Genetic Welfare Problems of Companion Animals

 

Newfoundland

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. About 10% of Newfoundlands develop DCM. Dogs with this heart disease – which causes progressive loss of heart function and abnormalities of heart 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.

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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, especially in the lungs (Dukes-McEwan 2000), and, secondly, it will develop dysrhythmia (abnormal heart beat) which may result in its sudden death due to inadequate blood circulation (Martin et al 2010). Newfoundlands often also have atrial fibrillation, an electrical defect of the heart (Dukes-McEwan 2000).

Newfoundlands 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) on ECG is the usual sign of the disease in Newfoundlands (Dukes-McEwan 2000).

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.

2. Intensity of welfare impact

Newfoundlands with DCM generally have a period of subclinical disease during which there are little or no welfare problems. If examined with ultrasound or ECG during this period, the changes in heart structure and function associated with DCM can be detected but there are no other clinical signs. However, affected dogs typically go on to develop failure of both sides of the heart. This tends to occur at an older age in Newfoundlands than in dogs of other giant breeds (Dukes-McEwan 2000).

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. In Newfoundlands with DCM there is usually a build up of fluid in the lungs and this causes breathing difficulty (Dukes-McEwan 2000) and also coughing. As 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 for welfare reasons at an earlier stage in this process to avoid this suffering.

Disturbances to heart rhythm (dysrhythmias) may contribute to congestive heart failure and may also have direct welfare effects when they cause acute cardiac insufficiency making the dog feel ill or faint and perhaps causing collapse or sudden death.

Investigations into the cause of heart failure and treatments administered to alleviate it may also have adverse effects on welfare through, for example, repeated travel to and from veterinary practices, hospitalisations and side effects of medications (which may, for example, cause gastrointestinal disease).

3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span in affected dogs. The progress of DCM in Newfoundlands tends to be slow (Dukes-McEwan 2000). The mean survival time of dogs of all breeds with DCM from their first presentation at a cardiorespiratory referral centre was found to be 19 weeks in one study (Martin et al 2009), and that of Newfoundlands has been reported to be around 6 months (Tidholm & Jonsson 1996).

4. Number of animals affected

The Newfoundland is one of the breeds of dog most commonly affected by DCM (Tidholm & Jonsson 1997, Menaut et al 2005, Borgarelli et al 2006, Martin et al 2009).  It has been established that Newfoundlands are predisposed to develop DCM (Dukes-McEwan 1998, 1999). Newfoundlands have the fifth 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 differentiation between different types of heart disease in this study, it is likely that DCM was the main reason for this. Dukes-McEwan (1999) found evidence of DCM in around 10% of Newfoundland dogs.

5. Diagnosis

DCM is usually diagnosed by ultrasound examination although this may be supported by findings from other cardiological examinations – physical examination, radiography of the chest and ECG (Vollmar 1999, Lee et al 2002, 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 is no genetic test for detection of DCM.

6. Genetics

It has been suggested that DCM has an autosomal dominant pattern of inheritance with incomplete penetrance (Dukes-McEwan 1998, 1999, Davidsson 2007), although the specific genes responsible have not yet been found (Davidsson 2007; Wiersma et al 2008). Autosomal dominant conditions affect both sexes equally and all individuals with the gene are at risk of developing the condition and passing it to their offspring. Other genes or environmental factors also may affect whether or not animals with the mutant genes for the disease develop it and how severely.

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

There is currently no genetic tests for DCM as the gene or genes involved have not been determined. It is not known whether carriers exist (ie whether the disease can be passed on to the offspring of animals which do not develop the disease themselves), but if the inheritance is autosomal with incomplete penetrance, then this may occur.

The only way to determine if an apparently normal dog is likely to develop clinical DCM, is by detecting heart abnormalities. The most sensitive methods for this are ultrasound examination and ECG. Annual screening of all Newfoundlands from 2 years old is recommended (Vollmar et al 2004).

8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no formal breeding schemes in operation aimed at reducing or eliminating this common condition from the Newfoundland breed, but there is an informal scheme operating in the UK.

In the absence of a genetic test, any scheme has to be based on detection of affected animals. Animals with clinical DCM should not be used 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 Newfoundlands, 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)

• Clinical and pathological effects
• Intensity of welfare impact
• Duration of welfare impact
• Number of animals affected
• Diagnosis
• Genetics
• How do you know if an animal is a carrier or likely to become affected?
• Methods and prospects for elimination of the problem
• Acknowledgements
• References

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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 around the lungs (Dukes-McEwan 2000), and secondly, it will develop 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 chambers (atria) and flows into the larger, lower chambers (ventricles). The ventricles have thick muscular walls. Between the atria and the ventricles are valves that prevent back flow of blood. 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.

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 flows through the tricuspid valve into the right ventricle and then as the right ventricle contracts, it is pumped through the pulmonary valves into the pulmonary arteries and on to 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, flows through the mitral valve into the left ventricle. Then, as the left ventricle contracts, it is pumped  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, including delivery of oxygen and nutrients and transport of 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 entire body, whilst the right hand side only has to supply the 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, and therefore thicker, than those of 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 it 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 chest (pleural fluid), abdomen (ascites) or in the body tissues generally (oedema).
2. As the heart shape changes as a result of DCM the valves can become distorted and leak. When the tricuspid or 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 and the problems, outlined above, associated with this.
3. In DCM, the abnormal heart 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 (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.

