Mitral Valve Disease (MMVD) in Dogs: Heart Murmur, Symptoms, and Treatment

In brief

There are five things you should know about mitral valve disease. First: MMVD (myxomatous mitral valve disease, formerly called “endocardiosis”) is the most common acquired heart disease in dogs—the mitral valve thickens and becomes deformed, so it no longer closes tightly and blood leaks backward. Second: it mainly affects small to medium-sized breeds (above all the Cavalier King Charles Spaniel), and the risk rises with age. Third: MMVD almost always gives itself away through a heart murmur that the veterinarian hears with the stethoscope—often years before the dog shows any symptoms at all. Fourth: MMVD cannot be cured, but in many cases it can be managed well for a long time; what matters is the stage at which it is detected. Fifth, and this surprises most people: coughing is a poor heart marker. In dogs with a heart murmur, the widely cited “cardiac cough” very often comes from the airways rather than the heart—the more reliable early warning sign is the resting respiratory rate.

For many owners, a heart murmur at the annual checkup is their first contact with the topic. This article explains what happens at the valve, which dogs are affected, how to recognize signs of progression, how the disease is diagnosed and treated depending on the stage, which complications can arise along the way—and how MMVD differs from the other major heart disease, DCM.

Note: This article is general information and does not replace a veterinary diagnosis. A heart murmur or a suspected heart condition should always be evaluated by a veterinarian, ideally a veterinary cardiologist.

👉 Prevention and health at a glance: dog health basics

1. What is MMVD—and what happens at the valve?

The mitral valve sits between the left atrium and the left ventricle. It works like a check valve: when the ventricle contracts, the valve is supposed to close tightly so that blood is pumped only forward into the body’s circulation and not back into the atrium.

In MMVD, the valve tissue changes slowly and progressively. The delicate valve leaflets thicken, become nodular, and lose their elasticity; the supporting cords (chordae tendineae) can be affected as well. The result: the valve no longer closes completely, and with every heartbeat part of the blood flows back into the left atrium—this is called mitral regurgitation, or a leaky valve. It is exactly this backflow that produces the typical heart murmur.

The body compensates for a long time, in two ways. Mechanically, the atrium and ventricle dilate to accommodate the blood that has leaked back. Hormonally, regulatory systems kick in that raise blood pressure and fluid retention to maintain cardiac output—useful in the short term, but in the long run an additional burden on a heart that is already overloaded. This is exactly where several of the drugs used later come in. That is why the disease can remain free of symptoms for years. Only when compensation is no longer enough does blood back up into the lungs, which can lead to pulmonary edema (“fluid in the lungs”) and thus to heart failure.

2. Which dogs are affected

MMVD is typically a disease of small to medium-sized breeds. The Cavalier King Charles Spaniel is affected particularly often and often early; in this breed the disease has a strong hereditary component and can appear at a comparatively young age. Dachshunds, Chihuahuas, miniature and toy poodles, small terriers, Maltese, and many other small breeds are also among those at risk.

Two patterns matter. First: the risk rises markedly with age—in older small-breed dogs, a heart murmur is nothing unusual. Second: males develop the disease somewhat earlier on average, and it often progresses faster in them than in females. That does not mean every small dog will develop it or that large breeds are never affected—but breed and age help put a heart murmur into context.

In practical terms, this tells you when listening to the heart becomes worthwhile. In a Cavalier King Charles Spaniel, the heart belongs in every routine exam from the start, not only in the senior years. In other small breeds, an annual check from middle age onward is a sensible starting point—and once a murmur has been heard, the question is no longer whether to monitor, but how often.

Conversely: a large dog whose stamina is declining is statistically more likely to have a different problem. That does not mean his heart is healthy—the other major heart disease covered in section 10 affects large breeds in particular and often makes no murmur.

