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Ettinger Cardiology > 252 Myocardial Disease > Flashcards

252 Myocardial Disease Flashcards

1
Q

What is canine dilated cardiomyopathy?

A

= a primary myocardial disease characterised by cardiac enlargement and impaired systolic function of one or both ventricles

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2
Q

What breeds is DCM most likely to occur in?

A
  • large and medium sized breeds.
  • US: Doberman Pinscher, Irish wolfhound, grea Dane, and cocker spaniel
  • European: Airedale terrier, Doberman Pinscher, Newfoundland, and English Cocker Spaniel.

The difference in breed prevalence suggests an influence of environmental factors, and genetic influences

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3
Q

How does DCM typically present?

A
  • Adult onset, except for Portuguese Water Dog and toy Manchester terrier who are diagnosed prior to 1 year
  • Clinical signs: coughing, dyspnea, tachypnoea, syncope, exercise intolerance, and occasionally ascites
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4
Q

What are the findings on physical exam of Dog with DCM?

A
  • soft systolic murmur consistent with mitral valve regurgitation +/- gallop sound (S3)
  • tachyarrhythmia of ventricular or atrial origin
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5
Q

What can be the ECG findings of a dog with DCM?

A
  • possibly tachyarrhythmia: AFib +/- vtach

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6
Q

What are the radiographic findings of a dog with DCM?

A

Depending on stage of disease, it could indicate atrial and ventricular enlargement (usually left side), +/- pulmonary venous distension and pulmonary oedema.
- some cases can have biatrial and biventricular enlargement.

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7
Q

What are the Echocardiographic findings of a dog with DCM?

A
  • left and sometimes right atrial and ventricular dilation
  • ventricular wall may be thin
  • concurrent left ventricular systolic dysfunction based upon decreased fractional shortening, ejection fraction, and increased end-systolic volume.
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8
Q

What cardiac biomarkers are useful for diagnosing DCM?

A

ANP = released in response to increased atrial pressure and stretch
-> increases in occult an overt dilated cardiomyopathy in Doberman’s. Other studies show not specific or sensitive enough to screen in other dog breeds

Cardiac troponin-1 (cTnI)= myocardial injury

  • > lack sensitivity and specificity to be used as early marker of DCM.
  • high sensitivity assay cTnI recentl available but utility to evaluate occult DCM is not reported

B-type natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP)= released when ventricles are dilated, hypertrophic or increased wall tension and cleaved into two polypeptides.

  • > sensitive screening even for dogs in occult stage of disease.
  • Doberman’s with DCM show elevated plasma concentrations up to 1.5 yrs prior to developing DCM
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9
Q

What is the cause of DCM in cocker spaniels? How is it managed & treated? What is the prognosis?

A

American CS

  • Cause= low plasma taurine levels in American Cocker Spaniels
  • Manage = taurine and l-carnations supplementation -> increase FS% & decrease left ventricular end diastolic and systolic diameter over 4 month period. Although myocardial function did not return.
  • Tx = 500mg of taurine and 1 gram of L-carnitine PO q 12h usually for life
  • Prognosis = if taurine deficiency not identified then prognosis is poor

English CS

  • Cause= English CS get DCM but taurine or carnations not identified. Can have a heritable component as most are from the same kennel.
  • Management= Some dogs die suddenly, but many live prolonged, mostly asymptomatic, or long survival with medical management
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10
Q

How do dalmatians present with DCM? How is it inherited? WHat are the ECG findings? What is the Duration of survival?

A

Inheritance = - male dogs appear over represented but no formal study done

  • Presentation = adult-onset and signs of left sided failure (cough, dyspnea) or syncope. Not biventricular heart failure
  • ECG findings = sinus rhythm, sinus tachycardia with occasional ventricular ectopy
  • Duration of survival= 1.5-30 months with euthanasia due to refractory CHF
  • 8/9 dogs fed low protein diets to prevent irate stones, but no L-carnitine or taurine deficiency
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11
Q

How do Doberman Pinscher present with DCM? Inherited? What can be done to detect it early?

A

Present =

  • left/and or right biventricular failure, often with atrial fibrillation or sudden cardiac death
  • occult stage = infrequent VPCs, mild ventricular dilation +/- systolic dysfunction +/- diastolic function
  • Overt stage = AFib, VPCs, and CHF
  • syncope is associated with VTach, and bradycardia associated with episodic weakness and syncope observed in cardiomyopathic Doberman Pinschers
  • Inherited = Familial inheritance - autosomal dominant mode of inheritance. USA identified a splice-site mutation in pyruvate dehydrogenase kinase 4 (PDK4)

Detection= measurement for early detection using NT-proBNP

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12
Q

How do Great Danes present with DCM? Inherited? ECG findings?

