Dilated Cardiomyopathy (DCM) in Dogs: Symptoms, Diagnosis and Treatment

In brief

There are four things you should know about DCM. First: in dilated cardiomyopathy, the heart muscle weakens, the heart enlarges, and it pumps less blood with every beat—which can lead to heart failure, arrhythmias and, in the worst case, sudden cardiac death. Serious, but in many cases very treatable. Second: it mainly affects large and giant breeds as well as a few specific breeds; the disease has a long silent (“occult”) phase in which the dog seems perfectly healthy even though the heart is already changing. Third: the single most important test is the cardiac ultrasound (echocardiogram)—painless and done without anesthesia; for at-risk breeds, early detection also includes rhythm monitoring (a 24-hour Holter ECG). Fourth: the much-discussed “nutritional DCM” has not been scientifically proven, but it should be taken seriously—in some dogs, heart function and test findings can improve after a change in diet, whereas genetic DCM usually cannot be reversed that way.

DCM is one of the most important heart diseases in dogs. This article explains what happens in the heart, which dogs are affected, how you can recognize the first signs, and how the condition is properly diagnosed and treated.

Note: This article is general information and does not replace a veterinary examination or diagnosis. If you suspect heart disease, have your dog seen by a veterinarian promptly. When DCM is suspected, an examination by a veterinarian experienced in cardiology is especially important, because the diagnosis requires a combination of cardiac ultrasound, rhythm monitoring and other findings.

👉 Prevention and health at a glance: Dog Health Basics

1. What is DCM—and what happens in the heart?

“Dilated” means enlarged. In DCM, the heart muscle loses its strength: because it no longer contracts forcefully enough, the heart chambers (especially the left ventricle) and the atrium stretch, and less blood is pumped into the circulation with every beat. At first the body compensates—which is why the disease goes unnoticed for a long time. At some point, compensation is no longer enough, and congestive heart failure develops, often with fluid backing up into the lungs or the abdomen.

Two things make DCM particularly treacherous. The first is arrhythmias: the diseased heart is prone to beating irregularly, which can lead to weakness, fainting (syncope) and—particularly in Dobermans and Boxers—sudden cardiac death, sometimes before any other symptoms were ever noticed. The second is the long silent phase: a dog can look perfectly fit on the outside while measurable changes have long been visible on a cardiac ultrasound.

This is exactly where the difference from the other major heart disease lies, and it is worth making early: in mitral valve disease, a valve leaks; in DCM, the heart muscle itself is weakened. That leads to the most important practical difference—a leaking valve almost always produces an audible murmur, a weakened muscle does not necessarily.

For early detection, this means two things. In valve disease, listening with a stethoscope provides a useful starting point, and ultrasound then establishes how severe it is. In DCM, that starting point is not reliable—if you wait for a murmur here, you do not have a screening method, you have a matter of chance.

👉 The other major heart disease: Mitral Valve Disease (MMVD) in Dogs

2. Which dogs are affected

DCM is primarily a disease of large and giant breeds, with a hereditary component. The classically predisposed breeds include the Doberman, Great Dane, Irish Wolfhound, Boxer and Cocker Spaniel, among others; the Newfoundland and Portuguese Water Dog are also mentioned. The list is not exhaustive, and the strength of the predisposition varies from breed to breed. In Dobermans, the disease is particularly common and has a long occult phase; for this breed, annual heart screening with cardiac ultrasound and a 24-hour ECG (Holter) is recommended starting at about three years of age.

Conversely: in a breed or an individual dog without a typical DCM risk, a DCM finding should be questioned especially critically and properly confirmed before it is accepted as established.

The Boxer is a special case: in this breed, a distinct form usually takes center stage, arrhythmogenic right ventricular cardiomyopathy (ARVC, “Boxer cardiomyopathy”). It shows up mainly as heart rhythm disturbances and, in the worst case, sudden cardiac death—often before the heart’s pumping strength visibly declines. That is why the 24-hour ECG (Holter) is the central screening method in Boxers, supplemented by cardiac ultrasound.

