Acquired Cardiac Disease Pathology

Question 1

Layers of the pericardium.

Answer 1

• Outer fibrous pericardium (coated by pleura).
• Serous pericardium parietal layer.
• Serous pericardium visceral layer = epicardium.
  Pericardial space normally contains a small amount of pericardial fluid - lubricates serosal surfaces.

Question 2

1. Pericarditis.
2. Pericarditis classification.

Answer 2

1. Inflammation of the pericardium or pericardial sac.
2. Based on morphological features and/or the type of exudate.
   Most commonly:
   - Fibrinous.
   - Suppurative (purulent)/fibrinopurulent.
   - Constrictive.

Question 3

Fibrinous pericarditis.

Answer 3

• A lot of fibrin present within the exudate.
• Contraction of endothelial cells due to inflammation – spaces between spaces, allowing escape of fluid and proteins into the surrounding tissues e.g. fibrinogen.
• Fluid accumulation on the serous layer surface within the pericardial space.
• Fibrinogen converted to fibrin by thrombin.
• Fibrin starts to polymerise together and create lots of matts – often yellowish or pinkish if contaminated with blood.
• Fibrin broken down by fibrinolysis or re-modelled and replaced by fibrous tissue (collagen laid down and leads to fibrous pericarditis).

Question 4

1. Fibrinous pericarditis most commonly seen in?
2. Examples of causes.

Answer 4

1. Farm animals.
   Due to bacterial septicaemias and haematogenous infections.
2. • Coli-septicaemia.
     - Mannheimiosis (Mannheimia haemolytica) in sheep and cattle.
     - Blackleg (Clostridium chauvoei) in sheep and cattle.
     - Glasser’s disease (Haemophilus parasuis) in pigs.

Question 5

1. Suppurative (purulent) pericarditis.
2. Most common in?
3. Appearance.

Answer 5

1. Infection w/ pyogenic bacteria causing purulent or fibrinopurulent exudate.
2. Cattle due to traumatic reticulopericarditis (“wire disease”).
3. Irregularly shaped.
   vv opaque.
   Markedly thickened pericardial sac, chronically fibrotic.
   Purulent exudate (pus) w/in pericardial cavity.
   Can start to be organised into fibrous tissue (very white and opaque).

Question 6

Consequence of fibrous tissue on the outside of the heart.

Answer 6

Constriction of the myocardium (constrictive pericarditis).
- Or constrictive pericarditis due to lots of adhesions surrounding the heart.
- Restricts the heart’s ability to relax.
– Impaired ventricular expansion.
–> Impaired diastolic filling.

Question 7

1. Hydropericardium.
2. Causes of hydropericardium.

Answer 7

1. Excess volume of translucent fluid (transudate or modified transudate) in the pericardial space.
2. Generalised oedema.
   - e.g. Congestive heart failure, hypoproteinaemia.
   Toxaemia or uraemia (capillary endothelial injury).
   Pericardial or cardiac neoplastic disease.
   - e.g. primary heart base tumours, cardiac lymphoma, pericardial metastatic neoplastic disease, mesothelioma.

Question 8

Cardiac haemangiosarcoma…
1. Most common in?
2. Location?

Answer 8

1. Dogs.
2. RA, esp. auricle.

Question 9

Heart-base tumours…
1. Most common in?
2. More common heart base tumours?
3. Less common?

Answer 9

1. Dogs.
2. Aortic body tumour (chemodectoma).
3. Ectopic thyroid tumours.

Question 10

1. Haemopericardium.
2. Causes of haemopericardium and/or haemorrhagic pericardial effusions.

Answer 10

1. Accumulation of pure blood in the pericardial cavity, NOT mixture of serous fluid and blood.
2. • Rupture of an atrium or blood vessel.
     - Clotting defect.
     - Neoplastic disease e.g. cardiac haemangiosarcoma or heart base tumours.
     - Idiopathic pericardial haemorrhagic effusion.

Question 11

Summary of causes of pericardial effusions.

Answer 11

Infectious agents – most common in FA.
Neoplastic disease – most common in dogs.
Idiopathic – most common in dogs.
CV disease – CHF (common); atrial or aortic rupture.
Metabolic/toxic – e.g. renal failure, hypoproteinaemia, clotting defect, toxaemia.
Trauma – traumatic reticulopericarditis in cattle.

Question 12

Cardiac tamponade.

Answer 12

Rapid accumulation of fluid in pericardial sac&raquo_space; compression and restriction of heart expansion and inhibition of venous return&raquo_space; impaired cardiac filling and reduced CO&raquo_space; could lead to death.

