Pathology of the Cardiovascular System 2

Question 1

NORMAL MICROANATOMY OF THE HEART

Answer 1

• Striated muscle
• Centrally located nuclei
• Branching myofibres
• Purkinje fibres- modified fibres which conduct electrical stimuli through the heart
• Intercalated discs- connect myofibres, allow for unified contraction of myofibres.

Question 2

SARCOMERE

Answer 2

Unit of muscular contraction, composed of actin (thin) and myosin (thick), running parallel to the LONG axis of the myofibre.
Z discs connect sarcomeres within the cell, for unified contraction.

Question 3

PHYSIOLOGICAL CHANGES TO MYOCARDIUM

Answer 3

ATROPHY- decreased cell size
HYPERTROPHY- increased cell size eg. athlete- physiological hypertrophy (can be seen pathologically as well)
Changes occur due to altered demands.
“The heart shape can further be described as eccentric or concentric during hypertrophic growth”

Question 4

MYOCARDIAL RESPONSES

Answer 4

To physiological changes… May become PATHOLOGICAL.
ATROPHY- reduced workload eg. bed rest, wasting diseases.
HYPERTROPHY- increased workload eg. hypertension, valvular stenosis.

Question 5

HYPERTROPHY

Answer 5

Increase in cell size.
Seen in the heart physiologically and pathologically.
In response to increased workload.
Leads to decreased space in the ventricles.
The heart can only compensate for so long in pathological hypertrophy, then it will go in to failure.

Question 6

ATROPHY

Answer 6

Decrease in cell size.
Seen in the heart physiologically and pathologically.
In response to decreased workload.
Can occur due to cell death eg. irreversible injury of myocytes.

Question 7

CONCENTRIC HYPERTROPHY

Answer 7

Increased myocyte width due to addition of sarcomeres in parallel.
Due to PRESSURE OVERLOAD eg. Valvular stenosis, systemic hypertension, lung disease.
Decreased lumen space in heart chambers.

Question 8

ECCENTRIC HYPERTROPHY

Answer 8

Increased myocyte length due to addition of myocytes in series- dilation as well as thickening.
Due to VOLUME OVERLOAD eg. valvular insufficiencies, septal defects.

Question 9

STAGES IN MYOCARDIAL HYPERTROPHY

Answer 9

1. INITIATION
2. STABLE HYPERFUNCTION
3. DETERIORATION OF FUNCTION- due to degeneration of hypertrophied fibres.

Question 10

PHYSIOLOGICAL HYPERTROPHY

Answer 10

Increase in heart function.

Normal gene expression.

Question 11

PATHOLOGICAL HYPERTROPHY

Answer 11

Initial increase in heart function, but long term, depressed cardiac function is seen due to cardiomyocyte damage- apoptosis, fibrosis. Associated with heart failure.
Foetal gene reactivation occurs- to activate gene expression pattern seen in embryonic development- hypertrophic gene markers are activated eg. BNP, ANP.

Question 12

MYOCARDIAL DISEASES

Answer 12

1. DEGENERATION- aging, nutritional, toxic
2. NECROSIS- nutritional, toxic, traumatic
3. MYOCARDITIS- viral, bacterial, parasitic
4. CARDIOMYOPATHIES- inherited or acquired.

Question 13

MYOCARDIAL DEGENERATION

Answer 13

1. LIPOFUSCINOSIS- ‘wear and tear’/old age pigment; brown atrophy; xanthosis. Clinically insignificant, seen in old/cachexic animals.
2. FATTY DEGENERATION- abnormal triglyceride accumulation.
3. MYOCYTOLYSIS- Myocyte lysis. Reversible in early stages.
4. VACUOLAR DEGENERATION- Hydropic changes.

Myocardial degeneration is sublethal.