For everyday life, this raises a simple question: starting when, and how often? In Dobermans, annual screening begins at roughly three years of age. For other predisposed breeds, a practice experienced in cardiology determines when to start and how often to repeat—the predisposition varies in strength from breed to breed, and there is no single rule that applies to all of them.

For mixed breeds with a recognizable share of an at-risk breed, the same principle applies in a weaker form: the risk is not zero, but it is not that of the purebred source population either. Screening here is a judgment call, not a given—and a good reason to actively raise the question once rather than never asking it at all.

3. Genetics and genetic testing

In many breeds—above all the Doberman—DCM has a hereditary basis. However, it is polygenic and multifactorial: several genes as well as non-genetic factors are involved in its development, and by no means all of them are known.

Commercial genetic tests are already available for Dobermans. In American Dobermans, two risk variants were identified (Meurs and colleagues, NC State): DCM1 in the PDK4 gene (energy metabolism of the heart muscle) and DCM2 in the titin gene (TTN, cardiac contraction). In the (American) populations studied, an estimated 37% or so of DCM1 carriers and around 50% of DCM2 carriers actually developed DCM, and more with both variants combined. What matters is incomplete penetrance: a carrier can develop the disease but does not have to—and some never do.

Two limitations are central for owners. First: a negative genetic test does not rule out DCM. Because the disease is polygenic, a dog can develop it even without the tested variants. Second, and especially relevant for dogs of European lines: DCM1 and DCM2 have so far not been confirmed in European Doberman populations—separate risk variants have been described there (DCM3 and DCM4; Niskanen et al. 2023). A genetic test is therefore valuable mainly for breeding decisions. As the central examination for early detection, cardiac ultrasound—supplemented by the 24-hour ECG in at-risk breeds—remains the most important standard.

👉 Another genetic topic for owners: The MDR1 Defect in Dogs

4. Symptoms—often late and nonspecific

In the early, occult phase there are usually no symptoms at all. When they do become visible, they are nonspecific at first: declining stamina and tiring more quickly, increased panting, coughing, faster or labored breathing, loss of appetite, an expanding belly (from fluid) and—as a warning sign of arrhythmias—brief fainting episodes. Because these signs are so general, they are easily put down to age or “a bad day.”

A simple, valuable marker you can track at home is the resting respiratory rate: count your dog’s breaths per minute while they are sleeping calmly (one rise and fall of the chest = one breath). A rate that stays above roughly 30 breaths per minute at rest is a reason to have your dog checked by a veterinarian promptly—especially if heart disease is already known.

5. The resting respiratory rate as a home measurement

Because the symptoms are so nonspecific, a value that can be collected at home and does not depend on interpretation is valuable.

Count while your dog is sleeping calmly—not dozing and not after exercise. One rise and fall of the chest is one breath; panting does not count.

As a rough guide, a rate that stays above about 30 breaths per minute at rest is a reason for a prompt checkup. More important than this guideline, however, is your dog’s own baseline: measure on three to five consecutive days while your dog is stable, and write the values down. A dog that is usually at 16 and suddenly at 28 stands out—even though 28 is still below the guideline.

Two limitations come with this. The value is nonspecific: fever, pain, excitement and respiratory disease raise it too. And a single elevated reading is not an emergency—what matters is a sustained rise across several measurements.

And one point that applies specifically to DCM: the resting respiratory rate picks up fluid congestion, not arrhythmias. In at-risk breeds, it therefore does not replace the rhythm monitoring described in the next section.

In practice, measuring is especially worthwhile in two phases: during the silent phase, as a baseline so that there is something to compare against later—and after treatment has started, because the trend shows whether the relief is working.

👉 When a dog truly comes to rest: Sleep and Learning in Dogs

6. Diagnosis: cardiac ultrasound and rhythm monitoring

When listening with a stethoscope, a heart murmur or an irregular rhythm can be a first clue—but DCM does not always cause a murmur, so it can be missed by listening alone. The most important test for assessing the heart’s structure and pumping function is echocardiography (cardiac ultrasound): it shows the size of the heart chambers and measures pumping strength, especially the so-called fractional shortening (FS). The big advantage: cardiac ultrasound is painless, noninvasive and does not require anesthesia.

