Dilated cardiomyopathy (DCM) is an enlarging or ballooning of the heart. It was first reported in 1970. The incidence seems to be increasing probably due to genetic selection and line breeding. DCM is probably not a single disease, but rather a result of different disease-producing processes, or defects, in the heart tissue metabolism. Some dogs have a deficiency of an amino acid L-carnitine or enzyme Q10; others perhaps may have muscular dystrophy or other diseases. Breeds involved include Dobermans, Boxers, English Cocker Spaniels, and giant breed dogs. DCM occurs primarily in young to middle age male dogs. As opposed to other breeds, Dobermans have ventricular arrhythmias (irregular heartbeat) more frequently and even poorer prognosis than other breeds. Signs include dyspnea (difficulty breathing), orthopnea (discomfort in breathing), or a soft cough sometimes with blood-tinged froth.
In DCM, the heart muscle loses its ability to contract (squeeze); therefore the heart is unable to distribute blood to the body. The muscular wall of the ventricle stretches out of shape over time until it is no longer able to pump blood at all.
Despite the dog's apparent good health at the time of an office visit, affected dogs deteriorate rapidly. Some dogs eventually suffer from poor appetite and weight loss due to reduced oxygen delivery to the body; the kidneys fail, the lungs fill up with fluid (pulmonary edema), and the abdomen may fill with fluid (ascites). Death normally results from heart arrhythmias, which eventually convert into ventricular fibrillation (ineffective random contractions). Sudden death is the regrettable end result once the heart goes into congestive heart failure.
Signs of DCM include combinations of weakness, weight loss, inappetence, lethargy, exercise intolerance, dyspnea, a soft cough, fainting episodes, or ascites. Sometimes veterinarians are able to detect heart rhythm abnormalities before the dog shows any signs of disease. The progression of clinical signs and weight loss may be unbelievably rapid.
Once suspected, thoracic (chest) radiographs may help to diagnose DCM. Typically, as the disease progresses, there is enlargement of the heart as well as pulmonary edema. Pleural effusion (free fluid in the chest cavity) or ascites may be seen on occasion.
Electrocardiography (ECG) can also be a useful tool. It can confirm cardiac arrhythmias, enlargement of the atria or ventricles, or myocardial (heart muscle disease). It can also be utilized to monitor treatment.
There are no laboratory tests to diagnose DCM; however, blood tests may be needed to monitor the secondary results of the disease on the body as the heart goes into failure.
Today, the “gold standard” for diagnosis relies on echocardiography. The dog is placed on a padded bed. Then the heart is harmlessly scanned to examine the heart while it is actually beating. In this way, we can look for anatomic abnormalities, watch the blood flow, and see if the muscle walls are in fact dilated and see how forcefully the muscle wall is able to contract.
Therapy of DCM is aimed at lessening signs of congestive heart failure; assist the heart rate, rhythm, the muscle's ability to contract, and the volume of blood pumped. Additional therapy is aimed at removing fluid from the lungs, chest cavity, and/or abdominal cavity. Vitamin E could possible retard the progression of DCM if administered early, by its ability to scavenge free oxygen radicals (a toxic substance to the heart which builds up when the heart operates under poor conditions).
New evidence suggests that there is high prevalence of myocardial dysfunction in normal dogs. Of one hundred-fifty Dobermans evaluated with echocardiography, greater than 50% showed evidence of reduced cardiac function. It appears that heart disease in Dobermans may be very common and that most are able to maintain a normal lifestyle regardless of a poorly functioning heart. However, by the time these dogs are clinical (showing signs), they soon die (i.e. the disease had been going on for a long time but it had gone undetected and finally the heart became unable to sustain life).
Michael O'Grady, DVM, MS has found that the prevalence of DCM in females equals that of males. It's not understood why females are underestimated in the literature. Perhaps it is due to the high incidence of sudden death in females. Perhaps these females suffered from DCM but died before it was detected due to a more rapid course of disease than in males.
Currently, prognosis is based on deterioration of the cardiac muscle's ability to function and electric alterations. Dobermans with mild dysfunction, but occasional abnormal beats, may do well for one to two years. Dobermans with severe dysfunction (with or without atrial fibrillations and occasional abnormal beats) may survive two to four months. Dobermans with mild dysfunction (but regular abnormal beats) usually die of sudden death. They may survive from six months to two years.
Presently there is no cure or prevention of DCM. More research is needed to determine why these hearts go into failure so we can best treat these dogs. For those of you purchasing from breeders, be sure to get a copy of the pups pedigree, before you buy, and research their lineage. Since Cardio is known to have a genetic component, if there is Cardio in the near generations, beware. For those of us that adopt foster dogs, be sure to have the heart listened to every 6-12 months.
Hopefully, we can some day reduce the incidence of DCM. Until then we can only hope to increase the quantity and quality of life for these dogs once they are sick.
© 2006 Margot B. Schwag, VMD. All rights reserved. For permission to reprint contact author at Landisville Animal Hospital, 3035 Harrisburg Pike, Landisville, PA 17538
by Margot Schwag, VMD
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