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Dilated cardiomyopathy in the dog: symptoms, treatment, and prognosis

Dilated cardiomyopathy in the dog

Dilated cardiomyopathy is one of the most common heart diseases, affecting mainly large and giant breed dogs.

It is characterized by a long, asymptomatic course, in the course of which pathological processes take place, leading to impaired function of the heart muscle.

Clinical symptoms appear late, already in the end stage of heart failure, and the ignorant owner cannot understand why he did not notice his dog developing the disease earlier.

Unfortunately, it is just like that dilated cardiomyopathy, and its main features are:

  1. Symptomatic or latent phase of various duration during which it is impossible to observe any irregularities in the behavior of the dog. Due to the lack of clinical symptoms, it is also difficult to make a diagnosis at this stage.
  2. High risk of development heart failure, and in seriously ill patients the frequent occurrence of an emergency cardiac death.
  3. The need for aggressive and comprehensive pharmacological treatment to relieve clinical symptoms.

In this article you will learn how to develop the disease, which dogs are most at risk, and how dilated cardiomyopathy is treated.

To better understand the mechanisms responsible for heart damage in this disease, let's start by explaining what we mean by cardiomyopathy.

  • What is cardiomyopathy?
  • Dilated Cardiomyopathy (DCM)
    • The essence of the disease
    • Which dogs are most at risk?
  • Causes of dilated cardiomyopathy in a dog
  • Pathophysiology or what happens to the heart in DCM?
  • Dilated cardiomyopathy symptoms
  • Course of illness
    • Phase I - asymptomatic.
    • Phase II - latent.
    • Phase III - clinically explicit.
  • Diagnosis of cardiomyopathy in dogs
    • Medical interview
    • Clinical examination
    • Ekg
    • Holter examination
    • Radiography
    • Echocardiography
    • Determination of the concentrations of atrial natriuretic peptide and B-type natriuretic peptide.
    • Measurement of the level of cardiac troponin I
  • Complications of dilated cardiomyopathy
    • Azotaemia
    • Electrolyte disturbances
    • Hypothyroidism
  • Interracial similarities and differences in the course of DCM
    • Great Dane, Irish Wolfhound and Bulmastiff cardiomyopathy
    • Doberman cardiomyopathy
    • Boxer cardiomyopathy
    • Cocker spaniel cardiomyopathy
  • Dilated cardiomyopathy treatment
    • Treatment of asymptomatic dilated cardiomyopathy (latent form)
    • Treatment of the clinically overt phase of dilated cardiomyopathy
    • Chronic treatment of patients after stabilization of acute heart failure
    • Management of refractory heart failure
    • Treatment of dcm associated with atrial fibrillation
  • Additional treatment
  • Dilated cardiomyopathy prognosis

What is cardiomyopathy?

Cardiomyopathies these are heart diseases that selectively damage the myocardium, leading to its failure.

They do not have an inflammatory background, and their special feature is the involvement of the myocardium without primary changes in:

  • endocarditis (valves),
  • coronary vessels,
  • pericardium.

The changes in the muscles are degenerative.

Cardiomyopathies are classified as follows:

  • Depending on the cause of the disease:
    • Idiopathic cardiomyopathies - this means that the cause of the disease is unknown:
      • further classification of cardiomyopathy is made on the basis of pathological and physiopathological changes:
        • dilated cardiomyopathy,
        • hypertrophic cardiomyopathy,
        • restrictive cardiomyopathy.
    • Secondary cardiomyopathies following poisoning, nutritional deficiencies, hormonal disorders, or infectious agents.

Dilated Cardiomyopathy (DCM)

The essence of the disease

In progress dilated cardiomyopathy it comes to enlargement of the heart cavities together with the simultaneous thinning of the walls of the chambers.

The fibers of the heart muscle succumb degeneration, fibrosis and necrosis.

The heart becomes less efficient, its ability to contract effectively decreases, and the amount of blood that should be pumped around the body's circumference and reaching all cells and tissues becomes insufficient to meet the body's oxygen and nutrient needs.

Colloquially, it can be said that the heart - from an efficient, resilient muscle pump - becomes a saggy, "rickety " bag, unable to supply the body with blood.

Initially, the body activates a number of compensation mechanisms to support the function of the heart.

And it does, but for a short time

Over time, this muscle suction pump becomes ineffective, symptoms of heart failure appear, and the disease eventually leads to death.

Which dogs are most at risk?

Cardiomyopathy predisposition

DCM the most common occurrence is u adult dogs of large breeds and is usually recognized between 6 and 8 years of age.

Sometimes the disease is diagnosed in younger dogs, approx 3 years old, and also in the elderly, aged 12 years.

The males get sick more often.

Dilated cardiomyopathy rarely affects small, weighing dogs < 15kg.

Dilated cardiomyopathy is extremely common in some breeds of dogs. These are:

  • dobermans (50% are males, 33% females),
  • Irish wolfhounds (approx 25%),
  • Scottish Greyhounds,
  • great dane,
  • boxers,
  • cocker spaniels,
  • springer spaniels,
  • irish setters,
  • German Shepherds,
  • St. Bernardine,
  • Portuguese water dogs (the disease develops at a much younger age - up to eight months of age),
  • bulmastiffy.