 

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 and fill 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 such that eventually the volume of blood that the heart can push forwards around the body also decreases. A further problem is that during relaxation the heart muscle itself receives blood via its coronary arteries so when it has to beat abnormally rapidly, its own oxygen supply may be compromised leading to death of heart muscle.

Inadequate blood flow from the heart can also cause 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 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, are likely to 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 and an elevated heart rate may be apparent on veterinary examination. The heart rate is measured by feeling the heart beat, or, more usually, by listening to the heart using a stethoscope. The pulse rate is measured by feeling the pulsing of blood flowing through a major artery - in dogs, usually the femoral artery in the upper inside leg. Normally heart and pulse rates are the same, but this is not always the case in 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 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 may be detected is a “gallop rhythm” (dysrhythmia). Normally a heart beat has two sounds, “lub – dub”. A gallop rhythm has three sounds 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 Newfoundlands 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 (Dukes-McEwan 2000). 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 disprupted 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 detection of atrial fibrillation (see above) on ECG examination is a typical sign of the disease in Newfoundlands.

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.

In animals with DCM, affected heart muscle cells have a reduced capacity to contract adequately. It is unclear if 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 (O’Brien et al 1992, O’Brien 1997, Meurs et al 2001, Spier et al 2001). The genes responsible for this disease in the Newfoundland have not been determined (Wiersma et al 2008).

DCM can also occur for other reasons including: nutritional deficiencies, drug side effects, viral infection, possibly hormonal imbalance, and autoimmune disease (Calvert & Meurs 2000, Rishniw 2004, Vollmar et al 2004, Buse et al 2008). It has been demonstrated that taurine deficiency can cause DCM in Newfoundlands eating commercial dog food. Supplementation may alleviate signs of DCM somewhat in some individuals (Dukes-McEwan et al 2003, Backus et al 2003, Willis et al 2003).

When heart tissue affected by DCM is examined at post-mortem under the microscope, two distinctive forms can be distinguished: (i) associated with fatty infiltration and degeneration and (ii) associated with wavy deformation of heart muscle fibres. The latter is the form usually seen in Newfoundlands (Tidholm et al 1997, 2000). It is not possible to determine which type of disease is present prior to death.

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2. Intensity of welfare impact

Newfoundlands with DCM generally have a period of subclinical disease during which there are little or no welfare problems. If examined with ultrasonography or ECG during this period the changes in heart structure and function associated with DCM can be detected but there are no other clinical signs.  However, affected dogs typically go on to develop failure of both sides of the heart: although, this tends to occur at an older age in Newfoundlands than in dogs of other giant breeds (Dukes-McEwan 2000).

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. In Newfoundlands with DCM there is usually a build up of fluid in the lungs and this causes breathing difficulty (Dukes-McEwan 2000) and also coughing. As 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 for welfare reasons at an earlier stage in this process to avoid this suffering.

Disturbances to heart rhythm (dysrhythmias) may contribute to congestive heart failure and may also have direct welfare effects when they cause acute cardiac insufficiency making the dog feel ill or faint and perhaps causing collapse or sudden death.

Investigations into the cause of heart failure and treatments administered to alleviate it may also have adverse effects on welfare through, for example, repeated travel to and from veterinary practices, hospitalisations and the side effect of medications (which may, for example, cause gastrointestinal disease).

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3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span in affected dogs. The progress of DCM in Newfoundlands tends to be slow (Dukes-McEwan 2000). The mean survival time of dogs of all breeds with DCM from their first presentation at a cardiorespiratory referral centre was found to be 19 weeks in one study (Martin et al 2009), and that of Newfoundlands has been reported to be around 6 months (Tidholm & Jonsson 1996).

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4. Number of animals affected

The Newfoundland is one of the breeds of dog most commonly affected by DCM (Tidholm & Jonsson 1997, Menaut et al 2005, Borgarelli et al 2006, Martin et al 2009). It has been established that Newfoundlands are predisposed to develop DCM (Dukes-McEwan 1998, 1999). Newfoundlands have the fifth 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 differentiation between different types of heart disease in this study, it is likely that DCM was the main reason for this. Dukes-McEwan (1999) found evidence of DCM in around 10% of Newfoundland dogs.

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5. Diagnosis

DCM is usually diagnosed by ultrasound examination although this may be supported by findings from other cardiological examinations – physical examination, radiography of the chest and ECG (Vollmar 1999, Lee et al 2002, 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 is no genetic test for detection of DCM.

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6. Genetics

It has been suggested that DCM has an autosomal dominant pattern of inheritance with incomplete penetrance (Dukes-McEwan 1998, 1999, Davidsson 2007), although the specific genes responsible have not yet been found (Davidsson 2007, Wiersma et al 2008). Autosomal dominant conditions affect both sexes equally and all individuals with the gene are at risk of developing the condition and passing it to their offspring. Other genes or environmental factors also may affect whether or not animals with the mutant genes for the disease develop it and how severely.

