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Cardiology > Canine myocardial disease > Flashcards

Canine myocardial disease Flashcards

1
Q

Primary canine cardiomyopathies

A

Idiopathic diseases

Dilated cardiomyopathy (DCM)

Arrhythmogenic right ventricular cardiomyopathy (ARVC)

Hypertrophic cardiomyopathy

Atrial myopathy

Restrictive cardiomyopathy

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2
Q

Dilated cardiomyopathy (DCM) - incidence

A

The most common canine cardiomyoathy with a prevalence of up to 60% in some breeds (Dobermann)

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3
Q

Arrhythmogenic right ventricular cardiomyopathy (ARVC) - breeds

A

Prevalent in boxers and english bulldogs

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4
Q

Hypertrophic cardiomyopathy - incidence

A

Rare in dogs

Terriers possibly over-represented

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5
Q

Atrial myopathy - incidence

A

Rare

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6
Q

Restrictive cardiomyopathy - incidence

A

Rare

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7
Q

Secondary canine cardiomyopathies

A

Arrhythmia-induced cardiomyopathy

Nutrition-associated cardiomyopathies

Congenital cardiac disease

Endocrinopathies

Chronic myocarditis

Systemic inflammation

Drug/toxin induced

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8
Q

Arrhythmia induced cardiomyopathy

A

Chronic tachycardia and arrhythmias can lead to a severe myocardial failure mimicking DCM.

This is potentially reversible with control of the arrhythmia

Increased myocardial oxyegn demand, reduced ventricular filling time and reduced coronary perfusion

Decreased systolic function and cardiac output, and left ventricular dilation

Severity of dysfunction dependent on the type of arrhythmia and duration

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9
Q

Nutrition-associated cardiomyopathies

A

Taurine deficiency:
- key roles in calcium handling and excitation-contraction coupling within the myocardium
- Deficiency may cause DCM phenotype
- Described in American Cocker spaniels, Golden retrievers, and Newfoundlands
- Potentially reversible with supplementation

Grain-free/legume rich diets:
- Increasing prevalence of DCM associated
- mechanism not understood
- diet change may give some improvement

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10
Q

Congenital cardiac disease (cardiomyopathy)

A

Any cardiac disease causing left-sided volume overload

May mimic DCM

E.g. mitral valve dysplasia, large left-to-right PDA, and left-to-right VSD

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11
Q

Endocrinopathies causing cardiomyopathy

A

Hypothyroidism (association rather than causation?)

Hyperadrenocorticism (possiblereverse remodelling with treatment)

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12
Q

Chronic myocarditis (cardiomyopathy)

A

Characterised by non-specific inflammation of the myocardium

Can result in DCM phenotype

Cardiac troponin I is typically markedly elevated

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13
Q

Systemic inflammation and cardiomyopathies

A

Left ventricular systolic dysfunction

Can occur in systemis inflammatory response syndrome and steroid responsive meningitis arteritis

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14
Q

Drug/toxin cardiomyopathies

A

Doxorubicin (chemotherapy) can have cardiotoxic effects

Manifests as myocardial failure and/or arrhythmias

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15
Q

Dilated cardiomyopathy

A

Second most common cardiac disease in dogs

Most prevalent in large and giant breeds

Presents with structural and/or electrical alterations

Charaterised by left ventricular dilation (+/- right) and systolic dysfunction

Diagnosis of exclusion

Occult/preclinical phase and then progressed to congestive heart failure

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16
Q

Occult or preclinical phase of DCM

A

Characterised by an abscence of clinical signs or ECG alterations

Duration of the phase is variable

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17
Q

What can cause sudden death in a dog suffering from DCM?

