Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

Rottweiler Rottweiler

Dilated Cardiomyopathy

Related terms: systolic heart failure, Primary Idiopathic Myocardial Failure (PIMF), Dilative cardiomyopathy, Primary idiopathic myocardial failure, DCM

Outline: Dilated cardiomyopathy (DCM) is disease of the heart muscle in which the heart becomes thin walled and dilated. Dogs with this heart disease – which causes progressive loss of heart function and abnormalities of heart beat rhythm – often show no obvious signs for several years and then may die suddenly or after several weeks or months due to progressive heart failure. Inadequate blood circulation results in fluid build up in the lungs or other parts of the body and can cause chronic malaise whose nature depends upon which parts of the body are affected. There is no genetic test but the disease can be detected in the early stages using ultrasound or 24 hour electrocardiographic monitoring. Breeding from affected dogs will perpetuate the problem.


Summary of Information

(for more information click on the links below)

1. Brief description

Dilated cardiomyopathy (DCM) is a disease of the heart muscle in which the heart becomes thin walled and dilated. There are two common, important consequences of this for the affected dog: first, it will experience congestive heart failure which leads to a build up of fluid in the body, especially the lungs, and second, it will show dysrhythmias (abnormal heart beats) which may result in its sudden death due to inadequate blood circulation (Martin et al 2010).

Rottweilers with heart disease may live for several years without heart failure. These dogs are likely to appear normal to their owners and have no welfare problems, but heart disease can be detected through electrocardiography (ECG) using a portable device, called a Holter monitor, strapped to the dog which records the electrical activity of the heart over an extended period of time.

The most powerful tool for examining the structure and function of the heart is ultrasonography. This enables measurement of the thickness of the heart muscle, the size of each of its chambers and the position and movement of each its valves.

The reason why some Rottweilers develop DCM is unknown. Genetic factors are likely to be important but the mechanism is unclear. Heart muscle cells have a reduced capacity to contract adequately but whether this is due to a defect in the cell structure, the proteins that make up the contractile apparatus, or in the cellular components that provide energy for contraction is not known (O’Brien et al 1992, O’Brien 1997, Meurs et al 2001, Spier et al 2001).

2. Intensity of welfare impact   

Rottweilers with DCM generally have a long period of subclinical disease during which there are no (or only slight) welfare problems. This subclinical phase typically lasts from the age of two to six years. If examined with ultrasound or by Holter ECG testing during this period the changes in heart structure and function associated with DCM can be detected but there are no other clinical signs at this time. Subsequently, dysrhythmia in affected dogs typically leads to episodes of weakness or collapse and/or sudden death. Some may go into congestive (backwards) heart failure from which survival for more than a few months is unusual. The time until death in these dogs is unpleasant due to fluid build up in the lungs which makes breathing laboured and difficult. It has been likened to slowly drowning. The affected dog is often euthanased at an earlier stage in this process because of this, to prevent further suffering.

3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span in affected Rottweilers. The duration of suffering for those dogs with the disease may be very short, with apparently healthy animals affected by the disease dying suddenly due to dysrhythmia. It can be much longer – weeks or months – in cases in which there is progressive congestive heart failure. A study has shown that the mean survival time after presentation of dogs of all breeds with DCM at a cardiorespiratory referral centre was 19 weeks (Martin et al 2009).

4. Number of animals affected

Rottweilers are frequently diagnosed with DCM (Borgarelli et al 2006, Petric & Tomsic 2008) but the number of Rottweilers affected with DCM is not known.

5. Diagnosis

Dilated cardiomyopathycan be diagnosed using ultrasound examination. Occult disease (the hidden form in which there are heart abnormalities but clinical signs have yet to become apparent) can also be detected using 24-hour Holter ECG monitoring. Currently there are no genetic tests for the disease available in the Rottweiler.

6. Genetics

The genetics of DCM in Rottweilers are unknown but in other breeds of dogs the condition has an autosomal dominant pattern of inheritance with incomplete penetration. This means that all dogs with at least one copy of the mutant gene have a tendency to be affected but the severity of the disease varies due to other genetic and environmental factors.

