Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

Great Dane 

Great Dane

Dilated Cardiomyopathy (DCM)

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: firstly, it will experience congestive heart failure which leads to a build up of fluid in the body and, secondly, it will show dysrhythmia (abnormal heart beat) which may result in its sudden death due to inadequate blood circulation (Martin et al 2010). Great Danes often also have atrial fibrillation, an electrical defect of the heart (Meurs et al 2001a, Menaut et al 2005, Martin et al 2009).

Great Danes with heart disease, but without heart failure, are likely to appear normal to their owners and will not have any welfare problems at that time. Heart disease can be detected through electrocardiography (ECG) which records the electrical activity of the heart as it beats. The presence of atrial fibrillation (AF, see above) on ECG is the usual sign of the disease in Great Danes (Menaut et al 2005).

The most powerful tool for examining the heart is ultrasonography (Vollmar 1999). 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. With colour-flow ultrasonography it is also possible to measure the speed and direction of blood flow in the heart and the great vessels.

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

2. Intensity of welfare impact

Great Danes with DCM generally have a period of subclinical disease during which there are no (or only slight) welfare problems. If examined with ultrasound or by 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 dysrhythmia 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 Great Danes with DCM develop a build up of fluid in the lungs (Meurs et al 2001a).  Heart failure also causes coughing. As this fluid accumulates, breathing becomes an 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 to avoid this suffering.

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.

3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span in affected dogs. 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). However, on average, Great Danes live only 5 weeks after developing signs of heart failure due to DCM (Martin et al 2010). It is likely that these dogs will be suffering to some extent during this period.

4. Number of animals affected

The Great Dane is one of the breeds of dog most commonly affected by DCM (Monnet et al 1995, Domanjko Petric et al 2002, Borgarelli et al 2006, Martin et al 2009). It has been established that there is a familial tendency and a genetic predisposition to DCM in Great Danes (Meurs et al 2001a). Great Danes had the third highest death rate from heart disease of all breeds of dog according to a Swedish survey of insured pedigree dogs (Egenvall et al 2006). Although there was no discrimination between different types of heart disease in this study it is likely that DCM was the main reason for this high rate of death.

5. Diagnosis

DCM is usually diagnosed by ultrasound examination but the diagnosis may be supported by findings from other cardiological examinations – physical examination, radiography of the chest and ECG (Vollmar 1999, Dukes-McEwan et al 2003).

ECG can be used to detect occult disease (eg heart rhythm abnormalities at a stage before the animal shows any clinical signs) (Menaut et al 2005).

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

6. Genetics

DCM in great Danes was thought to be a recessive X-linked condition (Meurs et al 2001a), which means that the mutant gene causing the disease is found on the X chromosome, of which male animals only have one. However, the specific genes responsible have not yet been determined and the genetic basis may not be simple.

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 have not been determined. If it was found to be an X-linked disease then there would be female carriers – that is females, who have two X chromosomes to males one, may be able to pass on the disease to offspring without developing the disease themselves.

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 ECG.

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 this breed, but the American breed society suggested that breeding animals should be examined by a cardiologist every two years and used for breeding only if there is no evidence of heart disease (http://www.gdca.org/health/cardio.htm). An informal scheme is operated at the UK’s University of Liverpool veterinary school, for examination to confirm whether or not older dogs are free of DCM (http://www.liv.ac.uk/sath/services/cardiology.htm). This is associated with the LUPA project to detect genes associated with the condition: http://www.eurolupa.org/index.php?option=com_content&view=article&id=21%3Abreeds-and-diseases-researched&catid=5%3Aveterinarians&Itemid=22&lang=en.

In the absence of a genetic test, any scheme to reduce the prevalence of this disease would have to be based on detection of affected animals by veterinary cardiologists.  

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

Since the disease is so common in Great Danes, there is concern that excluding all affected individuals from the breeding pool might limit the size of the breeding population to the extent that the risk of other genetic defects (of which several are known) might be significantly increased. Such problems could be avoided by out-breeding with dogs of other breeds unaffected by DCM.

 

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


1. Clinical and pathological effects

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 around the lungs (Vollmar 1999), and secondly, it will show dysrhythmia (abnormal heart beat) 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

The heart changes shape in animals with dilated cardiomyopathy. It becomes generally larger, the chambers have a greater volume and the muscle walls are thinned.

