Signs, Symptoms and Treatment for Dilated Cardiomyopathy (DCM) in Dogs


Dilated cardiomyopathy is a disease of predominantly large and giant breed dogs that results in progressive heart muscle dysfunction, chamber dilation, and eventual congestive heart failure or death of affected patients. The exact cause of the condition is unknown but genetic factors are presumed to play a role. There is no known effective preventative strategy for the condition. Treatment for affected individuals may improve their quality of life, delay the onset of heart failure symptoms, and potentially improve life expectancy. Treatment is not curative, however, and most affected individuals eventually die from the disease.


Dilated Cardiomyopathy (DCM) is a condition characterized by weakness of the heart muscle (poor contractility) that eventually leads to enlargement (dilation) of the heart chambers and complications of congestive heart failure, irregular heart rhythms (arrhythmias), and/or sudden death in affected individuals. The condition is infrequently diagnosed in dogs and is rare in cats. It is most common in large or giant breed dogs (i.e. Doberman Pinscher, Newfoundland, Great Dane, Irish Wolfhound, Boxer), with Cocker Spaniels being one notable exception. The prevalence in certain breeds suggests a genetic predisposition for the condition. It affects adult, usually middle-age or elderly patients.


Genetic factors seem to play a large role in the inheritance and development of DCM in the dog.  In fact, the definitive genetic mutation causing DCM in some breeds, such as the Doberman and Boxer, has now been discovered.  Several other systemic conditions can contribute to the development of a dilated, poorly contracting heart muscle including amino acid deficiencies (taurine,carnitine), a low thyroid level, inflammation of the heart muscle (myocarditis), prolonged rapid heart rates, and poor blood flow to the heart muscle (ischemia). In cats, the condition has for the most part been eliminated after a discovery in the late 1980’s of taurine deficiency as the primary cause in this species. Taurine is now supplemented in all commercial cat foods so the condition has become rare.

It is not uncommon for dogs with DCM to have a long pre-clinical phase  where that are no obvious symptoms. Weakness, fainting spells, difficulty breathing, distension of the abdomen with fluid, and coughing are all possible in the later stages of disease.  There are signs related to what is called “congestive heart failure.”  Some animals may die suddenly from an irregular heart rhythm without any previous symptoms.

The identification of DCM is initially based on physical exam findings and recognition of characteristic features (dilated, poorly contracting heart) on an echocardiogram. The echocardiogram is interpreted in conjunction with several other tests to rule out systemic  conditions that can cause similar echocardiographic  findings such as a low thyroid level, amino acid deficiency (taurine, carnitine), inflammation of the heart muscle (myocarditis), or decreased blood flow to the heart muscle (ischemic heart disease).  In some breeds (Boxer, Doberman pinscher), screening with a 24 hour ECG recording (Holter monitor) may be able to identify animals early in the course of the disease process so that they can be removed from the breeding population,   if they are potential breeding animals.   In other affected individuals, a Holter monitor may be recommended to determine the frequency and severity of irregular heart rhythms to help guide treatment.  Lastly, if the genetic mutation causing DCM is known in a certain breed (Doberman, Boxer), DNA from a cheek swab or blood sample can be used to screen for the disease.

There are no proven strategies for preventing the development of DCM, although many medical protocols and nutritional supplements have been proposed. Some medical therapies have been demonstrated to delay progression of DCM once a diagnosis is reached, and in patients with underlying conditions causing the heart muscle weakness (thyroid deficiency, taurine deficiency), supplementation with the appropriate therapies can halt or reverse the heart muscle changes. If congestive heart failure develops, a combination of diuretics, drugs to support heart muscle contraction, and medications to prevent fluid retention are all indicated. In patients that have irregular heart rhythms, drugs to stabilize the rhythm are also frequently added. There is no cure for DCM, and a heart transplant would be indicated in similarly affected people.

In patients with DCM that are asymptomatic, recheck echocardiograms, ECGs, radiographs, and Holter monitors are useful to assess therapy and document the rate of progression of disease. In symptomatic patients receiving heart failure therapy, these diagnostics are performed more frequently and combined with intermittent labwork (blood samples) to monitor for side effects of drug therapy and to monitor for other concurrent diseases.

Unfortunately, the overall prognosis for patients with DCM is poor. The individual prognosis varies to some degree with breed, with Cocker Spaniels having the longest clinical course (>1 year) and Doberman Pinschers having the shortest (< 1 year) once heart failure symptoms are apparent. Any affected breed is at risk for sudden death secondary to a lethal arrhythmia.

In breeds that are considered high risk (Doberman Pinscher, Boxer, Great Dane, Irish Wolfhound, Scottish Deerhound, Newfoundland, Cocker Spaniel), for individuals that are in an active breeding program, or for non-breeding individuals that have a family history of DCM, yearly screening with an echocardiogram and Holter monitor is recommended.