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Standards of Care May 2009 (Vol 11, No 4)

Canine Idiopathic Dilated Cardiomyopathy

by Gordon D. Peddle, VMD, Meg M. Sleeper, VMD, DACVIM (Cardiology)

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    Introduction

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    Idiopathic dilated cardiomyopathy (DCM) in dogs describes a primary myocardial disease characterized by systolic myocardial failure and ventricular chamber enlargement, with no known underlying cause. Numerous myocardial diseases that result in myocardial dysfunction and ventricular enlargement have been identified in dogs, including nutritional deficiency-associated cardiomyopathies (particularly taurine or l-carnitine deficiency), drug- or toxin-induced cardiomyopathies (e.g., adriamycin-induced cardiomyopathy), infectious or inflammatory cardiomyopathies/myocarditis, hypothyroidism, and familial cardiomyopathies (in which a definitive genetic relationship has been identified). When these causes of systolic dysfunction have been excluded, the diagnosis of idiopathic DCM is made.

    The clinical signs of idiopathic DCM result from contractile failure of the myocardium, which leads to eccentric hypertrophy (biventricular or left sided), activation of the renin-angiotensin-aldosterone system, and fluid retention with cardiac volume overload. Affected dogs present with congestive heart failure (CHF) and/or malignant ventricular or atrial arrhythmias (often manifested as syncope or sudden death).

    Diagnostic Criteria

    Historical Information

    Gender Predisposition

    • Males appear to develop symptomatic disease more frequently and with greater severity.

    Age Predisposition

    • Symptomatic disease is most common in middle-aged to older dogs.
    • A juvenile-onset form has been identified in Portuguese water dogs.
      — Occurs between 1 and 6 months of age (mean: 13 weeks).
      — Onset of clinical signs is usually extremely rapid (days) and refractory to conventional therapy.

    Breed Predisposition

    Adult DCM:

    • Doberman pinschers, cocker spaniels (English or American), Irish wolfhounds, Great Danes, Newfoundlands, boxers, Scottish deerhounds, German shepherds, Saint Bernards.
    • Doberman pinschers usually progress more quickly and are more likely to have a single, fatal collapse episode rather than multiple syncopal episodes.
    • Boxers are also more likely to suffer sudden death.

    Owner Observations

    • Cough.
    • Dyspnea/tachypnea.
    • Exercise intolerance.
    • Weight loss.
    • Syncope or sudden death.
    • Polydipsia.
    • Abdominal distention (ascites).

    Physical Examination Findings

    Subclinical Disease

    Soft heart murmurs, arrhythmias (with pulse deficits), and/or gallop sounds on auscultation.

    Symptomatic (CHF and/or Syncope)

    • Dyspnea/tachypnea.
    • Tachycardia, arrhythmias (with pulse deficits).
    • Soft systolic heart murmur (grade III/VI or less) over left apex of heart. Dogs with DCM often have some degree of mitral regurgitation due to dilation of the mitral annulus and papillary muscle displacement from eccentric left ventricular (LV) hypertrophy.
    • Harsh lung sounds with or without pulmonary crackles.
    • Cough.
    • Mucous membrane cyanosis.
    • Signs consistent with low cardiac output/poor peripheral perfusion:
      — Poor peripheral pulses.
      — Prolonged capillary refill time.
      — Decreased rectal temperature.
      — Cool extremities.
      — Dull mentation.
    • S3 gallop (low-frequency third heart sound; indicates increased LV diastolic pressure).
    • Cardiac cachexia.
    • Jugular pulsation.
    • Abdominal distention with or without a palpable abdominal fluid wave.
    • Hepatojugular reflux/positive abdominojugular test (pressure applied to cranial abdomen results in accentuated jugular pulsation).

    Laboratory Findings

    Abnormalities are not required for the diagnosis of CHF secondary to DCM.