A

Inherited=
- appears to be familial disease.
- one study showed mostly male dogs suggesting X-linked pattern of inheritance
Presentation=
- can present for weight loss +/- coughing
- left sided heart murmurs, a gallop and ascites were observed

  • ECG= AFib with VPCs
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13
Q

How do Irish Wolfhounds present with DCM? Inheritance? Outcome?

A

Inherited=

  • Familial trait
  • mode of inheritance is autosomal recessive with sex-specific alleles.

Presentation=
- AFib is commonly present in the majority

Outcome=

  • not well understood but appears slowly, then develops AFi preceding CHF by an average of 2 months
  • can die suddenly, commonly euthanised due to heart failure, - biventricular +/- chylothorax
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14
Q

How do Newfoundlands present with DCM? Inherited? ECG findings?

A

Inherited=
- adult onset with no gender predisposition

Presentation =

  • clinical presentation includes dyspnea, cough, innappetance and ascites with left or biventricular heart failure.
  • few have heart murmur
  • ECG= AFib or isolated VPCs
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15
Q

How do Portuguese Water Dogs present with DCM? Inherited?

A

Inherited=
- juvenile familial CM and inherited as autosomal recessive linked to chromosome 8.
Present/Outcome=
- Affected puppies from unaffected and died between 2-32 weeks of age, from sudden collapse and death without signs or development of CHF

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16
Q

How is DCM inherited in standard schnauzers present?

A

Inherited=
- Familial DCM due to deletion and frame-shift mutation in the RNA binding motif protein 20 (RBM20) gene was identified.

  • inherited in an autosomal recessive pattern.
17
Q

How do Toy Manchester Terrier present with DCM? Inherited?

A

Inherited=
- A rapidly progressive juvenile form of familial DCM reported in the Toy Manchester Terrier and similar to Portuguese Water Dog.

Presentation/outcome:
- Most dogs are less than 1 year of age and typically die suddenly without signs of overt congestive heart failure

18
Q

How can nutritional cardiomyopathy due to taurine deficiency result in DCM? What level is taurine deficiency? How is it managed?

A
  • low taurine and L-carnatine, but dog have greater ability to synthesise taurine than cats
  • common factor for dogs developing DCM is a diet of dr dog food with lamb meal, rice, or both as primary ingredient.
  • hypothesised that rice bran or whole rice products may result in decreased taurine levels

Deficiency =- A blood level of <150nmol/mL or plasma levels <4nmol/mL indicates diagnosis of taurine deficiency

Management=
Treat: variable dosages, but 100mg/day PO SID or BID. Inotropic medication such as pimobendan and treatment of heart failure.
- response to treatment is around and improvement in 3-6 months on echo.
- blood levels of taurine reevaluated in 1-2 months

19
Q

How is a dog with occult dilated cardiomyopathy managed?

A
  • There are few studies evaluating benefit of medical therapy for dogs diagnosed with occult stage DCM
  • ACEi: some benefit in dogs with dilation +/- systolic dysfunction
  • beta blockers: unknown not enough studies
  • pimobinden: PROTECT study, a multi Center double-blinded placebo controlled evaluation identified a survival benefit in Doberman Pinschers given pimobendan in occult stage of disease. Dobermans were given twice-daily pimobendan and time to onset of CHF or sudden cardiac death found significantly longer (718d V 441d)
20
Q

How are dogs with DCM and CHF treated?

A
  • Benefit form inotropic support-> ideally pimobendan
  • Pimobendan has balanced vasodilation and positive inotropic effects and has shown to increase survival (median of 130 days versus a median of 14 days for placebo in one study) in Doberman Pinschers with DCM when given at 025mg/kg PO q 12h
  • ACEi and diuretics should be started as needed
  • nutritional supplements like taurine
  • Fatty acids if in cachexia
  • Digoxin +/- diltiazem is used in toe management of atrial fibrillation and congestive heart failure
21
Q

How should dogs with DCM and ventricular arrhythmias?

A
  • Caution if systolic dysfunction is present: Sotalol (beta blocker + potassium channel blocker)
  • Mixelitine: 5-6 mg/kg PO q 8h can decrease arrhythmia
  • Amiodarone in Dobermans at a dose of 10mg/kg PO q 12h for 5 days then 5mg/kg q 24h
  • Evaluate serum drug concentrations, complete blood counts (neutropenia), and serum liver enzymes
22
Q

What are negative prognostic indicators?

A
  • Age of onset of clinical signs
  • pleural effusions
  • pulmonary oedema
  • ascites
  • atrial fibrillation
  • end systolic volume index
  • ejection fraction
  • restrictive pattern of trans mitral flow
23
Q

How is ARVC inherited in Boxer dogs? How do dogs present with clinical signs?

