Dilated Cardio Myopathy (DCM)

Dilated Cardio Myopathy (DCM) is most commonly seen in dogs and cats, and called canine dilated cardiomyopathy and feline dilated cardiomyopathy respectively.

Canine Dilated Cardiomyopathy

Canine dilated cardiomyopathy (DCM) is one of the most common acquired cardiovascular diseases of dogs. It is primarily a disease of older, male, large- and giant breed dogs such as Scottish Deerhounds, Dobermans, Boxers, Irish Wolfhounds, St. Bernards, Newfoundlands, Afghans, and Old English Sheepdogs.

Etiology

The cause of this disease is unknown, although its onset often follows myocardial insult from viral, bacterial, nutritional, or immune-mediated diseases. DCM results in impaired systolic function of the ventricles and, therefore, decreased stroke volume (the volume of blood ejected from the heart with each contraction).

Although DCM is primarily a disease of older dogs, Portuguese Water Dogs exhibit a juvenile onset of the disease, which is also genetic. Puppies anywhere from 2 to 32 weeks of age can be affected.

The cause of this dilation appears to be breed related. In Dobermans, the disease appears to be familial, related to an autosomal dominant gene. Great Danes and Irish Wolfhounds also demonstrate a genetic predisposition for this disease. In Cocker Spaniels, a taurine deficiency results in DCM. The disease in Cocker Spaniels appears to be related to diets high in lamb meat and rice and low in taurine.

Pathophysiology

The pathology of the disease involves dilation of all chambers of the heart. This dilation (caused by weak, thin, and flabby cardiac muscle) results in a decrease in cardiac output and an increase in cardiac after load (blood left in the heart in diastole).

The effect on the animal is one of low-output circulatory failure, exhibited by weakness, exercise intolerance, syncope, or shock.

Dogs with DCM frequently experience the development of atrial fibrillation (AF), which further contributes to a decrease in cardiac output. Signs of AF include rapid, irregular heart rhythms or sudden death. Patients may remain normal until the atria dilate excessively. The enlarged atria are unable to contract normally, and clinical signs of heart disease become evident.

Clinical Signs

• Right sided heart failure (ascites, hepatomegaly, weight loss, abdominal distension)
• Left-sided heart failure (coughing, pulmonary edema, syncope)
• Exercise intolerance
• Murmur of mitral regurgitation heard best on left chest

Diagnosis

• Based on clinical signs and history.
• Radiographs may be normal early in the disease. May show enlarged heart later in the disease time line; left ventricular enlargement, enlargement of both atria may be visible.
• Echocardiography test is the choice for examination of the heart. it demonstrate left and right atrial wall thinning along with left ventricular dilation.
• ECG may show widened QRS and P waves, rhythm disturbances but is fairly insensitive to changes seen in DCM.
• The use of cardiac biomarkers is gaining in popularity for diagnosis of DCM. These tests look for myocardial cell injury seen in DCM.
• Atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and pro-BNP blood tests are commercially available. In DCM, these values will be significantly increased.
• Troponin 1 (cTn1) will also be increased. (Whole blood is recommended over plasma for this test, but technicians should check with local laboratory before sample collection).

Treatment

• No cure exists for DCM; treatment is aimed at keeping the dog comfortable.
• Diuretics: Frusemide to decrease fluid load and reduce work of the heart.
• Enalapril: angiotensin-converting enzyme (ACE) inhibitor prevents the formation of angiotensin II, a potent vasoconstrictor; helps decrease vascular resistance and improve cardiac output.
• Beta-blockers (β-blockers): metoprolol, propranolol, are examples
• Pimobendan: a calcium sensitizer with inhibitory properties. It increases the calcium binding capability at cTn1 sites. The result is a more forceful contraction of the myocardial cell. The drug also has an antithrombotic effect and is a positive inotrope. Its use has been shown to slow the progression of the disease and to improve survival times.

Feline Dilated Cardiomyopathy

Feline Dilated Cardiomyopathy was one of the most frequent cardiac diseases reported in cats. After the association of the disease with taurine deficiency, additional taurine was added to commercial diets, and the incidence of the disease significantly decreased.

Etiology

Evidence has been found of a genetic predisposition to DCM in cats fed taurine-deficient diets.

Pathophysiology

The pathological condition is similar to DCM in dogs.

Clinical Signs

• Dyspnea
• Inactivity
• Anorexia
• Acute lameness or paralysis, usually in the rear limbs
• Pain and lack of circulation in the affected limbs
• Hypothermia

Diagnosis

• Based on clinical signs and history
• In ECG, increased QRS voltages, wide P waves, ventricular arrhythmia
• Echocardiography reveal dilated heart chambers

Treatment

• Oral taurine supplementation: 250 to 500 milligrams twice per day (mg/day)
• Frusemide to reduce fluid load on the heart
• Oxygen supplementation to increase oxygen levels to the cells.
• Digoxin to increase cardiac contractility and improve cardiac output
• Enalapril: ACE inhibitor to prevent the formation of angiotensin II and decrease vascular resistance; improves cardiac output.
• Pimobendan
• Hydralazine relaxes vascular smooth muscle and decreases peripheral resistance and improves cardiac output.
• Anticoagulants can be used to dissolve or prevent further blood clots.