PATHOLOGY OF CARDIOVASCULAR SYSTEM

Dr. Bikash Puri

Assist. Professor

Department of Veterinary Pathology and Clinics

9855052820

bpuri@afu.edu.np

• Recommended Textbook:
• Pathologic Basis of Veterinary

Medicine, Zachary & McGavin,

5^th ed. 2011

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• Complementary textbooks:
• Jubb, Kennedy & Palmer’s Pathology of Domestic Animals. Grant, 5^th ed. 2007
• Tumors in Domestic Animals, Meuten, 4^th ed. 2002
• Pathologic basis of disease, Kumar Abbas & Fausto, 8^th ed. 2005

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Introduction

• Cardiovascular system is a vitally life-sustaining organ
• Comprises- heart and blood vessels as two functional units of this system,
• Heart- primary function is to pump sufficient volume of blood to all organs in body to meet the varying metabolic needs of the organism.
• It is a biological pump which can be describe as an in series, 2-stage, rate variable , one way pump
• Depending upon the physiological demand it provide sufficient force to eject the blood it receive, respond to host needs by varying the amount of blood ejected per unit time and finally ensure on-way flow.
• When pathology supervenes, it will result in either diminution or complete cessation of function leading to devastating physiologic consequences.

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Any idea over an average 10 year lifetime of dog how many times will the heart beat?

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Histologically

The cardiac wall has 3 layers:

1. The epicardium, the outermost layer

2. The myocardium, the thick muscular middle layer

3. The endocardium, the innermost layer, which is continuous with the tunica intima of the great vessels entering and leaving the heart

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1- Epicardium

2- Myocardium

3- Endocardium

Epicardium

• Consist of a thin layer of mesothelium resting on elastic fiber rich connective tissue that merges with that of myocardium
• Epicardium is continuous with parietal pericardium, which consists of an inner mesothelial layer and a thick layer of collagen and elastic fibers.

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Myocardium

• Consist of striated muscles cells “cardiac myocytes” embedded in a well vascularized connective tissue frame work
• Identifying features:
• Branching of cardiomyocytes
• Centrally located nuclei with perinuclear halo
• Transversaly orientated intercalated discs

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Endocardium

• It is linned by endothelial cells and supported by a small amount of fibrious strom
• Contain small amount of adipose, lymphatic vessels and nerves

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Endocardium

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1. The endocardium is the inner surface of the heart.
2. It is composed of a thin layer of fibrous connective tissue with an overlying endothelial lining.
3. Purkinje fibers which are part of the conduction system of the heart are often present at the endocardial surface. 

CARDIAC PATHOPHYSIOLOGY

• The amount of blood that a heart pumps out in order to meet the needs of the organism at rest is called cardiac output.
• When the pathology intervene the cardiac output decreases
• The normal heart has a threefold to fivefold functional reserve capacity (ability of heart to respond above and below the cardiac output)
• This operate in both normal and diseased hearts in an attempt to meet both the short-term and long-term demands for adequate cardiac output.

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Component of cardiac reserve

• Increase contractibility
• Increase stroke rate

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Purpose:

• Increase cardiac output
• May be short or long term

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Pathogenesis:�

• Any lesion that brings change in the efficiency of heart also reduces the cardiac reserve.
• When the cardiac reserve is exhausted the need of animal at rest can’t be met.
• This increase the workload of heart.
• However, if the heart is forced to work against sustained overload, it eventually becomes unable to deliver a normal output of blood leading to cardiac enlargement (Dilation and hypertrophy).
• Cardiac hypertrophy: Develops when myocardium is healthy and adequate nutrition is available
• Cardiac Dilation: develops when myocardium is diseased and adequate nutrition is not available.
• This ultimately leads to decrease cardic output.

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Note:

When one side of the heart fails than it subsequently affect the other side too.

Congestive Heart Failure

Definition:

• Congestive heart failure is the inability of cardiac output to keep pace with venous return.
• Here heart cannot maintain an output adequate for the metabolic needs of the tissues and organs.
• It’s the end point of number of causes, rather than a specific disease and denotes a situation in which all compensatory mechanism have been exhausted.
• It is characterized by diminished cardic output or damming back of blood in venous side.

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Left sided congestive heart failure

Causes:

• loss of myocardial contractility associated with myocarditis, myocardial necrosis, or cardiomyopathy;
• dysfunction of the mitral or aortic valves; and
• several congenital heart diseases

Clinical signs:

• Dyspnea and shortness of breath
• Coughing
• Exercise intolerance

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Pathological findings

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1. Dilation & hypertrophy of the left ventricles and atrium
2. Pulmonary congestion and edema
3. Presence of haemosiderin laden alveolar macrophages (Heart failure cell)
4. Edema of the dependent part
5. In chronic cases there is fibrosis of the alveolar wall.

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Alveolar macrophages containing hemosiderin (blue) are present in the alveoli

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During heart failure, red blood cells gain access to alveoli where they are rapidly phagocytozed by pulmonary macrophages and the iron of the hemoglobin molecule is converted to hemosiderin. Hemosiderin gives a positive reaction for iron with the Prussian blue reaction.

Right sided congestive heart failure

Causes:

• Consequences of left-sided heart failure,
• Myocardial degeneration, Myocarditis,
• Primary disease of lungs e.g pulmonary hypertension, emphysema, pneumonia etc.
• Hydropericardium,
• Exudative pericarditis,
• Endocarditis
• Defective tricuspid & semilunar valves.