In DCM, however, echocardiography does not stand alone. Especially for early detection in at-risk breeds, rhythm monitoring is part of the workup, because arrhythmias can precede visible pumping weakness—which is why annual screening with echo and a 24-hour ECG (Holter) is recommended for Dobermans (Wess et al. 2017). Depending on the case, X-rays (heart size, lungs) and blood biomarkers (e.g., proBNP) are added. A sound DCM diagnosis belongs in the hands of someone experienced in cardiology and never rests on a single measurement, but on the overall picture of structure, function, rhythm, breed, age and the exclusion of other causes.

6.1 What a 24-hour ECG means in practice

The word “Holter” puts many people off, yet for the dog the procedure is less demanding than a cardiac ultrasound. A small recording device is carried in a vest or belly band, and the electrodes sit on shaved skin. The dog wears it through a normal day, at home, in everyday life.

That is exactly the point. An ECG at the clinic shows a few minutes—and of all things, under stress. Arrhythmias, however, occur irregularly, sometimes only a few times a day and often at rest or during excitement at home. A short recording can therefore miss them entirely.

What you need to do is manageable: keep to the usual daily routine, note down notable moments with the time—excitement, exertion, episodes of weakness—and keep your dog from chewing on the belt. Bathing and swimming are off the table that day.

Afterward, the number and type of abnormal heartbeats over 24 hours are analyzed. Above certain thresholds the finding is considered abnormal, and in at-risk breeds it can precede the pumping weakness on ultrasound—which is why it ranks equally alongside the echo in screening, not behind it.

One limitation that honesty requires: an unremarkable day does not rule out arrhythmias. It shows that nothing relevant occurred on that day. That is why repeating it at yearly intervals is part of the procedure, not an add-on.

7. What else could it be? Differential diagnoses

Many people end up on this topic because their dog is coughing or losing stamina. Both can have many causes—DCM is only one of them. A few common alternatives for context (this does not replace an examination):

• Mitral valve disease (endocardiosis, MMVD): the most common heart disease in dogs overall, but it mainly affects small to medium-sized breeds (classically the Cavalier King Charles Spaniel, but also, for example, Dachshunds or small terriers). The heart valves change, which almost always causes a clear heart murmur—unlike DCM, which does not necessarily produce a murmur.
• Kennel cough or tracheal collapse: coughing without heart disease that is easily mistaken for a heart problem. Kennel cough is infectious; tracheal collapse mainly affects small breeds and shows up as a typical “honking” cough.
• Age-related muscle loss or osteoarthritis: in large, older dogs, declining stamina and tiring more quickly are often blamed on the heart when joint pain or muscle wasting is actually behind them.

The distinction is not made from the symptom but through examination—listening to the heart, cardiac ultrasound and, depending on the case, X-rays or an ECG.

👉 Related to differential diagnosis: Recognizing Pain in Dogs

8. Caution with heart findings under anesthesia

A little-known but important point concerns heart findings that are noticed by chance during sedation or anesthesia—for example during dental treatment or surgery. The background: many anesthetic and sedative drugs depress the heart’s contractile force and alter circulatory conditions. As a result, exactly the measurements that are assessed in DCM can get worse.

This has been documented, among others, for alpha-2 agonists (e.g., medetomidine, dexmedetomidine), which are often used for sedation. They lower heart rate and pumping strength. Through changes in heart rate, preload and contractility, they then affect echocardiographic measurements—for example a lower fractional shortening and larger measured chamber diameters during systole. A true structural enlargement of the heart need not be present. In a study of healthy dogs, fractional shortening fell from around 41% to about 24% after dexmedetomidine—below the usual lower limit of normal of about 25% (Wang et al. 2016). Propofol can also markedly depress cardiac contraction, and general anesthesia with mechanical ventilation can likewise reduce measurable heart function.

What matters is putting this in proper perspective—and the wording here is deliberately cautious: anesthesia does not “create” DCM. It can, however, make heart function look worse than it is under normal conditions, and thereby complicate the assessment. A genuine DCM diagnosis is more than “poor pumping strength”: it involves actual enlargement of the chambers, systolic dysfunction, the risk profile from breed and age, often rhythm findings, and the exclusion of other causes.