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). When the right side is affected, the fluid builds up in the body and usually shows as fluid accumulating in 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 resulting in uncoordinated contractions (dysrhythmia or arrhythmia). Irregular heart beats can contribute to both forward and backward heart failure (Calvert et al 2007). 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 2

Figure 2. 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 2), 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).

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 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 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 murmurs 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 is a “gallop rhythm” (dysrhythmia). Normally a heart beat has two sounds, “lub – dub”. Where there is a 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.

One of the other problems that Great Danes commonly have, which is a marker for DCM and heart failure, is atrial fibrillation, in which there is abnormal electrical activity in the atria of the heart that causes problems with how it contracts (Meurs et al 2001a, Menaut et al 2005, Martin et al 2009). Normally an electronic impulse starts in an area of the upper heart called the sinoatrial node and spreads out in a controlled manner causing the various parts of the heart to contract. First the atria contract and then the impulse travels down to the ventricles causing them to contract. The process can be disrupted by disease at any point in the pathway, or if, as a result of disease, an impulse is generated elsewhere in the heart. All areas of the heart muscle have the capacity to act as a pacemaker and to generate electric pulses which can stimulate local muscle and which may spread around the heart. However, if this occurs, the heart is likely to contract abnormally and may fail to work properly as a pump, in which case either forward or backward heart failure (or both) may occur.

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). The presence of atrial fibrillation (see above) is the usual sign of DCM in Great Danes (Menaut et al 2005).

The most powerful tool for examining the heart is ultrasonography (Vollmar 1999). 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 Great Danes develop this disease is not fully understood but it is likely that genetic factors are important. Affected 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 2001b, Spier et al 2001) and the specific genes responsible have not yet been found.

Dogs can also be affected for other reasons including: nutritional deficiencies, drug side effects, viral infection and possibly hormonal imbalance, and autoimmune disease (Calvert & Meurs 2000, Rishniw 2004, Vollmar et al 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 but type ii is more common in Great Danes (Tidholm et al 2001).

Male Great Danes are more likely to be affected with DCM than females (Meurs et al 2001a, Martin et al 2009).

Return to top

2. Intensity of welfare impact

Great Danes with DCM generally have a period of subclinical disease during which there are no (or only slight) welfare problems. If examined with ultrasound or by 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 develop dysrhythmia (irregular heart beat) 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, in Great Danes with DCM fluid builds up in the lungs (Meurs et al 2001a). This causes coughing. As the 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 euthanised at an earlier stage in this process to prevent further suffering.

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 into and treatments of heart failure may also have adverse welfare effects related to travel to and from veterinary practices, hospitalisations and the side effects of medications – for example, medications may cause gastrointestinal disease.

Return to top

3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span. The mean survival time after presentation of dogs of all breeds with DCM at one cardiorespiratory referral centre was found to be 19 weeks. However survival time averaged only 5 weeks in Great Danes and with a maximum survival time of 39 weeks (Martin et al 2009, 2010). It is likely that the dogs will be suffering to some extent during this period.

Return to top

4. Number of animals affected

The Great Dane is one of the breeds most commonly affected by DCM (Monnet et al 1995, Domanjko Petric et al 2002, Borgarelli et al 2006, Martin et al 2009), although we are unaware of data on its prevalence. It has been established that there is a familial tendency and a genetic predisposition to DCM in Great Danes (Meurs et al 2001a). Great Danes were found to have the third highest death rate from heart disease of all breeds of dog in a Swedish survey of insured pedigree dogs (Egenvall et al 2006). Although this study did not differentiate between different types of heart disease, it is likely that DCM was the main reason for this for this high rate of death.

Return to top

5. Diagnosis

DCM is 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 (Vollmar 1999, Dukes-McEwan et al 2003).

ECG can be used to detect occult disease (eg heart rhythm abnormalities at a stage before the animal shows any clinical signs) (Menaut et al 2005).

Currently there are no genetic tests available.

Return to top

6. Genetics

DCM in great Danes was thought to be a recessive X-linked condition (Meurs et al 2001a), which means that the mutant gene causing the disease is found on the X chromosome, of which male animals only have one. However, the specific genes responsible have not yet been determined and the genetic basis may not be simple (Skelly 2003, Herbst 2007).