There has been considerable interest in searching for genes involved with DCM but studies have so far been inconclusive (Stabej et al 2004, Stabej et al 2005, Meurs et al 2008).

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

There are currently no genetic tests as the gene or genes involved have not been determined. If DCM is an autosomal dominant condition then there would be no silent carriers (ie animals that are unaffected themselves but which can pass it on to their offspring) but the genetics may be more complicated than this.

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 examinations. Because the condition can occur in dogs at quite an advanced age it may be necessary to determine that both the parents and all grandparents were without heart disease.

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8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no formal breeding schemes in operation aimed at reduce the prevalence of or eliminating this common condition from the Newfoundland breed. However, the UK breed society, working with the Veterinary Cardiovascular Society) has an informal scheme involving veterinary cardiac examinations using ECG and ultrasound (see http://www.thenewfoundlandclub.co.uk/health.htmand http://www.bsavaportal.com/vcs/Information/HeartTesting/HeartTestingonDogs.aspx). In the absence of a genetic test, any schemes have, at the present time, to be based on detection of affected animals by veterinary cardiologists.

Animals with clinical DCM should not be used for breeding. Nor should animals with occult DCM be used for breeding (when the disease in its early stages before it causes clinical signs) as this would perpetuate the problem. However, identification of such animals involves the regular monitoring of all breeding stock for early signs of disease: eg biannual examinations by a veterinary cardiologist.

Since the disease is so common in Newfoundlands, 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.

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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.

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10. References

Backus RC, Cohen G, Pion PD, Good KL, Rogers QR and Fascetti AJ (2003) Taurine deficiency in Newfoundlands fed commercially available complete and balanced diets. Journal of the American Veterinary Medical Association 223: 1130-1136

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, 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

Davidsson K (2007) Evaluation of genomic DNA from paraffin embedded tissue and desmin as candidate gene for dilated cardiomyopathy in Newfoundland dogs. PhD thesis. http://ex-epsilon.slu.se:8080/archive/00001514/01/290_Katarina_Davidsson.pdf accessed 28.6.2011

 Dukes-McEwan J (1998) Dilated cardiomyopathy in Newfoundlands - an epidemiological investigation, diagnostic criteria and an introduction to genetic linkage analysis. Proceedings of the Veterinary Cardiovascular Society April 2nd, 1998

Dukes-McEwan J (1999) Echocardiographic/Doppler criteria of normality, the findings of cardiac disease and the genetics of familial dilated cardiomyopathy in Newfoundlands. 108-116. PhD Thesis, The University of Edinburgh

Dukes-McEwan J (2000) Canine dilated cardionmyopathy 1. Breed manifestations and diagnosis. In Practice 22: 520-30

Dukes-McEwan J, Biourge V, Ridyard A, Corcoran BM, Rogers QR and Backus RC (2001) Dilated cardiomyopathy in Newfoundland dogs: association with low whole blood taurine level. Journal of Small Animal.Practice 41: 500

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

Lee B-H, Dukes-McEwan J and Corcoran BM (2002) Evaluation of a novel doppler index of combined systolic and diastolic myocardial performance in Newfoundland dogs with familial prevalence of dilated cardiomyopathy. Veterinary Radiology & Ultrasound 43: 154–165

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, 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-

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 M (2004) Systolic myocardial failure (Dilated Cardiomyopathy). VIN Associate accessed 3.11.2010

Skelly B (2003) Towards a molecular test for dilated cardiomyopathy in Newfoundlands. 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 and Jonsson L (1996) Dilated cardiomyopathy in the Newfoundland: a study of 37 cases (1983-1994). Journal of the American Animal Hospitals Association 32: 465-470

Tidholm A and Jonsson L (1997) A retrospective study of canine dilated cardiomyopathy (189 cases). Journal of the American Animal Hospital Association 33: 544-550

Tidholm A, Häggström J and Jönsson L (2000) Detection of attenuated wavy fibers in the myocardium of Newfoundlands without clinical echocardiographic evidence of heart disease. American Journal of Veterinary Research 61: 238-241

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

Wiersma AC, Stabej P, Leegwater PA, Van Oost BA, Ollier WE and Dukes-McEwan J (2008) Evaluation of 15 candidate genes for dilated cardiomyopathy in the Newfoundland dog. Journal of Heredity 99: 73-80

Willis R, Dukes Mc-Ewans J, Biourge V, Desprez G and Mellor D (2003) The role of taurine in dilated cardiomyopathy in Newfoundland dogs. Meeting of the Veterinary Cardiovascular Society, http://www.royalcanin.co.za/assets/images/library/taurine-in-dilated-cardiomyopathy-in-newfoundland-dogs.pdf   accessed 28.6.2011

http://www.thenewfoundlandclub.co.uk/health.htm accessed 28.6.2011

http://www.bsavaportal.com/vcs/Information/HeartTesting/HeartTestingonDogs.aspx accessed 29.6.2011

© UFAW 2011

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Credit for main photo above:

By SKern at the German language Wikipedia [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0  (http://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons