Acquired cardiovascular pathology

Question 1

Hydropericardium

Answer 1

Transudate fluid seen with congestive heart failure together with ascites and hydrothorax.

Fluid is clear to light yellow, watery.

Protein rich fluid often with fibrin clots seen in toxaemia due to endothelial damage.

Other causes include renal failure and hypoproteinaemia.

Large volumes of fluid within the pericardial sac (acute onset) leads to development of cardiac tamponade, which interferes with cardiac filling and venous return to the heart, and can lead to death.

Question 2

Haemorrhagic pericardial effusion

Answer 2

Idiopathic in large or giant breeds of dogs.

Not whole blood, just bloody fluid (haemorrhagic effusion).

Question 3

Haemopericardium

Answer 3

Accumulation of whole blood in the pericardial sac following rupture of heart.

Causes are spontaneous atrial rupture, following rupture of heart due to ulcerative endocarditis in uraemic dogs and atrial rupture in dogs with haemongiosarcoma.

Animals develop cardiac tamponade.

Question 4

Serous atrophy of fat

Answer 4

Occurs during chronic anorexia, starvation, cachexia.

Fat is catabolised to maintain energy balance.

Pericardial fat is gray and gelatinous.

Question 5

Pericarditis

Answer 5

Usually infectious aetiology

A variety of organisms are involved depending on the species affected

Haematogenous source or lymphatic spread from adjacent focus.

In animals fibrinous pericarditis is the most common type of pericardial inflammation and it is usually the result of haematogeneous spread of bacteria.

Question 6

Myocardial diseases

Answer 6

Fatty infiltration

Fatty degeneration

Hydropic degeneration

Lipfuscinosis

Myofibrillar degeneration

Myocardial mineralisation

Myocarditis

Myocardial degeneration, necrosis, and infarction

Hypertrophy and dilation/cardiomyopathies

Question 7

Fatty infilatration of myocardium

Answer 7

occurs when large numbers of lipocytes (adipocytes) are present between myocardial cells.

It needs to be distinguished from fatty degeneration.

Fatty infiltration is associated with obesity.

Question 8

Fatty degeneration of myocardium

Answer 8

Abundant lipid droplets are present in the cytoplasm of myocardial cells.

Grossly the myocardium is pale, soft, greasy and friable.

Cardiac fatty degeneration can be associated with anaemia, hypoxia, toxaemia and copper deficiency.

Question 9

Hydropic degeneration of myocardium

Answer 9

Heart muscle appears soft, pale, and flabby.

Microscopically myocardial cells show extensive vacuolization.

Hydropic degeneration can be seen in chronic administration of antineoplastic drugs (anthracyclines).

Question 10

Lipofuscinosis

Answer 10

Often occurs in aged animals, chronic wasting and malnutrition due to deposition of lipofuscin pigment in myocytes.

Affected hearts appear brown.

Microscopically cardiac muscle cells contain yellow-brown granules.

Question 11

Myofibrillar degeneration

Answer 11

It is a sublethal injury of myocardial cells, which are pale eosinophilic sarcoplasm and lack cross striations.

Not common in animals.

Question 12

Myocardial mineralisation

Answer 12

Multiple hard, white subendocardial lesions are present distributed randomly.

Two types:
a) Dystrophic – Calcium deposition occurs commonly following damage to myocytes by ischaemia or in vitamin E and selenium deficiency.

b) Metastatic - Occurs with elevated serum calcium in vitamin D toxicity and in secondary hyperparathyroidism.

Question 13

Myocarditis

Answer 13

Rarely a primary condition.

Common as part of a generalised infective disease or as a result of direct spread from endocardium or pericardium.

Often focal and patchy with oedema, fiber degeneration and variable cellular infiltrate

Question 14

Types of myocarditis

Answer 14

Suppurative (pyogenic bacteria)

Necrotizing (toxoplasmosis)

Haemorrhagic (Blackleg - Clostridium chauvoei)

Lymphocytic (Canine parvovirosis)

Eosinophilic (Sarcocystosis)

Question 15

Viral aetiologies of myocarditis

Answer 15

Canine parvovirus

Pseudorabies

Question 16

Bacterial aetiologies of myocarditis

Answer 16

Septicaemia

Question 17

Parasitic aetiologies of myocarditis

Answer 17

Toxoplasmosis

Neosporosis

Trypanosomiasis

Question 18

Canine parvovirus and myocardial disease

Answer 18

Affects rapidly dividing cells in alimentary tract, bone marrow and myocardium.