Causes of dilated cardiomyopathy in a dog

The etiology of canine idiopathic (primary) dilated cardiomyopathy is unknown.

Attempts are made to identify groups of causes that may be involved in the secondary pathogenesis of DCM. These are:

  • A metabolic defect on the basis of hereditary.

Dilated cardiomyopathy may run in families in some dog breeds (e.g. in Dobermans, Boxers, Cocker Spaniels), hence it is also likely genetic disease background.

  • Earlier viral infections, like for example. Parvo– or Coronavirus.
  • Immune disorders.

Autoantibodies have been found against several important structures found in heart muscle cells (e.g. against beta-adrenergic receptors, mitochondria, heavy chains of myosin).

However, these antibodies are also present in other diseases such as hypertrophic cardiomyopathy, myocarditis, for accompanying changes arterial hypertension, therefore they are not specifically related to DCM.

  • Hormonal and metabolic disorders (e.g. overactive adrenal cortex in dogs).
  • Poisoning chemical compounds (e.g. lead, cobalt, copper, argon). Certain drugs used in oncology (e.g. doxorubicin) are cardiotoxic.
  • Amino acid deficiency:
    • Deficiency taurine.

Contributes to the development of dilated cardiomyopathy in cocker spaniels, it can also cause disease in Dalmatians, labradors and golden retrievers.

The diagnosis of taurine deficiency is very important because its supplementation can improve heart function.

It is recommended that in patients with no familial predisposition to DCM serum taurine concentration test.

It happens that dogs with deficiencies of this amino acid are fed an appropriate meat diet, and yet they develop a deficiency of taurine.

This is most likely due to its malabsorption, metabolism, or secretion.

Unfortunately - in dogs predisposed to the development of DCM (Dobermans, Boxers, Great Danes, Irish Wolfhounds and Scottish Greyhounds) the disease does not respond to taurine administration

Most dogs with DCM due to taurine deficiency have plasma levels of this amino acid < 25 nmol/ml.

    • Deficiency L-carnitine

It is not the primary cause of DCM in dogs, but some taurine-deficient dogs require supplementation with both taurine and L-carnitine.

Measurement of plasma L-carnitine levels has little clinical significance, as this test does not reflect the concentration in muscle tissue. Diagnosis of L-carnitine deficiency requires myocardial biopsy.

Pathophysiology or what happens to the heart in DCM?

What happens to the heart at dcm?

During the development of dilated cardiomyopathy, the contractile function and contractility of the heart muscle are significantly impaired.

The diseased heart is not able to generate an adequate systolic pressure to maintain the cardiac output at an appropriate level.

To support the force of contraction, the heart muscle increases in size, but some blood remains in the ventricles and is not pumped out onto the periphery.

As a result, the preload of the heart increases, and his the chambers widen.

Unfortunately, this is not the end

Along with the weakening of the systolic function, the diastolic function of the heart muscle is also impaired.

As the compliance of the ventricular walls is reduced, the heart muscle does not relax properly:

it comes to impaired filling of the ventricular cavities with blood.

Further changes concern the remodeling of the heart and the expansion of the rings of the atrioventricular valves.

The blood flows back into the atria, they appear valvular insufficiency.

In the next stage:

  • blood pressure rises,
  • the atria are enlarged,
  • the venous pressure increases secondarily.

The culmination of these changes is congestive heart failure.

Dilated cardiomyopathy symptoms

Dilated cardiomyopathy symptoms

Dilated cardiomyopathy is a disease that is characterized by quite a lot long asymptomatic course.

The owner may not be aware that the dog has a cardiac problem, often the abnormalities are picked up accidentally during auscultation of the heart during a vaccination or other follow-up visit.

In many cases, however, the disease does not manifest itself until the end stage of heart failure, when clinical symptoms appear.

The most common reasons for a veterinary consultation in dogs with dilated cardiomyopathy are:

  • lethargy,
  • exercise intolerance,
  • weakness,
  • decreased appetite,
  • weight loss,
  • short breath,
  • cough,
  • enlargement of the abdominal volume.

Course of illness

Dilated cardiomyopathy - the course of the disease

Dilated cardiomyopathy develops slowly and initially has no noticeable clinical symptoms.

The moment symptoms manifest, in most cases the patient is already developing advanced heart failure.

Therefore, during the development of DCM in dogs, there are three stages of cardiomyopathy.

Phase I - asymptomatic.

There are no clinical symptoms at this stage and the examinations show neither morphological nor electrical changes in the myocardium.

The dog is apparently healthy.

Phase II - latent.

There are no visible clinical symptoms at this stage of the disease.

However, there are already some abnormalities that can be picked up by a doctor during a clinical examination.

Belong to them:

  • enlargement of the dimensions of the left ventricle and the left atrium, visible on X-ray or ultrasound of the heart,
  • increased contractility of the heart muscle (echo of the heart),
  • premature ventricular beats in ECG.