3. Symptoms—from a silent heart murmur to heart failure

For a long time, the heart murmur is the only sign—the dog notices nothing, and neither does the owner. This phase can last for years. As the leak progresses, symptoms gradually appear:

• faster or labored breathing, especially at rest—one of the most reliable signs of beginning fluid congestion
• reduced exercise tolerance, tiring faster on walks
• coughing—common, but far less meaningful than is generally assumed (see the next section)
• fainting episodes (syncope) during exertion or excitement
• in the advanced stage, signs of heart failure: marked shortness of breath, restlessness, pale or bluish mucous membranes

An especially valuable marker you can check at home is the resting respiratory rate. Count the breaths per minute while your dog is sleeping peacefully (one rise and fall of the chest = one breath). Persistently more than about 30 breaths per minute at rest in an otherwise stable dog—particularly one with known heart disease—is a warning sign of beginning fluid congestion and a reason to have your dog checked by a veterinarian promptly. What matters is that you really count a resting or sleeping dog, not one dozing after a walk.

👉 When your dog truly rests: sleep and learning in dogs

4. The resting respiratory rate: the most important value you collect yourself

This section is the most practically useful part of the whole article. Measuring the resting respiratory rate costs nothing, requires no equipment, and is one of the most reliable early indicators of fluid beginning to build up in the lungs.

4.1 How to measure

Count while your dog is sleeping peacefully—not dozing and not right after a walk. One rise and fall of the chest is one breath. Count for 30 seconds and double it, or count for a full minute if your dog is lying still enough.

It is important to know what does not count: panting is not a respiratory rate in this sense, and a dog that is dreaming, twitching, or has just fallen asleep will not give you a usable value. Wait until the breathing is steady.

4.2 Why your dog’s own baseline is worth more than the reference value

As a rough guideline, persistently more than about 30 breaths per minute at rest is considered a warning sign. More meaningful, however, is your dog’s individual baseline.

Measure it on three to five consecutive days while your dog is stable, and write the values down. A dog that normally sits at 16 and suddenly comes in at 28 is cause for attention—even though 28 is below the reference value. Another dog that always sits at 26 is not, at 28.

That is exactly why the measurement taken while your dog is stable is the more important one. If you only start counting when something seems wrong, you have nothing to compare against.

4.3 How often, and how to record it

In stage B1, once a week is enough; in stages B2 and C, daily measurements are common—your veterinary practice will decide. A simple list with date and value is all you need; a photo of it at the appointment says more than any description.

And one point that can save you some worry: a single elevated reading is not an emergency. What counts is a sustained increase over several measurements—or a very marked jump together with other signs.

5. The myth of the “cardiac cough”

Few ideas are as stubborn as this one: the small old dog is coughing, he has a heart murmur, so the cough must be coming from his heart. This equation appears in many textbooks—and according to current knowledge it does not hold up in this form.

The anatomical reason is simple: cough receptors are located in the large, upper airways. The fluid in pulmonary edema, by contrast, collects in the air sacs (alveoli) and the interstitial tissue—where there are hardly any cough receptors. Pulmonary edema therefore shows up mainly as rapid and labored breathing; coughing alone, however, is not a reliable indicator of heart failure.

The data so far support this. An analysis of 358 dogs with MMVD from two pre-existing studies suggests that existing heart failure does not reliably explain the likelihood of coughing: in that analysis, dogs with heart failure coughed about as often as dogs in the symptom-free stage. An increase appeared only with a severely enlarged left atrium, not with mild or moderate enlargement (Rishniw et al. 2026). And even this association is probably not mechanical: in a study in which four independent board-certified radiologists assessed 51 radiograph series, coughing and non-coughing dogs could not be distinguished by the degree of bronchial narrowing—the authors consider compression of the bronchi by the enlarged heart unlikely as the cause of the cough (van Opstal et al. 2025). An earlier study had already found no association between atrial size and airway collapse, but very frequent airway inflammation (Singh et al. 2012).

So what is causing the cough in many cases? Often the airways themselves are involved. Precisely the small, older dogs that develop MMVD are disproportionately likely to have chronic bronchitis, tracheal collapse, or bronchomalacia at the same time. Two diseases in the same dog—and the cough then often has nothing to do with the heart.

