Canine Myocardial Disease Flashcards

1
Q

What can cause primary myocardial disease in the dog?

A

–Dilated cardiomyopathy (DCM) is the most common thing we see

–Arrhythmogenic right ventricular cardiomyopathy (ARVC)

•Occurs more so in boxers

–Hypertrophic cardiomyopathy (rare)

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2
Q

What can cause secondary myocardial disease in the dog?

A

–Infective myocarditis

•Usually present as dogs with an explain sudden onset dysrhythmia and may go on to develop a DCM

–Deficiency diseases

•Identified in 80’s and 90’s – tend to be things that aren’t seen as much anymore as we are better at having things and not being deficient

–Toxic causes

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3
Q

What is dilated cardiomyopathy characterised by?

A

Characterised by impaired myocardial contractility with dilation of LV (+/-RV) – cannot reverse myocardial failure as we do not know what causes it

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4
Q

What kind of arrhythmia is common with dilated cardiomyopathy?

A

•Tachyarrhythmias are common

–Supraventricular and/or ventricular

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5
Q

What is the end stage of many cardiac diseases?

A

•DCM is an end stage of many cardiac diseases, primary DCM is a diagnosis of exclusion

–Animal suffers with some sort of myocardial insult and by the time we see it, we have this end stage heart

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6
Q

Which heart is affected with a cardiomyopathy here?

A

Both from great Danes:

Left – got hit by a car and died suddenly

Right – DCM, eccentric hypertrophy, external diameter has increased

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7
Q

What is the pathophysiology of dilated cardiomyopathy?

A
  • Eccentric hypertrophy of the LV
  • Systolic failure

–‘forward failure’

•Diastolic failure

–‘backward failure’ – congestion

  • LA dilation and increased LAP
  • Right side can also be affected
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8
Q

What is the histopathology of cardiomyopathy?

A

•Two distinct types of HP are reported these are thought to relate to the underlying mechanism of the disease:

–Narrow (attenuated) myocardial cells with a wavy appearance (Newfoundlands)

–Myofibre degeneration, myocyte atropy and lysis, fatty infiltration and fibrosis (Boxers, some Dobermans)

•Otherwise often non-specific and include:

–Scattered areas of myocardial necrosis

  • Myocardial degeneration and fibrosis
  • Inflammatory cell infiltrates are inconsistent but an active myocarditis is rare
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9
Q

With histopathology of cardiomyopathy, which type is most common in Newfoundlands?

A

Narrow (attenuated) myocardial cells with a wavy appearance (Newfoundlands)

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10
Q

With histopathology of cardiomyopathy, which type is most common in Boxers and some dobermans?

A

Myofibre degeneration, myocyte atropy and lysis, fatty infiltration and fibrosis (Boxers, some Dobermans)

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11
Q

What are some non-specific histopathology signs with cardiomyopathy?

A

•Otherwise often non-specific and include:

–Scattered areas of myocardial necrosis

  • Myocardial degeneration and fibrosis
  • Inflammatory cell infiltrates are inconsistent but an active myocarditis is rare
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12
Q

What is the pathophysiology of the OCCULT phase of cardiomyopathy?

A

Occult phase - no clinical signs

–CO falls

–Sympathetic, hormonal and renal compensatory mechanisms activated therefore

–These maintain CO by increasing HR, peripheral vasoconstriction and volume expansion

–Chronic NH activation also contributes to progressive myocardial damage and CHF

–Underlying myocardial disease, often will compensate for years but as time goes by, CO continues to fall and increasing levels of compensation and RAAS system etc. and as a consequence, we are asking the sick ventricle to work even harder, output falls, body vasoconstricts and retains fluid and then the ventricle has to deal with even more fluid and eject blood into a higher pressure system – contributing to the progression of the disease

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13
Q

What are the breed dispositions for cardiomyopathy?

A

•Breed predispositions – genetic basis

–Doberman, Newfoundland, IWH, St Bernards, Labradors, Great Dane, Cocker spaniels, Boxers (ARVC), GSD

•Most common breeds, presentation and progression is different in the different breeds.

–Boxers autosomal dominance inheritance pattern

–BUT different breeds have very different prognosis with the same disease

–Cocker spaniels – 2yrs with appropriate treatment

–Doberman – often a few weeks

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14
Q

What age, size and sex of dogs is most likely to be affected with cardiomyopathy?