The duration of this phase varies - it may vary from several months to several years.

As time goes by, the enlargement of the heart progresses and gets worse arrhythmias.

When the patient develops the first clinical symptoms, he enters the phase of clinically overt dilated cardiomyopathy.

Some dogs (especially dobermans) the first and only symptom may be sudden cardiac death (approx 40% cases).

Phase III - clinically explicit.

At this stage, noticeable symptoms already develop:

  • apathy and weakness, cooling of the peripheral parts of the body (ears, tail), pale mucous membranes, prolonged filling time of capillaries; these are symptoms of peripheral hypoxia as a result of decreased cardiac systolic output,
  • cough - usually dry, rough - as a result of pressure on the main bronchi by the enlarged heart,
  • exercise intolerance,
  • rapid breathing, shortness of breath, pulmonary edema as symptoms of pulmonary venous congestion,
  • fainting,
  • reluctance to eat,
  • breathing difficulties,
  • abdominal enlargement,
  • in the final stage of the disease, symptoms of peripheral venous stasis develop:
    • filling of the zygomatic veins,
    • pleural fluid,
    • fluid in the pericardial sac,
    • ascites.

Often there is an arrhythmia, usually in the form of premature ventricular disorders or atrial fibrillation.

As a rule, advanced heart failure is accompanied chronic respiratory failure, heavy exercise intolerance, lack of appetite and weight loss.

Many sick dog owners choose to be euthanized at this point.

Death can occur suddenly (dobermans) or as a result of advanced congestive heart failure, resistant to pharmacological treatment.

Despite the obvious features and symptoms indicating the disease, also in this phase it happens that they are underestimated for some time.

Remember that dilated cardiomyopathy usually affects older dogs.

Many owners notice the weakness of their charges, but they often blame it on age or accompanying diseases (e.g. joint problems).

Diagnosis of cardiomyopathy in dogs

Diagnosis of cardiomyopathy in dogs

Medical interview

The history of the disease is usually short and goes back only a few days to a few weeks.

The disturbing information reported to the doctor is usually:

  • weakness,
  • exercise intolerance,
  • fainting,
  • apathy,
  • reluctance to eat,
  • weight loss,
  • difficulty breathing - shallow, rapid breathing,
  • cough,
  • abdominal enlargement.

Clinical examination

Heart examination in a dog

In the asymptomatic phase, it can often be heard a soft, contractile murmur over the heart, and the rhythm can be irregular with a missing heart rate.

When such changes are found in patients predisposed to DCM, additional tests should always be ordered (even if the dog's owner does not report any alarming symptoms).

Sometimes it is audible at the apex of the heart on the left and / or right side of the chest during this phase diastolic gallop rhythm. It results from the enlargement of the chambers of the chambers and the reduction of the compliance of their walls.

Also possible to capture are:

  • reduced intensity of heart tones,
  • poor pulse quality in the femoral arteries,
  • widening of the external jugular vein,
  • positive venous pulse.

In the symptomatic phase - clinically evident - symptoms resulting from heart failure are manifested.

  • Irregular heart rhythm with a missing heart rate; gallop rhythm.
  • Low heart rate, compensatory increase in heart rate, decrease in peripheral blood flow (pale mucous membranes, peripheral parts of the body cold to the touch). These symptoms are due to a decrease in the minute volume of the heart (referred to as decreased heart rate) and decreased contractility of the heart.
  • Cough caused by pressure of the enlarged heart on the main bronchus.
  • Acute bronchoalveolar murmurs.
  • Reduced intensity of heart tones.
  • Weakness.
  • Usually an audible murmur typical of mitral and / or tricuspid valve regurgitation. Due to heart rhythm disturbances (e.g. atrial fibrillation) murmurs may be soft and difficult to distinguish. DCM differs from valve regurgitation in that, as long as it does not lead to clinical symptoms of heart failure, it does not produce a clearly audible heart murmur.
  • Increased breathing and shortness of breath due to pulmonary edema. This is the result of an increase in the volume of circulating blood and an increase in pressure in the precordial vessels (heart failure with retrograde stasis occurs).
  • Dilation of the external jugular vein or positive venous pulse, hepatomegaly, ascites and hydrocephalus as a result of right ventricular failure.
  • Pulmonary creaks.
  • Hypothermia.
  • Reduced awareness.


It is the test of choice for the detection of arrhythmias and it should be performed in any patient with evidence of abnormal auscultation.

In predisposed breeds, arrhythmias are often the first observable clinical sign and should be screened.

Routine ECG testing in the office often reveals arrhythmias in dogs for whom arrhythmias are fairly common.

However, arrhythmias do not occur in all dogs with cardiomyopathy or are transient and / or rare.

In such patients, it is recommended to perform Holter testing.

Record ecg as a rule, it indicates the features of enlargement of the heart, mainly of the left one.

The most common rhythm disturbance is atrial fibrillation.

Ventricular premature beats (often found in dobermans and boxers) may also be present.

