Canine myocardial disease Flashcards
Primary canine cardiomyopathies
Idiopathic diseases
Dilated cardiomyopathy (DCM)
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Hypertrophic cardiomyopathy
Atrial myopathy
Restrictive cardiomyopathy
Dilated cardiomyopathy (DCM) - incidence
The most common canine cardiomyoathy with a prevalence of up to 60% in some breeds (Dobermann)
Arrhythmogenic right ventricular cardiomyopathy (ARVC) - breeds
Prevalent in boxers and english bulldogs
Hypertrophic cardiomyopathy - incidence
Rare in dogs
Terriers possibly over-represented
Atrial myopathy - incidence
Rare
Restrictive cardiomyopathy - incidence
Rare
Secondary canine cardiomyopathies
Arrhythmia-induced cardiomyopathy
Nutrition-associated cardiomyopathies
Congenital cardiac disease
Endocrinopathies
Chronic myocarditis
Systemic inflammation
Drug/toxin induced
Arrhythmia induced cardiomyopathy
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
Nutrition-associated cardiomyopathies
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
Congenital cardiac disease (cardiomyopathy)
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
Endocrinopathies causing cardiomyopathy
Hypothyroidism (association rather than causation?)
Hyperadrenocorticism (possiblereverse remodelling with treatment)
Chronic myocarditis (cardiomyopathy)
Characterised by non-specific inflammation of the myocardium
Can result in DCM phenotype
Cardiac troponin I is typically markedly elevated
Systemic inflammation and cardiomyopathies
Left ventricular systolic dysfunction
Can occur in systemis inflammatory response syndrome and steroid responsive meningitis arteritis
Drug/toxin cardiomyopathies
Doxorubicin (chemotherapy) can have cardiotoxic effects
Manifests as myocardial failure and/or arrhythmias
Dilated cardiomyopathy
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
Occult or preclinical phase of DCM
Characterised by an abscence of clinical signs or ECG alterations
Duration of the phase is variable
What can cause sudden death in a dog suffering from DCM?
Typically due to ventricular arrhythmias
Aetiology of DCM
Primary DCM thouhgt to be inherited
Gene associations in in Dobermanns, boxers, and irish wolfhounds
Pathology of DCM
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
Histopathology of DCM
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)
Pathophysiology of DCM
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
Occult/preclinical phase of DCM
Presence of echocardiographic and/or electrical changes without signs of CHF
Slowly progressive over several years
Clinical phase of DCM
Progression to CHF
Staging of DCM
Very similar to staging of MMVD
(A, B1, B2, C, D)
Signalment of DCM
Adult dogs (usually 5-7)
Large and giant breeds
Portugese water dogs can get a juvenile onset form of DCM
History - preclinical DCM (stage B)
Family history of cardiac disease
Diet history
Most dogs will be asymptomatic
+/- exercise intolerance, collapse, syncope
History of clinical DCM (stage C: CHF)
Exercise intolerance, lethargy
Collapse/syncope
Elevated respiratory or effort
Cough
Abdominal distension (if right sided CHF)
Physical examination of pre-clinical DCM (stage B)
May be unremarkable
Soft murmur due to mitral regurgitation
Arrhythmias +/- pulse deficits may be present
Physical examination of clinical DCM (stage C: CHF)
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
Diagnostics for DCM
Echocardiography
Radiography
ECG
Holter
Cardiac biomarkers
Systolic blood pressure
Exclusion of disease mimickers
What is echocardiography used for in DCM?