A
  • familial disease and inherited as autosomal dominant trait
  • variable genetic penetrance and dogs have many different presentations including asymptomatic, syncope, sudden death, and systolic dysfunction.
  • homozygous mutant dogs exhibit severe forms of ARVC including higher number of ventricular arrhythmias, sudden death events, and rare structural heart disease (type III ARVC)
24
Q

What is the presentation and clinical signs of a dog with ARVC?

A

Presentation:

  • syncope, or episodes of syncope after period of exercise or excitement
  • Exercise intolerance or lethargy
  • Sudden death
  • 10% present with left or biventricular heart failure

Physical exam:

  • can be Normal
  • tachyarrhythmia
  • ventricular dilation and systolic dysfunction — termed type III ARVC
  • systolic murmur +/- gallop auscultation at left apex
  • signs of right heart failure - ascites & jugular distension
  • ** left basilar systolic murmu not indication of boxer ARVC
25
Q

How do biomarkers help with the diagnosis of Boxer ARVC?

A
  • variable value
  • Cardiac troponin I: significant elevated and correlated with VPC number and complexity of arrhythmia. BUT some dogs had lower levels of cTnI that overlapped with normal boxers
  • BNP is not a useful indicator of disease
26
Q

What are the ECG findings of a fog with ARVC?

A
  • A VPC may be singly, in pair and in runs of paroxysmal ventricular tachycardia
  • ## VPC’s have left bundle branch block in leads I, II, III, and AF consistent with right ventricular origin of this arrhythmia.
27
Q

What are the thoracic radiograph findings of boxers with ARVC?

A
  • usually in normal limits
  • small number with left ventricular dilation and systolic dysfunction (type III ARVC), generalised cardiomegaly and pulmonary oedema +/- pleural effusion
28
Q

What are the echo findings of a dog with ARVC?

A

Ventricular dilation and systolic dysfunction may occur but in most cases affected dogs have normal chamber sizes and systolic function.

29
Q

What are the indications for treatment in a boxer dog with ARVC?

A
  • if arrhythmia detected in asymptomatic dog then Holter monitor to evaluate arrhythmia. Treat if >1000 VPC/24hr period, runs of VTach, or evidence of RonT phenomenon.
  • Homozygous positive for the striating mutation may need treatment earlier as it is more severe
  • Treatment has no evidence for altering outcome, but will decrease PVC’s and syncopal episodes.

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30
Q

What treatments are indicated for boxers with ARVC?

A
  • Sotalol 1.5-3 mg/kg PO q12h
    OR
  • Mixelitine 5-6 mg/kg PO q 8h
  • In some cases both may improve to be effective.
  • Ideally Holter monitor placed before starting therapy and repeated 2-3 weeks after starting therapy to monitor effect of medication.
  • One study showed that fish oil supplementation orally 6 weeks reduced VPCs, but no to a degree that could be due to day-to-day variation.
  • If systolic dysfunction and ventricular dilation (from echo) treat DCM (pimobendan, ACEi, diuretic)+ supplement L-carnations 50mg/kg q 8-12h
31
Q

What is the prognosis of dogs with ARVC?

A
  • Risk of sudden death
  • many live for year on antiarrhythmics without clinical signs, but some develop ventricular dilation and systolic dysfunction.
32
Q

What is myocarditis?

A

= a myocardial disease characterised by presence of myocardial necrosis or degeneration and inflammation

33
Q

What causes myocarditis?

A

Overall a variety of physical, chemical, and infectious agents can damage the myocardial tissue and evoke inflammatory response -> results in chamber enlargement, myocardial dysfunction (similar to DCM), and tachyarrhythmia/bradyarrhythmia

  • Trypanosoma Cruzi (North America)
  • Leishmania
  • Parvovirus
  • West Nile virus
  • Fungal myocarditis (blastomyces)
  • bacteria: Bacillus pill form is, Citrobacter koseri, and Borreia burgdorferi
34
Q

What is atrial myocarditis?

A
  • Form of myocarditis limited to atria
  • unexplained arrhythmia including atrial fibrillation associated with inflammation or infection of right atria.
  • Intermittent asystole with syncope was observed in do with lymphocytes, macrophages, and neutrophils throughout right and lesser extent the left atrium.
35
Q

What is myocardial infarction? What causes it?

A
  • Acute myocardial infarction are uncommon rom of myocardial disease in dogs and most commonly associate with concurrent systemic or cardiac disease that lead to thromboembolic state.
  • Conditions include: endocarditis, neoplasia renal disease, IMHA, and pancreatic disease.

Ettinger Cardiology (11 decks)

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