Myocardial cells divide rapidly for up to 15 days post partum.

Virus infection occurs at this time but infection may take some time to become clinically apparent.

Two cardiac syndromes.
○ Sudden death in pups 3‑8 weeks old.
○ Pups of 8 weeks to two years of age develop dyspnoea, weakness, collapse and death within 24 hours.

Question 19

Sudden death in pups 3-8 weeks due to parvovirus

Answer 19

Gross appearance of cardiac failure with pulmonary oedema, swollen congested liver and a mottled pale myocardium.

Histologically ventricular myocardium shows multifocal myocardial necrosis and a mononuclear cellular infiltrate.

Some myocytes contain large basophilic intranuclear inclusion bodies.

Question 20

Parvovirus in pups 8 weeks - 2 years

Answer 20

Develop dyspnoea, weakness, collapse and death within 24 hours.

Pathologically there is cardiac failure associated with severe myocardial fibrosis.

Question 21

Myocardial degeneration, necrosis, and infarction

Answer 21

common lesion to encounter at post mortem.

The causes are many and varied, but ischaemia is probably the commonest.

Dilated and hypertrophied hearts are very susceptible to this type of change.

Arteriosclerotic and thrombotic disease may result in ischaemia.

Myocardial necrosis also arises from infectious processes, deficiency diseases and toxicities.

Question 22

Gross pathology of myocardial degeneration, necrosis, and infarction

Answer 22

Gross evidence of necrosis not present until 12 hours after injury.

By 18‑24 hours the area is grey brown and by 2‑4 days is ringed by an area of hyperaemia.

After 10 days there is gradual replacement by pale scar tissue.

Question 23

Acute infarction of myocardium

Answer 23

In the acute stages an area of infarction may be indicated by a fibrinohaemorrhagic thickening of the epicardium.

It is important to realise that quite large areas of myocardial necrosis may produce no functional disturbance but can be a complicating factor leading to chronic cardiac failure in a number of conditions.

Question 24

Acute necrosis of myocardium

Answer 24

due to deprivation of blood supply is known as infarction.

Less common in animals than in humans.

Due to thrombosis or embolism of the coronary arteries, atherosclerosis (hypothyroidism) and disseminated intravascular coagulation (DIC).

Question 25

Hypertrophy of myocardium

Answer 25

An increase in bulk due to increase size of cardiac muscle fibres, estimated by thickness and weight of wall.

Hypertrophy is generally secondary and is the result of compensatory response to increased workload.

Hypertrophy may be reversible on removal of the cause.

Right sided hypertrophy increases the width of the heart; left sided hypertrophy increases the length.

Bilateral hypertrophy produces a rounded shape.

Question 26

Concentric hypertrophy

Answer 26

Small ventricular chambers with thick walls.

It results from lesions that increase pressure load (valvular stenosis, systemic hypertension and pulmonary disease) and restrictive pericarditis.

Question 27

Eccentric hypertrophy

Answer 27

Hearts show enlarged ventricular chambers and walls of normal or decreased thickness.

It results from lesions that increase blood volume load.

Common with valvular insufficiencies and septal defects.

Question 28

Cardiac dilation

Answer 28

There is an increased chamber size.

Heart becomes globose with soft pliable ventricular wall.

Endocardium is often diffusely thickened.

Characteristically seen with chronic congestive heart failure.

Question 29

Cardiomyopathies

Answer 29

can be either primary or secondary.

There are several aetiologies and they represent important generalized myocardial diseases in animals.

Question 30

Primary or idiopathic cardiomyopathy

Answer 30

Heart muscle disease of unknown cause affecting only the heart.

Seen in dogs, cats and cattle.

They are progressive cardiac disease.

There are three morphologic types:
i) Hypertrophic
ii) Dilated (congestive)
iii) Restrictive

Question 31

Hypertrophic cardiomyopathy

Answer 31

The cat is the animal most commonly affected by cardiomyopathy. Maine coon, Persians

Wide age range 7 months to 24 years and varied symptoms including arrhythmias, tachycardias and dyspnoea.

About a third of cases present with thromboembolic hind leg ischaemia as a secondary effect but representing the ‘clinical horizon’.

Heart is enlarged with prominent hypertrophy of the left ventricle and interventricular septum.

The left ventricular cavity is markedly reduced in size and the left atrium is dilated.