A
  • Usually middle aged dogs (has been reported in puppies as young as 6m)
  • Usually dogs > 12kg
  • Males tend to be more severely affected but no gender predilection and they also tend to be affected earlier than females
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15
Q

What are the 2 phases of DCM?

A

Occult phase – may go on for years!

•no clinical signs usually

Symptomatic phase

  • usually CHF, typically LHS sometimes biventricular heart failure
  • Syncope – as a result of a poor output (fainting)
  • Weight loss – as a first clinical sign sometimes
  • Sudden death – can occur in some breeds
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16
Q

What are some screen programmes you can use to identify the occult phase of DCM?

A

–24 hour Holter monitor

•>50VPCs /24 hr abnormal but no clear exact number and depends on the morphology whether couplets / triplets

–Echocardiography

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17
Q

What are the clinical signs like for overt DCM?

A

•Onset of clinical signs can be sudden

–Weakness

–Lethargy

–Syncope

–Dyspnoea

–Exercise intolerance

–Cough

–Anorexia

–Ascites

–Cardiac cachexia

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18
Q

What would you find on clinical exam of a dog with DCM?

A
  • Variable depending on the degree of myocardial dysfunction
  • Pale mucous membranes
  • Sluggish CRT
  • Cool extremities
  • Tachycardia +/- arrhythmias – AF, VPCs, VT
  • Variable pulses +/- pulse deficits
  • Pulsus alternans
  • Signs of LCHF / RCHF
  • S3 gallop sound – if sinus rhythm

–Animals with dysrhythmias will not gallop

–Sinus tachcardia

•Soft MR / TR murmurs

–As heart is dilating, pulling valves apart so tricuspid and bicuspid valves leak, so a less hard murmur is heart

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19
Q

What investigations would you potentially use for the investiagion of DCM?

A
  • History
  • Clinical examination
  • Echocardiography

–Can confirm presence of DCM

  • Clinical pathology
  • Radiography
  • ECG
  • Blood pressure

–Increasingly interested in this, most interested in this one we have started treating them. BP should be reasonably normal, systemic arterial BP will be normal as that is why there are compensatory mechanisms.

•24hr Holter monitor

–To see what is going on when they are at home as in the clinic, there will be some impact of the sympathetic nervous system on rate and rhythm, want to know what this is like at home

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20
Q

Right parasternal short axis view

What is going on?

A

Eccentric dilation

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21
Q

Right Parasternal short axis view at the level of the aorta

Is the LA enlarged?

A

Aorta in the middle

LA enlargement – slug like left auricular appendange

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22
Q

What are some typical findings of echocardiography in a dog with DCM?

A

•Typical findings

–Large, round, poorly contractile LV

–Poor systolic function

–Diastolic dysfunction

–Dilated, round LA

–+/- MR small/moderate due to annulus dilation

–+/- right sided changes

23
Q

Zeus Dalton 6 mth Great dane

Which side of the heart does he have changes to?

What else can be seen?

A
  • Big LHS, tall cardiac. Also very wide, lots of RHS change
  • DCM could be PDA
  • Generalised cardiomegaly
  • Left atrial enlargement
  • Alveolar pattern
24
Q

What is enlarged on this radiograph?

What else can be seen?

A
  • Generalised cardiomegaly
  • Left atrial enlargement
  • Interstitial pattern
25
Q

What are often the finding likes on electrocardiography in a dog with DCM?

A

•Findings are very variable

–Normal

–Wide +/- tall complexes (occasionally small complexes)

  • Many DCM dogs have ventricular arrhythmias
  • TREAT HEART FAILURE
  • Treat arrhythmias if haemodynamically unstable
  • The rhythms will be made worse by the fact they aren’t oxygenating properly and the degree of sympathetic tone still persisting
26
Q

In a dog with DCM, on ECG how do they often present?

A

•Many dogs will present with atrial fibrillation

–Big dogs, with big atrium!

  • If in CHF the ventricular rate maybe very rapid
  • Rate control is the key

–Treat the CHF

–Treat the rate if necessary

27
Q

What are some situations that would want us to use a Holter Monitor? (a monitor that the dog wears for a period of time to get reports)

A
  1. To monitor for heart rate control – is it under control at home, when they are relaxed?
  2. Can also be used for unexplained syncope or collapse
  3. Arrhythmias
  4. Monitoring therapy

•Particularly rate control

28
Q

What would you see on haematology and biochemistry in dogs with cardiomyopathy?