Hence the practical rule: a heart finding that is noticed only under sedation or anesthesia is interpreted in light of the drugs used and, if DCM is suspected, confirmed by a targeted echocardiogram in the awake dog—with a follow-up exam if needed. Why this matters: an unconfirmed DCM diagnosis made under anesthesia can have real consequences—potentially unnecessary, long-term heart medication that is not free of side effects, unnecessary worry and restrictions for dog and owner, extra costs, and the risk that the actual cause is overlooked. The reverse is just as true: sometimes a genuine, previously unnoticed DCM becomes visible by chance during surgery. Both lead to the same conclusion—neither dismiss such a finding too quickly nor treat it too quickly, but clarify it properly in the awake dog.

9. The controversial “nutritional DCM”

Since a warning from the US Food and Drug Administration (FDA) in 2018, a possible link between certain diets—mainly grain-free foods and foods heavy in legumes or potatoes—and DCM has been under discussion, including in breeds with no known genetic predisposition. A note on terminology: the FDA coined the term “nutritional DCM”; in veterinary medicine today, the usual term is “diet-associated DCM,” to emphasize the uncertain causality. It does not refer to a separate disease, but to a possible subgroup of DCM.

Because proof of cause and effect is still lacking to this day. The data are contradictory, and the picture appears to be multifactorial—the original suspicion that taurine deficiency alone was to blame does not fully explain the cases, since many affected dogs had normal taurine levels. Factors under discussion today include the availability of sulfur-containing amino acids, bile acid and microbiome effects, and individual genetic susceptibility (Freeman et al. 2018; Freeman, Rush, Adin et al. 2022). The FDA itself stopped its regular updates at the end of 2022, noting that the reported cases alone do not establish a causal link—so the question remains open and is still being researched.

One aspect is especially relevant in practice: in some dogs with diet-associated DCM, heart function and test findings can improve after a change in diet (and taurine supplementation, if needed), whereas genetic DCM usually cannot be reversed by switching food. That is why feeding always belongs on the table when DCM is diagnosed. If a diet-associated form is suspected—especially in breeds without a typical DCM risk—it makes sense to measure the blood taurine level (and, depending on the case, carnitine) so that a deficiency can be treated specifically.

For balance, it should be said: “grain-free” is not automatically dangerous, and many such foods are complete and balanced. Caution is warranted mainly with recipes very heavy in legumes that lack solid feeding trials. If you are unsure, choose a nutritionally tested, complete and balanced food and, when in doubt, discuss the choice with your veterinarian.

👉 Keeping an eye on feeding: Ideal Weight for Dogs

9.1 What this means for choosing a food

An open research question cannot be turned into a feeding rule, and that is exactly where most advice articles on this topic fail—they turn a suspicion either into a warning or into an all-clear.

A middle path is defensible. For a healthy dog without DCM risk, there is no reason to switch away from a food that has worked well. Grain-free does not mean dangerous, and switching on a hunch does not solve a problem this dog does not have.

For a dog of a predisposed breed, the choice of food is one of several points that can be discussed at the screening appointment anyway. Restraint is warranted mainly with recipes very heavy in legumes for which no feeding trials exist.

For a dog with a confirmed DCM diagnosis—especially in a breed without a typical risk—feeding belongs on the table, including a taurine level. This is not about prevention, but about whether part of the finding is reversible.

What applies in all three cases: choosing between two complete and balanced foods is not a lever that can prevent heart disease. The levers that are backed by evidence are early detection and timely treatment.

10. Treatment

DCM usually cannot be cured, but it can be treated well—the goal is to support the heart muscle and relieve the strain on the heart. Which medications make sense depends on the stage. In the veterinary cardiology classification of chronic heart disease, dogs are roughly divided into at-risk animals without structural findings (stage A), dogs with structural heart disease but no symptoms (stage B), and dogs with current or past heart failure (stage C/D).

In the occult phase, not every dog automatically receives medication. For Dobermans with preclinical DCM, however, the PROTECT study showed that pimobendan—when defined echocardiographic criteria are met (markedly reduced pumping strength, enlarged left ventricle)—delays the onset of heart failure or sudden cardiac death and prolongs survival (Summerfield et al. 2012). Pimobendan improves pumping strength and relieves the load on the blood vessels.