7. How do you know if an animal is a carrier or likely to become affected?

There are currently no genetic tests for DCMas the gene or genes involved in the disease have not been determined in this breed. If this is an autosomal dominant condition, as is suspected, then it is likely that there are no silent carriers (ie animals that are unaffected themselves but which can pass it on to their offspring) – any individual with at least one copy of the mutant gene(s) are prone to develop the disease and can pass it on to their offspring.

The only way to determine if an apparently normal dog is likely to develop clinical DCM, is by detection of heart abnormalities. The most sensitive methods for this are ultrasound examination and 24-hour Holter ECG monitoring.

8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no formal breeding schemes in operation which aim to reduce or eliminate this condition from the Rottweiler breed. A genetic test would be very valuable as this would enable the detection and removal of affected individuals from the breeding pool.

Animals that have clinical DCM will not be suitable for breeding. Animals with occult DCM (the early stage of the disease before it causes clinical signs) may be capable of breeding but ideally should not be used as this would perpetuate the problem.


For further details about this condition, please click on the following:
(these link to items down this page)


1. Clinical and pathological effects

Dilated cardiomyopathy (DCM) is disease of the heart muscle in which the heart becomes thin walled and dilated. There are two common, important consequences of this for the affected dog: firstly, it will experience congestive heart failure which leads to a build up of fluid in the body, especially the lungs, and secondly, it will show dysrhythmias (abnormal heart beats) which may result in its sudden death due to inadequate blood circulation (Martin et al 2010).

The heart is a four-chambered pump which is divided into left and right sides. Each side has two chambers: blood enters into the thin-walled upper chamber (atrium). It then flows into the larger, lower chamber (ventricle). The ventricles have thick walls composed largely of heart muscle. Between the chambers of the atria and the ventricles there are valves that prevent blood flowing backwards from the latter to the former. On contraction, blood flows from the ventricles into the major blood vessels. There are also valves at the junction of the ventricles and these blood vessels that preventing blood flowing backwards.

Dilated Cardiomyopathy figure 1

Figure 1. The four chambers of the heart and direction of blood flow. Note the four valves, which in a normal healthy heart prevent the backflow of blood. (Image property of The Cardiomyopathy Association to whom we are grateful for permission for its reproduction here).

The right side of the heart receives blood from the whole of the body other than the lungs, via the venae cavae. The blood accumulates in the right atrium and during a heart beat it is sucked past the tricuspid valve into the right ventricle and then as the right ventricle contracts (squeezes) its muscular wall, the blood is pushed through the pulmonary valves into the pulmonary arteries that take it onto the lungs (to take up oxygen).

The left side of the heart receives this oxygenated blood from the lungs, via the pulmonary veins. The blood accumulates in the left atrium and during a heart beat it is sucked past the mitral valve into the left ventricle. Then, as the muscular wall of the left ventricle contracts, the blood is pushed through the aortic valves into the aorta and onto the other major arteries which carry it around the body to perform all the functions of blood circulation such as delivering oxygen and nutrients and sharing heat and metabolic products throughout the body. The part of the heart’s relaxation and contraction cycle (that together make up the ‘heart beat’) when contraction (squeezing of blood) is occurring is referred to as systole and the relaxation phase is called diastole.

So, the left hand side of the heart has to pump blood around the major organs of the body, whilst the right hand side only has to push blood through the adjacent lungs. This difference does not affect the structure and function of the atria very much but requires that the muscles of the left ventricle have to be much stronger than the right. As strength is largely a function of muscle size the muscle wall of the left ventricle is thicker than the right.

To co-ordinate the contractions of the different parts of the heart’s muscle there is a pathway for coordinating nerve impulses. These can be disrupted by damage to the heart muscle tissues through which they run. In dilated cardiomyopathy (DCM) the heart changes shape. It becomes generally larger, the chambers have a greater volume and the muscle walls are thinned.

Dilated Cardiomyopathy figure 2

Figure 2. In a normal healthy heart, nerve signals travel through the heart muscle to stimulate coordinated contractions. However if the muscle tissue becomes thinner, as occurs in dilated cardiomyopathy, the nerve signals are disrupted leading to a variety of detrimental effects (see below). (Image property of The Cardiomyopathy Association to whom we are grateful for permission for its reproduction here).