Clinical Sign:

• Generalized venous congestion
• Distention of jugular vein & other superficial veins
• Generalized edema

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Gross findings:

• Dilation & hypertrophy of the rt. ventricles and atrium
• Generalized venous congestion
• Spleenomegaly and hepatomegaly
• Liver on section display characteristic nutmeg pattern.
• Generalized edema example: Cow and horse (dependent subcutaneous edema); dog (Ascities); Cat (Hydrothorax)

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Ascitis

High Altitude

• Pulmonary hypertension 🡪
• Dilation-hypertrophy RV 🡪
• Right heart failure 🡪
• Ascites and subcutaneous edema

Note swelling of the pectoral region (arrow) due to extensive subcutaneous edema caused by right sided heart failure.

Liver with chronic passive congestion which translates into a zonal pattern caused by necrosis/fibrosis of the centrolobular regions. Affected livers have a hard texture.

Nutmeg

Livers with chronic passive congestion

Noah’s arkive

Nutmeg Liver

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Fluid admixed with fibrin

Rapid growing chickens

• Pulmonary hypertension
• Dilation-hypertrophy RV
• Right heart failure
• Ascites

Distended abdomen with fluid

Ascites

Microscopic findings:�

• Liver:
• Centrilobular congestion, degeneration, necrosis, and fibrosis of the liver.
• Hepatic sinosoids are dilated and congested.
• Chronic cases hepatic cirrhosis.

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• Spleen: The splenic red pulp becomes engorged

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• Lungs: Eventually, the effects of right heart failure are reflected in the left heart and lungs (if the animal lives long enough).

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What happen when there is myocardial infraction?

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What happen when there is myocardial infraction?

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What is Cor pulmonale?

• Right heart failure secondary to pulmonary disease, such as
• chronic obstructive pulmonary disease.
• Dirofilariasis
• Pulmonary thrombo-embolism
• Because the cardiovascular system is closed, failure of one ventricle will ultimately lead to failure of the other, culminating in global or biventricular failure.

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Cardiac Hypertrophy

• Cardiac hypertrophy is reversible increase in bulk of cardiac muscle (Mass) due to an increase in size of component fibers but not number of myocardial cells.

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• Occurs if the heart is forced to work against a sustained overload for long time.

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• Requirements for cardiac hypertrophy to develop
• Time
• healthy myocardium
• adequate nutrition (blood supply)

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• If these factors are lacking, dilatation in the absence of hypertrophy occurs.

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Gross findings:

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Increased thickness and rubbery firmness are best indication of cardiac hypertrophy

1. Eccentric hypertrophy

Definition:

• Hypertrophy is accompanied by dilation
• Leads to increase in mass with an increase in end diastolic volume (amount of blood in ventricle just before contraction)

Causes: Volume Overloads

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1. Right ventricular hypertrophy

• Tricuspid dysplasia

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2. Left ventricular hypertrophy

• Mitral valve endocardiosis
• Persistent ductus arteriosus

1. Valvular insufficiency
2. Increase in blood volume
3. May develop later in Concentric Hypertrophy

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Pathological findings

Gross findings:

• Heart globose in shape
• Increase size of ventricular chamber
• Thin ventricular walls
• Papillary muscle may be thin
• Endocardium may be white due to fibrosis related to hypoxia

Microscopic findings:

• Sarcomeres increase in length and width.

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2. Concentric hypertrophy

Definition:

• Hypertrophy is accompanied with narrowing of lumen of chamber.
• Increase in mass without an increase in end diastolic volume

Causes: Pressure Overloads

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1. Right ventricular hypertrophy

–Pulmonic stenosis

–Pulmonary hypertension

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2. Left ventricular hypertrophy

–Aortic stenosis

–Hyperthyroidism

Pathological findings

Gross

• Increase in thickness of ventricular wall
• Increase in size of papillary muscles and trabeculae carnae
• Decrease in ventricular chamber

Microscopic

• Increase in size of myocytes but increase in size of fibre is not uniform

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Eccentric

Concentric

Note thin ventricular wall (square) and distended ventricle (arrow).

Note thick ventricular wall (square) and reduced ventricular space (arrow).

Cardiac Dilation

• Response to an increase workload in both physiologic and pathologic states.

Causes

• same as those of hypertrophy in the presence of a myocardium which cannot undergo hypertrophy because there is
• not enough time,
• inadequate nutrition
• diseased myocardium.
• Detection at necropsy can be difficult.
• Often a terminal lesion in many cardiac disease processes.

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Pathological findings

Gross findings:

• Dilated heart is globose shaped
• Wall are soft, pliable and thin
• Endocardium is usually diffusedly thickened and opaque.

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Cardiac Dilation

Cardiac Hypertrophy

Notes:

• Hypertrophy affect left heart more frequently than right and ventricles more than atria.
• Hypertrophy of right heart muscles makes heart broader at base
• Hypertrophy of left heart increase length of heart
• Bilateral hypertrophy result in more round shape than normal.

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Congenital anamolies

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Classification of Congenital defect based on anatomic defect and functional effects

• Malformation causing systemic to pulmonary (left to right) shunting
• Atrial septal defect
• Atrioventricular septal defect
• Ventricular septal defect
• Patent ductus arteriosus
• Malformation of cardiac valves
• Pulmonic stenosis
• Tetralogy of fallot
• Dysplasia of right atrioventricular vulve
• Left atrioventricular valvular insufficiency or stenosis
• Transposition complexes
• Miscellaneous cardiac anamolies
• Vascular anomalies

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Atrial Septal Defect

• At embryonic stage blood directly moves form right atrium to left atrium through Foramen ovale.
• Functional closure occurs normally at birth due to increased left atrial pressure.
• Anatomical closure of the foramen ovale is complete within a week after birth
• The persistence of the opening between right and left atrium is called atrial septal defect.
• The defect is not significant as long as left atrial pressure exceeds right atrial pressure

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Interventricular Septal Defect

1. Primary R and L ventricles of the embryo communicate via the primary interventricular foramen;

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2. This opening get closed soon after birth.