In overt heart failure (stage C/D), a combination is used: diuretics (such as furosemide), ACE inhibitors (e.g., enalapril or benazepril), pimobendan and—if relevant arrhythmias are present—antiarrhythmics (e.g., sotalol or mexiletine). In diet-associated DCM, a change of food is part of the treatment.

Which combination is right is always individual and belongs in the hands of a cardiologist. The prognosis depends heavily on breed, stage and response—caught early, a great deal of quality of life and lifetime can often be gained.

11. Prognosis and life expectancy: how serious is DCM?

A DCM diagnosis is serious, but not a blanket death sentence—how much time remains depends heavily on stage, breed and cause. That is why only ranges can be given, not fixed numbers for an individual dog; the individual prognosis belongs in the hands of the treating cardiologist.

The decisive difference is whether it is caught early or late. DCM often progresses silently for years. If it only becomes visible once the dog is coughing, lethargic or short of breath, the heart muscle is usually already considerably damaged—the time from the first symptoms is then just the final phase of a long disease. If, on the other hand, it is detected during the silent phase through screening, progression can be delayed considerably: in the PROTECT study, pimobendan in preclinical Doberman DCM extended the median time to heart failure or sudden death from around 14 to about 24 months (Summerfield et al. 2012).

Once heart failure has developed, the prognosis becomes considerably more serious—in Dobermans in particular, DCM is then one of the heart diseases with the poorest prognosis. After the onset of heart failure, the prognosis is often considerably limited; older studies sometimes report very short survival times, although modern diagnostics and treatment can influence the course. Dogs of other breeds survive longer on average, with wide variation. Such figures are averages; an individual dog may do considerably better or worse, depending on how well they respond to treatment.

The unpredictable risk is sudden cardiac death. One reason the course is hard to predict is malignant arrhythmias. In Dobermans, sudden cardiac death plays a particularly important role; various studies show that a substantial proportion of affected dogs die of it—sometimes already in the silent phase, when the dog still looks perfectly fit on the outside. In Boxers (ARVC), this risk is likewise in the foreground. That is exactly why the annual 24-hour ECG (Holter) is so important in at-risk breeds: it can reveal such arrhythmias early so that they can be treated specifically—although whether this prevents sudden cardiac death in an individual dog is not established.

The big exception is the diet-associated form. When diet-associated DCM is detected early, the prognosis is fundamentally different: in many of these dogs, heart function can partially or largely recover after a change of food (and taurine/carnitine supplementation, if needed), and some dogs can improve markedly and remain stable for a long time. In breeds with a taurine connection—such as the Cocker Spaniel—the disease also often responds better.

The bottom line: the earlier DCM is detected—ideally by ultrasound in the awake dog and, in at-risk breeds, by Holter—the greater the chance of giving the dog a lot more good time. In the at-risk breeds, early detection is one of the most effective levers.

12. What you can do at home

Watch stamina, breathing and appetite, and measure the resting respiratory rate if in doubt. Always take fainting episodes seriously. Make use of the annual checkup—with targeted heart screening for at-risk breeds. And if anesthesia is coming up: have the heart assessed in the awake dog beforehand whenever possible.

👉 What matters when choosing one: Choosing a Good Veterinarian

Two more things belong in the daily life of a dog with a known finding. The first is managing exertion: exercise remains right and important; what goes are the peaks—the long, fast run, revving up in the heat, endlessly chasing the ball. Several calm, even sessions are the better way to split it up.

The second is keeping records. A simple list with the date, resting respiratory rate and anything unusual is worth more at the vet appointment than any recollection—especially for fainting episodes, which are rare and hard to describe after the fact.

13. When to see the vet immediately

DCM progresses quietly for a long time and can then turn quickly. Five situations do not allow waiting.

Fainting or near-fainting. A brief collapse, often during excitement or exertion, sometimes followed by completely normal behavior. Precisely because the dog seems like their usual self afterward, it is often dismissed—yet syncope in an at-risk breed is a sign of an arrhythmia and should be investigated the same day.