    CBC/Chemistry Profile/Urinalysis

    • Hyponatremia (in advanced disease; dilutional secondary to extracellular fluid retention).
    • Hypokalemia (dilutional or decreased intake).
    • Elevated blood urea nitrogen, creatinine (reduced glomerular filtration rate).
    • Increased urine specific gravity.
    • Elevated ALT, AST, ALP secondary to poor perfusion or hepatic congestion.
    • Stress leukogram.
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    Other Diagnostic Findings

    Arterial Blood Gas

    • Metabolic acidosis.
    • Decreased partial pressure of oxygen in arterial blood.
    • Decreased saturation of peripheral oxygen via pulse oximetry (SpO2).
    • Hypocapnia.

    Other Fluid Analyses

    • Elevated plasma lactate concentration (marker of poor peripheral tissue perfusion).
    • Pleural or abdominal effusions consistent with modified transudate or (less commonly) pure transudate.

    Thoracic Radiography $

    • Subclinical (or clinical for syncope only) DCM:
      — Increased vertebral heart size (normal range: 8.7-10.7 for most dogs).
      — LV or biventricular enlargement, left atrial enlargement.
    • Symptomatic DCM (CHF):
      — Interstitial, alveolar, or mixed pulmonary parenchymal pattern consistent with pulmonary edema. Perihilar or caudodorsal distribution is most common; atypical pulmonary patterns are possible.
      — LV or biventricular enlargement, left atrial enlargement.
      — Increased vertebral heart size.
      — Pulmonary venous distention/enlargement.
      — Left mainstem bronchus compression.
      — Pleural effusion (less common).
      — Enlarged caudal vena cava.
      — Ascites.
      — Hepatomegaly.

    Blood Pressure Measurement $

    • Decreased due to poor cardiac output and intravascular volume depletion.

    Echocardiography $$

    • The gold standard for diagnosing DCM.
    • Eccentric LV or biventricular hypertrophy (normal or decreased LV wall thickness with increased chamber size).
    • Increased LV internal dimension (>49 mm in Doberman pinschers).
    • LV or biventricular myocardial hypokinesis/systolic dysfunction.
      — Decreased fractional shortening (FS; <25%).
      • Some large- or giant-breed dogs have normal FS measurements between 20% and 25%.
      • FS <25% is considered below normal in most dogs.
      • Most dogs with CHF secondary to DCM have FS <15%.

      — Increased end-systolic LV dimension (>42 mm in Doberman pinschers).

    • Left atrial enlargement.
    • Mitral regurgitation, often centrally directed jet.
    • Evidence of diastolic dysfunction/relaxation abnormalities: Reversal of E and A waves on transmitral diastolic inflow patterns and mitral valve annulus tissue Doppler velocities.

    Electrocardiography $-$$

    • Atrial fibrillation: Some large- or giant-breed dogs have atrial fibrillation in the absence of structural cardiac disease, thus atrial fibrillation alone is not predictive of eventual onset of DCM.
    • Atrial premature contractions.
    • Ventricular arrhythmias (ventricular ectopy or ventricular tachycardia): >50 ventricular premature complexes on a 24-hour Holter monitor recording is suggestive of occult DCM in Doberman pinschers.
    • Increased P-wave amplitude or duration (evidence of right or left atrial enlargement).
    • Increased R-wave amplitude in lead II (supportive of LV hypertrophy).
    • Tachycardia (sinus tachycardia or atrial fibrillation; tachycardia almost always present when animal has CHF).

    Summary of Diagnostic Criteria

    • Echocardiographic evidence of myocardial hypokinesis (systolic dysfunction/failure) and ventricular dilation in the absence of other primary cardiac disease.
    • High index of suspicion for DCM based on breed may aid in diagnosis.
    • Surface electrocardiogram and 24-hour Holter monitor recordings are useful as screening tools in healthy dogs of predisposed breeds, asymptomatic/subclinical dogs of predisposed breeds, and dogs presenting for syncope/collapse.