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3. Failure of closure leads to condition known as interventricular septal defect.

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Persistent Ductus Arteriosus

• Shunt exist between pulmonary artery and aorta during embryonic life.
• It closes shortly after the birth (few min to one hour) but anatomial closure occur after 6^th or seventh day by ligamentum arteriosum
• Failure of closure leads to condition called persistent ductus arteriosus.

Consequences:

• This causes small amount of blood pumped into pulmonary artery during systole due to higher pressure in the aorta than the pulmonary artery.
• Decrease cardiac output and later CHF

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Transposition of great vessels

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The aorta & pulmonary artery may be transposed with the aorta arising from the right ventricle and the pulmonary artery from the left ventricle

Death of an animal

Persistent Right aortic arch

• Aorta normally forms from one of the left aortic arch
• This places the aorta and ductus arteriosus on the left of trachea and oesophagus.
• But if the aorta develops from one of right aortic arch aorta will be on the right side which displaces the oesophagus and trachea to the left.
• The ductus arteriosus connecting with aorta and pulmonary artery forms a ring around the trachea and oesophagus.

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Pulmonic Stenosis�

• Obstruction of pulmonary outflow.
• blood accumulates in the right ventricle leading to ventricular dilatation and hypertrophy.
• Subsequently, congestive heart failure may ensue.
• In addition, poststenotic dilatation of the pulmonary artery may occur, producing a rounded enlargement of the vessel resembling an aneurysm.

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Tetralogy of fallot

• Tetralogy of fallot consists of several individual anomalies occurring together.
• These include:
• Pulmonary stenosis (usually subvalvular).
• Ventricular septal defect (usually high).
• An overriding, dextropositioned aorta (that receives blood from both the left and right ventricles).
• Right ventricular hypertrophy (which is secondary to the other defects).

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The Eisenmenger complex is Tetralogy of Fallot without Pulmonic Stenosis

Abnormality of the position of the heart

Ectopic cordis:

• The entire heart lies outside the thoracic cavity.
• Most frequently seen in cattle
• Usually secoundary to sternal cleft or failure of thoracic cavity to close normally

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Dextrocardia:

• Heart is on the right side rather than the left
• Often associated with total or partial situs inversus

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Disease of pericardium

• The pericardium is the fibro-serous sac which encloses the heart.
• Primary diseases are rare
• Most diseases of the pericardium are secondary to disease processes in the heart, lungs, pleura, and other sites in the body.

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• Reaction is limited
• May provide clues

A. Non-Inflammatory Pericardial Disease

1. Hydropericardium
2. Hemopericardium
3. Serous atrophy of pericardial fat

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Hydropericardium

Defination:

• Refers to the accumulation of fluid (transudate) within the pericardial sac

Causes:

• Hypoproteinemia
• Congestive heart failure
• Neoplasia
• Systemic disease Example: Mulberry heart disease(Pig), Richettsial D/S (“heartwater”) and viral disease (African Horse Sickness, Bovine Ephemeral Fever, African Swine Fever)

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Significance

The volume of fluid that accumulates in the pericardial sac varies greatly

• Acute: (cardiac tamponade)
• If fluid accumulates rapidly,
• the pericardium is placed under considerable tension
• this is reflected in the pooling of venous blood (generalized venous congestion).
• Chronic: (extensible )
• When fluid accumulates slowly, there is time for the pericardium to stretch and adapt.
• Large amounts of fluid can accumulate before there is significant impediment to blood flow in the large veins and in the right side of the heart.

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1. Reversible if the cause can be removed.
2. Remember, a small increase in pericardial fluid occurs by transudation after death which is soon reddened by the products of postmortem hemolysis.

Hemopericardium

Defination:

• Hemopericardium refers to an accumulation of pure blood in the pericardial sac.

Etiology:

• Spontaneous rupture of the intrapericardial aorta of horses.
• In uremic dogs with ulcerative atrial endocarditis.
• Following rupture of the coronary artery.
• Iatrogenic
• Bleeding from a tumour within pericardial sac
• Cardiac tamponade refers to compression of the heart subsequent to the accumulation of any fluid within the pericardial sac.

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SEROUS ATROPHY OF PERICARDIAL FAT

Definition

• Progressive mobilization of depot fat, including that beneath the epicardium.
• Degeneration (atrophy) of adipose tissue with replacement by loose, edematous connective tissue.
• Subsequently, normal fat is converted to grayish-brown gelatinous masses.

Causes

• Inadequate nutritional supply
• Starvation
• Illness

Significance

–Condition of health

–Little effect on function

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Serous atrophy of epicardial fat

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Serous atrophy

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NORMAL SEROUS ATROPHY

INFLAMMATORY DISEASES OF THE PERICARDIUM

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Pericarditis

Defination:

• Pericarditis refers to inflammation of both the parietal and visceral surfaces of the pericardium.

Causes:

• Infectious: Infectious agent usually reaches the pericardium by extension from the surrounding structures or by way of hematogenous route.
• Trauma (Foreign bodies penetrating through reticulum): Example: Traumatic Reticulo Peritonitis

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Note: A true pericarditis is nearly always infectious with an accumulation of exudate within the sac

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FIBRINOUS PERICARDITIS

• Most common type of pericardial inflammation
• Characterized by an accumulation of fibrin within the pericardial sac.
• Exudation of fluid is not a prominent feature.