Serious suspicion of cardiomyopathy (in the case of latent phase) should be set when the following changes in the ECG record are detected:

  • the presence of one or more ventricular premature beats in boxer or doberman dogs,
  • features of left ventricular or atrial enlargement,
  • atrial fibrillation as an early symptom of the disease in Irish wolfhound dogs (in other breeds this arrhythmia usually occurs in the advanced stage of cardiomyopathy).

In the second phase of the disease may be present:

  • ventricular or supraventricular premature beats (occasional or frequent),
  • ventricular tachycardia,
  • features of left ventricular or atrial enlargement,
  • left bundle branch block.

Holter examination

Routine ECG examination in office conditions only provides information that is recorded at the time of examination of the dog, i.e in conditions unnatural for him.

If you have periodic heart rhythm disturbances during the day, these may not be detectable in your office.

Therefore, a 24-hour Holter recording in a normal environment and with the dog's normal activity makes it possible to detect arrhythmias with greater sensitivity.

Modern Holter cameras are digital recorders that record the electrical activity of the heart through 24 hours.

Some recorders have the option of recording even by 7 days.

Prepare the patient before putting on the braces.

In the places where the electrodes are attached, trim or shave the hair, wash and dry the skin.

Then special adhesive plasters are attached to these locations.

To protect the electrodes, wires and apparatus, bandage the chest.

A special vest or harness can be worn on a lightly but firmly applied headband.

These types of vests have pockets, thanks to which it is possible to stabilize the recording device.

Recording continues 24 hours.

During the Holter examination, the dog should be normally active - eat, go for walks, play, etc.

After 24 hours, the record is analyzed:

  • if the study states more than 100 ventricular premature beats occurs high probability of DCM or arrhythmogenic boxer cardiomyopathy,
  • from 50-100 ventricular premature beats may indicate an illness, however it is recommended to repeat the Holter test after 2-6 months,
  • some patients may have false-negative results - this may be the case when arrhythmias are of variable frequency; in such situations - if the Holter test does not allow for diagnosis - further Holter tests are recommended (especially in dogs with a family predisposition to DCM, as well as in those with syncope).

Holter examination is recommended especially in dogs at high risk of developing dilated cardiomyopathy (predisposed breeds, patients with a family predisposition).

It is especially recommended for the detection of the latent form of DCM in Dobermans, in which this test should be the gold standard in diagnostics.


X-ray examination

In the case of slight enlargement of the heart, X-ray examination is not very sensitive.

In Dobermans, this study is often misleading because enlargement of the heart is usually less pronounced than in dogs of other breeds with similar clinical severity.

In such a situation, it is more helpful to assess the size of the left ventricle and atrium ultrasound examination of the heart.

In boxers with arrhythmogenic cardiomyopathy (ARCV) the chest X-ray is often normal.

In the clinical phase of DCM, it is a key study to confirm the presence of congestive heart failure and to monitor response to treatment.

In the thoracic overview image, the following are in the foreground:

  • marked enlargement of the heart silhouette with rounded edges in the apex area,
  • enlargement of the left atrium,
  • features of stagnation in the pulmonary circulation.


The test is used to quantify cardiac enlargement and systolic function.

In the latent phase, this test is not particularly sensitive, but it has a great diagnostic value when the disease moves from the latent phase to the clinically overt.

In the early phase of the disease, echocardiographic findings may be normal even in the presence of ventricular arrhythmias.

For predisposed breeds (Dobermans, Irish Wolfhounds), even echocardiographic criteria have been developed, which are used to diagnose latent form of cardiomyopathy.

In boxers with ARCV, the result is usually normal.

However, as the disease progresses and the transition from asymptomatic to clinically overt echocardiography allows you to monitor cardiac enlargement, assess myocardial contractility, and identify possible mitral valve regurgitation.

Together with the X-ray examination, it allows you to decide when to start treatment.

Determination of atrial natriuretic peptide and B-type natriuretic peptide concentrations.

They are produced by the tissue of the atria and ventricles in response to the increased tension in their walls.

Concentrations natriuretic peptides are elevated in dogs with symptomatic DCM and reflect the severity of the disease.

Measurement of the level of cardiac troponin I

Troponin I it is released into the circulation as a result of damage or death of the heart muscle cells.

Its concentration increases in dogs with dilated cardiomyopathy and partially reflects the degree of left ventricular hypertrophy.

Important prognostic - dogs with troponin I in plasma > 0.20 ng / ml have a shorter survival time than those with a lower value.

A diagnosis of primary dilated cardiomyopathy should be made after excluding other conditions that may contribute to DCM-like symptoms.

This is very important as there are several disorders that can lead to the development of secondary DCM (which are treated first).

Therefore, the differential diagnosis should include:

  • heartworm,
  • pericardial diseases,
  • Osteoarthritis of the heart valves (these 3 diseases can cause heart failure similar to that associated with late stage primary dilated cardiomyopathy),
  • Hypothyroidism,
  • taurine deficiency (reported in Cocker Spaniels, Newfoundlands and Dobermans),
  • doxorubicin poisoning,
  • primary cardiac arrhythmia (e.g. permanent supraventricular tachycardia - this may be responsible for the DCM phenotype),
  • congenital conduction disturbances (e.g. additional conduction pathway) - reducing or treating arrhythmias can help restore the heart to normal.