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
Typical echo findings in DCM
Rounded, dilated left ventricle (increased volumes and diameter)
Left atrial dilation
Mild mitral regurgitation
Reduced ejection fraction and fractional shortening
Echo findings of Stage B1 DCM
Relatively normal or equivocal echo (but presence of arrhythmias)
Echo findings of Stage B2 DCM
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)
Echo of Stage C DCM
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
Radiography for DCM
Gold standard for diagnosis of pulmonary oedema and so CHF
Assesses for:
- cardiomegaly with left atrial enlargement
- distension of the pulmonary veins
- lung pattern
ECG for DCM
Common arrhythmias include:
Ventricular arrhythmias
- Ventricular premature complexes
- Ventricular tachycardia
Atrial fibrillation
Supraventricular premature complexes
Holter for DCM diagnosis
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
Cardiac biomarkers for DCM diagnosis
Ancillary screening tool (can’t replace echo and holter)
NT-proBNP
Cardiac troponin I
NT-proBNP for DCM diagnosis
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
Cardiac troponin I for DCM diagnosis
Indicator of myocardial cell damage
Prognostic indicator, monitor disease progression
Can be elevated in some non-cardiac disease
Systolic blood pressure in clinical DCM
120mmHg
Clinical pathology in DCM
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
Screening for DCM
Annual screening advised from three years old in at-risk breeds
Echo and 24-hr holter ECG
+/- cardiac biomarkers
Genetic testing
Sequelae of DCM
Left sided congestive heart failure
Forward failure
Right-sided congestive heart failure
Arrhythmias
- atrial fibrillation
- ventricular arrhythmias and sudden cardiac death
- sustained tachyarrhythmias
Treatment of pre-clinical DCM
Pimobendan
Antiarrhythmic therapy
Key points of CHF treatment
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
Acute CHF (in-hospital treatment)
Oxygen
Furosemide IV
Pimobendan
Sedation/antianxiety (butorphanol)
Additional hospital treatment for more advanced/refractory acute CHF cases
Vasodilators
- nitro-glycerine (venodilator)
- sodium nitroprusside CRI (ateriodilator and venodilator)
Further inotropic support
- Dobutamine CRI
Mechanical ventilation
At home treatment for chronic CHF
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
Treatment for ventricular arrhythmias
Lidocaine (mergency treatment of V tach)
Solatol (oral treatment)
Mexiletine (minimal depression of systolic dysfunction, may have marked GI effects)
Amiodarone (minimal myocardial depression)
Solatol
Oral treatment for chronoic ventricular arrhythmias
Peak effect within 2-4 hours of administration
Negative inotrope- use with care in severe systolic dysfunction
Mexiletine
Oral treatment for ventricular arrhythmias
Minimal effect on systolic function
Adverse effects: GI (anorexia, vomiting, diarrhoea)
Amiodarone
Oral therapy for ventricular arrhythmias
Takes several weeks to reach steady serum levels
Adverse effects: hepatopathy and thyroid dysfunction
Lidocaine
Treatment for sustained ventricular tachycardia
Na channel blocker
IV only
Amiodarone
Treatment for sustained ventricular tachycardia
Adverse effects: hepatic and thyroid dysfunction
Treatment for atrial fibrillation
Diltiazem
Digoxin
Diltiazem
Treatment for atrial fibrillation
Calcium channel blocker
Mild negative inotropic effect, so care of high doses in cases with CHF
Digoxin
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
Treatment for stage A DCM
No treatment
Treatment of stage B1 DCM
+/- Antiarrhythmics
Treatment of stage B2 DCM
Pimobendan
+/- antiarrhythmics
Treatment of stage C DCM
Diuretics
Pimobendan
ACE-i
Spironolactone
Treatment of stage D DCM
Diuretics
Pimobendan
ACE-i
Spironolactone
+ additional diuresis
+ K supplementation
Prognosis of DCM
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
Arrhythmogenic right ventricular cardiomyopathy ARVC
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
Aetiology of arrhythmogenic right ventricular cardiomyopathy (ARVC)
Likely to be genetic
Disease of the desmosome
Pathophysiology of ARVC
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
Signalment of ARVC
Best described in Boxers, also reported in English Bulldogs
Adult onset (usually 5-7)
Three clinical categories of ARVC
Asymptomatic
Symptomatic
Arrhythmias and DCM phenotype
Asymptomatic ARVC
Arrhythmias detected incidentally on clinical examination/ECG
Symptomatic ARVC
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
Diagnosis of ARVC
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
Treatment of ARVC
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
Prognosis of ARVC
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