Etiology:

• Cow: Mannheimia, (blackleg, coliform septicemias )

– Fetus – Brucella, Arcanobacter pyogenes

• Pig– Glasser’s disease, Streptococcus, Mycoplasma, Salmonella
• Horse – Streptococcal infections
• Birds – Psittacosis
• Sheep – Pasteurella, Streptococci

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Grossly�

• Both the visceral and parietal pericardial surfaces are covered by variable amounts of yellow fibrin deposits, which can result in adherence between the parietal and visceral layers.

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• Pericardium becomes thick and opaque

• When the pericardial sac is opened upon necropsy, these attachments are torn away (so-called bread-and-butter heart)

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Fibrinous pericarditis

Microscopically �

• An eosinophilic layer of fibrin with admixed neutrophils lies over a congested pericardium

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Eosinophilic fibrin deposits (left) on the epicardial surface (E)

Outcomes

• Variable outcomes
• Early death is frequent because many of these lesions result from infection by highly virulent bacteria and concurrent septicemia.
• When survival is prolonged, fibrous adhesions form between the pericardial surfaces after fibrous organization of the exudate.

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Purulent Pericarditis

• Characterized by the accumulation of pus in the pericardial sac

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Causes

• Pyogenic bacteria
• Pyothorax –horses, cats
• Traumatic reticulopericarditis

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Gross

• The pericardial surfaces are notably thickened by white, often rough, shaggy-appearing masses of fibrous connective tissue
• accumulation of white to gray, thick, foul-smelling, purulent exudate with in pericardial sac

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Microscopic

• Infiltration of moderate numbers of PMNS, macrophages and fibrous connective tissue.

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Constrictive Pericarditis

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Definition

• Chronic inflammation with fibrous adhesions of pericardial sac to epicardium
• Result from progressive organization

Result

• Compensatory cardiac hypertrophy
• leads to impaired diastolic filling and development of RCHF

PATHOLOGY OF �ENDOCARDIUM

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Endocardium

• Inner layer of the heart (lines the atria and ventricles
• Has 3 sublayers:
• Endothelium : simple squamous epithelium.
• Smooth Muscle and Connective Tissue - middle layer of the endocardium is mix of connective tissue (elastic fibre, collagen and fibroblast) and smooth muscle.
• Subendocardial Layer - outer layer ; loose connective tissue (collagen, elastic and fibroblast) joining the endocardium and myocardium.
• equivalent to tunica intima.

Endocarditis

Definition

• Endocarditis refers to inflammation of the endocardium
• Usually bacterial in cause, exceptional being occasionally parasitic or mycotic lesions.

Types: 2 types

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Mural

(Lesions located on lining of atrium & ventricles)

Valvular

(Lesions located on the vulves)

In domestic animals, valvular endocarditis occurs more frequently than mural.

Causes:�

1. Bacterial infection: Streptococci, Staphylococci, Corynebacterium pyogenes Actinomyces pyogenes, Erysipelothrix rhusiopathe
2. Parasites infestation: Strongylus vulgaris larvae
3. Mycotic infection
4. Uremia

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Location: Varies with species

• Cattle: right heart, tricuspid valve more affected followed by mitral, pulmonar and aortic vulve
• Horse, dog and Pig: Left heart , aortic vulve most frequently involved followed by mitral and finally pulmonary
• Dog and Pigs: lesion commonly observed in mitral valve followed by aortic, tricuspid and pulmonary valve

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Findings

Gross

• Vegetative/ cauliflower like growth on endocardium either in valves or in wall.
• “Valvular vegetations” are primilary composed of fibrin, few platelets and neutrophils.
• Initially, it is large, friable, yellow to gray masses of fibrin attached to the endothelium.
• They may even detach to produce emboli

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• In chronic lesions, the fibrin deposits are organized by fibrous connective tissue to produce irregular nodular masses termed “verrucae” (wartlike lesions).

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Microscopical

• Accumulated layers of fibrin and numerous embedded bacterial colonies underlain by a zone of infiltrated leukocytes and granulation tissue

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Fig: Vegetative valvular endocarditis

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Note: Abundant masses of fibrin and bacterial colonies (arrow)

Note:

• Remember, valvular thrombi are almost always serious since they tend
• To obstruct the normal flow of blood,
• Prevent perfect closure of the valves,
• Result in embolism.

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Congestive Heart Failure

Sequela

• Chronic lesions
• Organize by granulation from the base of the valve
• May undergo mineralization
• Complete resolution is uncommon
• Right Heart
• Valvular distortion = right heart failure
• Pulmonary thrombosis and abscessation (embolic pneumonia)

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Sequela

Left Heart

• Valvular distortion leading to left heart failure
• Thromboemboli (Kidney, spleen, brain, etc)
• Ruptured chordae tendinae
• Inflammatory induced septal defects or pericarditis can occur
• Not Common

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Vegetative Valvular Endocarditis / Right Sided Heart Failure / Cow

Note: hydrothorax due to right sided heart failure

Note large vegetative mass (arrow) on the tricuspid valve which was causing right heart failure, ventral edema, hydrothorax, ascites, and “nutmeg liver”

“nutmeg liver”

Vegetative Valvular Endocarditis / Embolic Pneumonia

Note the vegetative lesion in pulmonic valve (*) and multiple embolic foci in the lungs (arrows).

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Right ventricle

Pulmonary trunk

Fig. 10-61 Ulcerative endocarditis (uremia), heart, endocardium of left atrium, dog. Note the white-red, thick, wrinkled area (arrows) of endocarditis, mineralization, and fibrous tissue (scar) formation caused by uremia in this dog with chronic renal failure. Pathologic Basis of veterinary Diseases page 572

Ulcerative Endocarditis / Uremia / Dog

VALVULAR ENDOCARDIOSIS

• Also referred to as "verrucous endocardiosis" or "nodular fibrosis'',
• characterized by fibrous thickening of the heart valves.
• occurs primarily in dogs and the mitral valve is most frequently and severely affected.
• Incidence increases with age, and congestive heart failure may develop subsequent to the distorted valves.

