Genetic Welfare Problems of Companion Animals

An information resource for prospective pet owners

Doberman Pinscher

Doberman Pinscher

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 muscle of the heart. It has recently been found that the overall prevalence of dilated cardiomyopathy in Dobermans in Europe is greater than 50%. 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. A genetic test has recently become available for detection of dogs which have the mutant gene. The disease can be detected in the early stages using ultrasound or 24 hour electrocardiographic monitoring. Breeding from affected or carrier dogs will perpetuate the problem.


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. Firstly, it will develop congestive heart failure which leads to a build up of fluid in the body, especially around the lungs, and secondly, it will show dysrhythmias (abnormal heart beat) which may result in its sudden death due to a failure of the heart to pump blood adequately around the body (Martin et al 2010).

Dobermans with heart disease may live for several years without heart failure. These dogs are likely to appear normal to their owners and have no welfare problems, but heart disease can be detected by electrocardiogram (ECG– which records the electrical activity of the heart over an extended period of time (using a Holter monitor). This is a particularly valuable way of detecting DCM as sporadic dysrhythmia during a 24-hour recording is often the first detectable sign of disease (Calvert et al 1997a, Calvert et al 2000). The most powerful tool for examining the heart is ultrasonography. This enables measurement of the thickness of the heart muscle, the size of each chamber and the position and movement of each valve.

The reason why some Dobermans develop DCM is unknown. Genetic factors are certainly very important but the mechanism is unclear. Heart muscle cells have a reduced capacity to contract adequately but whether this is due to a defect in the cell structure, the proteins that make up the contractile apparatus, or in the cellular components that provide energy for contraction is unclear (O’Brien et al 1992, O’Brien 1997, Meurs et al 2001, Spier et al 2001).

2. Intensity of welfare impact    

Dobermans with DCM generally have a long period of subclinical disease during which there are no (or only slight) welfare problems. This subclinical phase typically lasts from the age of two to six years. If examined with ultrasound or by Holter ECG testing during this period the changes in heart structure and function associated with DCM can be detected but there are no other clinical signs at this time. Affected dogs then, typically, either die due to dysrhythmia, show an episode of weakness or collapse due to dysrhythmia, or go into backward (congestive) heart failure. Some dogs die quickly in congestive heart failure that does not respond to treatment, and survival for more than a few months is unusual. Dying from congestive heart failure is unpleasant. There is fluid build up in the lungs which makes breathing laboured and difficult. It is similar to slow drowning.

3. Duration of welfare impact

Dilated cardiomyopathy reduces life-span in the Doberman pincher. The duration of suffering for those dogs with the disease may be very short, when apparently healthy animals affected by the disease die suddenly due to dysrhythmia. It can be much longer – weeks or months – in cases in which there is progressive congestive heart failure.

4. Number of animals affected

A recent study by Wess et al (2010a) showed that the overall prevalence of DCM in Dobermans in Europe was 58%.

5. Diagnosis

DCM can be diagnosed using ultrasound examination. Occult disease (the hidden form in which there are heart abnormalities but before any clinical signs become apparent) can also be detected using 24-hour Holter ECG monitoring. A blood test has recently been developed for detection of animals which have the mutant gene (North Carolina State University 2011) for details of this see: http://www.cvm.ncsu.edu/vhc/csds/vcgl/dobe-dc.html.

6. Genetics

There is evidence that DCM is caused by an autosomal dominant gene in Dobermans (Meurs et al 2007). All individuals with the gene will be prone to develop disease and all will pass it on to all their offspring. 

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

Dogs with the mutant gene can be identified by a blood test (see above). As an autosomal dominant condition, it is likely that there are no silent carriers (ie animals that are unaffected themselves but which can pass it on to their offspring) – all individuals with the gene are prone to developing the disease and all will pass it on to their offspring.

Prior to the development of the genetic test, the only way to determine if an apparently normal dog would be likely to develop clinical DCM, was by detection of heart abnormalities and the most sensitive methods for this are ultrasound examination and 24-hour Holter ECG monitoring. These are examinations only available from specialist veterinary cardiologists. Annual screening of all dogs from 2 years old was recommended (Wess et al 2010a). However, the genetic test that is now available is likely to be the best way of detecting dogs at risk and which should not be used for breeding.