Question 32

Endomyocardial hypertrophic cardiomyopathy

Answer 32

Young cat

Subendocardiocardial inflammation and atrial thrombosis

Question 33

Symmetrical hypertrophic cardiomyopathy

Answer 33

Left ventricle, septum, and papillary muscles affected

Question 34

Assymetric hypertrophic cardiomyopathy

Answer 34

Asymmetric hypertrophy of septum especially the left outflow tract

20% have aortic thromboembolism

Question 35

Dilated cardiomyopathy

Answer 35

Common form in dog and cats.

In young middle-aged dogs of the large breeds e.g. St. Bernard, Wolfhound and Great Dane.

Sudden onset often with atrial fibrillation and congestive heart failure.

Affected cats and some dogs show low tissue concentrations of taurine.

Taurine supplementation results in reduction in cases.

Gross cardiomegaly with cardiac hypertrophy, dilation and poor contractile force.

Poor prognosis with 6‑12 months survival.

Question 36

Dilated cardiomyopathy in dobermans

Answer 36

Present with arrhythmias

Find lymphocytic infiltrates in ventricles

Question 37

Dilated cardiomyopathy in English cockers

Answer 37

Familial with high prevalence of sub clinical disease.

Ventricular hypertrophy progresses to muscular failure.

Question 38

Resrtictive cardiomyopathy

Answer 38

Occurs in cats but is infrequent.

Endocardial thickening and fibrosis leads to poor ventricular filling and left atrial dilation.

Aetiology of primary cardiomyopathy is unknown.

Question 39

Secondary cardiomyopathy

Answer 39

This group includes generalised myocardial diseases of known cause.

Hypertrophic cardiomyopathy is seen with hyperthyroidism in the cat due to thyroid nodular hyperplasia or neoplasia.

Question 40

Causes of secondary cardiomyopathy

Answer 40

Hyperthyroidism in the cat due to thyroid nodular hyperplasia or neoplasia.

nutritional deficiencies (selenium/vitamin E),

toxic (gossypol, uraemia),

Endocrine disorders (hypothyroidism, hyperthyroidism, diabetes mellitus),

Infectious disease (viral, bacterial, mycotic, parasitic),

immune-mediated,

myocardial lymphoma,

chronic renal disease.

Question 41

Valvular endocardiosis (myxomatous valve disease)

Answer 41

This is the most common cardiovascular lesion in dogs.

Often encountered at post mortem as an incidental age-related cardiac disease of middle-aged to old dogs.

Question 42

Aetiology of valvular endocardiosis (myxomatous valve disease)

Answer 42

The aetiology of the condition is not known.

It is suggested that there may be a genetically influenced degeneration of connective tissue.

This disease is very similar to the prolapsed mitral valve syndrome of humans, which is associated with abnormalities of collagen metabolism.

Question 43

Signalment of valvular endocardiosis (myxomatous valve disease)

Answer 43

Small and toys breeds are more affected.

Breeds with high incidence include: cavalier King Charles spaniel, cocker spaniel, beagle, poodle, Chihuahua, Doberman pinscher, fox terrier, Boston terrier, Pekingese and other chondrodystrophic breeds.

Males of certain breeds are most frequently affected.

Question 44

Sequelae of valvular endocardiosis

Answer 44

valvular incompetence and clinical left sided heart failure.

In dogs more than 9 years of age 75% have lesions and 40% will have a degree of valvular incompetence.

The left A‑V valves (mitral) are chiefly affected (Myxomatous mitral valve disease - MMVD), the right less so and the aortic and pulmonary valves are rarely affected.

Question 45

Lesion of of valvular endocardiosis (myxomatous valve disease)

Answer 45

occurs in the spongiosa and fibrosa layers of the valve leaflet.

Collagen in the fibrosa degenerates and loose fibroblastic tissue and glycosaminoglycan is laid down in the spongiosa.

This type of change is known as mucoid or myxomatous degeneration.

Cartilagenous and bony metaplasia can be seen.

Microscopically, the thickened valves have increased fibroblastic proliferation and deposition of acid mucopolysaccharides.

Question 46

Pathology of myxomatous valve disease

Answer 46

The valve becomes thickened and the edge of the leaflet may roll over.

In the earliest stages the leaflet may contain only small nodules but gradually large plaques form and these may eventually be rupture of the chordae tendinae and gross distortion of the valve cusps.

The valves become incompetent and dilation of the atria occurs together with ventricular dilation.