Causes:

• constant mechanical injury to the edges of the valves as they strike against each other

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Findings

Grossly:

• The Mitral valve cusps are shortened and thickened (Nodular)
• Thickening of the leaflet may be more or less uniform with rounded edge or prominent nodular thickening of valve leaflet.
• Valves are opaque and white with smooth and glistening surface with out inflammation
• Chordae tendineae – thickened and occasionally ruptured allowing eversion of leaflet into atrium
• Valvular annulus may be enlarged.

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• Nodular
• Smooth surface

Myxomatous Valvular Degeneration (Endocardiosis)

Findings

Microscopically:

• The thickened valves have notably increased fibroblastic proliferation and deposition of acid mucopolysaccharides

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Fig: Valvular endocardiosis, cusp of right atrioventricular valve, heart, dog.

The valve is thickened and nodular from an increase in myxomatous tissue supported by a fibrous stroma.

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A. Normal valve leaflet.

B. Affected leaflet.

Myxomatous degeneration of the stratum spongiosum of the AV valve.

C. The increase in glycosaminoglycans in the affected valve leaflet is high- lighted by staining with Alcian blue.

CALCIFICATION OF THE ENDOCARDIUM

• CVS is unusually susceptible to mineralization because of its high elastin content. Mineralization is more common in endocardium and tunica intima of vessels
• Susceptible species: dogs, cattle, sheep, and horses.
• Causes: Any diseases leading to an imbalance of Ca:P

Example: 1. Metabolic disease

• Renal failure
• Hyperphosphatemia
• Pseudohyperparathyroidism
• Nutritional: Deficiency of vitamin E and Se (white muscle disease, Excess phosphate in diet)

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PATHOLOGY OF CARDIOVASCULAR SYSTEM

2. Toxic substances

• intake of excessive amounts of vitamin D and from intoxication by calcinogenic plants (Cestrum diurnum, Trisetum flavescens, Solanum malacoxylon, Solanum torvum) that contain vitamin D analogs.

3. In healed lesions of left atrial ulcerative endocarditis associated with a prior uremic episode

4. Chronic debilitating disease example: Paratuberculosis

5. “jet lesions” (The jet lesion is a raised, rough, firm streak of endocardial fibrosis resulting from long-term trauma by a jet of blood leaking through the damaged valve in the closed position.)

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Gross:

• Presence of white, elevated, firm gritty plaques generally in subendocardial location.

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Figure: Extensive subendocardial mineralization in the left atrium and ventricle of a horse following ingestion of Solanum glaucophyllum (vitamin D analogue toxicosis).

(Courtesy A. P. Loretti.)

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Microscopic:

• Accumulations of basophilic, acellular material usually with little or no inflammatory cells
• Stain positive with Von Kossa stain for calcium

white-red, thick, wrinkled area (arrows) of endocarditis, mineralization, and fibrous tissue (scar) formation caused by uremia in this dog with chronic renal failure

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Ulcerative endocarditis

Johne’s disease

The left atrial (LA) endocardium is white, thick, and wrinkled from mineralization

Gross findings

Diseases of Myocardium

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Myocardium

• Consist of striated muscles cells “cardiac myocytes” embedded in a well vascularized connective tissue frame work
• Identifying features:
• Branching of cardiomyocytes
• Centrally located nuclei with perinuclear halo
• Transversaly orientated intercalated discs

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Diseases of Myocardium

• Myocarditis is the inflammation of myocardium, the middle layer of heart.
• It may be suppurative, eosinophlic or lymphocytic depending on the type of the exudates.

Etiology:

1. Infectious:
• Viral (Canine parvovirus, encephalomyocarditis, FMD, Pseudorabies, Canine distemper, Newcastle disease, Avian encephalomyelitis)
• Bacterial: (Blackleg, listeriosis, Tuberculosis, disseminated infection by actinobaillus equuli, Staphylococcus sp. Corynebacterium, pseudomaonas etc.)
• Protozoan: Toxoplasmosis, Sarcocystosis, Trypanosomiasis, etc
• Parasitic: Cysticercosis, trichinosis,
• Idiopathic: Eosinophilic myocarditis

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Types of Myocarditis

• Suppurative: Results from localization of pyogenic bacteria in the myocardium. There is typical abscess formation with neutrophilic infiltration.
• Examples: Streptococcus, staphylococcus, etc.
• Necrotizing: Charaterized by the necrosis of myocardium
• Examples: toxoplasmosis,
• Hemorrhagic: Characterized by hypermia and hemorrhage of myocardium.
• Examples: Blacklegs
• Lymphocytic: Characterized by infiltration of lymphocytes at site of inflammation
• Examples: Viral infection (Parvovirus)
• Eosinophilic: Characterized by infiltration of eosinophils at inflammatory sites.
• Example: Sarcocystosis.

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Hemorrhagic myocarditis

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Area of hemorrhagic myocarditis (arrows) in the wall of the ventricular myocardium. This disease is caused by Clostridium chauvoei,

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Multifocal to coalescing myocarditis in ventricle wall, caused by Blastomyces dermatitidis in a dog.

Parvovirus myocarditis

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multifocal pale areas (arrow) in the ventricular myocardium

An intranuclear basophilic inclusion body is in a myocyte (arrow)

Grossly:

• Colour of myocardium may become dark red or cyanotic due to accumulation of blood.
• In suppurative myocarditis, one can find abscesses in myo-cardium from where yellow/green pus oozes out.
• Yellowish white streaks of necrosis in myocardium.
• Presence of cyst encapsulated by fibrin in case of cysticercosis.
• Hyperemia and haemorrhages in myocardium.
• Heart become pale and flabby.