8. Methods and prospects for elimination of the problem

As far as we are aware, there are currently no formal breeding schemes operating which aim to reduce or eliminate this common condition from the Doberman pinscher breed. A genetic test would be very valuable as this would enable the detection and removal of affected individuals from the breeding pool. However, because the condition is so common in Dobermans, there is concern that removal of all affected individuals from the breeding pool might cause excessive restriction in the choice of Dobermans to breed from, and hence a reduction in the size of the breed’s gene pool with the risk that other genetic defects may inadvertently increase in frequency. Such problems could be avoided by out-breeding with dogs of other breeds.


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


1. Clinical and pathological effects

Dilated cardiomyopathy (DCM) is disease of the heart muscle in which the heart becomes thin walled and dilated. There are two common, important consequences of this for the affected dog: firstly, it will experience congestive heart failure which leads to a build up of fluid in the body, especially the lungs, and secondly, it will show 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 made largely of heart muscle. Between the atria and the ventricles 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 to prevent blood flowing backwards.

Dilated 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. This 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), the blood is pushed past the pulmonary valves into the pulmonary arteries that take it to the lungs (to take up oxygen).

The left side of the heart receives this oxygenated blood from the lungs, via the pulmonary veins. As described for the right side, it pumps blood around the body via the major arteries to deliver oxygen and nutrients and to remove heat and metabolic waste products.

So, the right side of the heart only has to pump blood to the lungs while the left side has to service all other parts of the body. This difference does not affect the structure and function of the atria very much but requires that the left ventricle is much stronger than the right. Muscle strength is largely is a function of size so the left ventricle’s muscle wall is thicker than the right.

The contraction phase of the heart beat cycle is called systole and the relaxation phase is called diastole.

Muscle contraction throughout the heart are coordinated by nerve signals. These can be disrupted by damage to the heart muscle tissues through which they run. In dilated cardiomyopathy (DCM) the heart changes shape. It becomes generally larger, the chambers have a greater volume and the muscle walls are thinned.

The heart is a complex, sophisticated 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.

Dilated figure 2

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

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 to build up in the lungs (pulmonary oedema) and this is the usual problem in Dobermans with DCM. When the right side is affected, the fluid builds up in the body and usually shows as fluid accumulating in the chest cavity (pleural fluid), the abdomen (ascities) or in the body tissues generally (oedema).

 As the heart shape changes the valves can become distorted and leak. When the valves between the ventricles and atria are affected, they may allow blood to flow backwards which causes further back pressure 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.

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

Dilated figure 3

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

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, the high heart rate may compromise capacity for the ventricles to relax as there is less time between each contraction for the ventricles; time in which the ventricles relax and fill. This can cause backward heart failure to worsen and eventually the rate at which blood can be pushed forward around the body also drops. A further problem is that it is during relaxation that the heart muscle itself receives its own blood supply via its coronary arteries so when beating quickly its own oxygen supply can drop 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. In response, hormones are released 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, may appear normal to their owners and the dog will not have any welfare problems at that time. An owner might detect a fast heart beat if feeling the dog’s chest, and this rapid heart or pulse rate is apparent on clinical examination. In a normal individual the heart rate and pulse rate are the same – each heart beat produces a pulse; but this is not always the case in heart failure – sometimes an ineffectual heart beat occurs that does not generate a detectable pulse. 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.

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

Electrocardiography(ECG) to record the electrical activity of the heart as it beats is carried out in dogs without sedation or anaesthesia and can provide information about the presence of heart disease (or of heart failure). Some individuals may occasionally have irregular heart beats whilst being normal most of the time. These dogs can experience fainting episodes during the periods of irregularity but when being examined in the veterinary surgery may appear completely normal. Normal ECGs record the electrical activity for a few minutes only and can miss problems that occur infrequently despite these problems possibly being very significant when they do happen (Wess et al 2010b). Such intermittent problems can be detected using a device that records ECG over an extended period (a Holter monitor). This is a particularly valuable way of investigating DCM in Dobermans as sporadic dysrhythmia during a 24-hour recording is often the first detectable sign of disease (see below) (Calvert 1995, Calvert et al 1997b, Calvert et al 2000). Dobermans are particularly susceptible to dysrhythmias (Martin et al 2009, Wess et al 2010a). 