Complications of dilated cardiomyopathy

Hypothyroidism in a dog

During moderate to severe dilated cardiomyopathy, certain systemic disorders develop, which may substantially affect the further progression of the disease.

These include, among others:


Prerenal azotaemia quite often it appears in the dogs they receive diuretics.

If it is mild (level urea in blood < 60 mg/dl and creatinine < 2,5 mg/dl) - does not require special treatment or drug dose reduction.

However, in the event that urea exceeds 80 mg / dL and creatinine 3.0 mg / dl is developing already severe azotemia, which may increase the morbidity of patients.

Therefore, doses should be reduced ACE inhibitors (angiotensin-converting enzyme - angiotensin converting enzyme) and diuretic drugs.

Periodic periods are also often recommended parenteral fluid therapy.

In patients receiving digoxin, Azotemia may increase the predisposition to poisoning with this drug.

Serum digoxin levels should be measured in them, especially if the dog has:

  • appetite disorders,
  • vomiting,
  • diarrhea,
  • frequent arrhythmias.

Electrolyte disturbances

They appear quite frequently in dogs with congestive heart failure associated with dilated cardiomyopathy.

Usually there are irregularities in the levels potassium and sodium.

Most of them are mild and do not require specific treatment.

  • Mild hypokalemia (lowering potassium levels below physiological norms) where potassium is in the range 2.5-3.0 mEq / l, it is often the result of administering high doses of diuretics to patients and does not require treatment.
  • Severe hypokalemia (potassium < 2,5 mEq/l) can cause heart rhythm disturbances and cause muscle weakness. Then it is recommended to reduce the doses of potassium "rinsing out" drugs (eg. furosemide) or the administration of potassium-sparing drugs (e.g. an ACE inhibitor, spironolactone).
  • Clinically significant hyperkalemia (increase in potassium levels above physiological norms) is rare. It is usually associated with decreased cardiac output, poor perfusion of the kidneys and renal failure.
  • Mild reduction in sodium levels (hyponatraemia) occurs frequently. This is the effect of blood thinning due to water retention in the body and an increase in plasma volume (despite the increase in total sodium in the body). It does not require specific treatment.
  • With severe hyponatraemia (sodium < 130 mEq/l) the prognosis is bad. Belongs reduce the doses of diuretics and supplement sodium in your diet.


It is quite common in middle-aged and older dogs, especially Dobermans.

Supplementing thyroid hormones does not spectacularly improve survival, but it essentially reduces the symptoms associated with it endocrinopathy, therefore, appropriate additional thyroid treatment should be given.

Interracial similarities and differences in the course of DCM

Cardiomyopathy unequal.

It is clearly visible especially in breeds strongly predisposed to its development.

Below is a brief description of the types of DCM found in each breed.

Great Dane, Irish Wolfhound and Bulmastiff cardiomyopathy

Classic dilated cardiomyopathy, affecting giant breed dogs.

Arrhythmia is common in these dogs atrial fibrillation, and the failure concerns as a rule right heart, less often the left one.

It happens more often than in other breeds decreased appetite and weight loss.

However, after starting treatment these breeds have a better prognosis than others predisposed to DCM, and dogs with congestive heart failure can live at least a year from the moment of diagnosis.

The response to treatment is also more satisfying than that of Dobermans and boxers.

Doberman cardiomyopathy

They appear frequently in Dobermans with DCM cardiac arrhythmias, and sudden cardiac death.

They usually show symptoms left-sided heart failure.

There is usually no noticeable weight loss at the outset of the disease and dogs are in good condition, however, during the course of the disease, there may be losing weight and appearing muscle atrophy.

The average survival time for congestive heart failure is 4-6 months.

Routine echocardiography and Holter examinations are recommended for all dogs of this breed, regardless of the presence of signs of heart failure.

Boxer cardiomyopathy

Dilated boxer cardiomyopathy is called the most common arrhythmogenic right ventricular cardiomyopathy (ARVC - arrhytmogenic right ventricular cardiomyopathy).

Some boxers show the typical features of DCM and develop frequently congestive heart failure.

Other individuals, on the other hand, present the correct dimensions and systolic heart rate values, yet suffer from severe ventricular arrhythmias, which in turn contributes to an increased risk of faint and sudden cardiac death.

Even in asymptomatic boxers, premature ventricular syndromes can develop, so routine echocardiography and Holter examinations are required in this breed of dog.

Cocker spaniel cardiomyopathy

The breed is more predisposed to heart valve disease.

Usually when DCM is present, the response to treatment is satisfactory.

Dilated cardiomyopathy treatment

Dilated cardiomyopathy treatment

It is used in the treatment of idiopathic dilated cardiomyopathy symptomatic treatment.

