Dilated cardiomyopathy in dogs

Dilated cardiomyopathy is a primary disease affecting the cardiac muscle (myocardium). Hearts affected by this disease have difficulty pumping blood to the rest of the body, also known as systolic dysfunction. One or both of the ventricles could be affected. As a result, the cardiac chambers become distended and this will eventually cause congestion of the blood at this site (congestive heart failure). Heart rhythm can be affected and become irregular.

Breed, age and gender predisposition

This condition is usually reported in adult dogs (4-10 years old) with the exception of the Portuguese water dog and the Manchester terrier where it can be found in puppies ranging from the age of several weeks to several months. It is found more often in male than females.

Large and giant breeds are predisposed such as the Doberman pinscher, Irish wolfhound, Great Dane, Scottish deerhound, Boxer, Afghan hound, English Shepherd and the Dalmatian. There are also a variety of spaniel breeds that are at risk. A taurine (essential fatty acid) deficiency can be the cause in Cocker spaniels and Golden Retrievers whereas a diet poor in protein can be associated with this disease in Dalmatians. However, it is most often due to a genetic component. Other more rare causes have been suggested such as viral infections, auto-immune disease and toxicity.

This disease is rare in cats, but the breeds at risk are Abyssinian, Burmese and Siamese. For these breeds, a taurine deficiency is usually the cause.

Clinical Presentation

The disease may present itself in different forms: occult (usually at the beginning), congestive heart failure, cardiac arrhythmia and sudden death. The symptoms are variable depending on the form:

  • No symptoms
  • Tachypnea (rapid respiration), cough, respiratory distress, nasal discharge
  • Abdominal distension, ascites (liquid in the abdomen), hepatomegaly (enlarge liver) 
  • Lethargy, depression, weight loss/cachexia
  • Loss of appetite
  • Irregular heart rhythm, heart murmur, syncope, attenuated heart noises due to the presence of pleural effusion (presence of liquid between thoracic cage and the lungs), pulmonary crackling at auscultation (if there is pulmonary edema)
  • Distended jugular vein



In order to diagnose the problem, a minimum of tests are proposed such as thoracic x-rays to detect an enlarged heart, pulmonary edema, pleural effusion and/or enlarged vena cava. An electrocardiogram (EKG) will help in detecting different types of arrhythmias in order to adjust the treatment. A blood test and urine analysis will detect any concomitant conditions and control the effect of the treatments. A pro-BNP test may be recommended to help orient the diagnosis. If pleural effusion is present, an analysis of the liquid can be done to evaluate its content (the type of liquid will confirm the nature of the cardiac condition).
Other tests may be added to confirm the diagnosis if necessary. These include a cardiac ultrasound (including its vessels), measurement of taurine concentrations and biopsy.


The goals of treatment are to reduce and, if possible, eliminate the congestion of blood in the heart, stabilize the cardiac rhythm and improve the patient’s quality of life.

If the animal is respiratory distress upon presentation, oxygen will be administered and treatment for pulmonary edema will begin if it is present. In the case of pleural effusion, the liquid must be removed by aspiration with a syringe to improve breathing. Various types of medication may be added according to the severity of the condition and the patient’s response to the first treatments.

In the long term, diuretics may be necessary to control pulmonary edema (this will eliminate the liquid in the lungs that is preventing the patient from breathing properly. Other medication may be prescribed to decrease the blood pressure located at the exit of the heart allowing it to work less hard to pump the blood to the rest of the body. Also, some medication allows to increase the force of contraction of the heart. Arrhythmias must also be treated.

In terms of nutrition, we recommend to decrease sodium content with a specially formulated diet such as Hill’s H/D. Taurine supplements are recommended for all cats whereas L-carnitine may be considered for certain breeds of dogs. Omega-3 fatty acids may help to increase the appetite and decrease cachexia.


Follow-up exams in the future will be necessary in order to follow the evolution of the disease and to adjust the treatments. Unfortunately, the patient will decease generally between 3 and 24 months following the diagnosis. More specifically, following symptoms of heart failure, patients do not live more than 3 months. However, if there is a good response to the initial treatment, 25 to 40% of affected dogs will live more than 6 months. It is estimated that between 7.5 and 28% will live 2 years following the diagnosis.

Accelerated cardiac rhythm, arrhythmias (atrial fibrillation), pleural effusion, ascites and pulmonary edema are associated to a decreased prognosis.

The prognosis is generally worse in breeds such as the Portuguese water dog and the Doberman pinschers despite the fact that some Dobermans will still live several months to several years following the diagnosis. The prognosis for Irish wolfhounds, however, is not good.

In cats where the disease is not associated to a deficiency in tauring, the prognosis is generally poor.


References :
Côté, Étienne, Clinical veterinary advisor Dogs and Cats, Mosby, Missouri, 2007, pp.302-304.
Nelson, Richard W. and C. Guillermo Couto, Small Animal Internal Medicine, 3rd ed., Mosby, Missouri, 2003, pp. 106-115.