Why this matters in practice: if the cough is wrongly interpreted as a cardiac cough, the dog is given diuretics it does not need. The tricky part is that this often seems to work anyway. Furosemide does not only remove fluid; it is also credited with anti-inflammatory and cough-suppressing properties, while a bronchodilating effect has so far been described mainly in cats and humans and has not been established in dogs. The cough can therefore improve even though there was never any pulmonary edema. The apparent treatment success can then confirm the wrong diagnosis, while the actual airway disease goes untreated and the dog is dehydrated unnecessarily.

What this means for you: coughing alone does not prove heart failure, and a heart murmur alone does not turn a cough into a cardiac cough. The distinction is made through examination—resting respiratory rate, chest radiographs, echocardiography—not by how the cough sounds. And human cough suppressants from your own medicine cabinet are especially dangerous here: they suppress a symptom whose cause nobody knows.

👉 Why this is dangerous: never give your dog medications from your own medicine cabinet

6. What else could it be? Differential diagnoses

Many people come to this topic because their small dog is coughing, having trouble breathing, or no longer keeping up the way he used to. All of this can have many causes—MMVD is only one of them, and frequently just one of several present at the same time. A few common alternatives to help you put things in context, none of which replaces an examination:

Tracheal collapse and chronic bronchitis: the most important differential diagnoses of all, because they affect the same small, older breeds. Tracheal collapse classically shows up as a dry, “honking” cough, often during excitement or when the dog pulls against the collar.

Laryngeal paralysis: more common in larger dogs, typically with a harsh breathing noise, hoarseness, and problems in the heat and during exertion.

Pulmonary hypertension: can be a consequence of MMVD, but can also develop on its own as a result of airway disease—and likewise causes exercise intolerance and fainting episodes.

Osteoarthritis and age-related muscle loss: in old dogs, declining stamina is quickly blamed on the heart, even though joint pain may be what is really holding the dog back.

The distinction cannot be made from the symptom; it is made through examination—auscultation, radiographs, echocardiography, and, depending on the case, further airway diagnostics.

👉 The underestimated brake in older dogs: recognizing pain in dogs

7. Diagnosis: from heart murmur to staging

The first step is usually auscultation, listening with the stethoscope: in MMVD, a heart murmur over the left apex of the heart is almost always present, and its loudness gives a rough indication of severity. Murmurs are commonly graded from 1 to 6, with louder grades on average going along with a more severe leak. “On average” is meant literally here: the stage cannot be read from loudness alone. Unlike DCM, which does not necessarily produce a murmur, the heart murmur in MMVD is at least a very reliable first marker that something is wrong with the valve at all.

The most important test for a precise assessment is echocardiography (cardiac ultrasound): it shows the altered valve, the extent of the backflow, and—crucial for treatment—whether the atrium and ventricle are already enlarged. Standardized measurements are used for this, including the ratio of the left atrium to the aorta and the ventricular diameter normalized to body size. These are supplemented by chest radiographs (heart size via the vertebral heart score, pulmonary congestion, airways) and blood biomarkers such as NT-proBNP. Biomarkers are pointers, not decision-makers: an elevated value supports the suspicion of cardiac strain but replaces neither ultrasound nor radiographs. The echocardiogram itself is painless, non-invasive, and as a rule does not require anesthesia.

These findings determine the stage according to the ACVIM guidelines (Keene et al. 2019), which guides treatment:

• Stage A: an at-risk breed with no detectable change to the heart (e.g., a young, healthy Cavalier).
• Stage B1: leak and heart murmur present, but normal-sized or only slightly enlarged heart chambers that do not meet the B2 criteria—no treatment needed yet.
• Stage B2: leak with an enlarged heart (defined ultrasound and radiographic criteria), but still without symptoms—this is where drug treatment begins.
• Stage C: current or past heart failure (e.g., pulmonary edema).
• Stage D: heart failure that is refractory despite standard treatment.

This staging is more than theory: it decides whether and when medication makes sense. That is why the frequency of checkups in stage B1 is not a formality—it is meant to catch the transition to B2, and that transition does not announce itself through symptoms.

8. Treatment—depending on the stage

MMVD cannot be cured, but it can be treated well. The goal is to delay the transition to heart failure and, once it has occurred, to relieve the strain on the heart.

In stage B1, the disease is not treated but monitored—usually with regular follow-up examinations so that the transition to B2 is not missed.