Question 14

MYOCARDIAL NECROSIS

Answer 14

Injury to normal cardiac muscle cells eg. toxic insult, nutritional deficiency, physical insult, infarction causes:
HYALINE NECROSIS- loss of cross striations, cells become translucent.
-> MACROPHAGE INVASION -> HEALING WITH FIBROSIS (scar formation)
eg. White Muscle Disease in calves (selenium/vitamin E deficiency)

Question 15

VIRAL MYOCARDITIS

Answer 15

Myofibre degeneration and loss
Reactive fibroplasia
Mononuclear, mostly lymphocytic infiltrate.
eg. Canine Parvovirus- viral myocarditis can be seen weeks/months after the first signs of viral infection.
Myocardial pallor (CPV)
Intranuclear inclusion bodies (CPV)

Question 16

BACTERIAL MYOCARDITIS

Answer 16

eg. Traumatic reticulitis- wire penetration.
Localised suppurative inflammation will occur.
The body will try and wall off the lesion with fibrous connective tissue.
This forms an abscess, which AFFECTS HEART FUNCTION.
The abscess is a large area with no function.
The heart muscle hypertrophies to compensate for this.
Depending on its location, the abscess may move heart valves, causing valvular insufficiency.

Question 17

PARASITIC MYOCARDITIS

Answer 17

eg. Cysticercus bovis (T. saginata cystic stage), Cysticercus ovis (T. ovis).
PUBLIC HEALTH SIGNIFICANCE.
All skeletal muscles are also affected- carcass condemnation.
Cysts can have a greenish tinge- eosinophils.

Question 18

CONSEQUENCES OF MYOCARDIAL NECROSIS/MYOCARDITIS

Answer 18

1. SUDDEN DEATH.
2. MYOCARDIAL SCARRING- consequence of this depends on scar location. Can result in sudden death, chronic hart failure, or a clinically normal animal.

Question 19

BIOCHEMICAL MARKERS OF MYOCARDIAL DAMAGE

Answer 19

Various biochemical markers may be detectable from 1-3 hours to 10- 14 days after damage occurs.

eg. Creatine kinase
eg. Troponins- these can be used to measure the reversibility of the damage (increased levels indicate cardiac muscle cell death)

Question 20

HEART MUSCLE DISEASES (CARDIOMYOPATHIES)

Answer 20

MYOCARDITIS
HYPERTROPHIC CARDIOMYOPATHY
DILATED CARDIOMYOPATHY

Question 21

MYOCARDITIS

Answer 21

Inflammation of the heart muscle

Question 22

HYPERTROPHIC CARDIOMYOPATHY

Answer 22

Heart muscle is hypertrophied/thickened

Question 23

DILATED CARDIOMYOPATHY

Answer 23

Heart muscle is atrophied/weakened, leading to dilated chambers.

Question 24

PRIMARY CARDIOMYOPATHIES

Answer 24

Idiopathic, some are inherited/familial.
-HYPERTROPHIC- seen most commonly in cats (also dogs, pigs, hamsters)

• DILATED- seen most commonly in dogs (large breeds), also cattle and cats (decreased incidence since taurine now supplemented in food)
• CAT- Arrhythmogenic Right Ventricular Cardiomyopathy/Disease (ARVC/ARVD)- Rare but seen in cats and more rarely in dogs and horses.

Question 25

SECONDARY CARDIOMYOPATHIES

Answer 25

CATS- Hypertrophic Cardiomyopathy (HCM) seen secondary to hyperthyroidism.
-Dilated Cardiomyopathy (DCM), Taurine Responsive Cardiomyopathy (TRCM) seen with taurine deficiency- uncommon now due to supplementation of food.

OTHER SPECIES- Cardiomyopathies seen secondary to drug/toxin/nutritional disorders.

Question 26

FELINE HYPERTROPHIC CARDIOMYOPATHY

Answer 26

Marked left ventricular hypertrophy and interventricular septum thickening.

• > Left atrial enlargement (harder to push blood through to ventricle so it builds up)
• > Pulmonary oedema and pleural effusion (blood backs up in to pulmonary vein and pulmonary system)
• > Progresses to either congestive heart failure or sudden death.