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Microscopically:

• Infiltration of neutrophils, eosinophils or lymphocytes.
• Coagulative necrosis of muscle fibers.
• In chronic cases, proliferation of fibrous connective tissue.

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Pathology of veins, arteries and lymphatics

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Pathology of Veins

• Arteriovenous fistulas
• Is an abnormal channel between an artery and a vein
• Normally, blood flows from arteries into capillaries and then into veins.
• With arteriovenous fistulas, some blood flows directly from an artery into a vein, bypassing capillaries.
• It may be-
• Congenital
• Acquired

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• Near surface of skin, it appear swollen and reddish blue.
• If larger veins are involved, large volume of blood flows under high pressure from the artery into vein. As vein walls are not strong enough to withstand such high pressure and vein become enlarged and bulge.
• Large amount of blood get accommodated in vein and to compensate for fall in blood pressure heart has to pump forcefully and rapidly. Eventually leading to heart failure
• If large volume of blood get diverted, it cause numbness, pain and cramping, bluish discoloration and severe cases even skin sores can develop.

Consequences:

Protosystemic anastomoses

Persistent ductus venosus

• In utero, the ductus venosus connects the left portal vein to the inferior vena cava, allowing portion of the venous blood to by pass the liver and return to the heart.
• After birth, the ductus venosus closes due to change in intracardiac pressure and decrease in endogenous prostaglandin.
• Failure of this closure leads to condition called persistent ductus venosus
• Allow portal blood , with its absorbed toxic substances, such as ammonia, to by pass liver causing hepatic encephalopathy
• Common in dog and cat

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Phlebectasia

• It’s the dilation of vessels
• Causes:
• Congenital defects likes- venous diaphragm, agenesis, hypoplasia or ectopia or
• secoundary to surgery, trauma or neoplasia.
• Initial dilation causes insufficiency of the venous valves and the vein become dilated, elongated and tortuous

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Telangiectasis �

• Dilatation of small vessels causing threadlike red lines or pattern on the skin or the surface of organ is called Telangiectasis
• Also know as spider veins because of their fine and web like appearance.
• They appear grossly as small, red to bluish blood-filled spaces
• Example: sinusoidal capillaries in one or more lobules in liver.

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Phlebitis

• is the inflammation of veins
• Characterized by presence of inflammatory exudate, thickening of the wall and dilation of the lumen.
• Less common then arteritis
• May lead to thrombosis; it is likely to soften, disintegrate and produce emboli

Etiology/ Occurrence

• Mechanical: repeated venipuncture
• Chemical: injection of irritant solution
• Infectious:
• Naval infection in calves; Uterine infections; feline infectious peritonitis; Schistosomiasis (bilharziasis)

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�Varicose Veins�

• Dilated and elongated veins are referred to as varicose veins
• produced by prolonged increase in intraluminal pressure and loss of vessel wall support.
• Such veins follow an irregular and tortuous course and hold an abnormally large amount of blood.
• Varicose veins are less common in animals than in man.

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• _Findings:
• Varicose veins show wall thinning at the points of maximal dilation with smooth muscle hypertrophy and intimal fibrosis in adjacent segments;
• Degeneration of elastic tissue and spotty medial calcifications (phlebosclerosis)
• Focal intraluminal thrombosis (due to stasis) and venous valve deformities (rolling and shortening) are common.

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Pathology of arteries

• Aneurysm
• ARTERITIS
• ARTERIOSCLEROSIS

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Pathology of arteries

Aneurysm

• Aneurysm is a localized dilation or out pouching of a thinned and weakened portion of a vessel.
• Usually large elastic arteries are affected but the lesion can also occur in veins.
• Consequences are rapidly fatal as large arteries are typically involved.

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Etiology

• Copper deficiency in pigs (necessary for normal development of elastic tissue)
• Parasitic infestation (Spirocerca lupi in dog; Strongylus vulgaris.
• Infectious emboli.
• Weak vessel wall due to rupture.
• Necrosis of medial layer of large blood vessel.

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• An aneurysm is a localized abnormal dilation of a blood vessel or the heart
• When an aneurysm involves all three layers of the arterial wall (intima, media, and adventitia) or the attenuated wall of the heart, it is called a "true" aneurysm.
• False aneurysm (also called pseudoaneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space ("pulsating hematoma").
• An arterial dissection arises when blood enters the wall of the artery, as a hematoma dissecting between its layers.
• Both true and false aneurysms as well as dissections can rupture, often with catastrophic consequences.

Dissecting aneurysm, copper deficiency, heart, pulmonary artery, right ventricle (RV), pig

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The dark, blood-filled, bulging segment of the wall of the pulmonary artery (arrows) has resulted from disruption of elastic fibers

Macroscopic features�

• Fracture or necrosis of medial layer of large blood vessels permitting parallel blood circulation till the next division of blood vessel is called as Dissecting aneurysm or false aneurysm.
• Formation of sac in artery due to dilation, also known as True aneurysm.

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Microscopic features

• Rough intimal layer.
• Wall of blood vessel damaged with inflammatory exudate.

