Dilated cardiomyopathy (DCM) is one of the most common heart diseases in dogs. It involves dilation (enlargement) of the left ventricle or both ventricles, along with a reduction in the heart muscle’s ability to contract.
DCM is the second most common heart disease in dogs, after mitral valve endocardiosis (see related article). There is a genetic predisposition in all large and giant breeds, particularly in Dobermans, Boxers, Portuguese Water Dogs, Great Danes, Irish Wolfhounds, Bobtails, Dogues de Bordeaux, Deerhounds, Labrador Retrievers, Leonbergers, Newfoundlands, and PONs. Cocker Spaniels are also affected. Male dogs are affected more frequently than females.
In Dobermans and Portuguese Water Dogs, there is a juvenile form of DCM that occurs before the age of one. The adult form develops between the ages of two and seven, depending on the breed.
DCM is generally classified into three forms:
DCM progresses through three stages and ultimately leads to heart failure (see related article).
The cellular phase proceeds unnoticed in all forms of DCM. During this phase, damage to the myocardium leads to the death of heart muscle cells. Subsequently, connective tissue forms in the affected area, which impairs the function of the heart muscle. To compensate, the heart wall thickens outward, so that cardiac output remains within the normal range for a long time. Affected animals show no symptoms. Even with imaging diagnostics (see related article), no findings can be detected.
The cellular phase then transitions into the subclinical phase, during which myocardial insufficiency (= heart muscle weakness) continues to develop. This phase progresses differently depending on the type of DCM. In DCM Type I, the internal volume of the heart increases. In most cases, only the left ventricle is affected. At the same time, the contractile force decreases. This leads to volume overload of the ventricle, resulting in mitral valve regurgitation (leakage of the heart valve between the left atrium and the left ventricle). Subsequently, the left atrium also enlarges, and blood backs up into the lungs.
The clinical phase of DCM usually begins with the onset of mitral valve regurgitation. Symptoms then become apparent. As a result of myocardial overdistension and hypoxia (insufficient oxygen supply), cardiac arrhythmias, extrasystoles (additional heartbeats outside the normal rhythm), and atrial fibrillation (uncoordinated atrial contractions; see related article) occur.
In Type II DCM, cardiac arrhythmias develop as early as the subclinical phase, and in some cases even during the cellular phase. It is believed that fat deposits act like pacemakers, triggering the extrasystoles. Dogs with Type II DCM often die of sudden cardiac death during the subclinical phase, that is, without having shown any prior symptoms.
DCM can be primary or secondary, resulting from another condition.
Primary causes are genetic mutations in the dog breeds mentioned above. These lead to DCM types I and II.
Secondary causes predominantly lead to degenerative-inflammatory DCM type III. High hormone levels, such as those seen in hyperthyroidism (=overactive thyroid, see related article) or a pheochromocytoma (=rare adrenal gland tumor), cause damage to the heart muscle cells due to a chronic increase in heart rate and blood pressure. However, severe hypothyroidism (=underactive thyroid, see related article) can also cause DCM.
Furthermore, infections with various bacterial and viral pathogens, such as parvovirus (see related article) in puppies, can result in myocarditis (inflammation of the heart muscle), which can progress to DCM.
A deficiency in carnitine or taurine is a common cause of secondary DCM in Labradors, Boxers, American and English Cocker Spaniels, Golden Retrievers, Newfoundlands, and Portuguese Water Dogs. A long-term low-protein diet—such as one prescribed for the treatment of urinary stones, or vegetarian diets and lamb-based diets—can also lead to a deficiency in carnitine and taurine in other dog breeds, thereby causing DCM.
Symptoms usually do not appear until DCM has been present for several years. In DCM types I and III, patients may then experience shortness of breath, coughing, difficulty breathing, or ascites (fluid accumulation in the abdomen).
In DCM type II, fatigue and brief loss of consciousness occur. Unfortunately, this type of DCM often leads to sudden cardiac death without prior symptoms.
After taking your history, your veterinarian will perform a thorough physical examination, including auscultation (listening) of the heart and lungs, as well as a blood pressure measurement. An X-ray examination allows the veterinarian to obtain clear findings during the clinical phase. In the subclinical phase, however, the X-ray images are almost always unremarkable. An ECG (see related article), preferably a 24-hour ECG, should always be recorded. Echocardiography (heart ultrasound; see related article) allows for a detailed examination of the heart structures and blood flow. It can also be used to rule out other conditions that similarly lead to heart failure. A blood test can measure carnitine, taurine, hormones, and specific DCM laboratory markers.
Genetic tests are available for various breeds. These can be used to identify carriers of the genetic predisposition. However, a positive genetic test result does not indicate whether the affected dog will actually develop clinical symptoms.
The goal of treating subclinical DCM is to delay the progression to the clinical phase for as long as possible. This requires increasingly higher doses of medication as the disease progresses. Initially, a medication is used that strengthens the heart muscle and dilates the blood vessels. This reduces the resistance against which the heart must pump. If there is a carnitine or taurine deficiency, this must be corrected with appropriate dietary supplements. Additionally, any underlying conditions must be treated. Affected dogs may still be exercised at a limited to normal level. Veterinary check-ups are scheduled every three to six months.
As soon as clinical symptoms appear, treatment must be intensified with additional blood pressure-lowering, diuretic, and heart medications. Omega-3 fatty acids and magnesium are used as supportive measures to strengthen heart muscle function, reduce arrhythmias, and dilate blood vessels. From now on, the dog must be spared physical exertion and undergo veterinary checkups at shorter intervals.
The prognosis for DCM is generally poor. It is better for dogs with DCM types I and III than for dogs with DCM type II. About 25 to 30 percent of Doberman Pinschers with DCM type II die of sudden cardiac death. There are also breed differences: Doberman Pinschers have the poorest prognosis, while life expectancy in Cocker Spaniels is higher than in other breeds.
Because of its genetic component, DCM cannot be completely prevented in dogs. However, especially in breeds genetically predisposed to the condition, regular heart examinations by a veterinary cardiologist can ensure that changes are detected and treated early. In addition, you can prevent carnitine and taurine deficiencies by feeding your dog a balanced diet with an appropriate protein content.
It is particularly important to identify carriers as early as possible and exclude them from breeding. For some breeds, there are special DCM screenings available, consisting of genetic testing, cardiac ultrasound, and an ECG.
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