A

•Routine haematology

–usually WNL but ensure no other concurrent disease

•Routine biochemistry

–Pre-renal azotaemia is common – these dogs are struggling to maintain perfusion

–Elevation in liver enzymes esp ALP not uncommon due to hepatic venous congestion

–Hypoproteinaemia in CHF

–Electrolyte disturbances – particularly when we start treating them

29
Q

Other than haematology and biochemistry, what other clinical pathology parameters could/should you check in dogs with cardiomyopathy?

A

•Cardiac troponin I – may be increased?

–Already usually have diagnosis, all it tells you is that the myocardial cells have been damaged and released into circulation

•Check T4/TSH level?

–Predisposed to hypothyroidism. If they have this on top of DCM, will make them worse

30
Q

In dogs with cardiomyopathy, what does blood pressure often show?

A
  • This is frequently very low with Systolic pressure <100mmHg – but a lot will be normal due to the compensatory mechanisms!
  • Rule out hypertension
  • Important to monitor with therapy – diuretics and vasodilators which will try to reverse compensatory mechanisms that have been trying to keep BP up, so we can sometimes make animal hypotensive with treatment
  • Aim to maintain BP >100mmHg
31
Q

What is the treatment for cardiomyopathy?

A
  • Treat the LCHF
  • Treat immediate life threatening arrhythmias – haemodynamically significant
  • IF treat LCHF many arrhythmias resolve or do not require treatment
  • Rate control of Atrial Fibrillation – digoxin/diltiazem/BB (only if not in heart failure)
32
Q

Arrhythmogenic right ventricular cardiomyopathy is also know as what? e,g, what breed is affected?

A

“Boxer cardiomyopathy”

33
Q

Arrhythmogenic right ventricular cardiomyopathy - what damage is done at a molecular level?

A

Myofibre atrophy, fibrosis and fatty infiltration within myocardium

34
Q

What are the 3 stages of Arrhythmogenic right ventricular cardiomyopathy (in boxers mainly)?

A
  1. Asymptomatic with ventricular arrhythmias
  2. Symptomatic – normal heart size and LV function but dogs are syncopal/weak from ventricular arrhythmias
  3. CHF – poor myocardial function, CHF and ventricular arrhythmias
35
Q

What are the clinical signs of of Arrhythmogenic right ventricular cardiomyopathy?

A
  • Can appear any age mean age 8yrs
  • Ventricular arrhythmias
  • Supra-ventricular arrhythmias
  • >500 VPCs / 24hrs
  • But spontaneous variation of up to 80%
  • Syncope
  • Sudden death
36
Q

How would you investiage Arrhythmogenic right ventricular cardiomyopathy?

A
  • Investigations as listed previously but 24 hour Holter monitor is necessary:
  • History
  • Clinical examination
  • Echocardiography

–Can confirm presence of DCM

  • Clinical pathology
  • Radiography
  • ECG
  • Blood pressure
  • 24hr Holter monitor
  • May need further physiological monitoring
  • Ideally consider referring these cases as they can be complex
  • BUT never underestimate a syncopal/collapsing Boxer
37
Q

What is the treatment for Arrhythmogenic right ventricular cardiomyopathy?

A
  • Treat any other underlying cases
  • Treat LCHF as necessary
  • Anti-arrhythmic medication often used:

–Sotalol BID

38
Q

What is secondary Myocardial Disease?

A

Viral aetiology – rarely associated with DCM in dogs

39
Q

What drug can cause secondary Myocardial Disease?

A

•Doxorubicin – acute and chronic cardiotoxicity

–Anti-cancer drug used quite a lot and is toxic to myocytes

–Dogs who have this often have an echo to make sure we aren’t damaging the myocardium

40
Q

What can cause secondary myocardial disease?

