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Genetic Welfare Problems of Companion Animals
An information resource for prospective pet owners
Miniature Schnauzer
Mitral Valve Disease (MVD)
Related terms: myxomatous mitral valve degeneration (MMVD), mitral valve disease (MVD), degenerative valve disease (DVD), degenerative mitral valve disease (DMVD), endocardiosis, mitral regurgitation (MR), chronic valve (valvular) disease, chronic mitral valve disease, valvular insufficiency, acquired mitral regurgitation, chronic valvular degeneration, chronic valvular fibrosis
Outline: Mitral valve disease is a serious, progressive disease of the heart, caused by the deterioration of one of its valves. It is the most common heart disease of adult dogs and is more prevalent in the Miniature schnauzer than the average dog. It has a serious impact on welfare, causing respiratory and other difficulties, with severe discomfort due to breathlessness and coughing. Unless animals are euthanased, the disease causes death by chronic heart failure.
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Summary of Information
(for more information click on the links below)
1. Brief description
Mitral valve disease is a disease of the heart, caused by the deterioration of one of its valves. It is a common disease in Miniature schnauzers. Because of the damage to the valve, with each heart beat some blood is forced backwards from one chamber into another rather than out of the heart (mitral regurgitation).
One effect of this backflow of blood is that the heart enlarges and the knock on effects of this interfere with breathing and cause the dog to cough. At the same time, as less oxygenated blood is being pumped around the body, any exertion can result in the dog panting heavily and struggling for breath. As the disease progresses the lungs become increasingly fluid filled resulting in further breathlessness and coughing. Affected dogs may be reluctant to sit or lie down, because of the extra pressure this puts on the chest, and may also show appetite and related weight loss (Prošek 2007). They may faint at exercise. Most dogs die or are euthanased when the disease has progressed to this stage.
Dogs with mitral valve disease, but without heart failure, appear normal to their owners and do not have any welfare problems at that time, although they generally have a detectable heart murmur on auscultation (listening with a stethoscope). Most develop heart failure within several years of the onset of mitral valve disease (Häggström et al 2009).
Surgical repair of the valves is rarely a feasible option. Combination drug therapy can usually help to control the early stages of heart failure but the prognosis is guarded (French 2005). Most dogs die less than two years after the onset of heart failure (Kittleson and Kienle 1998).
2. Intensity of welfare impact
Mitral valve disease has a serious impact on the welfare of affected dogs as a result of respiratory and other difficulties. The progressive heart failure causes discomfort associated with breathlessness and coughing. Unless animals are euthanased, they are likely to die of chronic heart failure.
3. Duration of welfare impact
Mitral valve disease is progressive. Treatment is usually aimed at relief of the symptoms rather than cure. The period from when heart failure begins to develop and animals first show adverse welfare signs (eg coughing breathlessness) to death or euthanasia can be years.
4. Number of animals affected
Mitral valve disease is the single most common heart disease of dogs (Egenvall et al 2006. Miniature schnauzers are recognised as one of the breeds most commonly affected with mitral valve dysplasia (Abbott 2003, Rishniw 2005). Individuals of this breed are 4.4 times more likely to be affected than the average dog (Gough & Thomas 2010). However, we are unaware of data on the proportion of Miniature schnauzers that are affected.
5. Diagnosis
Initial diagnosis is by detection of a characteristic heart murmur with a stethoscope, and can be confirmed by ultrasound investigation. Other diagnostic tools may also be used to determine the severity of the disease and the presence of heart failure including ECG (electrocardiogram) recordings, chest radiography, blood tests and full physical examination.
6. Genetics
The known predisposition of Miniature schnauzers to develop mitral valve disease is evidence for a genetic influence on this disease in the breed. It is known that most of the variation in severity of mitral valve disease in some other breeds is genetic, for example, in the Cavalier King Charles spaniel in the UK (Lewis et al 2010) and the Dachshund (Olsen et al 1999). The genetics have not been studied in the Miniature schnauzer.