These changes lead to various ‘knock on’ problems which, at some stage prevent the heart from functioning normally. Exactly what happens in an individual depends on which parts dilate, how fast and to what degree, whether or not the valves are affected, and the degree to which conduction of heart beat signals are interfered with. The consequences of various manifestations of the disease are outlined below.

  1. The thin heart wall contracts poorly so the heart may fail to empty. This causes a backflow problem so that blood cannot enter the heart normally. This is backward or congestive heart failure. When the left side of the heart is affected, the result is fluid build up in the lungs (pulmonary oedema) and this is the usual problem in Rottweilers with DCM. When the right side is affected, the fluid builds up in the body and usually shows as fluid accumulating in the chest cavity (pleural fluid), the abdomen (ascites) or in the body tissues generally (oedema).
  2. As the heart shape changes the valves can become distorted and leak. When the valves, the tricuspid and mitral valves, between the ventricles and atria are affected, they may allow blood to flow backwards into the atria during contraction which causes further backwards (back pressure) heart failure problems and the problems, outline above, associated with this.
  3. The abnormal muscle often contains scar tissue or fatty infiltrates which interfere with the conduction of nerve signals through the heart resulting in uncoordinated contractions (dysrhythmia or arrhythmia). Irregular heart beats can contribute to both forward and backward heart failure. Forwards heart failure occurs when the left ventricle provides inadequate blood flow to the body and this can lead to weakness, collapse, fainting and sudden death. In DCM the weakness of the heart muscle also contributes to forward heart failure.

Dilated Cardiomyopathy figure 3

Figure 3. In cases of dilated cardiomyopathy, the ventricles dilate and become larger, and the cardiac muscle surrounding them becomes thinner causing the heart to change shape. This in turn impedes the muscle contraction and effectiveness of the valves, which can lead to irregular heartbeats and the backflow of blood (labelled mitral regurgitation in Figure 3), leading to further complications such as a build up of fluid in the lungs or the rest of the body. (Image property of The Cardiomyopathy Association to whom we are grateful for permission for its reproduction here).

Dysrhythmia may occur when a dog with occult DCM is anaesthetised (Calvert et al 2004).

The body is able to compensate, to some extent, for impending heart failure using various mechanisms although some of these can themselves lead to further problems.

When there is inadequate blood flow from the heart, heart rate is increased so that blood supply to the organs is maintained. However, this raised heart rate may further restrict the ability of the ventricles to relax as there is less time between each contraction; time in which the ventricles can relax and fill. Increasing heart rate can cause backward heart failure to worsen and eventually the amount of blood that the heart can push forwards around the body also decreases. A further problem is that it is during relaxation that the heart muscle itself receives blood via its coronary arteries so when beating quickly its own oxygen supply can decrease and heart muscle can die.

Inadequate blood flow from the heart also causes the body to react as though there has been a loss of circulating blood volume. Hormones are released in response, which cause fluid to be retained even though there actually has been no loss of blood. The amount of fluid in the body thus increases and this is one of the reasons that fluid accumulates in the lungs (pulmonary oedema) or elsewhere in the body (pleural fluid or oedema).

Dogs with heart disease, but without heart failure, will very likely appear normal to their owners and will not have any welfare problems at that time. An owner might be able to detect a fast and abnormally strong heart beat if feeling their dog’s chest. Similarly, a veterinary surgeon may notice a high heart rate or pulse rate when examining a dog. The heart rate is measured by feeling the heart beat, or, more usually, listening to the heart beating using a stethoscope. The pulse rate is measured by feeling the pulsing of blood flowing through a major artery. In dogs it is usually the femoral artery in the upper inside leg that is felt. In a normal individual the heart rate and pulse rate will be the same – each heart beat produces a pulse; but this is not always the case with heart failure – sometimes an ineffectual heart beat occurs that does not generate a pulse that can be detected. This is called a pulse deficit.