The most powerful tool for examining the heart is ultrasonography. This enables measurement of the thickness of the heart muscle; the size of each chamber, and the position and movement of each valve. With colour-flow ultrasonography it is also possible to measure the speed and direction of blood flow in the heart and the great vessels. The reason why some Dobermans develop this disease is not known. Genetic factors are certainly very important but the mechanism is unclear. Heart muscle cells have a reduced capacity to contract adequately but whether this is due to a defect in the cell structure, the proteins that make up the contractile apparatus, or in the cellular components that provide energy for contraction is unclear (O’Brien et al 1992, O’Brien 1997, Meurs et al 2001, Spier et al 2001)

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

When heart tissue affected by DCM is examined post-mortem under the microscope two distinctive forms can be distinguished: (i) the fatty infiltration-degenerative type and (ii) the attenuated wavy fibre type – in which heart muscle cells are deformed. Both forms are seen in Dobermans which is further evidence that there may be more than one causes of DCM in this breed. It is not possible to determine which type of disease is present in an individual dog prior to death (Tidholm et al 2001).

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2. Intensity of welfare impact

Dobermans with DCM will have a long period of subclinical disease with no welfare problems; this typically lasts from the ages of two to six years. If examined with ultrasound or by Holter ECG testing during this period the existence of DCM can be detected but there are no clinical or welfare issues at this time. Subsequently, they typically either die due to a dysrhythmia, have an episode of weakness or collapse that is due to a dysrhythmia, or they go into backward (congestive) heart failure.

DCM causes a reduction in life-span for Dobermans. Sudden death due to dysrhythmia typically occurs at 6-9 years (range 3-12 years) and death from congestive heart failure at 7-10 years (range 1-15 years) (Calvert & Meurs 2000). A reduced life-span in itself may be considered a significant welfare problem.

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 Dobermans with DCM develop left-sided congestive heart failure (affecting the left side of the heart most). This leads to fluid building up in their lungs which makes breathing difficult. It also causes coughing. As this fluid accumulates, breathing becomes an ever increasing struggle and the dog effectively dies from drowning in its own body fluids. This is a severe welfare problem although the affected dog is often euthanised at an earlier stage in this process.

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

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

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3. Duration of welfare impact

DCM causes a reduction in life-span for Dobermans. 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 survival time of Dobermans is usually suggested to be lower (Domanjko-Petric et al 2002, Calvert et al 1997), although as a result of advances in treatment some dogs may survive for a year or two (Tidholm et al 1997, Luis Fuentes et al 2002, O’Grady et al 2008). Dogs that develop signs at a younger age are may tend to deteriorate more rapidly (Tidholm et al 1997) but this was not been confirmed in a more recent study (Martin et al 2010).

Sudden death due to dysrhythmia typically occurs in affected Dobermans at 6-9 years (range 3-12 years) and death from congestive heart failure at 7-10 years (range 1-15 years) (Calvert & Meurs 2000).

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4. Number of animals affected

A recent study by Wess et al (2010a) showed that the overall prevalence of DCM in Dobermans screened using both 24 hour Holter monitoring and ultrasound examination was 58%. This varied from 3% of dogs 1-2 years old, 10% of dogs 2-4 years, 12.5% at 4-6 years, 44% at 6-8 years and 44% over 8 years old. These figures are higher than those suggested in earlier reports and this is probably a reflection of better methods of detecting DCM.

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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 (Dukes-McEwan et al 2003).

ECG can be used to detect occult disease (eg heart rhythm abnormalities at a stage before animals show any clinical signs) but short-term recordings are less sensitive than 24-hour Holter monitoring (Wess et al 2010b). The stage of disease can be estimated from the results of 24-hour Holter monitoring, physical examination and chest radiographs. There has been some interest in using a blood test to detect evidence of heart muscle damage but this has not yet become well established (Wess et al 2010c).

A blood test has recently been developed for detection of animals which have the mutant gene (North Carolina State University 2011) for details of this see: http://www.cvm.ncsu.edu/vhc/csds/vcgl/dobe-dc.html.

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6. Genetics

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 (Dukes-McEwan et al 2003).

ECG can be used to detect occult disease (eg heart rhythm abnormalities at a stage before animals show any clinical signs) but short-term recordings are less sensitive than 24-hour Holter monitoring (Wess et al 2010b). The stage of disease can be estimated from the results of 24-hour Holter monitoring, physical examination and chest radiographs. There has been some interest in using a blood test to detect evidence of heart muscle damage but this has not yet become well established (Wess et al 2010c).