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. The gene or genes involved have not been determined. It has been suspected to be an X-linked disease – ie the genes responsible may be on the X chromosome (of which females have two and males one) – and if this proves to be the case then females may be able to carry the disease and pass it to their offspring without developing the disease themselves.

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 ECG.

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 this breed but the American breed society has suggested that breeding animals should be examined by a cardiologist every two years and used for breeding only if there is no evidence of heart disease (http://www.gdca.org/health/cardio.htm). An informal scheme is operated at the UK’s University of Liverpool veterinary school to examine older dogs to confirm whether or not they are free of the disease (http://www.liv.ac.uk/sath/services/cardiology.htm). This is associated with the LUPA project aimed at determining the genes associated with the condition (http://www.eurolupa.org/index.php?option=com_content&view=article&id=21%3Abreeds-and-diseases-researched&catid=5%3Aveterinarians&Itemid=22&lang=en).

In the absence of a genetic test, any scheme to reduce the prevalence of the disease would have to be based on detection of affected animals by veterinary cardiologists.

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

Since the disease is so common in Great Danes, there is concern that excluding all affected individuals from the breeding pool might limit the size of the breeding population to the extent that the risk of other genetic defects (of which several are known) might be significantly increased. Such problems could be avoided by out-breeding with dogs of other breeds unaffected by DCM.

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, Chiavegato D, D’Agnolo G, Zanatta R, Mannelli A and Tarducci A (2006) Prognostic Indicators for Dogs with Dilated Cardiomyopathy. Journal of Veterinary Internernal Medicine 20: 104–110

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

Calvert CA, Hall G, Jacobs G and Pickus C (1997) Clinical and pathologic findings in Doberman pinschers with occult cardiomyopathy that died suddenly or developed congestive heart failure: 54 cases (1984-1991). Journal of the American Veterinary Medical Association 210: 505-11

Domanjko Petric A, Stabej P and Zemva A (2002) Dilated cardiomyopathy in Doberman pinschers, survival, causes of death and pedigree review in a related line. Journal of Veterinary Cardiology 4: 17-24

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

Egenvall A, Bonnett BN and Haggström J (2006) Heart Disease as a Cause of Death in Insured Swedish Dogs Younger Than 10 Years of Age. Journal of Veterinary Internal Medicine 20: 894–903

Herbst SM (2007) Genetic analysis of dilated cardiomyopathy in the great dane. PhD thesis. http://repository.tamu.edu/bitstream/handle/1969.1/ETD-TAMU-2515/HERBST-DISSERTATION.pdf?sequence=1 accessed 28.6.2011

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

Menaut P, Belanger MC, Beauchamp G, Ponzio NM and Moise NS (2005) Atrial fibrillation in dogs with and without structural or functional cardiac disease: A retrospective study of 109 cases. Journal of Veterinary Cardiology 7: 75-83

Meurs KM, Miller MW and Wright NA (2001a) Clinical features of dilated cardiomyopathy in Great Danes and results of a pedigree analysis: 17 cases (1990-2000). Journal of the American Veterinary Medicine Association 218: 729-732

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

Monnet E, Orton EC, Salman M and Boon J (1995) Idiopathic dilated cardiomyopathy in dogs: survival and prognostic indicators. Journal of Veterinary Internal Medicine 9: 12–17

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-

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

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

Skelly B (2003) Towards a molecular test for dilated cardiomyopathy in great danes. Journal of Small Animal Practice 44: 196-197

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, 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

Vollmar AC (1999) Use of echocardiography in the diagnosis of dilated cardiomyopathy in Irish wolfhounds. Journal of the American Animal Hospital Association 35: 279-283

Vollmar A, Fox PR, Keene BW, Biorge V, Distl O and Broschk C (2004) Heart screening results of more than 1000 Irish Wolfhounds: Prevalence of DCM, survival characteristics, whole blood taurine & DCM inheritance. http://www.eiwc.org/pdf/Heart_Problems_DCM.pdf; accessed 24/06/2011.

http://www.gdca.org/health/cardio.htm accessed 28.6.2011

http://www.eurolupa.org/index.php?option=com_content&view=article&id=21%3Abreeds-and-diseases-researched&catid=5%3Aveterinarians&Itemid=22&lang=en accessed 28.6.2011

© UFAW 2011


Credit for main photo above:

By Fainomenon (Own work) [CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0)], via Wikimedia Commons