In order for it to be effective and significantly improve the clinical condition and comfort of the patient's life, it should meet the following criteria:

  1. Medications should reduce and then control cardiovascular stasis and cardiac preload.
  2. Drugs should improve the systolic function of the heart and increase its output.
  3. In the presence of arrhythmias, medications should suppress the abnormal heart rhythm.

Treatment depends on the race, condition of the patient, and the presence or absence of congestive heart failure or arrhythmias.

It should be tailored individually and the response to therapy should be regularly monitored to allow for early possible modifications.

The main groups of drugs used to treat dilated cardiomyopathy are:

  • Diuretics:
    • Furosemide - a strong loop diuretic that is routinely used in symptomatic patients. Mild azotaemia and hypokalemia may occur with prolonged use.
    • Hydrochlorothiazide, belongs to the group of thiazide diuretics. Weaker than furosemide but with a longer half-life, it also acts elsewhere and provides additional diuresis in patients already receiving loop diuretics.
    • Spironolactone  (a weak potassium-sparing diuretic), typically given in combination with a thiazide. Its effectiveness is more related to the additional anti-proliferative effect and reducing the remodeling of the heart (the so-called. remodeling) and ventricular fibrosis.

The main task of diuretics is to reduce the clinical symptoms associated with blood stasis.

  • Drugs having a positive intotropic effect. Their action is aimed at improving the contractility of the heart muscle.
    • Digoxin. It is relatively weak as a strength enhancer and is not used in an emergency. However, it is effective in abnormal heart rhythms by slowing the ventricular rate in patients with atrial fibrillation.
    • Beta-adrenergic antagonists (e.g. dopamine, dobutamine). Same as milrinone are given as a continuous infusion into a vein for emergency treatment.
    • Phosphodiesterase inhibitors (e.g. milrinone).
    • Calcium sensitizers (e.g. pimodendan). Pimodendan has a positive inotropic effect and dilates blood vessels. He is credited with a significant improvement in the quality of life and long survival.
  • Vasodilator drugs. Vein dilators reduce preload and arterial dilators reduce afterload.
    • Angiotensin converting enzyme inhibitors (ACE). In addition to reducing the activity of the renin-angiotensin-aldosterone system and the retention of water and sodium in the body, they also cause mild dilatation of the arteries. They increase the survival rate and improve the quality of life of dogs with DCM. In the presence of severe heart failure and poor renal perfusion, azotaemia may develop while taking ACEI (especially if high doses of diuretics are used concomitantly).
    • Sodium nitroprusside - it dilates the arterial and venous vessels and is very effective in life-threatening heart failure. It is given as a constant infusion and your blood pressure should be monitored regularly (risk of hypotension with this medicine).
    • Nitroglycerin. When administered topically, it minimally dilates venous vessels in dogs as it is poorly absorbed and achieves low blood levels.
  • Antiarrhythmic drugs. They are designed to suppress life-threatening arrhythmias. They slow down the ventricles in atrial fibrillation.
    • In the presence of ventricular arrhythmias, drugs of the following class are applicable:
      • In P. lidocaine, mexiletine),
      • II (beta blockers),
      • III (e.g. sotalol).
    • In atrial fibrillation, drugs from the following class are used:
      • II and IV (calcium channel blockers)
      • digoxin.
  • Beta-adrenergic blockers. They inhibit the activity of the sympathetic system (i.e. tachycardia, cardiac arrhythmias, damage to myocytes, ventricular remodeling, increased activity of the renin-angiotensin-aldosterone system). However, their excessive use may worsen congestive heart failure.
  • Inodilators - increase the contractility of the heart muscle and dilate the blood vessels:
    • Pimodendan - is an inodilator that sensitizes heart muscle cells to calcium, thanks to which it increases the heart's response to this element. Used in dogs with symptomatic disease that have already received conventional treatment.

The use of particular groups of drugs depends on the stage of the disease and the coexistence of possible complications.

Treatment of asymptomatic dilated cardiomyopathy (latent form)

Both in medicine and in veterinary medicine, the detection of most diseases at an early stage and the early introduction of treatment allows to slow down their course, which usually ensures cure, or at least extends the survival time.

Unfortunately, this is not the case with dilated cardiomyopathy

With this disease entity, there are no known treatment options that would significantly and 100% slow down the progression of the disease in its latent phase.

However, in 2009, the results of a study with Dobermans were published documenting that administration benazeproil (ACEI) significantly prolongs the asymptomatic period of the disease.

The same was true for Dobermans treated in the preclinical stage pimobendan, the administration of which also resulted in an increase in survival time.

Another study was conducted on a group of 75 Irish Greyhounds also in the asymptomatic phase of the disease.

The dogs are divided into 3 groups:

  1. Receiving pimobendan.
  2. Receiving benazepril.
  3. Receiving methyldigoxin.

It was observed that the best therapeutic effect (understood as the rarest occurrence of sudden cardiac death) was achieved with the administration of pimobendan.

Pharmacological treatment is not able to cure dogs with dilated cardiomyopathy, but it is worth considering introducing therapy already in the asymptomatic phase of DCM in order to extend the time of disease development.

Current treatment recommendations are based on the results of studies conducted in both dogs and humans.

