Acquired cardiovascular pathology Flashcards
Hydropericardium
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.
Haemorrhagic pericardial effusion
Idiopathic in large or giant breeds of dogs.
Not whole blood, just bloody fluid (haemorrhagic effusion).
Haemopericardium
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.
Serous atrophy of fat
Occurs during chronic anorexia, starvation, cachexia.
Fat is catabolised to maintain energy balance.
Pericardial fat is gray and gelatinous.
Pericarditis
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.
Myocardial diseases
Fatty infiltration
Fatty degeneration
Hydropic degeneration
Lipfuscinosis
Myofibrillar degeneration
Myocardial mineralisation
Myocarditis
Myocardial degeneration, necrosis, and infarction
Hypertrophy and dilation/cardiomyopathies
Fatty infilatration of myocardium
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.
Fatty degeneration of myocardium
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.
Hydropic degeneration of myocardium
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).
Lipofuscinosis
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.
Myofibrillar degeneration
It is a sublethal injury of myocardial cells, which are pale eosinophilic sarcoplasm and lack cross striations.
Not common in animals.
Myocardial mineralisation
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.
Myocarditis
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
Types of myocarditis
Suppurative (pyogenic bacteria)
Necrotizing (toxoplasmosis)
Haemorrhagic (Blackleg - Clostridium chauvoei)
Lymphocytic (Canine parvovirosis)
Eosinophilic (Sarcocystosis)
Viral aetiologies of myocarditis
Canine parvovirus
Pseudorabies
Bacterial aetiologies of myocarditis
Septicaemia
Parasitic aetiologies of myocarditis
Toxoplasmosis
Neosporosis
Trypanosomiasis
Canine parvovirus and myocardial disease
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.
Sudden death in pups 3-8 weeks due to parvovirus
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.
Parvovirus in pups 8 weeks - 2 years
Develop dyspnoea, weakness, collapse and death within 24 hours.
Pathologically there is cardiac failure associated with severe myocardial fibrosis.
Myocardial degeneration, necrosis, and infarction
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.
Gross pathology of myocardial degeneration, necrosis, and infarction
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.
Acute infarction of myocardium
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.
Acute necrosis of myocardium
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).
Hypertrophy of myocardium
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.
Concentric hypertrophy
Small ventricular chambers with thick walls.
It results from lesions that increase pressure load (valvular stenosis, systemic hypertension and pulmonary disease) and restrictive pericarditis.
Eccentric hypertrophy
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.
Cardiac dilation
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.
Cardiomyopathies
can be either primary or secondary.
There are several aetiologies and they represent important generalized myocardial diseases in animals.
Primary or idiopathic cardiomyopathy
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
Hypertrophic cardiomyopathy
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.
Endomyocardial hypertrophic cardiomyopathy
Young cat
Subendocardiocardial inflammation and atrial thrombosis
Symmetrical hypertrophic cardiomyopathy
Left ventricle, septum, and papillary muscles affected
Assymetric hypertrophic cardiomyopathy
Asymmetric hypertrophy of septum especially the left outflow tract
20% have aortic thromboembolism
Dilated cardiomyopathy
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.
Dilated cardiomyopathy in dobermans
Present with arrhythmias
Find lymphocytic infiltrates in ventricles
Dilated cardiomyopathy in English cockers
Familial with high prevalence of sub clinical disease.
Ventricular hypertrophy progresses to muscular failure.
Resrtictive cardiomyopathy
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.
Secondary cardiomyopathy
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.
Causes of secondary cardiomyopathy
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.
Valvular endocardiosis (myxomatous valve disease)
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.
Aetiology of valvular endocardiosis (myxomatous valve disease)
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.
Signalment of valvular endocardiosis (myxomatous valve disease)
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.
Sequelae of valvular endocardiosis
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.
Lesion of of valvular endocardiosis (myxomatous valve disease)
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.
Pathology of myxomatous valve disease
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.
Valvular endocarditis
Usually due to bacterial infection arriving via the blood stream and usually affects the valves.
Portals of entry for valvular endocarditis
Haematogenous dissemination
Parasitic migration
Intravenous and intra cardiac catheters (long-term)
Uraemia-induced
Immune induced
Pathology of valvular endocarditis
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).
What do thrombi of the valves look like in valvular endocarditis?
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.
What causes death in valvular endocarditis?
Congestive cardiac failure and the effects of embolisation
Where do valvular endocarditis lesions occur in dogs?
Particularly on the mitral valves, sometimes the aortic and pulmonary.
Large vegetations produce septic emboli in various organs but particularly the kidney causing infarcts.
Ulcerative endocarditis
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.
Endocardial and endothelial mineralisation
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.
Pathology of endocardial and endothelial mineralisation
multiple, large, rough, white, firm plaques within fibroelastic tissue in the endocardium and intima of large elastic arteries
Endocardial haemorrhage
Haemorrhages can be found in septicaemias, viraemias, and toxaemias
Arterial thrombosis
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.
Aneurysm
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.
Blood vessel hypertrophy
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.
Arteriosclerosis
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.
Atherosclerosis
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
Fibrinoid necrosis
A microscopic term with a brightly eosinophilic change in the media
Seen in three situations:
- uraemia in the dog
- endothelial damage
- vasculitis
Fibrinoid necrosis in uraemia
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.
Fibrinoid necrosis with endothelial damage
entry and accumulation of serum proteins that following fibrin polymerization in the vessel wall e.g. dogs with uremia.
Predisposing factors to thrombosis
a. Endothelial injury,
b. Altered blood flow,
c. Hypercoagulability
Thrombosis
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.
Embolism
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).
Pathogenesis of Disseminated Intravascular Coagulation (DIC)
Endothelial damage, intravascular activation of coagulation process
-> exposure of subendothelial collagen
-> platelet aggregation
-> DIC
Vascultitis
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.
Phlebitis
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.
Viral causes of vasculatitis
Infectious canine hepatitis
Canine distemper
Bacterial causes of vasculitis
Septicaemia diseases
Mycotic causes of vasculitis
Aspergillosis
Parasitic causes of vasculitis
Dirofilariosis (heartworm in dog) and spirocercosis in dogs, and aelurostrongylosis in cats.
Immune mediated causes of vasculitis
Type III hypersensitivity reactions.
Feline infectious peritonitis in cat.
Aleutian disease in mink and systemic lupus erythematosus.
Venous dilation and thrombosis
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
Varicocele
when the pampiniform plexus in the spermatic cord is affected by venous dilation and thrombosis
Lymph vessel dilation
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
Physical injury of lymph vessels
Rupture of thoracic duct as a result of trauma or from spontaneous disruption produces chylothorax/chylopericardium.
Lymphangitis
a feature of many diseases processes, related mainly with inflammation in any tissue, e.g. distal limbs.