In stage B2, that is, an enlarged heart without symptoms, the EPIC study provided important evidence: the drug pimobendan markedly delays the onset of heart failure—the median symptom-free period was extended from about 766 to 1,228 days, or by roughly 15 months (Boswood et al. 2016). Pimobendan strengthens the contraction of the heart muscle and at the same time dilates the blood vessels, lowering the resistance the heart has to pump against. Starting pimobendan at this stage is standard today.

In stage C (heart failure), a combination is used that acts at different points: diuretics such as furosemide flush out the fluid buildup, pimobendan supports pumping function, and an ACE inhibitor and often spironolactone dampen the hormonal regulatory systems that put additional long-term strain on the heart—spironolactone acts specifically as an antagonist of the hormone aldosterone, which otherwise promotes water and salt retention and fibrotic remodeling of the heart muscle. This combination often restores quality of life quickly. That dogs with existing heart failure lived longer on pimobendan than on the ACE inhibitor benazepril (each in addition to the other therapy) had already been shown by the QUEST study in 260 dogs (Häggström et al. 2008). In stage D, doses are adjusted, the diuretic may be switched, and further drugs are added. We deliberately do not give specific doses here: they depend on weight, kidney function, blood values, and concurrent diseases and belong in the hands of your veterinarian, tailored to your dog.

For selected cases, surgical mitral valve repair is now available—open-heart surgery on cardiopulmonary bypass and the only option with a potentially curative aim. The valve ring is tightened and ruptured chordae are replaced with artificial ones (Uechi 2012). It is offered at only a few specialized centers worldwide, is technically demanding, involves considerable cost, and requires careful selection of suitable patients.

Results at experienced centers are good but depend heavily on the stage: dogs in earlier stages come through the procedure considerably more reliably than dogs with far-advanced, refractory heart failure. The team’s experience probably plays a role as well: during the documented build-up of a European program, short-term outcomes improved markedly as the program progressed (Brockman et al. 2025)—consistent with a learning curve, even though a single clinic cannot separate out which factors exactly were behind it. If you are considering this route, it is worth asking the center specifically about its case numbers.

In addition, a much less invasive procedure has become established: in TEER (transcatheter edge-to-edge repair), a clip is placed on the beating heart through a small incision in the chest wall; it fastens the valve leaflets together and thereby reduces the leak—without cardiopulmonary bypass. It is an option for a narrower group of dogs, depending among other things on body weight and valve anatomy, and is now offered at a number of specialized centers.

For the vast majority of dogs, medical treatment remains the way forward.

9. Complications along the way

MMVD usually progresses slowly, but it can lead to complications that suddenly change its course. Four are relevant for putting things in context.

Ruptured chorda (chordae tendineae rupture): if one of the supporting cords that guide the valve leaflet tears, the leak suddenly gets much worse. The typical picture is a dog who is markedly worse overnight even though he was stable the day before—often with acute shortness of breath.

Left atrial tear: a severely stretched atrium can tear. If blood leaks into the pericardial sac, an acutely life-threatening situation develops, with sudden weakness, pale mucous membranes, and collapse. Rare, but an emergency.

Pulmonary hypertension: the backup into the pulmonary blood vessels can raise the pressure there permanently. Pulmonary hypertension is not uncommon in MMVD and is associated with a worse prognosis (Borgarelli et al. 2015). Important for treatment: if the pulmonary hypertension is caused by the left-sided heart disease itself—group 2 in the ACVIM classification—relieving the left heart takes priority. In this situation, vasodilating drugs such as sildenafil are explicitly not the first choice (Reinero et al. 2020). That does not rule out their use in individual cases, but it makes it a decision for the cardiologist rather than an automatic step.

Strain on the kidneys: heart and kidneys are closely linked. Diuretics are indispensable in heart failure but can worsen kidney values—especially in old dogs, who often already have reduced kidney function. That is why monitoring of blood and kidney values is part of ongoing treatment; it is always a balance between sufficient fluid removal and protecting the kidneys. In practical terms for you: water must be freely available at all times—never combine diuretics with restricting how much your dog drinks—and markedly increased thirst, loss of appetite, vomiting, or unusual tiredness should be checked promptly.

