Flashcards in Pathology of the Cardiovascular System 2 Deck (37):
NORMAL MICROANATOMY OF THE HEART
-Centrally located nuclei
-Purkinje fibres- modified fibres which conduct electrical stimuli through the heart
-Intercalated discs- connect myofibres, allow for unified contraction of myofibres.
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.
PHYSIOLOGICAL CHANGES TO MYOCARDIUM
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"
To physiological changes... May become PATHOLOGICAL.
ATROPHY- reduced workload eg. bed rest, wasting diseases.
HYPERTROPHY- increased workload eg. hypertension, valvular stenosis.
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.
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.
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.
Increased myocyte length due to addition of myocytes in series- dilation as well as thickening.
Due to VOLUME OVERLOAD eg. valvular insufficiencies, septal defects.
STAGES IN MYOCARDIAL HYPERTROPHY
2. STABLE HYPERFUNCTION
3. DETERIORATION OF FUNCTION- due to degeneration of hypertrophied fibres.
Increase in heart function.
Normal gene expression.
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.
1. DEGENERATION- aging, nutritional, toxic
2. NECROSIS- nutritional, toxic, traumatic
3. MYOCARDITIS- viral, bacterial, parasitic
4. CARDIOMYOPATHIES- inherited or acquired.
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.
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)
Myofibre degeneration and loss
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)
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.
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.
CONSEQUENCES OF MYOCARDIAL NECROSIS/MYOCARDITIS
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.
BIOCHEMICAL MARKERS OF MYOCARDIAL DAMAGE
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)
HEART MUSCLE DISEASES (CARDIOMYOPATHIES)
Inflammation of the heart muscle
Heart muscle is hypertrophied/thickened
Heart muscle is atrophied/weakened, leading to dilated chambers.
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.
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.
FELINE HYPERTROPHIC CARDIOMYOPATHY
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)
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.
CANINE DILATED CARDIOMYOPATHY
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).
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.
1. Developmental anomalies
2. Degeneration- valvular endocardiosis- degenerative structural change.
3. Inflammation- valvular endocarditis.
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.
ENDOCARDIOSIS- POSSIBLE CONSEQUENCES
massive right atrial expansion and possibly rupture due to mitral regurgitation.
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.
VALVULAR ENDOCARDITIS- GROSS APPEARANCE
Friable yellow and grey masses or vegetations seen on affected valves.
Layers of fibrin with embedded bacterial colonies stuck on to valves.
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"
CONSEQUENCES OF VALVULAR DISEASE
-RUPTURED CHORDAE TENDINAE- severe incompentence.
Failure of valve to open.
Impedes forward flow.
Failure of valve to close.
Reversed flow- regurgitation- heart murmurs.