosis

Patent ductus arteriosus.

Atrioventricular septal defect.

Transposition of great arteries.

Truncus arteriosus.

Total anomalous pulmonary venous connection.

Tricuspid atresia.

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.

Review questions

Explain pathophysiology of atherosclerosis.

Mention five (5) causes of aneurysms.

List three (3) complications of aortic dissection.

Mention five (5) risk factors of deep venous thrombosis.

List five (5) causes of secondary lymphedema.

References

Goljan E.;(2007): Rapid Review Pathology (2th 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 (6th 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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Session 26 Cardiovascular Pathology

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Lecture Notes