7. How do you know if an animal is a carrier or likely to become affected?
Dogs that will become affected cannot be detected in earlier life. Because the problem affects middle-aged or older dogs, if the parents of a dog appear unaffected, this does not mean that the individual or its parents are free of the condition. Choosing a dog born to older parents (perhaps 5 years plus) which have not themselves developed mitral valve disease has been advocated (Swenson et al 1996, Häggström 2004a). Knowing that grandparents and great grandparents are free of heart murmurs and heart failure is probably helpful.
8. Methods and prospects for elimination of the problem
Neither the genes involved with mitral valve disease nor the inheritance pattern have been determined. This, plus the late onset of signs makes control currently rather difficult. Currently there are no guidelines or schemes developed to help reduce mitral valve disease in Miniature schnauzers.
Buyers should ask breeders whether the parents have any signs of mitral valve disease and how old they are. A cardiac examination by a veterinary surgeon should be made prior to breeding any dog and if a heart murmur is found then this should be investigated (not all heart murmurs indicate significant disease).
Research is currently underway (for example at the Universities of Minnesota, Missouri and Davis in the USA; the University of Toronto in Canada, and at The Animal Health Trust in England) to improve understanding of the genetic basis of mitral valve disease in various breeds. This is the LUPA project (http://www.eurolupa.org/). The development of genetic tests to help identify the genes involved in the condition may help to eliminate this
For further details about this condition, please click on the following:
(these link to items down this page)
- Clinical and pathological effects
- Intensity of welfare impact
- Duration of welfare impact
- Number of animals affected
- Diagnosis
- Genetics
- How do you know if an animal is a carrier or likely to become affected?
- Methods and prospects for elimination of the problem
- Acknowledgements
- References
1. Clinical and pathological effects
Mitral valve disease is the most common heart disease of adult dogs (Häggström 2004a). When functioning normally, the mitral valve prevents backflow of blood from the left ventricle – the chamber of the heart which pumps blood around the body – back into the smaller left atrium, which receives blood from the lungs. In mitral valve disease, the valve degenerates becoming thicker and less flexible so that it does not close fully. As a result, some blood is forced backwards from the ventricle into the atrium during contractions. As the disease progresses and the valve becomes increasingly distorted, more and more blood gets forced backwards during each contraction and consequently less and less blood is pumped out, around the body (this process is known as mitral regurgitation (Rishniw 2005)).
The backward flow of blood causes a heart murmur, - a change to the normal ‘lubb-dupp’ heart sound (detectable using a stethoscope). This is often the first sign of the condition. In the final stages of the disease, the tendons supporting the valve snap and the valve fails completely (Corcoran 2009, Häggström 2004a), causing heart failure and death.
It is the effect that this valve failure has on the normal functioning of the heart that causes the problems. One effect of the backflow of blood under high pressure from the left ventricle into the left atrium is compensatory enlargement of the atrium. In time, the enlarged heart can begin to interfere with breathing, through increasing pressure on the windpipe, causing coughing. Because the pumping of oxygenated blood around the body is compromised, the heart has to pump harder and faster and any exertion can result in the dog panting heavily and struggling for breath (Merck 2009). Circulation to other parts of the body is weakened as blood flow to the vital organs, such as the brain and lungs, is conserved. Also, because of the higher pressure in the atrium because of the back flow, blood flow from the lungs into the heart is compromised and fluid leaks from the blood vessels of the lungs into the chest and lungs themselves, resulting in further breathlessness and coughing – which in severe chronic heart failure may include coughing up blood-tinged sputum. These signs often imminently precede death (Rishniw 2005).
Affected dogs may be reluctant to sit or lie down, because of the extra pressure this puts on the chest cavity, and may hold their elbows away from their body in an attempt to reduce this. Affected dogs may also show appetite and related weight loss and have a distended abdomen (Häggström 2004a, Prošek 2007). They may even faint on exercise.
Dogs with mitral valve disease, but without heart failure, appear normal to their owners and do not have any welfare problems. Most dogs go on to develop heart failure within several years of the onset of mitral valve disease (Häggström et al 2009).
Other signs of heart disease (before it becomes apparent due to heart failure) can be detected using more sophisticated equipment. Radiographs (x-rays) of the chest may show evidence of heart enlargement and other signs of heart failure.