Treatment is introduced that supports the functions of the heart.

In this phase of the disease, 3 groups of drugs are considered in the treatment:

  • ACEI,
  • spironolactone,
  • antiarrhythmic drugs - introduced in the latent phase of the disease, mainly in Dobermans and boxers.

Treatment of the clinically overt phase of dilated cardiomyopathy

  • Life-threatening treatment congestive heart failure:
    • In the case of ascites or pleural fluid, the fluid accumulated as a result of heart failure should be evacuated first. This treatment will improve the patient's breathing and comfort, as well as eliminate shortness of breath.
    • Furosemide in dose 3-8 mg / kg m.c. intravenously or intramuscularly. If the respiratory rate does not decrease and dyspnoea continues, repeat the administration after 2 hours and - if necessary - repeat. In severe renal failure, the dose of furosemide should be reduced and the drug administered less frequently.
    • Sodium nitroprusside (2-5 μg / kg m.c./ min) - it dilates vessels very effectively. Blood pressure should be monitored during its use.
    • Intravenous intotropic positive drugs, which will help increase cardiac output:
      • dopamine 2-10μg / kg m.c./ min by intravenous infusion;
      • dobutamine 5-15 μg / kg m.c./ min by intravenous infusion;
      • milrinone - a strong drug increasing the force of heart contraction, also stimulating the beta-adrenergic receptors of the heart muscle. It increases contractility in patients receiving beta blockers and in non-responders dopamine or dobutamine.
      • In situations where intravenous intotropic positive drugs cannot be used, oral administration may be beneficial pimobendan (0.25 mg / kg m.c. every 12 hours)
    • Oxygen therapy in the form of an oxygen cage or in the form of intranasal.
  • Treatment arrhythmia:
    • Premature ventricular beats and short-term attacks of ventricular tachycardia, occurring at a relatively slow heart rate () usually do not require treatment. They often resolve spontaneously after the patient has stabilized (recovery from congestive heart failure and hypoxia).
    • Sudden attacks of ventricular arrhythmias that are life-threatening and cause symptoms such as weakness, fainting, hypotension, pale mucous membranes:
      • lidocaine administered intravenously (2 mg / kg m.c. as an intravenous bolus followed by continuous intravenous infusion 40-80 μg / kg m.c./ min),
      • procainamide (6-8 mg / kg m.c. as an intravenous bolus followed by continuous intravenous infusion 20-40 μg / kg m.c./ min).
    • Sudden cardiac death is common in boxers and Dobermans, and is therefore recommended for these breeds aggressive antiarrhythmic therapy (especially with fainting). After stabilization, it is administered sotalol or connection mexiletine and atenolol.

Chronic treatment of patients after stabilization of acute heart failure

With aggressive emergency treatment during acute heart failure, improvement is seen in 75% of patients.

There is a significant improvement in comfort and breathing in the dog over time 48 hours.

If the condition does not stabilize after this time has elapsed, prognosis worsens.

After the emergency is controlled, the doses of drugs are gradually reduced, intravenous drugs are discontinued and replaced by oral drugs.

The patient's hydration, weight, appetite, breathing pattern, electrolyte levels and kidney function should be monitored.

  • Intravenous administration furosemide it stops as soon as the respiratory rate stabilizes and the shortness of breath is resolved. Is moving in oral furosemide in dose 1-2 mg / kg m.c. every 8-12 hours.
  • Slowly - on 12-24 hours feeding decreases nitroprusside and dopamine (or dobutamine) and replaces them an ACE inhibitor (enalapril 0.5 mg / kg m.c. every 12 hours or benazepril 0.5 mg / kg m.c. every 12 hours) and digoxin (0.003 mg / kg m.c. every 12 hours) or pimodendan (0.25 mg / kg m.c. every 12 hours). Sometimes - due to the risk of side effects (lack of appetite, vomiting) - the initiation of treatment with an ACE inhibitor and digoxin is introduced on different dates. In patients with atrial fibrillation, it is important to promptly introduce digoxin; after 5-7 days the ACEI is added.
  • Within 12-24 hours the dose is reduced lidocaine and procainamide. It is introduced as a placeholder sotalol (1.5-2.5 mg / kg m.c. every 12 hours) or combination mexiletine (5 mg / kg m.c. every 8 hours.) and atenolol (0.3-0.4 mg / kg m.c. every 12 hours).
  • It is recommended to limit intake sodium in the diet (40-70 mg Na / 100 kcal).

Management of refractory heart failure

Sometimes - despite the use of high doses of loop diuretics - it is not possible to properly stabilize the patient's condition.

It is then recommended to introduce additional diuretics that work in a different part of the nephron than furosemide.

  • Hydrochlorothiazide (1-4 mg / kg m.c. every 12-48 hours.) - a medium-strength diuretic with a longer half-life than furosemide. It is given initially in combination with furosemide and then gradually increased in dose.
  • Hydrochlorotiad Also available as a combined tablet with spironolactone (dose 2-4 mg / kg m.c. every 12-24 hours).

