Genetic Welfare Problems of Companion Animals

 

Irish Wolfhound

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. Around one third of Irish wolfhounds develop DCM. 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 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 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 develop 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 dysrhythmias (abnormal heart beats) which may result in its sudden death due to inadequate blood circulation (Martin et al 2010). The abnormal heart beat activity in Irish wolfhounds with this condition is atrial fibrillation (AF) (Brownlie & Cobb 1999, Vollmar 2000, Vollmar et al 2004).

The heart is a complex organ and 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.

• 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) but fluid accumulation in the chest cavity (pleural fluid) is the usual problem in Irish wolfhounds with DCM (Vollmar et al 2004).
• 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 (or back pressure) heart failure problems and the problems, outline above, associated with this.
• 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.

The reason why some Irish wolfhounds develop this disease is not fully understood but it is known that a number of genetic factors are very important (Vollmar et al 2004, Distl et al 2007). Affected heart muscle cells have a reduced capacity to contract adequately.

Dogs can 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   

Irish wolfhounds 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 develop dysrhythmia or congestive (backwards) heart failure. The average age for an Irish wolfhound to show clinical signs of DCM is four years (Vollmar et al 2004).

DCM is a significant cause of death in Irish wolfhounds and has been shown to cause early death (Vollmar et al 2004).

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 Irish wolfhounds with DCM develop fluid building up in the pleural cavity – between the chest wall and the lungs leading to compression of the lungs and difficulty in breathing (Vollmar 1999). This is a severe welfare problem although the affected dog is often euthanased at an earlier stage in this process.

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). The mean time between diagnosis and death from DCM in a group of Irish wolfhounds was 5 months although the majority of dogs diagnosed were still alive 15 months after diagnosis (Vollmar 2000).

Death due to congestive heart failure typically occurs in Irish wolfhounds at 4-5 years (Vollmar et al 2004).

4. Number of animals affected

Vollmar (2000) and Vollmar et al (2004) found that 24% of Irish wolfhounds presenting to her practice had dilated cardiomyopathy on ultrasound examination (most also had atrial fibrillation - abnormal electric activity of the heart - found on ECG) and another 10% were found, using ECG, to have AF but had normal ultrasound appearance. Distl et al (2007) found an overall prevalence of DCM in Irish wolfhounds, screened using ultrasound examination, of 26%.

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 animals show any clinical signs) (Brownlie & Cobb 1999, Vollmar 2000, Vollmar et al 2004).

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

6. Genetics

There is evidence that it is a polygenic condition in Irish wolfhounds, with some genes playing a more important role in its development than others, one of which may be sex linked as there is a higher prevalence of DCM in males (Vollmar et al 2004, Distl et al 2007). However, the specific genes responsible have not yet been found (Philipp et al 2007a, 2007b, 2008).

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. 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. Annual screening of all dogs from 2 years old is recommended (Vollmar et al 2004). Around half of the offspring of an affected parent are likely to themselves develop DCM (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 to reduce or eliminate this common condition from the Irish wolfhound breed. However, an informal screening programme is run by the UK breed society based on diagnosis by ECG and ultrasound examinations (http://www.irishwolfhoundsociety.co.uk/heartregional.htm).

In the absence of a genetic test, any scheme would have to be based on detection of affected animals by veterinary cardiologists. Vollmar et al (2004) have suggested breeding protocols to tackle the condition (see below), but as far as we are aware these have not been widely implemented.

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)

• 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 (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.

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. In dilated cardiomyopathy (DCM) the heart changes shape. 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.

• 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) but fluid accumulation in the chest cavity (pleural fluid) is the usual problem in Irish wolfhounds with DCM (Vollmar et al 2004)..
• 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 (or back pressure) heart failure problems and the problems, outline above, associated with this.
• 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 (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).

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 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.