Question 13

Cardiac tamponade with example of atrial rupture.

Answer 13

Atrial rupture&raquo_space; rapid haemopericardium&raquo_space; cardiac tamponade&raquo_space; shock&raquo_space; sudden death.

Question 14

What if accumulation of pericardial fluid is slow?

Answer 14

Pericardium can stretch to accommodate larger volumes of fluid compared to when rapid accumulation of fluid occurs.

Question 15

1. Cardiomyopathies.
2. Primary.
3. Secondary.

Answer 15

1. Disease of the myocardium.
2. • sometimes referred to as idiopathies.
     - genetic or suspected genetic cause (some breed dispositions).
     - genetically determined abnormalities identified in a few breeds.
3. • Generalised myocardial diseases of known cause other than genetic e.g. nutritional deficiency, endocrine disorder, hypertension.
     - May have similar morphological appearance to primary cardiomyopathies.

Question 16

3 main pathological forms of primary cardiomyopathies.

Answer 16

• Dilated cardiomyopathy (DCM).
• Hypertrophic cardiomyopathy (HCM).
• Restrictive cardiomyopathy (RCM).

Question 17

DCM.

Answer 17

• Reduced myocardial contractility
• Chamber dilation.
• Affects systolic function.
• Causes include myocarditis, cardiotoxins, dietary taurine deficiency.
• Mainly affecting dogs.

Question 18

HCM.

Answer 18

• Ventricular hypertrophy, esp. affecting LV.
• No obvious explanation.
• Reduced wall compliance.
• Affects diastolic function.
• Causes include hyperthyroidism, acromegaly.
• Mainly affecting cats.

Question 19

RCM.

Answer 19

• Characterised by pathological changes such as endocardial and/or myocardial fibrosis that reduce ventricular wall compliance.
• Affects diastolic function.
• Mainly affecting cats.

Question 20

1. Main size of dogs affected by DCM?
2. Main age of dogs affected by DCM?
3. DCM most common in which sex?
4. Why was DCM a problem for cats previously but no longer a problem now?

Answer 20

1. Medium and large/giant.
2. Middle aged and older, but can be seen in young dogs.
3. Males.
4. Found to be due to a lack of dietary taurine which has now been rectified for many cats.

Question 21

DCM pathophysiology.

Answer 21

Impaired myocontractility&raquo_space; impaired systolic function in one or both ventricles&raquo_space; cardiac enlargement w/ progressive dilation of the heart chambers on one or both sides of the heart.

Question 22

DCM gross features.

Answer 22

• Heart appears dilated – ventricle and atrium (atrial dilation due to ventricular wall stretching and annulus of AV valve stretching and AV valve cannot shut properly, so regurgitation).

Question 23

Potential consequences of DCM.

Answer 23

Chronic CHF.
Left and/or right side heart failure.
Heart murmur due to valve insufficiency.
Arrhythmias.
Sudden death.

Question 24

1. Genetic factor of HCM.
2. HCM gross features.

Answer 24

1. Some breed-specific (Maine coon and ragdoll) genetic mutations in cardiac myosin binding protein have been identified.
2. • Hypertrophy of left ventricular free wall and interventricular septum.
     - Dilation of LA.
     - Variable hypertrophy:
     – symmetrical.
     – Asymmetrical:
     –> septum.
     –> LV free wall.
     – segmental, particularly affecting basal regions of ventricular septum.

Question 25

1. At what heart weight should HCM or other causes of ventricular hypertrophy be considered in the cat post mortem?
2. HCM pathophysiology?

Answer 25

1. > 20g.
2. Abnormal cardiomyocyte hypertrophy and fibrosis affect cardiac function, esp. LV&raquo_space; impaired diastolic relaxation and filling so increased diastolic filling pressure&raquo_space; transmits to cause left atrial dilation&raquo_space; transmits to cause pulmonary oedema etc. and left sided CHF.

Question 26

Other potential functional effects of HCM.

Answer 26

Dynamic obstruction of the left ventricular outflow tract:
- narrowing of outflow tract.
- systolic anterior motion (SAM) of the mitral valve.
Arrhythmias.
Sudden death (most common cause of sudden death in cats).
Atrial thrombus due to dilation and therefore stasis of blood.
- Part can break off and become lodged in the aortic trifurcation (Feline Aortic/Arterial Thromboembolism):
– Severe pain, off one or both hindlegs, cold and cyanotic hindlegs (obstruction of blood flow to iliac arteries)

Question 27

What is RCM caused by?
What can it cause?

Answer 27

Extensive fibrosis of the endocardium and myocardium.
- Ventricular stiffness w/ impaired diastolic filling and increased diastolic pressure.

