Many large breeds of dogs may develop dilated cardiomyopathy as young as four years of age, although some smaller breeds are affected by it as well. The cause is unknown but is likely genetic in most cases.

In this common genetic heart problem, which encompasses several different diseases, the heart muscle is diseased and gradually becomes dysfunctional. The heart enlarges as the muscle itself thins out and becomes too loose to contract properly. When the diseased heart muscle no longer pumps enough blood throughout the heart, the dog will develop congestive heart failure.

Warning Signs

If you happen to notice that your dog is slowing down and is not his usual peppy self, it's wise to look for other signs of cardiomyopathy. Early detection will help obtain treatment for your dog. The signs include:

• Depression and lethargy

• Fainting, stumbling, or collapse

• Little interest in food or eating

• More time sleeping

• Overall weakness

• Reluctance to get up and down or to climb stairs

• Shortness of breath, coughing, and wheezing

• Swelling in limbs

• Pale gums

• Increased heart rate

Dry, hacking coughing at night may be due to pulmonary congestion (fluid in the lungs and chest cavity) and/or due to enlargement of the atrium.

Treatment

Conventional treatment for heart disease includes medications. When drugs are used, dogs need to be closely monitored for serious side effects, such as kidney disease.

Veterinarians may prescribe heart medications, along with diet recommendations, herbs, supplements, and acupuncture. Diuretics may be prescribed to remove excess water from the body. ACE (angiotensin-converting enzyme) inhibitors are used to lower blood pressure. Calcium channel blockers decrease the contraction of the heart and widen the arteries to make it easier for the heart to pump blood. Digoxin increases the ability of the heart to contract and reduces heart rate. A new drug called Pimobendan is becoming the drug of choice for many cases of DCM that have resulted in congestive heart failure. It opens up the blood vessels and returns blood to the heart, which reduces pressure on the muscle. Discuss this option with your veterinarian.

The side effects of these medications should be seriously considered before giving them to your dog. Diuretics require monitoring to avoid electrolyte imbalances. ACE inhibitors may reduce appetite, cause diarrhea and vomiting, or lead to kidney insufficiency. Digoxin and Pimobendan may cause loss of appetite, vomiting, diarrhea, lack of coordination, depression, and abnormal heart rhythms.

These medications are frequently and routinely combined by cardiologists, but blood parameters must be followed to ensure proper kidney function at the start of treatment. An overdose of calcium channel blockers will cause an abnormal drop in blood pressure, heart failure, and an overall slowing of the heart.

Adding Taurine and Carnitine

In some breeds, nutritional deficiencies in the amino acid taurine have been linked to the development of DCM. Some Boxers with cardiomyopathy have responded to treatment with supplemental L-carnitine. Not all dogs respond to supplementation; successful treatment largely depends on the underlying cause of disease.

Several giant and large breeds are genetically predisposed to DCM. These include Boxers, Doberman Pinschers, Newfoundlands, Portuguese Water Dogs, and Great Danes. If you have one of these breeds consider supplementing your dog's diet with carnitine and taurine under a veterinarian's supervision. If there is a deficiency, providing extra carnitine improves heart rate and protects against heart muscle weakness. Extra carnitine won't have any impact if there is no deficiency. Dogs often show improvement in heart muscle function with the added amino acid.

Dogs with valvular disease have a high enough level of taurine and wouldn't benefit from the additional amino acid. A supplement of carnitine may or may not help valvular disease, although the combination of taurine and carnitine has been shown to improve life expectancy in some dogs with DCM.