Regurgitation of blood into the atria at systole produces ‘jet’ lesions on the atrial endocardium, which in severe cases may lead to atrial tears and haemopericardium, and rupture of the chordae tendinae.

The dilated left ventricle may eventually fail and back pressure on the lung leads to pulmonary oedema.

The enlarged left atrium compresses the left bronchus between the aorta and the heart wall leading to coughing.

Focal myocardial necrosis and fibrosis may occur in the dilated left ventricle and may lead to impaired cardiac conduction arrhythmias and eventual congestive heart failure.

Question 47

Valvular endocarditis

Answer 47

Usually due to bacterial infection arriving via the blood stream and usually affects the valves.

Question 48

Portals of entry for valvular endocarditis

Answer 48

Haematogenous dissemination

Parasitic migration

Intravenous and intra cardiac catheters (long-term)

Uraemia-induced

Immune induced

Question 49

Pathology of valvular endocarditis

Answer 49

Affected valves are thickened with adhering, friable, yellow to gray exudate (vegetations- vegetative endocarditis).

In chronic cases exudate organizes as fibrous connective tissue forming nodular masses (verrucae).

Question 50

What do thrombi of the valves look like in valvular endocarditis?

Answer 50

Begins as loose thrombus of platelets and fibrin on the atrial side of the A‑V valves.

Soon large crumbly cauliflower-like vegetations build up on the leaflet.

Bacterial colonies occur in the mass and there is an attempt to organise the mass from the leaflet, which becomes ulcerated.

Unless the lesions are very small healing probably never occurs and there may be rupture of the chordae tendinae with spread to the mural endocardium.

Question 51

What causes death in valvular endocarditis?

Answer 51

Congestive cardiac failure and the effects of embolisation

Question 52

Where do valvular endocarditis lesions occur in dogs?

Answer 52

Particularly on the mitral valves, sometimes the aortic and pulmonary.

Large vegetations produce septic emboli in various organs but particularly the kidney causing infarcts.

Question 53

Ulcerative endocarditis

Answer 53

occurs most commonly in renal failure in dogs and is restricted to the left atrium of the heart although lesions also occur in the aorta and pulmonary artery proximal to the valves.

Question 54

Endocardial and endothelial mineralisation

Answer 54

May occur when there is an elevated serum level of calcium

Other tissues such as lung, arteries and bowel mucosa may also be affected.

Also occurs following chronic dilatation of the heart or associated with “jet” lesions resulting from turbulence or abnormal flow.

Calcium and phosphorus are deposited on damaged fibro‑elastic tissue.

Uremic dogs can have ulcerative endocarditis and dystrophic mineralisation.

Question 55

Pathology of endocardial and endothelial mineralisation

Answer 55

multiple, large, rough, white, firm plaques within fibroelastic tissue in the endocardium and intima of large elastic arteries

Question 56

Endocardial haemorrhage

Answer 56

Haemorrhages can be found in septicaemias, viraemias, and toxaemias

Question 57

Arterial thrombosis

Answer 57

It occurs in dog and cat with idiopathic cardiomyopathies.

Thrombosis may be followed by episodes of embolisation with impaction in the terminal aorta, particularly in the cat.

Clinically there is a syndrome of sudden hind leg paralysis with cold hind limbs and absence of femoral pulse.

Embolisation may occur elsewhere but is often clinically silent.

Question 58

Aneurysm

Answer 58

Local abnormal dilation of a thinned and weakened vessel.

Causes: idiopathic

Partial rupture of the wall may allow blood to track within the wall producing a dissecting aneurysm.

Uncommon in animals.

Causes include Spirocerca lupi larvae in dogs.

Aneurysms can rupture leading to sudden death.

Question 59

Blood vessel hypertrophy

Answer 59

Occurs as response to sustained increases in pressure or volume loads.

Medial hypertrophy of the pulmonary arteries in the cat can be associated with parasites such as Aelurostronylus abstrusus and Toxocara sp., however, arterial hypertrophy occurs in the absence of parasites.

Enormous increase in the thickness of the media often visible macroscopically.

No apparent clinical effect.

Question 60

Arteriosclerosis

Answer 60

Very rare in domestic animals.

Represents a heterogenous group of conditions where the changes are either hyperplastic or hyaline (amorphous eosinophilic change).

Non-inflammatory chronic change with induration, loss of elasticity and narrowing of the vessel wall.

Usually affects the intima and media, characterised by intimal fibrosis of large elastic arteries and results in ischaemia of tissue supplied.