In some patients the absorption and delivery of furosemide to the kidneys may be limited.

This occurs especially in the case of right-sided heart failure or with severely reduced cardiac output.

Then replacing the tablet with the injection form may restore its effectiveness.

  • Pimobendan in dose 0.25 / kg m.c. every 12 hours often helps in the treatment of heart failure, and also increases appetite and improves well-being in patients with refractory disease.
  • In the final stages of DCM, there is often a lack of appetite and weight loss. Sometimes an introduction can help anabolic steroids for some time (stanozolol 1-2 mg per dog every 12 hours).

Treatment of dcm associated with atrial fibrillation

Atrial fibrillation is a common arrhythmia found in the advanced phase of DCM.

It usually occurs in giant dog breeds (Great Dane, Irish Wolfhound), but less often in Dobermans and boxers.

The goal of treating this arrhythmia is to slow down the ventricles.

The following drugs are used:

  • Digoxin (0.003 mg / kg m.c. every 12 hours). In most cases, it is the drug recommended in the first place because of its action to improve the contractility of the heart muscle. However, if a reduction in heart rate is not achieved after its use, it is recommended to be included in the treatment diltiazem or atonolol.
  • Diltiazem (0.5-2.0 mg / kg m.c. every 8 hours) or Diltiazem XR (1.5-4.0 mg / kg m.c. every 12 hours)
  • Atenolol (0.25 - 1.0 mg / kg m.c. every 12 hours).

A 24-hour period is recommended during treatment ECG monitoring using the Holter method.

Additional treatment

In combination with diuretic treatment, ACE inhibitors and pimobendan, in some cases, treatment with other drugs is introduced:

  • Beta-adrenergic blockers (e.g. metoprolol, carvedilol):
    • used as anti-arrhythmic drugs, but also to slow the enlargement of the heart and the progression of systolic dysfunction,
    • they are introduced in patients with clinically stable heart disease,
    • the initiation of drug administration may cause a sharp deterioration in contractility, therefore their dose should be gradually increased over 4-8 weeks,
    • it takes several months to achieve effective action, and therefore the use of these drugs in patients at the end of the disease is impractical; the best results are achieved with the introduction of these drugs in the early stages of the disease.
  • Aldosterone antagonists (spironolactone) - they have a mild diuretic effect, but the more important role is to inhibit the proliferation of aldosterone within the heart muscle and blood vessels.
  • Some breeds of dogs (e.g. American Cocker Spaniel) are deficient in amino acids:
    • addition taurine (500 mg orally every 12 hours) is recommended in dogs with low plasma levels,
    • simultaneous supplementation L-carnitine (1 g every 12 hours in cocker spaniels) is recommended in dogs deficient in taurine; its addition should also be considered in boxer dogs with left ventricular dilatation (50 mg / kg m.c. orally every 8-12 hours)
  • In case of symptoms such as: decreased appetite, weight loss, loss of muscle mass - supplement fish oil can improve the wasting condition.
  • Coenzyme Q10  and vit. E, A and C added as a supplement can improve quality of life.

Dilated cardiomyopathy prognosis

Dilated cardiomyopathy prognosis

The prognosis depends on several factors, including:

  1. From the moment of diagnosis of the disease. It has been established that the average survival time from diagnosis is approx. 6 months. The time it takes for the disease to progress from the latent phase to the symptomatic phase varies and can be as high as several years.
  2. From the stage of the disease. In the presence of congestive heart failure, the prognosis is worse, and in the presence of congestive heart failure, which cannot be controlled and controlled, death occurs.
  3. From the breed of the animal. Dobermans have the worst prognosis: the survival time from the onset of clinical symptoms is from several days to several weeks. Usually these animals they don't live a year. Some dogs (Great Danes, Cocker Spaniels, German Shepherds) respond to treatment with radical clinical improvement. The average time they survive is 1-2 years.
  4. From comorbid arrhythmias. 80% of dogs, diagnosed with atrial fibrillation die before the expiry 6 months. Some dogs (especially Dobermans and Boxers) may experience a sudden death as a result of ventricular arrhythmias


Dilated cardiomyopathy in the dog

Although many dogs manage to control symptoms for a while, there is usually not a complete cure, and most patients with DCM and congestive heart failure eventually win the disease.

The diagnosis of asymptomatic dilated cardiomyopathy remains a challenge for veterinarians.

The matter is further complicated by the fact that the image of changes in dogs is significantly influenced by breed differences.

Therefore, in predisposed breeds, routine screening is extremely important and should be introduced as the gold standard in the management of dogs at risk of developing DCM.

Annual prophylactic echocardiography in dogs from the age of two and in some breeds Holter testing may reduce the incidence of this disease.

It is worth noting that early detection of the disease is the best way to ensure a good quality of life for patients with dilated cardiomyopathy.

Currently, research is being conducted on slowing the course of DCM by means of stem cell therapy administered directly into the coronary vessels.

Although the published research results did not bring satisfactory results, it is hoped that the rapid progress of regenerative medicine may be a milestone in the future dilated cardiomyopathy in dogs.

Sources used >>

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