One of the other problems that Irish wolfhounds 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 (Brownlie & Cobb 1999, Vollmar 2000, Vollmar et al 2004). Normally an electronic impulse starts in an area of the upper heart called the sinoatrial node and spreads out in a set and controlled manner causing the various parts of the heart to contract. There is a pathway that conducts the nerve impulses that induce contractions. First the atria contract and then the impulse travels down to the ventricles which contract. The contraction process can go awry if there is disease at any point in the pathway that prevents the impulse from flowing or if there is disease somewhere in the heart that itself generates another pulse. All areas of the heart muscle are intrinsically able to act as a pacemaker and to generate an electric pulse which will cause activity in the local muscle and may spread around the heart. But when the heart contracts in an abnormal way it may cease to work properly as a pump and either forward or backward (or both) heart failure will 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 Irish wolfhounds (Brownlie & Cobb 1999, Vollmar 2000, Vollmar et al 2004).

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 major arteries and veins.

The reason why some Irish wolfhounds develop DCM is not fully understood but it is known that a number of genetic factors are very important (Vollmar et al 2004, Distl et al 2007). 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 2001, Spier et al 2001) and the specific genes responsible have not yet been found (Philipp et al 2007a, 2007b, 2008).

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 (Tidholm et al 2001).

Male Irish wolfhounds are more likely to be affected than females (Distl et al 2007).

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2. Intensity of welfare impact

Irish wolfhounds 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 signs of dysrhythmia (irregular heart beat) or congestive (backwards) heart failure. The average age for an Irish wolfhound to show clinical signs of DCM is four years (Vollmar et al 2004),

DCM is a significant cause of death in Irish wolfhounds and has been shown to cause early death (Vollmar et al 2004).

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 Irish wolfhounds with DCM develop fluid build up in the pleural cavity – between the chest wall and the lungs leading to compression of the lungs and difficulty in breathing (Vollmar 1999). Heart failure also causes coughing. As the fluid accumulates, breathing becomes an ever increasing struggle, fluid within the lungs also appears 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 into and treatments of heart failure may also have adverse welfare effects related to travel to and from veterinary practices, hospitalisations and medications – for example, medications may cause gastrointestinal disease.

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3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span. In one study of dogs of all breeds it was found that mean survival time after presentation with DCM at a cardiorespiratory referral centre was 19 weeks (Martin et al 2009). The mean time between diagnosis and death from DCM in a group of Irish wolfhounds was 5 months although the majority of dogs diagnosed were still alive 15 months after diagnosis (Vollmar 2000).

Death due to congestive heart failure typically occurs in Irish wolfhounds at 4-5 years (Vollmar et al 2004).

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4. Number of animals affected

The genetic predisposition of Irish wolfhounds for DCM is well established (Cobb et al 1996, Urfer et al 2007). Irish wolfhounds had a higher death rate from heart disease than any other breed of dog according to a survey of insured pedigree dogs performed in Sweden (Egenvall et al 2006). Although different types of heart disease were not discriminated in this study, it is likely that DCM was the main reason for these figures.

Vollmar (2000, et al 2004) found that 24% of Irish wolfhounds presenting to her practice had DCM on ultrasound examination (most also showed atrial fibrillation - abnormal electric activity of the heart - on ECG) and a further 10% were found, using ECG, to have AF but had a normal ultrasound appearance. Distl et al (2007) found an overall prevalence of DCM in Irish wolfhounds screened using ultrasound examination of 26%. They found that the prevalence in males (34%) was significantly higher than that in females (19%).

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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 animals show any clinical signs) (Brownlie & Cobb 1999, Vollmar 2000, Vollmar et al 2004).

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

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6. Genetics

There is evidence that it is a polygenic condition in Irish wolfhounds, with some genes playing a more important role in its development than others, one of which may be sex linked as there is a higher prevalence of DCM in males (Vollmar et al 2004, Distl et al 2007). However, the specific genes responsible have not yet been determined (Philipp et al 2007a, 2007b, 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. 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. Annual screening of all dogs from 2 years old is recommended (Vollmar et al 2004). Around half of the offspring of an affected parent are likely to themselves develop DCM (Vollmar et al 2004).