Left atrial or bi-atrial dilation and heart failure.
May cause arrhythmia and/or atrial thrombosis.

Question 28

1. 2 types of endocardial disease.

Answer 28

1. Endocardiosis (degenerative).
   Endocarditis (inflammation).

Question 29

1. Valvular endocardiosis.
2. Breed dispositions.

Answer 29

1. Myxomatous mitral valve disease (MMVD).
   Most common CV disease in dogs.
   Slowly progressive degenerative condition.
   Prevalence increases with age (mainly middle aged/older dogs.
2. Small to medium breeds (<20kg).
   CKCS.

Question 30

1. Which valves affected by MMVD?
2. Valvular endocardiosis in the horse.
3. Valvular endocardiosis in pigs.

Answer 30

1. Mostly left AV valve (mitral).
   Sometimes right AV valve (tricuspid) (1/3 cases).
2. Most common acquired valvular pathology in horses.
   Aortic and left AV valve most commonly affected.
   May have generalised or nodular thickening, or thickened chordae tendineae.
   Clinical significance variable.
3. May affect left AV valve.
   Often not clinically significant.

Question 31

Valvular endocardiosis.

Answer 31

Generalised or nodular thickening of the valves.
Nodules can be singular, multiple, coalescing.
Smooth.
Opaque surface.

Question 32

Valvular endocardiosis.

Answer 32

Distortion and disruption of normal organised layered structure of valve leaflet.
Blue staining of mucopolysaccharides.
Collagen fibres disorganised and fragmented because too much interstitial matrix laid down.

Question 33

Valvular endocardiosis pathophysiology.

Answer 33

Distortion of valve leaflets can cause valvular insufficiency.
Regurgitation of blood back into the atrium during systole.
Subsequent increased blood into ventricle.
Secondary adaptive changes:
- Dilation of ventricle and hypertrophy of the ventricle (eccentric hypertrophy).
- Atrial dilation.
- Eventually exceed ability for ventricle to adapt and ventricle dilation continues but ventricular wall thins out – terminal decline.

Question 34

1. What does the red and blue indicate on echocardiogram?
2. What does the green indicate on echocardiogram.

Answer 34

1. Normal flow of blood.
2. High velocity turbulent blood flow.

Question 35

Other possible consequences of valvular endocardiosis.

Answer 35

• “Jet lesion” – high pressure jets of blood squirting through the distorted valve leaflets can traumatise atrial endocardium causing endocardial fibrosis.
• Chordae tendineae rupture (leads to flail leaflet / elongation. – exacerbates regurgitation of blood back into the atrium.
• Atrial tear or rupture – caused by sudden increases in volume, eventual thinning of the atrial wall, or thinning or weakening due to jet lesions.

Question 36

Classifications of endocarditis.

Answer 36

Valvular endocarditis - inflammation affecting one or more of the heart valves.
Mural endocarditis - inflammation of the endocardium lining the walls of the cardiac chambers.

Question 37

Valvular endocarditis…
1. Spp. more commonly affecting.
2. Usually caused by?
3. Valves affected?

Answer 37

1. FA.
2. Bacterial agents e.g. Staphylococcus, Streptococcus, Trueperella pyogenes, Erysipelothrix rhusiopathiae.
3. Any can be affected.
   Most commonly left sided heart valves in most spp.
   Right AV valve most commonly affected in cattle.

Question 38

Gross features of valvular endocarditis.

Answer 38

Multiple raised irregular pale yellow (fibrin) plaques on atrial surface of the valve leaflets w/ rough surfaces and multiple small red areas.
Vegetative lesions.

Question 39

Valvular endocarditis pathogenesis.

Answer 39

Bacteraemia + disruption of valve endothelium > bacterial invasion of valve > inflammation and thrombus formation on the valve leaflet w/ blood, fibrin and bacteria > buildup of these depositions into layers forms vegetative lesions.

Question 40

Valvular endocarditis potential consequences.

Answer 40

• Insufficiency.
• Stenosis.

Question 41

Valvular stenosis potential comsequences.

Answer 41

Of ventricular outflow tract e.g. aortic or pulmonic.
- Systole – increased amount of pressure needed to push blood out of the ventricle (pressure overload) so concentric hypertrophy.
Of AV valve e.g. mitral or tricuspid.
- Diastole – build up of blood in the atrium so increased diastolic filling pressure due to obstruction of blood flow into ventricle so atrial enlargement.
–> may get translation of this build up to the pulmonary circuit.

Question 42

Valvular insufficiency potential consequences.
1. AV valve.
2. Outflow tract valve.