A blood test has recently been developed for detection of animals which have the mutant gene (North Carolina State University 2011) for details of this see: http://www.cvm.ncsu.edu/vhc/csds/vcgl/dobe-dc.html.

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

Dogs with the mutant gene can be identified by a blood test (see above). As an autosomal dominant condition, it is likely that there are no silent carriers (ie animals that are unaffected themselves but which can pass it on to their offspring) – all individuals with the gene are prone to developing the disease and may pass it on to their offspring.

Prior to the development of the genetic test, the only way to determine if an apparently normal dog would be likely to develop clinical DCM, was by detection of heart abnormalities and the most sensitive methods for this are ultrasound examination and 24-hour Holter ECG monitoring. These are examinations only available from specialist veterinary cardiologists. Annual screening of all dogs from 2 years old was recommended (Wess et al 2010a). However, the genetic test that is now available is likely to be the best way of detecting dogs at risk and which should not be used for breeding.

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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 Doberman pinscher breed. (But see http://www.dobermannbreedcouncil.co.uk/dcm2.html).

Prior to the development of the genetic test selection had to be based on detection of affected animals by veterinary cardiologists.

Animals that have clinical DCM will not be suitable for breeding. Animals found to have the mutant gene or 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 common in Dobermans, breeding only from unaffected animals that have been tested and found to be negative for the mutant gene may narrow the breeding pool considerably and there may be a risk of increasing the prevalence of other genetic diseases (of which several are known). This could be avoided by out-breeding Dobermans with dogs of other breeds.

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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 finding suitable illustrations for it.

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10. References

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 (1995) Diagnosis and management of ventricular tachyarrthythmias in Doberman pinschers with cardiomyopathy. In: Kirk’s Current Veterinary Therapy XII editor J.D. Bonagura, WB Saunders, Philadelphia. pp 799

Calvert CA, Hall G, Jacobs G andPickus C (1997a) 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

CalvertCA, Pickus CW, Jacobs GJ and Brown J (1997b) Signalment, survival, and prognostic factors in Doberman Pinschers with end-stage cardiomyopathy. Journal of Veterinary Internal Medicine 11: 323-326

CalvertCA, Jacobs GJ, Smith DD, Rathbun SL and Pickus CW (2000) Association between results of ambulatory electrocardiography and development of cardiomyopathy during long-term follow-up of Doberman Pinschers. Journal of the American Veterinary Medical Association 216: 34-39

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

Domanjko-Petric A, Stabej P and Zemva A (2002) Dilated cardiomyopathy in the Dobermann dog: survival, causes of death and a 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

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

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

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

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

Meurs KM, Fox PR, Norgard M, Spier AW, Lamb A, Koplitz SL and Baumwart RD (2007) A Prospective Genetic Evaluation of Familial Dilated Cardiomyopathy in the Doberman Pinscher. Journal of Veterinary Internal Medicine 21: 1016–1020

Meurs KM, Hendrix KP and Norgard MM (2008) Molecular evaluation of five cardiac genes in Doberman Pinschers with dilated cardiomyopathy 69 8 1050-1053

North Carolina State University College of Veterinary Medicine (2011) Genetic mutation testing service for Doberman Pinscher dilated cardiomyopathy. http://www.cvm.ncsu.edu/vhc/csds/vcgl/dobe-dc.html.

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

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

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

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

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

Stabej P, Imholz S, Versteeg SA, Zijlstrc C, Stokhof AA, Domanjko-Petric A, Leegwater PAJ and van Oost BA (2004) Characterization of the canine desmin (DES) gene and evaluation as a candidate gene for dilated cardiomyopathy in the Dobermann. Gene 340: 2241-249

Stabej P, Leegwater PAJ, Imholz S, Versteeg SA, Zijlstra C, Stokhof AA, Domanjko-Petriè A and van Oost BA (2005) The canine sarcoglycan delta gene: BAC clone contig assembly, chromosome assignment and interrogation as a candidate gene for dilated cardiomyopathy in Dobermann dogs. Cytogenetics and Genome Research 111: 140-146

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

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

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

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

Wess G, Simak J, Mahling M and Hartmann K (2010C) Cardiac Troponin I in Doberman Pinschers with Cardiomyopathy. Journal of Veterinary Internal Medicine 24: 843–849

© UFAW 2011