HISTOLOGICALLY- Hypertrophy and disarray of myocytes (enlarged, but same length)
-Interstitial fibrosis.

HCM is the most common primary heart disease diagnosed in cats, but is rare in dogs.
DCM is rare in cats since the introduction of taurine supplementation.

Question 27

CANINE DILATED CARDIOMYOPATHY

Answer 27

Cardiac dilation and contractile dysfunction of the ventricles.

• > Left sided heart failure- pulmonary oedema
• > Progression to chronic heart failure with dilation of all chambers- globular shaped heart.

DCM is one of the most prevalent ACQUIRED heart diseases of dogs.
It is a major cardiovascular cause of morbidity and mortality.
It is only surpassed by endocardiosis (degenerative valvular disease) and heartworm disease (in some parts of the world).

Question 28

RESTRICTIVE CARDIOMYOPATHY

Answer 28

LEAST COMMON cardiomyopathy.
Characterised by increased ventricular stiffness, usually caused by abnormal fibrosis (can be due to ventricular deposits)
Left ventricular compliance is decreased- Restrictive filling and reduced diastolic volume (reduced preload).
Reduced cardiac output and stroke volume.

Question 29

VALVULAR DISEASES

Answer 29

1. Developmental anomalies
2. Degeneration- valvular endocardiosis- degenerative structural change.
3. Inflammation- valvular endocarditis.

Question 30

VALVULAR ENDOCARDIOSIS

Answer 30

Degenerative disease of older dogs, especially medium/small breeds (Cavalier King Charles Spaniel classic example)
-Bluish, myxoid/mucoid degeneration of valves (connective tissue)
-Degeneration is slowly progressive and often subclinical
-Structural change- changes occur within the valve material as well as on the surface.
-Smooth, pearl-white round thickenings on valve leaflets +/- chordae thickening
-MOST FREQUENT ON MITRAL VALVES
Causes MITRAL INSUFFICIENCY, MITRAL REGURGITATION.
Commonest cause of congestive heart failure in adult dogs.

Question 31

ENDOCARDIOSIS- POSSIBLE CONSEQUENCES

Answer 31

massive right atrial expansion and possibly rupture due to mitral regurgitation.

Question 32

VALVULAR ENDOCARDITIS

Answer 32

Inflammation.

eg. Bacterial infection of valves.
- CATTLE- Right AV (tricuspid) valve is most commonly affected- infection can spread to pulmonary veins -> lungs, causing pulmonary thromboembolism.

• PIGS, SHEEP, DOGS- Left AV (mitral) valve- can cause infarct (systemic circulation- kidneys, liver, spleen)
• HORSES- Aortic valve (semilunar)- can cause infarct.

Question 33

VALVULAR ENDOCARDITIS- GROSS APPEARANCE

Answer 33

Friable yellow and grey masses or vegetations seen on affected valves.
Layers of fibrin with embedded bacterial colonies stuck on to valves.
Inflammatory exudate.
Septic embolisation can occur to the lungs, heart and kidneys- LOOK FOR LESIONS AROUND THE BODY AS WELL!
Circulating factors promote thromboembolic disease- “it’s not simply the vegetation”

Question 34

CONSEQUENCES OF VALVULAR DISEASE

Answer 34

• STENOSIS
• INCOMPETENCE
• RUPTURED CHORDAE TENDINAE- severe incompentence.

Question 35

STENOSIS

Answer 35

Failure of valve to open.

Impedes forward flow.

Question 36

INCOMPETENCE

Answer 36

Failure of valve to close.

Reversed flow- regurgitation- heart murmurs.

Question 37

JETTING LESIONS

Answer 37

Endocardial roughening/thickening seen in response to repeated impact from high velocity blood, seen due to valvular incompetence-> regurgitation.
Causes necrosis and mineralisation.
Occasionally, the damage to the endocardium is enough to permit mural thrombi to develop.