Answer 42

1. Systole - AV valve regurgitation causing atrial enlargement
   Diastole - Volume overload on ventricle due to added flow of blood that was regurgitated back into the ventricle on top of normal volume that would flow in so get eccentric hypertrophy.
2. Diastole - May get backflow of blood from the artery into the ventricle, causing a degree of volume overload and eccentric hypertrophy

Question 43

Other potential consequences of valvular endocarditis.

Answer 43

Septic embolism, bacteraemia.
- E.g. Brain abscess caused by endocarditis in the aortic valve or left AV valve.
- e.g. Lung abscessation caused by endocarditis in the pulmonic or right AV valve.

Question 44

Contributions to heart failure.

Answer 44

• Pericardial disease:
  – cardiac tamponade.
  – restrictive pericarditis.
• Congenital shunts and anomalies:
  – PDA.
  – Septal defects.
  – Endocardial cushion (AV canal) defects.
• Arrhythmias and conduction disturbances.
• Valvular disease:
  – pulmonic/aortic stenosis.
  – valvular dysplasia.
  – Endocardiosis.
  – Valvular endocarditis.
• Myocardial diseases:
  – DCM, HCM, RCM.
  – Myocarditis.
  – Myocardial necrosis.

Question 45

1. Basic requirements of heart function.
2. Basic reason for heart failure?

Answer 45

1. • Ability to eject sufficient blood to meet tissue perfusion requirements and metabolic demands.
     - Ability to receive blood to provide adequate drainage from pulmonary and systemic venous and capillary beds.
2. Failure to meet one or both of the basic requirements of heart function.

Question 46

1. Define acute heart failure.
2. Profound acute heart failure.
3. Other signs of acute heart failure.

Answer 46

1. Rapid onset of new or worsening symptoms/signs of heart failure.
   - Resulting from new condition.
   - OR resulting from acute decomposition of pre-existing chronic heart failure.
2. Profound changes in BP and HR cause cardiac syncope where collapse and unconsciousness and sometime death occur.
3. Arrhythmia.
   Cardiac tamponade.
   Rupture of a structure.
   Myocardial injury.

Question 47

Chronic heart failure.

Answer 47

Slow development over time.
End point of any type of progressive cardiac disease.
Often referred to as chronic congestive heart failure.
Loss of cardiac reserve +:
- forward failure – inadequate CO and decreased perfusion of the peripheral tissues.
- backwards failure – failure to deal w/ venous return and congestion of venous and capillary beds –> Characterised by pulmonary and/or systemic vascular congestion and oedema.

Question 48

Left sided heart failure pathophysiology…
1. Forward failure.
2. Backward failure.

Answer 48

1. Reduced tissue/organ perfusion: hypoxia/ischaemia - weakness, fatigue, or hypotension and shock in severe cases.
2. Pulmonary congestion and oedema - Dyspnoea and cough.
   *congestive signs are the most important from clinical and treatment viewpoint.

Question 49

Right sided heart failure…
1. Forward failure.
2. Backward failure.

Answer 49

1. Reduced output to the lungs and left side of the heart.
2. Systemic tissue/organ congestion and oedema - Ascites, pleural effusion, peripheral oedema, visceral congestion (spp. variation).

Question 50

Right sided heart failure species differences.

Answer 50

Ascites esp. in dogs.
Pleural effusion esp. in cats.
Peripheral oedema esp. in ruminants and horses.
- Oedema gravitates downwards to be on ventral surface of chest, abdomen, neck etc.

Question 51

Hepatic congestion.

Answer 51

Nutmeg liver due to pattern.
Passive congestion of liver often related to right sided heart failure.
Hepatomegaly.

Question 52

Chronic congestive heart failure pathophysiology.

Answer 52

Reduced perfusion of tissues and CO is perceived by body as a drop in effective circulating blood volume even though the blood volume is adequate or even excessive.
- sympathetic system increases HR and contractility and arteriolar constriction.
– arteriolar constriction increases the systemic pressure that the heart has to work against and so increases afterload and therefore increases the stress on the heart, which could contribute to congestion.
- sympathetic system increases venous tone, pushing more blood back to the heart but also increasing the pressure in the venous system.
- sympathetic system increases blood flow to the kidneys to promote sodium and water absorption, increasing circulating blood volume and exacerbating the congestion and oedema associated with the heart failure.
- Renin-Angiotensin-Aldosterone system.
– vasoconstriction.
– sodium and water retention –> increased circulating blood volume, exacerbating congestion.
– exposure to hormones that can promote degradation of cardiac function.
- ADH.
- Endothlins.
- Natriuretic peptides.