Marked difficulty breathing at rest. Labored abdominal breathing, an outstretched neck, a dog that no longer wants to lie down.

Pale, gray or bluish mucous membranes. Check the gums.

A rapidly expanding belly combined with declining stamina. This can be fluid building up in the abdomen.

A sustained rise in the resting respiratory rate above your dog’s own baseline, especially together with restlessness or loss of appetite.

A word of context that matters at this point: sudden cardiac death in Dobermans and Boxers cannot be foreseen through observation. That is exactly why screening, not waiting for symptoms, takes priority in these breeds—if you wait for signs, in some dogs you are waiting for something that never comes before the event occurs.

14. Limits and when to see a specialist

This article cannot replace an examination. If your dog is coughing, losing stamina, breathing abnormally or fainting, have them seen promptly. A suspicion of DCM—and all the more so a chance finding under anesthesia—should be clarified with a cardiology echocardiogram in the awake dog. And because the nutrition question in particular is still evolving scientifically, it pays to rely on current veterinary assessments on this topic rather than on sweeping verdicts about food.

15. Conclusion

DCM is a serious but treatable heart muscle disease with a long silent phase—which is why early detection by cardiac ultrasound and, in at-risk breeds, a 24-hour ECG is crucial. Just as important is putting findings in proper perspective: not every enlarged, “weak” heart finding is automatically DCM. When in doubt, a cardiac ultrasound in the awake dog—in hands experienced in cardiology—confirms the diagnosis before it turns into lifelong therapy. That way, two mistakes can be avoided at once: the overlooked genuine disease and the unnecessary treatment of a healthy heart.

If you take away just one thing from this article: in a predisposed breed, it is not observation that decides, but the appointment. DCM shows up on ultrasound and on the 24-hour ECG long before it shows up in behavior—and in some dogs it only shows up in behavior when it is too late.

And if a heart finding comes from anesthesia: do not dismiss it, but do not treat it either until it has been confirmed in the awake dog.

Key takeaways on DCM in dogs

The silent phase is the real problem. A dog can look perfectly fit on the outside while measurable changes have long been visible on cardiac ultrasound. That is why, in at-risk breeds, screening is what counts, not watching for symptoms.

DCM does not necessarily cause a heart murmur. Unlike mitral valve disease, it can be missed by listening alone—that is the most important practical difference between the two diseases.

In Boxers, a distinct form takes center stage. Arrhythmogenic right ventricular cardiomyopathy shows up mainly as arrhythmias, often before pumping strength declines. That is why the 24-hour ECG is the central screening method there.

A negative genetic test does not rule out DCM. The disease is polygenic, and the variants DCM1 and DCM2 described for American Dobermans have so far not been confirmed in European populations (Niskanen et al., 2023). Genetic tests are valuable mainly for breeding decisions.

Heart findings under anesthesia should be read with caution. Under dexmedetomidine, fractional shortening in healthy dogs fell from around 41 to about 24 percent (Wang et al., 2016)—below the usual lower limit of normal. Such a finding should be confirmed in the awake dog before treatment begins.

“Nutritional DCM” is not proven and should still be taken seriously. Proof of cause and effect is lacking, the data are contradictory, and taurine deficiency alone does not explain the cases. In some dogs, findings improve after a change in diet—genetic DCM usually cannot be reversed that way.

Pimobendan delays here, too. For Dobermans with preclinical DCM, the PROTECT study showed a benefit in the silent phase, provided defined ultrasound criteria are met.

Syncope is not a harmless incident. Even if the dog seems like their usual self afterward, a brief collapse in an at-risk breed is a sign of an arrhythmia.