Examination with a stethoscope may reveal a heart murmur. This is often the way in which the disease is first detected. Murmurs are caused by abnormally turbulent blood flow. They usually indicate the presence of a structural abnormality of the heart, for example, in DCM they may be caused by an abnormal valve allowing backflow of blood.

On detection of a murmur, further investigations should be carried out to find their cause and to determine the health of the heart. Another change that a veterinary surgeon may detect when listening to a dog’s heart is a “gallop rhythm” (dysrhythmia). Normally a heart beat has two sounds, “lub – dub”. With a, so-called, gallop rhythm three sounds are heard and this is a reliable indication that heart disease is present.

Other signs of heart disease (before it becomes apparent due to heart failure) can only be detected using more sophisticated equipment. Radiographs (x-rays) of the chest may show evidence of heart enlargement but this is a relatively crude method. (chest radiographs are very useful for detecting common signs of heart failure – see below). A disadvantage of chest radiographs is the need for heavy sedation or a general anaesthetic.

Electrocardiography (ECG) to record the electrical activity of the heart as it beats is carried out in dogs without sedation or anaesthesia and can provide information about the presence of heart disease (or of heart failure). Some individuals may have irregular heart beats on occasions whilst being normal most of the time. These dogs experience fainting episodes during the periods of irregularity but when being examined in the veterinary surgery may appear completely normal. Normal ECGs record the electrical activity for a few minutes only and can miss problems that occur infrequently despite these problems possibly being very significant when they do happen (Wess et al 2010b). Such intermittent problems can be detected using a device that records ECG over an extended period (a Holter monitor).

The most powerful tool for examining the heart is ultrasonography. This enables measurement of the thickness of the heart muscle; the size of each chamber, and the position and movement of each valve. With colour-flow ultrasonography it is also possible to measure the speed and direction of blood flow in the heart and the great vessels.

The reason why some Rottweilers develop this disease is not known. Genetic factors are certainly very important but the mechanism is unclear. Heart muscle cells have a reduced capacity to contract adequately but whether this is due to a defect in the cell structure, the proteins that make up the contractile apparatus, or in the cellular components that provide energy for contraction is unclear (O’Brien et al 1992, O’Brien 1997, Meurs et al 2001, Spier et al 2001)

DCM can also occur for other reasons including: nutritional deficiencies, drug side effects, viral infection and possibly hormonal imbalance, and autoimmune disease (Calvert & Meurs 2000, Rishniw 2004, Buse et al 2008).

When heart tissue affected by DCM is examined post-mortem under the microscope two distinctive forms can be distinguished: (i) a fatty infiltration-degenerative type and (ii) an attenuated wavy fibre type – in which heart muscle cells are deformed. It is not possible to determine which type of disease is present in an individual dog prior to death (Tidholm et al 2001).

Return to top

2. Intensity of welfare impact

Rottweilers with DCM generally have a long period of subclinical disease during which there are no (or only slight) welfare problems. This subclinical phase typically lasts from the age of two to six years. If examined with ultrasound or by Holter ECG testing during this period the changes in heart structure and function associated with DCM can be detected but there are no other clinical signs at this time Subsequently, they typically then go on to experience dysrhythmias or congestive (backwards) heart failure.

Some dogs die in hours to days from congestive heart failure that does not respond to treatment and survival for more than a few months is unusual. Usually Rottweilers with DCM develop left-sided congestive heart failure (affecting the left side of the heart most). This leads to fluid building up in their lungs which makes breathing difficult. It also causes coughing. As this fluid accumulates, breathing becomes an ever increasing struggle and the dog effectively dies from drowning in its own body fluids. This is a severe welfare problem although the affected dog is often euthanased at an earlier stage in this process.

Dysrhythmias may cause or contribute to congestive heart failure occurring and the welfare implication described above. They also directly cause welfare problems by making the dog feel ill, faint or collapse and lead to its sudden death.

Investigations for heart failure and treatments may also cause welfare issues related to travel to and from veterinary practices, hospitalisations and medications; for example heart medications may cause gastrointestinal disease.

