Chapter 55 - Dilated Cardiomyopathies Flashcards

1
Q

How is dilated cardiomyopathy characterized ?

A
  • Primary systolic dysfunction or “pump” failure of the left ventricle
  • Thinning of the left ventricular walls, and cardiac chamber dilation

Common sequelae of DCM include congestive heart failure (CHF), arrhythmias, and sudden death.

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2
Q

What are the etiologies of DCM ?

A
-	Idiopathic
o	Genetic mutation (boxer)
o	Myocarditis
o	Parvovirus (2-4 wo)
o	Chaga’s disease
o	Doxorubicin
o	Taurine deficiency
o	Tachycardia induced cardiomyopathy 2dary to persistent tachyarrythmias (reversible)
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3
Q

Signalment, prevalence, incidence of DCM ?

A
Doberman pinschers (45–62% in the US and Canada, and 58.2% in Europe), Irish wolfhounds (24.2%), Great Danes, Newfoundlands (17.6%), Scottish deerhounds, German shepherds, St Bernards, airedales, and boxers. Cocker spaniels and juvenile PWD (first 6 months of life) may also develop DCM secondary to taurine deficiency. 
Dogs between the ages of 4 to 9 years, with an increase in incidence with advancing age;
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4
Q

What are the 3 stages of DCM ?

A

●● Stage I: asymptomatic dogs with no detectable morphological or electrical abnormalities; currently no
test to detect dogs within this stage.
●● Stage II: occult stage; asymptomatic with development of electrical or structural abnormalities. Early, preclinical stage. May be characterized by only ventricular premature complexes (VPCs), only echocardiographic changes, or both with the absence of clinical signs.
NT-proBNP testing may also assist in the detection of dogs with structural changes.
●● Stage III: overt stage; symptomatic dogs with clinical signs of heart failure, syncope, or sudden death.

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5
Q

What are the clinical signs ?

A
  • Initial clinical signs such as exercise intolerance or fatigue : subtle, often unnoticed.

Most commonly diagnosed when clinical signs of CHF develop:
- left-sided CHF: tachypnea and dyspnea or cough
- right-sided CHF: jugular venous distension and ascites (abdominal distension)
Biventricular heart failure possible.
- syncope
- sudden death secondary to tachyarrhythmias

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6
Q

What are the physical examination findings?

A
  • Soft low-grade holosystolic left apical murmur secondary to mitral regurgitation may be heard. Intensity of the murmur typically reduced due to systolic dysfunction and/or the presence of pleural effusion.
  • S3 gallop
  • Arrhythmia
  • Jugular venous or abdominal distension
  • Femoral pulses may be of poor or weak quality and pulse deficits may occur if arrhythmias are present.
  • Dyspnea, tachypnea, increased bronchovesicular sounds, crackles
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7
Q

What are the electrocardiogram findings associated with DCM?

A
  • Sinus tachycardia
  • Arrhythmias such as atrial fibrillation:
    • Rapid, irregularly irregular rhythm with the absence of P-waves
    • Undulating baseline with fibrillation waves may be seen (unconsistent finding)
  • Ventricular arrhythmias (can lead to sudden death): single isolated ventricular premature contractions (VPCs), couplets, with or without R-on-T morphology, or ventricular tachycardia, ventricular ectopic beats (wide and bizarre complexes) of left or right ventricular origin, or multifocal.
  • Atrial premature contractions

(10-years retrospective study:
- On 39 Irish wolfhounds, 46% had atrial fibrillation at time of their first examination
- 100% developed atrial fibrillation by the time they presented in CHF with overt DCM.
=> atrial fibrillation should always prompt further diagnostic investigation.)

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8
Q

What is diagnostic for the early phase of DCM in Dobermans?

A

2017 guidelines :

  • More than 300 VPCs in a 24h period
  • or between 50- 300 VPCs on 2 subsequent recordings within a year
  • or any couplets or runs of ventricular tachycardia

A cut-off of at least one VPC on evaluation of a 5-minute ECG was found to have a sensitivity of 64.2% and specificity 96.7% for the diagnosis of DCM.

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9
Q

Useful additional tests other than imagery ?

A
  • Genetic testing : PDK4 (mitochondrial protein) gene in Dobermans and the striatin gene mutation in boxers
  • Dogs predisposed to taurine-deficiency DCM (cocker spaniels or dogs fed a vegetarian/vegan or lamb and rice diet): whole-blood and plasma taurine levels
  • NT-proBNP Testing
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10
Q

Treatment for DCM?

A

Standard triple therapy:

  • Pimobendan,
  • ACE inhibitor (enalapril, benazepril, lisinopril, etc.),
  • Furosemide
  • Additional diuretics such as spironolactone or torsemide may be added in dogs with refractory CHF
  • Diltiazem, digoxin, or amiodarone (refractory ventricular tachycardia only) in case of atrial fibrillation with a rapid ventricular response. Combination of oral digoxin+ diltiazem more effective in lowering heart rate than either of these drugs alone.
  • Frequent or complex ventricular ectopy: intravenous lidocaine, procainamide, amiodarone, sotalol, mexiletine, flecainide, and beta-blockers
  • Low-dose beta-blockers in humans: reduction in mortality and morbidity. Should not be started in patients with active congestive heart failure (negative inotropic and chronotropic effects).
  • Taurine or L-carnitine supplementation if indicated
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11
Q

What is the prognosis associated with DCM?

A
  • variable: disease stage, severity, breed, etiology, concurrent diseases
  • asymptomatic phase (occult DCM) up to 2–4 years
  • Sudden death secondary to ventricular tachycardia-fibrillation: first clinical sign of disease in >25–30% cases
  • Overt DCM: prognosis guarded to poor, reported median survival times of 2–6 months. Case fatality rate after 1 year is > 90% in some studies.
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12
Q

Negative prognostic indicators:

A
  • young age at onset of clinical signs ( < 5 years),
  • presence of pleural effusion,
  • pulmonary edema,
  • ascites,
  • atrial fibrillation,
  • higher plasma creatinine,
  • greater than 50–100 VPCs in 24 hours.
  • increased end-systolic volume index, restrictive transmitral inflow pattern, short E-wave deceleration time (< 80 msec)
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