Rarely causes thrombosis.

In the dog seen in pulmonary vessels, and commonly in the myocardium and may contribute to myocardial fibrosis and cardiac failure in that species.

Question 61

Atherosclerosis

Answer 61

It involves deposition of lipid (atheroma) in vessel wall, greatest importance in human beings, but in veterinary medicine only infrequently.

Seen in dogs ‘with hypothyroidism due to the hypercholesterolaemia caused by this condition

Luminal narrowing and loss of elasticity

Question 62

Fibrinoid necrosis

Answer 62

A microscopic term with a brightly eosinophilic change in the media

Seen in three situations:

1. uraemia in the dog
2. endothelial damage
3. vasculitis

Question 63

Fibrinoid necrosis in uraemia

Answer 63

Affects the small muscular arteries of the gastric submucosa, gall bladder, and urinary bladder.

Lesions are focal or circumferential medial necrosis, mineralisation and subendothelial accumulations of fibrin.

May lead to gastric ulceration due to ischaemia and infarction.

With chronic renal failure the proliferative component may be more prominent.

Question 64

Fibrinoid necrosis with endothelial damage

Answer 64

entry and accumulation of serum proteins that following fibrin polymerization in the vessel wall e.g. dogs with uremia.

Question 65

Predisposing factors to thrombosis

Answer 65

a. Endothelial injury,
b. Altered blood flow,
c. Hypercoagulability

Question 66

Thrombosis

Answer 66

Represents the process of intravascular coagulation during life.

More often arterial then venous in animals.

Examples include caudal aortic thromboembolism in dogs and cats (primary cardiomyopathy) and pulmonary thrombosis in dogs with dirofilariasis.

Question 67

Embolism

Answer 67

the occlusion of arteries with foreign bodies, e.g. bacteria, neoplastic cells, fragments of thrombi (endocarditis, verminous arteritis), parasites (dirofilariasis), air bubbles, hair fragments, fibrocartilagenous tissue and fat from the bone marrow (fractures).

Question 68

Pathogenesis of Disseminated Intravascular Coagulation (DIC)

Answer 68

Endothelial damage, intravascular activation of coagulation process

-> exposure of subendothelial collagen

-> platelet aggregation

-> DIC

Question 69

Vascultitis

Answer 69

When all types of vessels are affected with an inflammatory process and arteritis if only arteries are affected.

Inflammation of the vessel wall distinguished from degenerative changes by the presence of inflammatory cells within and around the vessel wall.

Main results are increased permeability leading to oedema, haemorrhage and thrombosis.

Petechial or echymotic haemorrhages in the mucosa are characteristic.

Question 70

Phlebitis

Answer 70

Inflammation of veins

A common vascular lesion and is often complicated by thrombosis and occasionally haemorrhage.

E.g. intravenous injections of irritant solutions and feline infectious peritonitis.

Question 71

Viral causes of vasculatitis

Answer 71

Infectious canine hepatitis

Canine distemper

Question 72

Bacterial causes of vasculitis

Answer 72

Septicaemia diseases

Question 73

Mycotic causes of vasculitis

Answer 73

Aspergillosis

Question 74

Parasitic causes of vasculitis

Answer 74

Dirofilariosis (heartworm in dog) and spirocercosis in dogs, and aelurostrongylosis in cats.

Question 75

Immune mediated causes of vasculitis

Answer 75

Type III hypersensitivity reactions.

Feline infectious peritonitis in cat.

Aleutian disease in mink and systemic lupus erythematosus.

Question 76

Venous dilation and thrombosis

Answer 76

A venous dilation from weakened vascular walls is termed a varicosity and phlebectasia if a generalised alteration occurs. In animals is uncommon.

Tendency to thrombosis and sclerosis

Question 77

Varicocele

Answer 77

when the pampiniform plexus in the spermatic cord is affected by venous dilation and thrombosis

Question 78

Lymph vessel dilation

Answer 78

Lymphangiectasis is dilation of lymph vessels, following obstruction, e.g. lymphangiectasia in bowel and obstruction of lymph drainage by invading masses of malignant neoplasms.

Intestinal lymphangiectasis in digs can lead to PLE

Question 79

Physical injury of lymph vessels

Answer 79

Rupture of thoracic duct as a result of trauma or from spontaneous disruption produces chylothorax/chylopericardium.

Question 80

Lymphangitis

Answer 80

a feature of many diseases processes, related mainly with inflammation in any tissue, e.g. distal limbs.