A

Typically due to ventricular arrhythmias

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18
Q

Aetiology of DCM

A

Primary DCM thouhgt to be inherited

Gene associations in in Dobermanns, boxers, and irish wolfhounds

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19
Q

Pathology of DCM

A

Dilation of the left ventricle and left ventricular systolic dysfunction

Metabolic dysfunction or defects in contractility at a cellular level

Leads to overt systolic dysfunction and eccentric ventricular hypertrophy

Dilation of the mitral annulus can lead to mitral regurgitation

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20
Q

Histopathology of DCM

A

There are two distinct described in DCM:

A fatty infiltration- degenerative type (mainly in Dobermanns and Boxers)

An attenuated wavy fibre type (more common in giant breeds)

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21
Q

Pathophysiology of DCM

A

Impaired systolic function -> progressive eccentric hypertrophy of L ventricle -> reduced CO -> activation of compensatory mechanisms (RAAS) -> further myocardial hypertrophy and chamber dilation

Increased left-sided volumes result in progressively increased left atrial pressures -> pulmonary oedema

Ventricular arrhythmias and atrial fibrillation are common

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22
Q

Occult/preclinical phase of DCM

A

Presence of echocardiographic and/or electrical changes without signs of CHF

Slowly progressive over several years

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23
Q

Clinical phase of DCM

A

Progression to CHF

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24
Q

Staging of DCM

A

Very similar to staging of MMVD

(A, B1, B2, C, D)

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25
Q

Signalment of DCM

A

Adult dogs (usually 5-7)
Large and giant breeds

Portugese water dogs can get a juvenile onset form of DCM

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26
Q

History - preclinical DCM (stage B)

A

Family history of cardiac disease

Diet history

Most dogs will be asymptomatic

+/- exercise intolerance, collapse, syncope

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27
Q

History of clinical DCM (stage C: CHF)

A

Exercise intolerance, lethargy

Collapse/syncope

Elevated respiratory or effort

Cough

Abdominal distension (if right sided CHF)

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28
Q

Physical examination of pre-clinical DCM (stage B)

A

May be unremarkable

Soft murmur due to mitral regurgitation

Arrhythmias +/- pulse deficits may be present

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29
Q

Physical examination of clinical DCM (stage C: CHF)

A

Murmur - soft

Tachycardia, arrhythmias, pulse deficits, weak pulses

Tahcypnoea +/- dyspnoea

Pulmonary crackles

Reduced/absent lung sounds

Jugular distension, positive hepatojugular reflux, abdominal distension with fluid thrill

Weakness, collapse

Cardia cachexia

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30
Q

Diagnostics for DCM

A

Echocardiography

Radiography

ECG

Holter

Cardiac biomarkers

Systolic blood pressure

Exclusion of disease mimickers

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31
Q

What is echocardiography used for in DCM?

A

Assess the severity of systolic dysfunction

Assess the severity of left ventricular +/- left atrial dilation and the likelihood of CHF

Assess the right heart also

Monitor progression of the disease

Exclude secondary causes of a DCM phenotype

32
Q

Typical echo findings in DCM

A

Rounded, dilated left ventricle (increased volumes and diameter)

Left atrial dilation

Mild mitral regurgitation

Reduced ejection fraction and fractional shortening

33
Q

Echo findings of Stage B1 DCM

A

Relatively normal or equivocal echo (but presence of arrhythmias)

34
Q

Echo findings of Stage B2 DCM

A

Evidence of left ventricular systolic dysfunction (reduced ejection fraction, fractional shortening and end systolic volume)

As disease advances: progressive left ventricular dilation (increased end diastolic volume and diameter) and progressive left atrial dilation (increased LA:Ao)

35
Q

Echo of Stage C DCM

A

Same as B2 but more advanced dilation and systolic function, large left atrium, and evidence of elevated left sided filling pressures.