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Dissecting aneurysm

ARTERIOSCLEROSIS

• It is a degenerative change which literally means hardening of arteries
• Characterized by fibrous thickening, loss of elasticity and narrowing of the lumen of arteries resulting from proliferative and degenerative, rather than inflammatory changes of the media and intima
• “Atherosclerosis” is a subtype of arteriosclerosis which refers to the buildup of fats, cholesterol and other substances in and on the artery walls

Etiology:

• Exact cause is not known
• Hypertension
• Hyperlipidemia (Increase Blood concentration of LDL)
• Increase in glucose concentration in blood (Diabetic patients)
• Homocysteinemia
• Circulating reactive oxygen sps example: smoke, air pollution

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Pathogenesis

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Release of chemoattractant

Example:  Cytokinine

Endothelial Injury

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Release of cell surface adhesion moleules

Example: VCAM-1,

Change in shape of endothelium,

Attract the monocytes and T-Lymphocytes at the site of injury

Adhere the monocytes and T-lymphocytes between the endothelial cell

Tight junction between endothelial cells loosen

Monocytes migrate to the intima by squeezing in between the endothelial wall

Monocytes convert to marcrophages

Entry of LDL into the arterial wall

Oxidation of LDL in presence of NO, Macrophage & lipoxygenase

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• Uptake of oxidise LDL by the macrophages
• This lipid laden macrophages are called “Foam Cells”
• Aggregate of foam cells appear grossly as small elevated fatty streaks in the arterial luminal surface; which eventually evolves into the wax like, fatty plague.
• In progressive expanding lesion foam cells become necrotic and liberate free lipids which incite fibrosis and calcification.

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Fig: Growing Atheroma

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• The right side of the artery has a fairly normal appearance, but an atherosclerotic plaque has evolved on the left side.

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• The mass of the "atheroma" is composed of a mixture of lipid and subintimal smooth muscle cells.

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• Note that much of the lumen of the artery is occupied by this growing lesion.

Gross findings

• Arteries of the heart, mesentery, and kidneys are prominently thickened, firm, and yellow white
• Fatty streaks running parallel in the direction of the artery.
• Intimal layer of aorta/ coronary arteries is elevated due to plaques which are white/yellow, fIbrous and occluding the lumen of vessel.

Note:

• Occlusion of artery may lead to ischemia and infarction.

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Coronary atherosclerosis�

The affected coronary arteries are prominent and cordlike (arrows) with thickened walls.

Johne’s disease, arteriosclerosis, aorta, cow.

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Multiple prominent, white, mineralized foci are in the tunica intima and media (arrows)

Microscopic features�

• Macrophages are filled with lipid droplets including cholesterol, fatty acids, triglycerides and phospholipids.
• Fragmented internal elastic lamina in the intimal layer of artery
• Proliferation of altered smooth muscles may become metaplastic to macrophages. .
• Deposition of mucoid ground substance and collagen fIbers
• Hyalinization of connective tissue " Fibrous plaques".
• Presence of some fat droplets in between the lesion

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Microscopically,

• lipid globules accumulate in the cytoplasm of smooth muscle cells and macrophages, often termed “foam cells,” in the media and intima
• Necrosis and fibrosis develop in some arterial lesions.

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Fig: Atherosclerosis, meningeal artery, horse

extensive accumulation of lipid-laden (clear vacuoles) “foam cells” throughout the thickened media

ARTERITIS

• Arteritis is the inflammation of arteries
• characterized by infiltration of neutrophils, lymphocytes and macrophages in the media and intima of arterial wall

Etiology

• Infectious: Viral (Equine viral arteritis, swine fever, bluetongue, equine infectious anaemia, BVD etc.); Bacterial (Erysipelas, Haemophius sps,); Mycotic (Asperfillosis); Parasitic (Strongylus vulgaris, Dirofilaria immitis, )
• Immune mediated diseases (Rheumatioid arthritis, polyarteritis nodosa, drug induced hypersensitivity)

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Macroscopic features

• Equine viral arteritis (Grossly, severe oedema of the interstitial wall and mesentery accompanied by marked accumulation of serous fluids in the body cavities.)
• Occlusion of lumen of arteries due to thickening of wall.
• Parasitic arteritis the vessel is enlarged and its wall is firm and fibrotic.

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Microscopic features

• Presence of thrombi in artery involving intimal layer.
• Equine viral arteritis virus causes fibrinoid necrosis, extensive oedema and leukocytic infiltration in media.
• In case of parasitic arteritis there is eosinophilic infiltration of the intima and later on proliferation of fibroblasts through the wall.

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Findings

Macroscopic feature

• Wall of vein is thickened.
• Vein contain large thick necrotic material
• Lumen dialated
• Inner surface of vein is rough and hyperemic.

Microscopic features

• Infiltration of neutrophils in the wall of veins
• Sometimes calcification may also present.
• Wall of vein becomes thick due to inflammatory cells and/proliferation of fibrous tissue

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Pathology of Lymphatics

Lymphedema

• Is a swelling of a part of body by an increased quantity of lymph resulting from a lymphatic system disorder.
• Two types-
• Primary lymphedema: due to anomalous development of lymphatic system (congenital )
• Secondary lymphedema: due to obstruction of previously normal lymphatics, resulting from inflammation, neoplasia, surgery or trauma
• Prolonged lymphedema leads to fibrosis

Lymphocele

• It is a lymph filled space that does not have a distinct endothelial lining
• Result due to disruption of lymphatics by trauma or surgery.

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Congenital anamolies

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Dilation of epicardial lymphatics in a foal

Congenital lymphedema, esp. of limbs of a calf

Lymphangiectasis

• Dilation of lymphatic vessels.

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• Causes:
• Congenital
• obstruction of lymph drainage by invading masses of malignant neoplasms, thrombosis or post surgical scarring
• protein-losing enteropathy (in dog). Example:Intestinal lymphangiectasis

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• Findings:
• Prominently dilated lymph vessels.