10. MMVD or DCM? The difference at a glance

Because both are the most common heart diseases in dogs and both can lead to heart failure, they are often confused. The core difference: in MMVD, a valve is leaking; in DCM, the heart muscle itself is weakened.

This gives rise to practical distinguishing features. MMVD mainly affects small to medium-sized breeds and almost always causes a distinct heart murmur. DCM mainly affects large and giant breeds (the Doberman being the classic example) and does not necessarily produce a murmur—it can be missed by listening alone and sometimes first becomes apparent through arrhythmias or sudden cardiac death. The screening path differs as well: in MMVD, the murmur that is heard leads to the ultrasound; in breeds at risk for DCM, active annual screening with ultrasound and Holter monitoring (24-hour ECG) is needed, because there is no reliable warning sign to listen for.

👉 The big counterpart of this disease: dilated cardiomyopathy (DCM) in dogs

11. Prognosis and life expectancy

Overall, the prognosis for MMVD is better than for many other heart diseases—and strongly dependent on the stage. Many dogs live completely unburdened with a stage B leak for years; quite a few small dogs eventually die with their MMVD, not of it. What matters is that the transition to the phase that needs treatment is recognized and treated in time.

Once heart failure (stage C) has set in, the prognosis becomes more serious but remains very individual: many dogs stay stable and full of life on combination therapy for quite some time, while others progress more quickly. How much time remains depends on the response to treatment, the degree of atrial enlargement, accompanying complications such as pulmonary hypertension or a ruptured chorda, and kidney function. Fixed numbers for an individual dog cannot responsibly be given—that assessment belongs with the treating cardiologist.

12. Everyday life, feeding, and what you can do at home

Take a heart murmur found at a checkup seriously and have it evaluated, even if your dog seems fit—especially in the silent phase, the right monitoring decides how things go from there.

The most important value you collect at home is the resting respiratory rate. It is easy to measure, costs nothing, and is one of the most reliable early warning signs of beginning fluid congestion. Even more meaningful than the reference value is your dog’s individual baseline: measure the resting respiratory rate on three to five consecutive days while your dog is stable, and write it down. Later, you compare against his own normal value instead of a textbook figure and will notice a deviation much earlier.

Keep your dog lean—excess weight puts additional strain on a heart that is already working hard. Conversely, in the advanced stage the opposite applies: weight loss without a diet is a warning sign, because heart disease can break down muscle mass. Both are worth keeping an eye on.

Exercise remains allowed and worthwhile. What goes are peaks of exertion: instead of one long, fast outing, several calm, steady walks are better, and you should cut back considerably in the heat. A harness instead of a collar is often more comfortable for dogs that also have airway problems. A particularly low-sodium special diet is not necessary in stage B according to current knowledge; what makes sense is a balanced diet and avoiding heavily salted snacks.

👉 Easing the heart also means: how to recognize your dog’s ideal weight

13. When to see the vet immediately

MMVD usually progresses slowly. Some situations, however, are acute and cannot wait until the next business day.

Marked shortness of breath at rest. Labored abdominal breathing, an outstretched neck, a dog who no longer wants to lie down or will only sit upright.

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

Collapse or near-collapse. Even if your dog recovers afterward.

A sudden decline overnight in a dog who was stable the day before. This is the typical picture after the rupture of a chorda described in section 9.

A marked, sustained rise in the resting respiratory rate above your dog’s own baseline—especially together with restlessness or reduced exercise tolerance.

The last two points reflect the connection from section 9: a heart that has compensated for years can lose that compensation within a short time. What was a gradual course yesterday is then an emergency.

14. Limits of the evidence

As well researched as MMVD is, open questions remain. The best time to start treatment in the gray zone between B1 and B2 is not always clear-cut in the individual case, and even the criteria for an “enlarged heart” are debated among specialists. Whether an ACE inhibitor in addition to pimobendan is beneficial as early as stage B2 has not been conclusively resolved.