Return to top

3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span in affected animals. The duration of suffering for those dogs with the disease may be very short, with apparently healthy animals affected by the disease dying suddenly due to dysrhythmia. The mean survival time after presentation of dogs of all breeds with DCM at a cardiorespiratory referral centre was 19 weeks in one study (Martin et al 2009); although, as a result of advances in treatment some dogs may survive for a year or two (Tidholm et al 1997, Luis Fuentes et al 2002, O’Grady et al 2008). Another study suggested dogs that develop signs at a younger age tend to deteriorate more rapidly (Tidholm et al 1997) but this was not confirmed in a more recent study (Martin et al 2010).

Return to top

4. Number of animals affected

Rottweilers are frequently diagnosed with DCM (Borgarelli et al 2006, Petric & Tomsic 2008) but,  is far as we are aware, there are no data on the proportion affected.

Return to top

5. Diagnosis

Dilated cardiomyopathyis usually diagnosed by ultrasound examination although the diagnosis may be supported by findings from other cardiological examinations – physical examination, radiography of the chest and ECG (Dukes-McEwan et al 2003).

ECG can be used to detect occult disease (eg heart rhythm abnormalities at a stage before animals show any clinical signs) but short-term recordings are less sensitive than 24-hour Holter monitoring (Wess et al 2010b). Holter monitoring is not available directly at most practices. It is available at specialist cardiac veterinary practices and Holter monitoring equipment can be hired via any veterinary practice (www.holtermonitoring.co.uk). The stage of disease can be estimated from the results of 24-hour Holter monitoring, physical examination and chest radiographs.

Currently there are no genetic tests available for detection of affected animals in this breed.

Return to top

6. Genetics

The genetics of DCM in Rottweilers are unknown but in other breeds of dogs the condition has an autosomal dominant pattern of inheritance with incomplete penetration. This means that all dogs with at least one copy of the mutant gene have a tendency to be affected but that severity depends on other genetic and environmental factors.

Return to top

7. How do you know if an animal is a carrier or likely to become affected?

There are currently no genetic tests for DCM as the gene or genes involved in the disease have not been determined. If DCM in Rottweilers is an autosomal dominant condition, as is suspected, then there will be no actual carriers (ie animals that are unaffected themselves but which can pass it on to their offspring) – any individuals with at least one copy of the mutant gene are prone to developing the disease and can pass it on to their offspring.

The only way to determine if an apparently normal dog is likely to develop clinical DCM, is by detection of heart abnormalities. The most sensitive methods for this are ultrasound examination and 24-hour Holter ECG monitoring (see above). Annual screening of all dogs from 2 years old is recommended in other breeds and is to be advised in Rottweilers as well (Wess et al 2010a).

Return to top

8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no formal breeding schemes in operation to reduce or eliminate this common condition from the Rottweiler breed. In the absence of a genetic test any scheme would have to be based on detection of affected animals by veterinary cardiologists. The age of onset of disease and its severity do vary between affected individuals and the detection of more mildly affected animals that are yet to develop clinical disease may well be important but is currently difficult.

Animals that have clinical DCM will not be suitable for breeding. Animals with occult DCM (the disease in its early stages before it causes clinical signs) may be capable of breeding but ideally should not be used as this would perpetuate the problem.

Return to top

9. Acknowledgements

UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section and to Stephanie Kaufman for assistance in illustrating it.

Return to top

10. References

Borgarelli M, Santilli RA, Chiavegata D, D'Agnolo G, Zanatta R, Mannelli A and Tarducci A (2006) Prognostic indicators for dogs with dilated cardiomyopathy. Journal of Veterinary Internal Medicine 20: 104-10

Buse C, Altmann F, Amann B, Hauck SM, Poulsen Nautrup C, Ueffing M, Stangassinger M and Deeg CA (2008) Discovering novel targets for autoantibodies in dilated cardiomyopathy. Electrophoresis 29: 1325–1332

Calvert CA and Meurs KM (2000) CVT update: Doberman pinscher occult cardiomyopathy. In: Kirk’s Current Veterinary Therapy XIII editor JD Bonagura, WB Saunders, Philadelphia. pp 756

Calvert CA, Jacobs GJ, and Pickus CW (2004) Unfavorable influence of anesthesia and surgery on Doberman pinschers with occult cardiomyopathy. Journal of the American Animal Hospital Association 32: 57-62