References

• Wess, G., Domenech, O., Dukes-McEwan, J., Häggström, J. & Gordon, S. (2017): European Society of Veterinary Cardiology screening guidelines for dilated cardiomyopathy in Doberman Pinschers. Journal of Veterinary Cardiology 19(5): 405–415. https://doi.org/10.1016/j.jvc.2017.08.006 (ESVC screening guideline: echo + Holter, annual screening from 3 years of age)
• Summerfield, N. J., Boswood, A., O'Grady, M. R., Gordon, S. G., Dukes-McEwan, J., Oyama, M. A. et al. (2012): Efficacy of pimobendan in the prevention of congestive heart failure or sudden death in Doberman Pinschers with preclinical dilated cardiomyopathy (the PROTECT Study). Journal of Veterinary Internal Medicine 26(6): 1337–1349. https://doi.org/10.1111/j.1939-1676.2012.01026.x (in occult Doberman DCM, pimobendan delays heart failure/sudden death and prolongs survival)

• Freeman, L. M., Stern, J. A., Fries, R., Adin, D. B. & Rush, J. E. (2018): Diet-associated dilated cardiomyopathy in dogs: what do we know? Journal of the American Veterinary Medical Association 253(11): 1390–1394. https://doi.org/10.2460/javma.253.11.1390

• Freeman, L. M., Rush, J. E., Adin, D. B. et al. (2022): Prospective study of dilated cardiomyopathy in dogs eating nontraditional or traditional diets and in dogs with subclinical cardiac abnormalities. Journal of Veterinary Internal Medicine 36(2): 451–463. https://doi.org/10.1111/jvim.16397 (recent prospective study on diet-associated DCM)
• U.S. Food and Drug Administration (2019): FDA Investigation into Potential Link between Certain Diets and Canine Dilated Cardiomyopathy. https://www.fda.gov/animal-veterinary/outbreaks-and-advisories/fda-investigation-potential-link-between-certain-diets-and-canine-dilated-cardiomyopathy
• Wang, H.-C., Hung, C.-T., Lee, W.-M., Chang, K.-M. & Chen, K.-S. (2016): Effects of intravenous dexmedetomidine on cardiac characteristics measured using radiography and echocardiography in six healthy dogs. Veterinary Radiology & Ultrasound 57(1): 8–15. https://doi.org/10.1111/vru.12305 (fractional shortening fell from ~41% to ~24%, chamber dimensions increased—evidence of the influence of sedation on echo measurements)
• Meurs, K. M., Lahmers, S., Keene, B. W., White, S. N., Oyama, M. A., Mauceli, E. & Lindblad-Toh, K. (2012): A splice site mutation in a gene encoding for PDK4, a mitochondrial protein, is associated with the development of dilated cardiomyopathy in the Doberman pinscher. Human Genetics 131(8): 1319–1325. https://doi.org/10.1007/s00439-012-1158-2 (original paper behind the test marketed as “DCM1”: 16 base pairs are missing at the splice site of intron 10 of the PDK4 gene on chromosome 14; American Dobermans)
• Meurs, K. M., Friedenberg, S. G., Kolb, J. et al. (2019): A missense variant in the titin gene in Doberman pinscher dogs with familial dilated cardiomyopathy and sudden cardiac death. Human Genetics 138(5): 515–524. https://doi.org/10.1007/s00439-019-01973-2 (original paper behind the test marketed as “DCM2”; the family studied did not carry the PDK4 variant)
• Owczarek-Lipska, M., Mausberg, T. B., Stephenson, H., Dukes-McEwan, J., Wess, G. & Leeb, T. (2013): A 16-bp deletion in the canine PDK4 gene is not associated with dilated cardiomyopathy in a European cohort of Doberman Pinschers. Animal Genetics 44(2): 239. https://doi.org/10.1111/j.1365-2052.2012.02396.x (the DCM1 variant was not associated with the disease in a European cohort)
• Niskanen, J. E., Ohlsson, Å., Ljungvall, I. et al. (2023): Identification of novel genetic risk factors of dilated cardiomyopathy: from canine to human. Genome Medicine 15(1): Article 73. https://doi.org/10.1186/s13073-023-01221-3 (540 Dobermans from Germany, Finland, the Netherlands, Slovenia and Sweden; two independent risk loci on chromosome 5 with the candidate genes RNF207 and PRKAA2; at the loci marketed as DCM1 (PDK4) and DCM2 (TTN), no signal was found in this European cohort, and they were not predictive of disease risk; ventricular premature complexes as the sole abnormality were not associated with either locus)

Frequently asked questions about DCM in dogs

What owners ask most often