May see B lines suggestive of pulmonary oedema

May have signs of right-sided CHF

36
Q

Radiography for DCM

A

Gold standard for diagnosis of pulmonary oedema and so CHF

Assesses for:
- cardiomegaly with left atrial enlargement
- distension of the pulmonary veins
- lung pattern

37
Q

ECG for DCM

A

Common arrhythmias include:

Ventricular arrhythmias
- Ventricular premature complexes
- Ventricular tachycardia

Atrial fibrillation

Supraventricular premature complexes

38
Q

Holter for DCM diagnosis

A

24hr holter advised

Can detect VPCs

Presence of over 300 VPCs in 24hrs in a Dobermann is diagnostic (or two holters in 12mo with 50-300)

Signs of malignancy used to determinewhether antiarrhythmic treatment is required
- coupling intervals (R-R intervals) exceeding 260/minute
- frequent couplets or triplets

39
Q

Cardiac biomarkers for DCM diagnosis

A

Ancillary screening tool (can’t replace echo and holter)

NT-proBNP

Cardiac troponin I

40
Q

NT-proBNP for DCM diagnosis

A

Indicator of myocardial stretch and strain

May help assess the severity of disease and monitor disease progression

Identify dogs that would benefit from further screening

False positives are possible

Poor sample handling may lead to reduced levels

Daily variation and breed variation

41
Q

Cardiac troponin I for DCM diagnosis

A

Indicator of myocardial cell damage

Prognostic indicator, monitor disease progression

Can be elevated in some non-cardiac disease

42
Q

Systolic blood pressure in clinical DCM

A

120mmHg

43
Q

Clinical pathology in DCM

A

Pre-renal azotaemia is a common finding

Elevated liver enzymes due to liver congestion (in right-CHF)

Consider T4/TSH and basal cortisol

Consider plasma or whole blood taurine

44
Q

Screening for DCM

A

Annual screening advised from three years old in at-risk breeds

Echo and 24-hr holter ECG

+/- cardiac biomarkers

Genetic testing

45
Q

Sequelae of DCM

A

Left sided congestive heart failure

Forward failure

Right-sided congestive heart failure

Arrhythmias
- atrial fibrillation
- ventricular arrhythmias and sudden cardiac death
- sustained tachyarrhythmias

46
Q

Treatment of pre-clinical DCM

A

Pimobendan

Antiarrhythmic therapy

47
Q

Key points of CHF treatment

A

Standard therapy: pimobendan, diuresis, RAAS inhibition

Aims are to reduce preload (diuretics, venodilators), provide inotropic support (pimobendan) and reduce RAAS stimulation

Furosemide and torasemide are licensed in dogs

Renal parameters and electrolytes should be monitored

ACE-inhibitors in combination with spironolactone, can be initiated once recovered from acute CHF event

48
Q

Acute CHF (in-hospital treatment)

A

Oxygen

Furosemide IV

Pimobendan

Sedation/antianxiety (butorphanol)

49
Q

Additional hospital treatment for more advanced/refractory acute CHF cases

A

Vasodilators
- nitro-glycerine (venodilator)
- sodium nitroprusside CRI (ateriodilator and venodilator)

Further inotropic support
- Dobutamine CRI

Mechanical ventilation

50
Q

At home treatment for chronic CHF

A

Pimobendan

Diuretics
- furosemide PO
- torasemide PO
- thiazides considered in refractory cases

ACE-i
- benazepril
- combined with spironolactone

Spironolactone
- potassium sparing (aldoseterone antagonist)
- Combined with benazepril

51
Q

Treatment for ventricular arrhythmias

A

Lidocaine (mergency treatment of V tach)

Solatol (oral treatment)

Mexiletine (minimal depression of systolic dysfunction, may have marked GI effects)

Amiodarone (minimal myocardial depression)

52
Q

Solatol

A

Oral treatment for chronoic ventricular arrhythmias

Peak effect within 2-4 hours of administration

Negative inotrope- use with care in severe systolic dysfunction

53
Q

Mexiletine

A

Oral treatment for ventricular arrhythmias

Minimal effect on systolic function

Adverse effects: GI (anorexia, vomiting, diarrhoea)