Some individuals may have irregular heartbeats – arrhythmias which can be detected by electrocardiography (ECG) or using a stethoscope. 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, shape 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. This will show mitral regurgitation.
Many dog breeds are susceptible to mitral valve disease, especially small dog breeds such as Cavalier King Charles spaniels, Cocker spaniels, Toy and Miniature poodles, Papillons, Chihuahuas, Dachshunds, Shih tzus and Lhasa apsos (French 2005, Rishniw 2005, Lundin and Kvart 2010). Typically, it is diagnosed from six to seven years of age onwards (Häggström 2004b).
Surgical treatment of mitral valve disease is unlikely to be practically or economically feasible (Griffiths et al 2004, Orton 2004, Orton et al 2005, Williams et al 2008, Borgarelli and Häggström 2010). A combination drug therapy protocol, including diuretics, ACE inhibitors, inodilators such as pimobendan, and others depending on the individual and stage of disease, is commonly used to control heart failure (Häggström et al 2009, Borgarelli and Häggström 2010). However, drugs therapy, at best only works for a time (Gordon 2004, Häggström et al 2009).
Once the degenerative process associated with mitral valve disease begins, it is unstoppable and worsens with time. The process from asymptomatic heart murmurs to valve failure may take several years ((Häggström et al 2009, Corcoran 2009). A life-threatening stage may be reached within 1-3 years of diagnosis (Kittleson and Kienle 1998). Once severe congestive heart failure has developed, survival has been found to average about seven months, with 75% mortality within a year (French 2005).
2. Intensity of welfare impact
Mitral valve disease has a serious impact on the welfare of affected dogs as a result of respiratory and other difficulties.
As the disease progresses (murmur graded 3-4), the condition starts to affect the dog’s ability to exercise, with the extra work required of the heart during exercise resulting in respiratory distress, seen as rapid breathing and breathlessness, even after exercise has ceased. Humans who experience such breathlessness report that it is very unpleasant and talk about feelings of suffocation and nausea and it is likely that the dog experiences it similarly. Further progression of the disease, as fluid begins to accumulate in the lungs, results in increasing dry, hacking coughing and persistent laboured breathing, even during rest. This is most common when the dog is lying down. Dogs may feel generally tired or fatigued.
Towards the latter stages of the disease, with the heart failing, the dog may faint, collapse and/or show signs of general weakness. Exercise tolerance becomes extremely limited and exercise may cause great distress. Breathing difficulty is becomes constant and animals may be reluctant to lie down because extra pressure on the chest causes increased difficulty with breathing. Affected dogs may remain standing until the point of collapse Kidney and/or liver function becomes seriously impaired and there fluid congestion occurs in the heart, lungs, and abdominal cavity. All of effects seriously add to the impact on the animal’s welfare. At or before this stage, euthanasia is generally recommended.
The progressive heart failure causes discomfort associated with breathlessness and coughing. Unless animals are euthanased, they are likely to die of chronic heart failure.
3. Duration of welfare impact
Mitral valve disease is a progressive disease. During the early stages, when murmurs are at their weakest (graded 1 or 2), the condition has relatively little impact on welfare (Merck 2009). A life-threatening stage may be reached within 1-3 years of diagnosis (Kittleson and Kienle 1998). Once severe congestive heart failure has developed, survival has been found to average about seven months, with 75% mortality within a year (French 2005). In these late stages the adverse welfare effects become constant rather than episodic.
4. Number of animals affected
Mitral valve disease is the single most common heart disease of dogs (Egenvall at al 2006). Miniature schnauzers are recognised as one of the breeds most commonly affected with mitral valve dysplasia (Abbott 2003, Rishniw 2005): individuals of this breed are 4.4 times more likely to be affected than the average dog (Gough & Thomas 2010). As far as we are aware there are no data on the proportion of Miniature schnauzers that are affected.