The last word on coughing has not been spoken either: that heart failure alone does not explain the cough is supported by several studies, but why a severely enlarged atrium in particular goes along with more coughing, if mechanical compression is not the reason, remains open. In addition, some of the available studies are small or retrospective.

The home value from section 4 has its limits, too. The resting respiratory rate is well established as a monitoring measure, but it is nonspecific: fever, pain, excitement, and airway disease raise it as well. So it tells you that something is wrong—not what.

And in general: the major studies refer to particular breeds, weight classes, or starting situations—not every figure can be transferred one-to-one to every dog. The guidelines provide a very good framework, but the specific decision belongs in experienced cardiological hands.

15. Conclusion

MMVD is the most common acquired heart disease in dogs and mainly affects small to medium-sized breeds such as the Cavalier King Charles Spaniel. It reveals itself early through a heart murmur, then runs a silent course for a long time, and can be managed well using the ACVIM stages: in the symptom-free phase with an enlarged heart (B2), pimobendan delays the onset of heart failure; once heart failure is present (C), combination therapy stabilizes quality of life. Two things are worth remembering: take a heart murmur seriously and have it properly classified by ultrasound rather than missing the right time to start treatment—and do not be quick to blame a cough on the heart, but use the resting respiratory rate as the more reliable value.

For everyday life, a simple sequence remains: have the murmur evaluated, even if your dog seems fit. Establish your dog’s own resting respiratory rate baseline while everything is stable. And do not be quick to blame a cough on the heart—in these dogs, the more common explanation often lies in the airways themselves.

👉 What matters when you choose: what makes a good veterinarian

Key takeaways on mitral valve disease

A heart murmur is a finding, not a disease. The silent phase can last for years, and many small dogs eventually die with their MMVD, not of it. What matters is not missing the transition to the stage that needs treatment.

The stages guide treatment, not the symptoms. In stage B2—an enlarged heart, but no clinical signs—medication begins. This stage does not announce itself through symptoms, only through monitoring (Keene et al., 2019).

Pimobendan measurably delays onset. The median symptom-free period was extended from about 766 to 1,228 days, or by roughly 15 months (Boswood et al., 2016).

The “cardiac cough” does not hold up in this form. Cough receptors are located in the upper airways, while pulmonary edema collects in the alveoli. An increase appeared only with a severely enlarged left atrium, not with existing heart failure as such.

Small older dogs often have two diseases at once. Chronic bronchitis, tracheal collapse, and bronchomalacia affect the same group. If the cough is attributed to the wrong cause, the dog is given diuretics it does not need.

The resting respiratory rate is the most important value to track at home. More meaningful than any reference value is your dog’s own baseline, measured while he is stable—if you only start counting when things get serious, you have nothing to compare against.

Pulmonary hypertension is associated with a worse prognosis and calls for different treatment depending on whether it is a consequence of the left-sided heart disease or has developed independently (Borgarelli et al., 2015; Reinero et al., 2020).

Heart and kidneys are linked. Diuretics are indispensable in heart failure and can worsen kidney values. Ongoing monitoring is therefore part of treatment.

References

• Keene, B. W., Atkins, C. E., Bonagura, J. D., Fox, P. R., Häggström, J., Luis Fuentes, V., Oyama, M. A., Rush, J. E., Stepien, R. & Uechi, M. (2019): ACVIM consensus guidelines for the diagnosis and treatment of myxomatous mitral valve disease in dogs. Journal of Veterinary Internal Medicine 33(3): 1127–1140. https://doi.org/10.1111/jvim.15488 (the authoritative guideline, including stages A/B1/B2/C/D and treatment)

• Boswood, A., Häggström, J., Gordon, S. G., Wess, G., Stepien, R. L., Oyama, M. A. et al. (2016): Effect of Pimobendan in Dogs with Preclinical Myxomatous Mitral Valve Disease and Cardiomegaly: The EPIC Study – A Randomized Clinical Trial. Journal of Veterinary Internal Medicine 30(6): 1765–1779. https://doi.org/10.1111/jvim.14586 (in stage B2, pimobendan delays the onset of heart failure; 1,228 vs. 766 days)

