Introduction

• Common acquired disease, especially large and giant breeds in middle age, some spaniels.
• Cause: systolic (contractility) failure of left ventricle in classic form, occasionally Arrhythmogenic right ventricular cardiomyopathy (ARVC) form seen.
• Signs: exercise intolerance, weight loss, dyspnea, cough, arrhythmia. The occult/pre-clinical phase is not associated with clinical signs.
• Diagnosis: ECG, radiography, echocardiography.
• Treatment: manage cardiac failure, support myocardial function and control arrhythmias.
• Prognosis: guarded, survival usually months rather than years but varies with breed.

Use the interactive tool from ROYAL CANIN® UKto explain dog anatomy and disease conditions to your client. Visit Royal Canin Natom Explorer to find out more.

Pathogenesis

Etiology

Undefined

• Idiopathic, see also secondary dilated cardiomyopathy.
• Nutritional (taurine Taurine /carnitine deficiency Carnitine deficiency ).

Genetic

• Pure bred dogs are over-represented implying a familial or genetic component.
• May be autosomal dominant inheritance in some Newfoundland, Boxers and Irish Wolfhound families.
• Boxer ARVC may be associated with abnormal ryanodine function secondary to calstabin.

Metabolic

• L-carnitine deficiency Carnitine deficiency within the cardiomyocytes (some Boxers); and possibly other breeds may respond to carnitine supplementation.
• Carnitine transports long chain fatty acids across mitochondral membranes → energy for myocardium.
• Deficiency may exist in up to 40% of dogs with cardiomyopathy but most of these have normal plasma carnitine levels.
• Can only be assessed by endocardial biopsy so treatment may be initiated on a trial basis however the supplement may be expensive.
• Taurine Taurine is the most abundant free amino acid in the heart.
• Normal plasma level 63 nmol/l (range 44-224 nmol/l).
• Taurine deficiency Taurine deficiency most likely to occur in dogs on vegetarian diet, but also seen in some dogs on normal proprietary diets.
• Low plasma taurine levels recorded in Golden Retrievers Retriever: Golden , American Cocker Spaniels American Cocker Spaniel and Newfoundlands Newfoundland with cardiomyopathy (<60 nmol/l).
• American Cocker Spaniels American Cocker Spaniel may be taurine Taurine and carnitine deficient. Respond to supplementation.

Toxic

• Anthracycline cytotoxic drugs Chemotherapy: general principles , eg doxorubicin Doxorubicin , epirubicin Epirubicin (may be less toxic), monensin, salinomycin.

Physical

• Hyperpyrexia or hypothermias Hyperthermia.

Other

• Toxoplasma gondii Toxoplasma gondii , parvovirus Canine parvovirus , borrelia burgdorferi Borrelia burgdorferi.
• Lymphoma Lymphoma infiltration of myocardium.
• Tachycardia - supraventricular and ventricular tachycardias can result in a cardiomyopathy if uncontrolled.
  Dilated cardiomyopathy is by definition an idiopathic disease. In cases where an underlying cause has been identified, they should be titled according to the cause, eg tachycardiomyopathy, infiltrative cardiomyopathy.

Predisposing factors

General

• Breed.
• Family.

Factors which worsen congestive failure

• Exertion.
• Stress.
• Sudden increase in salt intake.
• Development of an arrhythmia, eg atrial fibrillation.

Specific

• Familial basis (breed).
• Age.

Pathophysiology

• Metabolic or biochemical lesion affecting cardiac myocyte → failure of contractility/increased work for myocardium → :
  • Increased end-diastolic left ventricular volume and pressure → dilation and non-compensatory eccentric hypertrophy of left ventricle → compromised papillary muscle function and passive dilation of atrioventricular annulus causing mitral regurgitation → increased left atrial pressures → left atrial enlargement → increased pulmonary venous (capillary wedge) pressure and pulmonary edema.
  • Poor cardiac output (CO) due to decreased stroke volume (SV) → increased sympathetic drive → increased heart rate (HR), especially if atrial fibrillation present.
  • Reduced cardiac output with arteriolar constriction to increase vascular resistance (mediated through sympathetic tone, active renin-angiotension-aldosterone system (RAAS) and increased vasopressin release); also venoconstriction → increased venous return → increased stretch of myocardium (preload).
  • Arteriolar constriction increases afterload (left ventricle wall stress) and myocardial workload → further myocardial dysfunction, further dilation.
• Signs of poor systolic function and vasoconstricted state:
  • Poor pulse.
  • Pale mucous membranes.
  • Delayed capillary refill time.
  • Cold extremities, etc.
• Left atrial stretch may → supraventricular dysrhythmias, eg atrial fibrillation Heart: atrial fibrillation.
• Increased myocardial wall stress, poor coronary perfusion of myocardium and diseased myocytes may result in ventricular dysrhythmias Heart: dysrhythmia.
• Right-sided failure may also result due to myocardial involvement or secondary to the left congestive failure → ascites, hepatomegaly, hepatojugular reflex, pleural effusion Pleural: effusion , pericardial effusion Pericardial disease.
• Salt and water retention by kidney due to poor renal perfusion → increased sympathetic drive and activation of the RAAS (increased aldosterone) leads to increased venous return (preload) and venous pressure, further stretch of myocardium and predisposition to edema.

Timecourse

• Weeks-months from onset of signs.
• Dobermann: rapid, usually <6 weeks survival after diagnosis without ACE inhibition; sudden death common 50% dead in 3 months, 10% live >1 year. Survival may be improved by addition of pimobendan Pimobendan to medication regime.
• Boxer: variable, may be sudden death from dysrhythmia, may present with congestive heart failure Heart: congestive heart failure.
• Irish Wolfhound: variable dysrhythmias and progressive cardiac dilatation over several years or sudden death.

Other breeds

• Survival depends on breed.
• Cocker Spaniels may survive >12 months.
• Giant breeds may survive for months to years after diagnosis.

Diagnosis

Treatment

Prevention

Outcomes