Dilated cardiomyopathy (DCM) is disease of the muscle of the heart. It has recently been found that the overall prevalence of dilated cardiomyopathy in Doberman(n)s in the U.S. and 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.  

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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.

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Doberman(n)s 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. 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 Doberman(n)s 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.

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Doberman(n)s 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 labored and difficult. It is similar to slow drowning.

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Dilated cardiomyopathy reduces life-span in the Doberman(n). 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.

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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.

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There is evidence that DCM is caused by an autosomal dominant gene in Doberman(n)s (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. 

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Dogs with the mutant gene can be identified by a blood test.  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.

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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.  However, the genetic test that is now available is likely to be the best way of detecting dogs at risk.

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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(n) 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(n), there is concern that removal of all affected individuals from the breeding pool might cause excessive restriction in the choice of Doberman(n)s 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.