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Congential lymphangiectasia, epicardium, young horse

• tortuous appearance of the epicardial lymphatic vessel .
• lymph vessels fail to make connections with other vessels or are obstructed because of anomalous development

Findings

Macroscopic

• Distension of subcutaneous lymph vessels, nodules of lymphoid aggregates
• Edema due to failure of lymphatic drainage.

Microscopic

• Lymphoid aggregation around lymphatics.
• Lymphatics distended
• Edema of dependent tissue.

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Chylothorax

• Result of leakage or rupture of the thoracic ducts
• Occurs frequently in dog and cats

Causes:

• Thoracic trauma
• Neoplasia
• Right sided heart failure
• Dirofilariasis
• Thrombosis of cranial vena cava,
• lung lobes torsion
• Obstruction of thoracic duct drainage

Gross findings:

• Pleural fluid is opalescent to opaque, milky-white to yellow and on standing forms a top layer of cream(chylomicron fat) that is ether soluable

Microscopically:

• Fluid contain large number of lymphocytes, a few neutrophils, red cells , plasma cells and fat globules

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�LYMPHANGITIS�

• Lymphangitis is the inflammation of lymph vessels
• characterized by aggregation of lymphocytes around lymphatics, oedema of dependent parts and distension of lymphatics.

Etiology/ Occurrence

• It is the feature of many diseases like-
• Bacterial: Bacillus anthracis, Mycobacterium Paratuberculosis, Actinobacillus lignieresii, Pseudomonas mallei, Dermatophilus congolensis, , etc
• Mycotic: Histoplasma farciminosum, Sporothrix schenckii
• Parasitic: Brugia spp. Infection of dogs and cats

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Types of lymphangitis

• Ulcerative lymphangitis
• Epizootic lymphangitis
• Sporadic lymphangitis

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Lymphangitis, forelimb, lymphatic vessels, horse.

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• Red , painful subcutaneous streaks with painful enlargement of the draining lymph nodes
• Affected vessels often located in the distal limbs and are thick, cordlike structures
• Nodular suppurative lesion of lymphangitis often ulcerate and discharge pus onto the surface of skin

Tumors of the cardiovascular system

• Tumor is any type of abnormal growth whether benign or malignant
• Tumor in heart may be-
• Primary (benign or malignant): tumor that originate in heart
• Metastatic (always malignant): cancer that develped in another organ and thenspread to the heart
• Both primary and metastatic tumors may develp in the-
• Tissue lining the inside of chamers of the heart (endocardium)
• Heart muscles (myocardium)
• Heart valves
• Sac that surround the heart (Pericardium)

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Consequences

• Tumors in the endocardium and heart valves can block blood flow through the heart
• Cause blood clots that can break off and go to other parts of the body (embolism).
• Tumors in the myocardium can affect heart function and lead to heart failure
• Affect the heart's electrical conduction system and cause abnormal heart rhythms.
• Tumors in the pericardium may squeeze (constrict) the heart, preventing it from filling properly leading to heart failure.

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Some common types of CVS tumors in animal include-

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Cardiac myxomas-

• most common benign tumor;
• Often develop in the heart’s left upper chamber (atrium)
• Most are pedunculated , but some are board based and sessile
• Grossly:
• myxomas appears gelatinous (“myxoid”)
• Histologically:
• composed of spindle shaped cells surrounded by loose myxoid matrix

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Fig: Cardiac myxoma.. These tumors can have a lobulated, smooth surface o

Myxoma cells are the diagnostic hallmark of cardiac myxoma. These bland, spindle-shaped cells occur both singly and in small clusters.

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Cardiac myxoma: light microscopy.

Lymphosarcoma

• Neoplastic cell infiltration can be diffuse or nodular and involve the myocardium and pericardium.
• Grossly:
• Tissue appear as white masses that resemble deposite of fat
• Microscopically:
• Extensive infiltration of neoplastic lymphocytes are present between myocytes
• Atrophy and loss of myocytes

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Lymphosarcoma, heart, myocardium, cow.

Chemodectoma

• Chemoreceptor in CVS include aortic and carotid bodies. Neuroendocrine tumors involving these organ are called chemodectomas.
• Mostly benign but can have a malignant behave
• Common in dog
• Microscopically:
• the neoplastic cells are polyhedral with vaculated cytoplasm and supported by abundant fine connective tissue stroma

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Chemodectoma (heart base tumor), aortic body, dog. Note the large mass (arrow) at the base of the

heart (H). L, Lungs. (

Hemangiosarcoma

• Important neoplasm of dogs
• Usaully seen in the wall of right atrium (occassionaly in rt. Ventricle)
• Grossly:
• protruding red to red-black blood containing masses on the epicardial surface
• Microscopically:
• composed of scattered, spindle cells with large, round to oval nuclei and numerous mitotic figures;
• presence of hemosiderin pigments

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Fig: A dark-red hemangiosarcoma protrudes from the wall of the right atrium (RA),

Cardiac angiosarcoma

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The infiltrating mass within the right atrioventricular groove (white arrow) may rupture and bleed into the pericardial space leading to hemopericardium (white asterisk) and tamponade.

Fibrinous pericarditis

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Greatly thickened pericardial sac and extensive fibrinous exudate loosely attached to the epicardium, accompanied by epicardial hemorrhage

Chronic constrictive pericarditis in a cow, typical of traumatic reticulopericarditis.

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Note the wide band of fibrosis on the surface of the epicardium (arrow)

Myocardial necrosis in a calf.

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Figure: Focal necrosis of cardiac myocytes showing eosinophilia, loss of cross striations, and

absence of nuclei (arrowhead). Extensively mineralized necrotic cardiac myocytes (arrow). Some normal cardiac myocytes remain in lower portion. H&E.