Dukes-McEwan J, Borgarelli M, Tidholm A, Vollmar AC, Häggström J and The ESVC Taskforce for Canine Dilated Cardiomyopathy (2003) Proposed Guidelines for the Diagnosis of Canine Idiopathic Dilated Cardiomyopathy. Journal of Veterinary Cardiology 5: 7-19

Luis Fuentes V, Corcoran B, French A, Schober KE, Kleemann R and Justus C (2002) A double-blind, randomized, placebo-controlled study of pimobendan in dogs with dilated cardiomyopathy. Journal of Veterinary Internal Medicine 16: 255-261

Martin MWS, Stafford Johnson MJ and Celona B (2009) Canine dilated cardiomyopathy: a retrospective study of signalment, presentation and clinical findings in 369 cases. Journal of Small Animal Practice 50: 23–29

Martin MWS, Stafford Johnson MJ, Strehlau G and King JN (2010) Canine dilated cardiomyopathy: a retrospective study of prognostic findings in 367 clinical cases. Journal of Small Animal Practice 51: 428–436

Meurs KM, Magnon AL, Spier AW, Miller MW, Lehmkuhl LB and Towbin JA (2001) Evaluation of the cardiac actin gene in Doberman Pinschers with dilated cardiomyopathy. American Journal of Veterinary Research 62: 33-36

O'Brien PJ (1997) Deficiencies of myocardial troponin-T and creatine kinase MB isoenzyme in dogs with idiopathic dilated cardiomyopathy. American Journal of Veterinary Research 58: 11-16

O'Brien PJ, O'Grady M, McCutcheon LJ, Shen H, Nowack L, Horne RD, Julian RJ, Grima EA, Moe GW et al 1992 Myocardial myoglobin deficiency in various animal models of congestive heart failure. Journal of Molecular and Cell Cardiology 24: 721-730

Petric AD and Tomsic K (2008) Diagnostic methods of cardiomyopathy in dogs - old and new perspectives and methods. Slovenian Veterinary Research 45: 5-14

O'Grady M, Minors S, O'Sullivan M and Horne R (2008) Effect of Pimobendan on Case Fatality Rate in Doberman Pinschers with Congestive Heart Failure Caused by Dilated Cardiomyopathy. Journal of Veterinary Internal Medicine 22: 897–904

Rishniw (2004) Systolic myocardial failure. VIN Associate accessed 3.11.2010

Spier AW, Meurs KM, Coovert DD, Lehmkuhl LB, O'Grady MR, Freeman LM, Burghes AH and Towbin JA (2001) Use of Western immunoblot for evaluation of myocardial dystrophin, alpha-sarcoglycan, and beta-dystroglycan in dogs with idiopathic dilated cardiomyopathy. American Journal of Veterinary Research 62: 67-71

Tidholm A, Svensson H and Sylven C (1997) Survival and prognostic factors in 189 dogs with dilated cardiomyopathy. Journal of the American Animal Hospital Association 33: 364-368

Tidholm A, Haggstrom J, Borgarelli M and Tarducci A (2001) Canine idiopathic dilated cardiomyopathy. Part I: Aetiology, clinical characteristics, epidemiology and pathology. Veterinary Journal 162: 92-107

Wess G, Schulze A, Butz V, Simak J, Killich M, Keller L, Maeurer J and Hartmann K (2010a) Prevalence of Dilated Cardiomyopathy in Doberman Pinschers in Various Age Groups. Journal of Veterinary Internal Medicine 24: 533–538

Wess G, Schulze A, Geraghty N and Hartmann K (2010b) Ability of a 5-Minute Electrocardiography (ECG) for Predicting Arrhythmias in Doberman Pinschers with Cardiomyopathy in Comparison with a 24-Hour Ambulatory ECG. Journal of Veterinary Internal Medicine 24: 367–371

© UFAW 2011


Credit for main photo above:

By rostdi (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html), CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/) or CC-BY-2.5 (http://creativecommons.org/licenses/by/2.5)], via Wikimedia Commons