    Diagnostic Differentials

    • Infectious or inflammatory cardiomyopathies/myocarditis.
    • Secondary cardiomyopathies:
      — Blood or plasma taurine testing should be considered in dogs with unusual signalment for DCM.
      — Thyroid testing.
    • Chronic degenerative atrioventricular valve disease.
    • Pericardial effusion (cardiomegaly in a large-breed dog).
    • Arrhythmogenic right ventricular cardiomyopathy in boxers.
    • Heartworm disease in patients with right-sided enlargement.

    Treatment Recommendations

    Occult Disease

    • Discrete evidence for definitive therapy in occult DCM is lacking.
    • Use of β-blockers (atenolol, metoprolol, or carvedilol), angiotensin-converting enzyme (ACE) inhibitors (enalapril, benazepril), or spironolactone in early systolic dysfunction should be considered.

    Acute Congestive Heart Failure (Table 1)

    • First-line therapy:
      — Oxygen supplementation as needed.
      — Furosemide.
      — Pimobendan.
    • Second-line therapy:
      — Dobutamine.
      — Nitroprusside. Monitor blood pressure carefully; causes vomiting in some patients; cyanide toxicity with prolonged use.
      — Hydralazine. Monitor blood pressure carefully.

    Maintenance Treatment of Chronic CHF Due to DCM

    • CHF patients should begin chronic therapy after improvement of clinical signs and discharge from the hospital.
    • Loop diuretic therapy: Furosemide: 1-2 mg/kg PO q12h initial dose. $
      — Use the lowest effective dose that controls congestion.
      — Some degree of resistance to furosemide eventually develops in most patients.
    • ACE inhibitors are indicated in all patients receiving diuretics. $
      — Enalapril maleate: 0.5 mg/kg PO q12h.
      — Benazepril: 0.5 mg/kg PO q24h.
    • Pimobendan: 0.25 mg/kg PO q12h. $-$$
    • Digoxin: $
      — Useful adjunct therapy for systolic failure.
      — Trough serum levels (therapeutic range: 0.5-2.0 ng/mL) should be checked 6 to 8 hours after administration at least 4 to 5 days after beginning therapy, particularly if anorexia is noted by the owner.
      — Digoxin toxicity manifests primarily as gastrointestinal signs, but development of tachy- or bradyarrhythmias is possible.

    SOC Table 1: Canine Idiopathic Dilated Cardiomyopathy

    Alternative/Optional Treatments

    • Aldactazide (hydrochlorothiazide/spironolactone; Pfizer): 0.5-2.0 mg/kg PO q12h. $
      — Begin at low dose and/or reduce furosemide dose when initiating therapy with this drug.
      — Combined thiazide and potassium-sparing diuretic/aldosterone antagonist (spironolactone).
      — Indicated in cases of CHF that become refractory to furosemide therapy or require very large doses of furosemide.
      — Monitor for hyperkalemia and azotemia.
    • Afterload reducers/antihypertensives:
      — Indicated in patients with systemic hypertension.
      — May improve forward blood flow in normotensive patients with severe mitral regurgitation.
    • Cough suppressants (indicated in patients with controlled CHF but intractable coughing). $
      — Hydrocodone: 0.25 mg/kg PO q6-24h prn.
      — Butorphanol tartrate: 0.5 mg/kg PO q6-12h prn.
    • Mild dietary sodium restriction may be beneficial in patients with CHF, particularly early in the disease.
    • Taurine with or without l-carnitine supplementation may be considered for any dog with DCM and is recommended in atypical breeds until normal plasma taurine levels are confirmed. If improved systolic function is not recognized within 3 months, response is unlikely.
      — Taurine: <25 kg: 0.5-1.0 g PO q12h. 25-40 kg: 1-2 g PO q8-12h.
      — L-carnitine: <25 kg: 1 g PO q8h. 25-40 kg: 2 g PO q8h.