• Häggström, J., Boswood, A., O'Grady, M., Jöns, O., Smith, S., Swift, S. et al. (2008): Effect of pimobendan or benazepril hydrochloride on survival times in dogs with congestive heart failure caused by naturally occurring myxomatous mitral valve disease: the QUEST study. Journal of Veterinary Internal Medicine 22(5): 1124–1135. https://doi.org/10.1111/j.1939-1676.2008.0150.x (260 dogs with heart failure due to MMVD; treatment of established heart failure)

• Borgarelli, M., Savarino, P., Crosara, S. et al. (2008): Survival characteristics and prognostic variables of dogs with mitral regurgitation attributable to myxomatous valve disease. Journal of Veterinary Internal Medicine 22(1): 120–128. https://doi.org/10.1111/j.1939-1676.2007.0008.x (558 dogs from 36 breeds; prognostic data)

• Borgarelli, M., Abbott, J., Braz-Ruivo, L. et al. (2015): Prevalence and prognostic importance of pulmonary hypertension in dogs with myxomatous mitral valve disease. Journal of Veterinary Internal Medicine 29(2): 569–574. https://doi.org/10.1111/jvim.12564 (pulmonary hypertension in MMVD: frequency and prognostic significance)

• Reinero, C., Visser, L. C., Kellihan, H. B., Masseau, I., Rozanski, E., Clercx, C., Williams, K., Abbott, J., Borgarelli, M. & Scansen, B. A. (2020): ACVIM consensus statement guidelines for the diagnosis, classification, treatment, and monitoring of pulmonary hypertension in dogs. Journal of Veterinary Internal Medicine 34(2): 549–573. https://doi.org/10.1111/jvim.15725 (group 2 = pulmonary hypertension due to left heart disease; PDE5 inhibitors not the first choice there)

• Rishniw, M., Borgarelli, M., Ferasin, L. & Menciotti, G. (2026): Severe left atrial enlargement, but not congestive heart failure, increases the probability of coughing in dogs with mitral valve disease. Journal of the American Veterinary Medical Association 264(5). https://doi.org/10.2460/javma.25.07.0507 (358 dogs from two studies; heart failure did not increase the probability of coughing, only severe atrial enlargement did)

• Uechi, M. (2012): Mitral valve repair in dogs. Journal of Veterinary Cardiology 14(1): 185–192. https://doi.org/10.1016/j.jvc.2012.01.004 (overview of the technique: annuloplasty and artificial chordal replacement)

• Uechi, M., Mizukoshi, T., Mizuno, T., Mizuno, M., Harada, K., Ebisawa, T. et al. (2012): Mitral valve repair under cardiopulmonary bypass in small-breed dogs: 48 cases (2006–2009). Journal of the American Veterinary Medical Association 240(10): 1194–1201. https://doi.org/10.2460/javma.240.10.1194

• Brockman, D. J., Greensmith, T. D., Rossanese, M., Young, A., Carey, S. L., Boswood, A. et al. (2025): Improvement in short-term outcome over time, in a single center embarking on a canine mitral valve repair program using a structured multidisciplinary approach. Veterinary Surgery. https://doi.org/10.1111/vsu.14229 (learning curve of a European center: better results as the program progressed)

• van Opstal, K. Y., Kittleson, M. D., Teske, E., Auriemma, E., van den Broek, H., Spattini, G., Vilaplana Grosso, F. R. & Szatmári, V. (2025): No Correlation Between Chronic Cough and Radiographic Signs of Bronchial Narrowing in Dogs with Cardiomegaly and Left Atrial Dilation Secondary to Primary Mitral Valve Regurgitation. Animals 15(17): 2510. https://doi.org/10.3390/ani15172510 (bronchial compression by the enlarged heart unlikely as the cause of cough)

• Singh, M. K., Johnson, L. R., Kittleson, M. D. & Pollard, R. E. (2012): Bronchomalacia in Dogs with Myxomatous Mitral Valve Degeneration. Journal of Veterinary Internal Medicine. https://doi.org/10.1111/j.1939-1676.2012.00887.x (no association between atrial size and airway collapse; airway inflammation common)

Frequently asked questions about MMVD in dogs