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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 to reduce or eliminate this common condition from the Irish wolfhound breed. However, a n informal screening programme is run by the UK breed society using ECG and ultrasound examinations (http://www.irishwolfhoundsociety.co.uk/heartregional.htm).

In the absence of a genetic test, any scheme would have to be based on detection of affected animals by veterinary cardiologists. There is a scheme in place for collection and storage of blood samples from Irish wolfhounds to aid in future research and there are research programmes underway to search for the important genes e.g http://heart.ohsu.edu/HTMLs/iwhsProjectInfo.pdf. (NB. It is not legally permissible to take a blood sample just for research but it may be permissible for any surplus remaining after collection of blood for clinical tests to be used for this purpose (http://www.iwhealthgroup.co.uk/bloodrep.html).

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 should not be used as this would perpetuate the problem.

The following suggestions regarding breeding were made by Vollmar et al (2004) for the control of the condition. However, as far as we are aware these have not been widely implemented.

'1) All breeding dogs should have heart examinations performed on an annual basis not only as long as they are used for breeding but also later in life to make sure they do not develop DCM.  Having proven healthy (> 8 yrs old) parents and grandparents is the most valuable information we can get concerning the likelihood for not developing DCM in an individual dog used for breeding today.

2) Heart examinations must be performed in a standardized fashion and all results must be centrally registered and become available for official publication.

3) The number of litters produced by an individual dog preliminarily must be restricted to a maximum (suggestion: 5 litters).

Today it is possible to preserve semen from sires which can be used again later, after it is proven that the dog has not developed DCM.

More litters could be permitted for dogs with a proven healthy heritage ie both parents or all 4 grandparents had normal hearts (i.e. dogs were re-examined and still normal at/after 8 yrs. of age).'

Since the disease is so common in Irish wolfhounds, 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 Irish wolfhounds 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

Brownlie SE and Cobb MA (1999) Observations on the development of congestive heart failure in Irish wolfhounds with dilated cardiomyopathy. Journal of Small Animal Practice 40: 371–377

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

Cobb MA, Brownlie S, Pidduck SE and Batt RM (1996) Evidence for genetic involvement in dilated cardiomyopathy in the Irish wolfhound. British Small Animal Veterinary Association Congress Proceedings pp 215

Distl O, Vollmar AC, Brosclk C, Hamann H and Fox PR (2007) Complex segregation analysis of dilated cardiomyopathy (DCM) in Irish wolfhounds. Heredity 99: 460-5

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

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-

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

Philipp U, Vollmar A and Distl O (2007a) Evaluation of candidate genes for dilated cardiomyopathy in Irish wolfhounds. Animal Genetics 39: 88-9

Philipp U, Broschk C, Vollmar A and Distl O (2007b) Evaluation of Tafazzin as candidate for dilated cardiomyopathy in Irish wolfhounds. Journal of Heredity 98: 506-9

Philipp U, Vollmar A and Distl O (2008) Evaluation of Titin-Cap gene (TCAP) as candidate for dilated cardiomyopathy in Irish wolfhounds. Animal Biotechnology 19: 231-6

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, 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

Urfer SR, Gaillard C and Steiger A (2007) Lifespan and disease predispositions in Irish wolfhounds: a review. Veterinary Quarterly 29: 104-113

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 AC (2000) The prevalence of cardiomyopathy in the Irish wolfhound: a clinical study of 500 dogs. Journal of the American Animal Hospital Association 36: 125-132

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.irishwolfhoundsociety.co.uk/heartregional.htm accessed 24.6.2011

http://www.iwhealthgroup.co.uk/hearttesting.html accessed 24.6.2011

http://heart.ohsu.edu/HTMLs/iwhsProjectInfo.pdf accessed 24.6.2011

© UFAW 2011

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Credit for main photo above:

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