    Acute (in-hospital) Arrhythmia Management

    • Atrial fibrillation >160 bpm (or other supraventricular tachycardias).
      — Esmolol: Class II (β-blocker) antiarrhythmic, 50-100 µg/kg IV slow bolus or 50-200 µg/kg/min CRI (if responsive).
      — Diltiazem: Class IV (calcium channel blocker) antiarrhythmic, 0.05-0.25 mg/kg IV slow bolus, repeat boluses at lower doses q2-3min, maximum dose 0.25 mg/kg; maintenance CRI 2-6 µg/kg/min. Use caution when using β-blockers and calcium channel blockers in dogs with significant systolic dysfunction.
    • Ventricular tachycardia.
      — Lidocaine: Class Ib antiarrhythmic, 2-4 mg/kg IV slow bolus, repeat q2-3min as necessary up to three times; maintenance CRI 40-100 µg/kg/min.
      — Procainamide: Class Ia antiarrhythmic, 3-5 mg/kg IV slow bolus, repeat q5-8min up to 20 mg/kg maximum total dose if necessary; maintenance CRI 20-50 µg/kg/min if responsive.
      — Sotalol: Class II (β-blockade) and III antiarrhythmic properties, 0.5-2.0 mg/kg PO q12h.

    Chronic Arrhythmia Management

    • Supraventricular.
      — Digoxin (increases parasympathetic tone at the AV node; see above for dosing and other recommendations) $
      — β-blockers:
      • Atenolol: 0.25-1.5 mg/kg PO q12-24h (β1 selective β-blocker). $
      • Propranolol: 0.2-1.0 mg/kg PO q8h (nonselective β-blocker). $
      — Calcium channel blockers:
      • Diltiazem: 0.5-2 mg/kg PO q8h. $
      • Diltiazem extended release: 1.5-6 mg/kg PO q24h.
    • Ventricular arrhythmias.
      — Treatment of ventricular tachyarrhythmias may reduce the frequency of sustained tachyarrhythmias and overall ectopy.
      — Mexiletine: 5-8 mg/kg PO q8h (class Ib). $
      — Procainamide: 10-30 mg/kg PO q8h (sustained release) or q6h (regular formulation). $
      — Sotalol: 0.5-2.0 mg/kg PO q12h. $
      — Amiodarone (properties of classes I-IV): Loading dose of 10 mg/kg PO q12h for 1 week, thereafter 5 mg/kg PO q12-24h; last resort for ventricular arrhythmias. $

    Supportive Treatment

    • Therapeutic abdominocentesis is indicated in any patient with right-sided CHF in which significant ascites is causing respiratory distress.
    • Therapeutic thoracocentesis is indicated in any patient with CHF with significant pleural effusion or respiratory compromise.
    • Oxygen therapy is indicated in any dyspneic CHF patient until it is stable and breathing room air.

    Patient Monitoring

    Patients Hospitalized for CHF

    • Respiratory rate and effort, lung auscultation: Decreases in respiratory rate and/or effort can occur with severe respiratory fatigue and may not always be indicative of clinical improvement.
    • Heart rate, pulse rate, and pulse quality.
    • SpO2 goal, >95% on room air; arterial blood gas analysis provides more definitive assessment of patient's oxygenation capability but is not necessary.
    • Systemic blood pressure monitoring (particularly if vasodilator therapy is initiated).
    • Rectal temperature.
    • Serial monitoring of renal parameters and electrolytes q12h with aggressive diuretic therapy.
    • Hydration status (mucous membranes, skin turgor, packed cell volume/total protein).
    • Mentation.
    • Continuous electrocardiography, particularly in patients with arrhythmias.
    • Assessment of rate of ascites recurrence following abdominocentesis in patients with right-sided CHF.

    Chronic Management

    • Renal parameters should be reevaluated within 1 week after discharge from the hospital and initiation of chronic diuretic/ACE inhibitor therapy.
    • Owners should be encouraged to keep daily logs of respiratory rate (and heart rate if possible, particularly in dogs with atrial fibrillation) so that they will recognize early signs of pulmonary congestion.
    • Owners of dogs with right-sided CHF should monitor the rate of recurrence of abdominal distention at home; therapeutic abdominocentesis should be performed as necessary to reduce respiratory compromise from diaphragmatic compression.
    • A recheck of thoracic radiographs and/or empirical diuretic therapy adjustment is indicated if clinical signs recur at home; more severe clinical signs warrant readmission to the hospital.
    • Evaluation of renal parameters is indicated after any medication changes or every 6 to 12 months if owners report signs of lethargy/inappetence.

    Patients with Severe Tachyarrhythmias

    • Owners should monitor patients for recurrence or development of clinical signs of syncope or collapse.
    • Serial auscultation and surface electrocardiography should be performed in patients with atrial fibrillation to assess if the target heart rate is being achieved with therapy or maintained without therapy. Target heart rate in stable patients with atrial fibrillation is <160 bpm at rest.
    • Serial surface electrocardiograms and/or 24-hour Holter monitor recordings may be useful in assessing the effect of antiarrhythmic therapy on frequency of ventricular ectopy/arrhythmias.
    • If digoxin is used, serum levels should be rechecked if clinical signs consistent with digoxin toxicity become evident (reduced appetite or anorexia).

    Treatment Cautions/Contraindications

    • Drugs that increase afterload (i.e., α-agonists such as phenylephrine) and negative inotropes are contraindicated in patients with severe systolic dysfunction.
    • Intravenous fluid use, in general, is contraindicated in patients with CHF. If severe dehydration or electrolyte depletion necessitates fluid administration, conservative use of reduced-sodium agents (0.45% sodium chloride or D5W) should be implemented with careful monitoring of respiratory status, body weight, laboratory parameters, and central venous pressure.

    Prognosis

    • The prognosis for dogs with subclinical DCM is guarded as this stage may last for years before the onset of clinical signs.
    • The prognosis for dogs with CHF secondary to DCM is poor, and patients often do not live beyond 6 months from diagnosis.
    • The prognosis for DCM patients with ventricular arrhythmias is guarded to poor as these patients are at risk for fatal arrhythmias and sudden death.

    Favorable Criteria

    • Subclinical or occult DCM carries a more favorable prognosis than symptomatic DCM.

    Unfavorable Criteria

    • Clinical signs.
    • Presence of pulmonary edema, pleural effusion, or ascites.
    • Predisposed breed (i.e., Doberman pinschers).
    • Young age at onset of disease carries a worse prognosis.
    • Presence of bilateral CHF.

    Abbott JA. Beta-blockade in the management of systolic dysfunction. Vet Clin North Am Small Anim Pract 2004;34:1157-1170.

    Borgarelli M, Tarducci A, Tidholm A, et al. Canine idiopathic dilated cardiomyopathy. Part II: Pathophysiology and therapy. Vet J 2001;162:182-195.

    Gordon SG, Miller MW, Saunders AB: Pimobendan in heart failure therapy—a silver bullet? JAAHA 2006;42:90-93.

    O'Grady MR, Minors SL, O'Sullivan ML, et al. Effect of pimobendan on case fatality rate in Doberman Pinschers with congestive heart failure caused by dilated cardiomyopathy. J Vet Intern Med 2008;22:897-904.

    O'Grady MR, O'Sullivan ML. Dilated cardiomyopathy: An update. Vet Clin North Am Small Anim Pract 2004;34:1187-1207.

    Sisson D, O'Grady MR, Calvert CA. Myocardial diseases of dogs. In: Fox PR, Sisson D, Moise NS, eds. Textbook of Canine and Feline Cardiology. 2nd ed. Philadelphia: WB Saunders; 1999:581-620.

    Tidholm A, Haggstrom J, Borgarelli M, et al. Canine idiopathic dilated cardiomyopathy. Part I: Aetiology, clinical characteristics, epidemiology and pathology. Vet J 2001;162:92-107.

    Tilley LP, Smith FW, Oyama MA, et al. Common cardiovascular drugs. In: Tilley LP, Smith FW, Oyama MA, Sleeper MM, eds. Manual of Canine and Feline Cardiology. 4th ed. St. Louis: Saunders Elsevier; 2008:402-413.

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