54
Q

Amiodarone

A

Oral therapy for ventricular arrhythmias

Takes several weeks to reach steady serum levels

Adverse effects: hepatopathy and thyroid dysfunction

55
Q

Lidocaine

A

Treatment for sustained ventricular tachycardia

Na channel blocker

IV only

56
Q

Amiodarone

A

Treatment for sustained ventricular tachycardia

Adverse effects: hepatic and thyroid dysfunction

57
Q

Treatment for atrial fibrillation

A

Diltiazem

Digoxin

58
Q

Diltiazem

A

Treatment for atrial fibrillation

Calcium channel blocker

Mild negative inotropic effect, so care of high doses in cases with CHF

59
Q

Digoxin

A

Treatment for atrial fibrillation

Narrow therapeutic window

Check serum levels 5-7 days post initiation of treatment, or dose change 6-8hrs post pill

Lower doses required in patients with renal disease

Monitor potassium

60
Q

Treatment for stage A DCM

A

No treatment

61
Q

Treatment of stage B1 DCM

A

+/- Antiarrhythmics

62
Q

Treatment of stage B2 DCM

A

Pimobendan
+/- antiarrhythmics

63
Q

Treatment of stage C DCM

A

Diuretics
Pimobendan
ACE-i
Spironolactone

64
Q

Treatment of stage D DCM

A

Diuretics
Pimobendan
ACE-i
Spironolactone

+ additional diuresis
+ K supplementation

65
Q

Prognosis of DCM

A

Highly variable due to long pre-clinical phase

Prognosis of DCM with CHF is generally guarded, median survival times following progression to CHF of typically 6-12months

Median survival is shorter when there is concurrent atrial fibrillation

Sudden caridac death affects up to 25-30% of dogs with DCM

66
Q

Arrhythmogenic right ventricular cardiomyopathy ARVC

A

Myocardial disease primarily affecting right ventricle
- may involve LV

Progressive loss of myocytes with fatty or fibro-fatty replacement

Best described in Boxers (and english bulldogs)

Primarily an electrical disease sometimes associated with myocardial dysfunction

Results in ventricular arrhythmias

High risk of syncope and sudden cardiac death

67
Q

Aetiology of arrhythmogenic right ventricular cardiomyopathy (ARVC)

A

Likely to be genetic

Disease of the desmosome

68
Q

Pathophysiology of ARVC

A

Fibrofatty tissue replacement particularly in the right ventricle

Fatty tissue and scarring may be seen grossly

Replacement of cardiomyocytes with adipose, fibrosis, and inflammatory cells

Right +/- left ventricular dilation and systolic dysfunction seen in some

69
Q

Signalment of ARVC

A

Best described in Boxers, also reported in English Bulldogs

Adult onset (usually 5-7)

70
Q

Three clinical categories of ARVC

A

Asymptomatic

Symptomatic

Arrhythmias and DCM phenotype

71
Q

Asymptomatic ARVC

A

Arrhythmias detected incidentally on clinical examination/ECG

72
Q

Symptomatic ARVC

A

Present with clinical signs associated with ventricular arrhythmias (syncope, weakness, collapse, exercise intolerance)

Echocardiography may show right ventricular dilation and reduced right ventricular function

Left ventricular size and function remain normal

73
Q

Diagnosis of ARVC

A

Family history or history of syncope warrants screening

Echocardiography - normal or signs of right ventricular dilation

Holter - identifies the presence of ventricular arrhythmias and assess the severity of these. Annual holter advised in breeding dogs and those with family history

74
Q

Treatment of ARVC

A

Palliative

Aims at controlling ventricular arrhythmias and ameliorating any associated clinical signs

Solatol - first line antiarrhythmic

Pimobendan - indicated in cases with structural or functional changes

75
Q

Prognosis of ARVC

A

Syncope seen in approx 1/3 of Boxers with ARVC - associated with worse prognosis

Risk of sudden death

Many dogs without significant echo changes can have good long term prognosis

Cardiology (10 decks)

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