A

•Doxorubicin – acute and chronic cardiotoxicity

–Anti-cancer drug used quite a lot and is toxic to myocytes

–Dogs who have this often have an echo to make sure we aren’t damaging the myocardium

•Metabolic / nutritional deficiencies

–L-carnitine

•Some familes of dogs, particularly Dobermans, that have problems with this and can result in a DCM

–Taurine

  • Ischaemic heart disease
  • Tachycardia induced cardiomyopathy
  • Infective myocarditis
  • Non-infective myocarditis
41
Q

What can doxorubicin do to the heart?

How can we reduce risk of dogs that need this medication?

A

•Acute toxicity

–Arrhythmias

–Anaphylaxsis

  • Can cause chronic cardiotoxicity à DCM
  • Histamine, catecholamine release and free radical production are suggested to be involved.
  • To reduce risk

–Close monitoring when administering drug

–Echocardiography prior to first treatment and then repeat echo serially

42
Q

What can taurine deficiency do?

Why do some dogs get taurine deficiency?

A
  • Causes or contributes to myocardial failure in a small proportion of dogs
  • Unknown mechanism
  • Most abundant free amino acid in the heart
  • Found in American Cocker spaniels
  • Low taurine levels have been seen in Labs, Dalmations and others with DCM
  • Vegetarian, home made lamb and rice diets often deficient in taurine
  • Will improve systolic function in most dogs and very markedly in some cocker spaniels
  • Test plasma levels and supplement as necessary
  • NB care in measuring levels
  • Should always measure levels especially in atypical breeds of dog with DCM
43
Q

What is L-carnitine and what does it do?

A

–Essential component of the mitochondrial membrane transport system for fatty acids (hearts primary energy source)

–Also binds and transports toxic metabolites out of mitochondria

44
Q

What can high levels of metabolites do to the levels of L-carnitine?

What has it been associated with?

A

–High levels of metabolites can lead to depletion

–Has been associated with DCM in some families of Boxers, Dobies, IWH, Newfies and Cockers

45
Q

How common is ischaemic heart disease in dogs?

When are dogs at risk of this?

A
  • Rare in dogs
  • Dogs at risk due to a disease which predisposes them to thromboembolic disease

–Bacterial endocarditis

–Neoplasia

–Renal disease

–IMHA

–DIC etc.

  • Atherosclerosis – hypothyroidism, diabetes mellitus
  • Clinically – acute onset arrhythmias, ST depression on ECG
46
Q

What is tachycardia induced cardiomyopathy?

Is it reversible?

When is it most frequently seen?

A
  • Rapid incessant tachycardia leads to myocardial dysfunction and failure
  • Depending on severity can be reversible
  • Most frequently seen with SVT due to an accessory pathway
47
Q

What is wrong with this ECG?

A

Tachycardia induced cardiomyopathy

48
Q

How common is hypertrophic cardiomyopathy in the dog?

What is the cause?

A
  • Rare in the dog
  • Cause unknown – genetic basis suspected
49
Q

What is the signalment for hypertrophic cardiomyopathy and what are often the clinical signs?

A
  • Young to middle aged large breed dogs
  • Male predisposition
  • Syncope / sudden death
  • CHF
  • S4 heard in some dogs
50
Q

What is canine hypertorphic cardiomyopathy also referred to as?

A
  • Dynamic obstruction of the left ventricular outflow tract
  • Dynamic subvalvular aortic stenosis
51
Q

What are the typical features of canine hypertrophic cardiomyopathy?

A

•Typical features

–Distinct

  • Symmetric hypertrophy
  • No myofiber disarray
  • LVOT obstruction
  • Abnormal mitral valve apparatus

–Elongated anterior leaflet

–Abnormally orientated papillary muscles

–Similar

•Small vessel disease

52
Q

What is the aetiology of canine hypertrophic cardiomyopathy?

A

•Uncertain

–Genetic

  • Polygenic or autosomal recessive pattern of inheritance
  • Several gene have been identified in Humans
  • Cardiac myosin binding protein C in Maine Coon cats
53
Q

What are the conclusions for hypertrophic cardiomyopathy?

A
  • HCM does occur in dogs although it is RARE
  • Rule out other causes before making a diagnosis

–Hypertension

–Aortic stenosis

–Renal disease

–Pseudohypertrophy secondary to dehydration, hypovolaemia etc..

•Ventricle walls may be underfilled and may just look hypertrophied. Ensure they are not hypovolaemic etc. before you make the diagnosis

–Hyperthyroidism

–Other systemic disease

•Consider Referral