5. Diagnosis
Initial diagnosis is by stethoscope. Murmurs are categorised on a six point scale from grade 1, the mildest and least audible, which can be heard with a stethoscope only in a quiet room, to grade 6, the loudest and most turbulent, which can be heard with the stethoscope not touching the chest, or even without using the stethoscope. The loudness of the murmur is thought to increase with the severity of the valve leak. If a murmur is detected, then confirmation through further stethoscopic examination or, more definitively, using ultrasound examination is recommended; this should occur within 3-6 months from first detection of a murmur. Using ultrasound, heart size, function including the direction and speed of blood flow, and valve appearance can be evaluated. Other diagnostic tools used to determine the severity of the disease and the presence of heart failure, include: ECG recordings (electrocardiogram), blood tests, chest radiography and full physical examination.
Current research is aimed at earlier diagnosis of mitral valve disease before the development of a heart murmur. Such research seeks to measure concentrations of circulating hormones - natriuretic peptides - secreted by areas of the heart that regulate the excretion of sodium in the urine. Elevated blood levels of these natriuretic peptides are found in dogs with heart problems and when the heart is having to work harder, eg because of mitral valve leakage. (MacDonald et al 2003). However, whilst testing for these peptides is non-invasive, it remains to be shown that their measurement offers a means of diagnosing mitral valve disease significantly sooner than by listening for a heart murmur.
6. Genetics
The known predisposition of Miniature schnauzers to develop mitral valve disease is evidence for a genetic influence on this disease in the breed. It is known that most of the variation in severity of mitral valve disease in some other breeds is genetic, for example in the Cavalier King Charles cavalier spaniel in the UK (Lewis et al 2010) and the Dachshund (Olsen et al 1999). The genetics have not been studied in the Miniature schnauzer.
7. How do you know if an animal is a carrier or likely to become affected?
Dogs that will become affected cannot be detected in earlier life. Because the problem affects middle-aged or older dogs, if the parents of a dog appear unaffected, this does not mean that the individual or its parents are free of the condition. Choosing a dog born to older parents (perhaps 5 years plus) which have not themselves developed mitral valve disease has been advocated (Swenson et al 1996, Häggström 2004a). Knowing that grandparents and great grandparents are free of heart murmurs and heart failure is probably helpful.
8. Methods and prospects for elimination of the problem
Neither the genes involved with mitral valve disease nor the inheritance pattern have been determined. This, plus the late onset of signs makes control currently rather difficult. Currently, we are unaware of any guidelines or schemes to help reduce this disease in Miniature schnauzers.
Buyers should ask breeders whether the parents have any signs of mitral valve disease and how old they are. A cardiac examination by a veterinary surgeon should be made prior to breeding any dog and if a heart murmur was found then this should be investigated (not all heart murmurs indicate significant disease).
Research is currently underway (for example at the Universities of Minnesota, Missouri and Davis in the USA; the University of Toronto in Canada, and at The Animal Health Trust in England) to improve understanding of the genetic basis of mitral valve disease in various breeds. This is the LUPA project (http://www.eurolupa.org/). The development of genetic tests to help identify the genes involved in the condition may help to eliminate this condition in the future.
9. Acknowledgements
UFAW is grateful to Rosie Godfrey BVetMed MRCVS and David Godfrey BVetMed FRCVS for their work in compiling this section.
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10. References
Abbott JA (2003) Canine Mitral Valve Disease-Current Therapy. American College of Veterinary Internal Medicine Conference Proceedings http://www.vin.com/Members/Proceedings/Proceedings.plx?CID=acvim2003&PID=pr03868&O=VIN accessed 18.10.2011
Borgarelli M and Häggström J (2010) Canine degenerative myxomatous mitral valve disease: natural history, clinical presentation and therapy. Veterinary Clinics of North American Small Animal Practice 40: 651-63
Cochron BM (2009) Understanding mitral valve disease. http://www.thecavalierclub.co.uk/health/hearts/reports/MVD_Report_Mar_09.pdf accessed 19.10.2011
Egenvall A, Bonnett BN and Haggstrom J (2006) Heart disease as a cause of death in insured Swedish dogs younger than 10 years of age. Journal of Veterinary Internal Medicine 20: 894-903
French A (2005) Mitral Valve disease in the Cavalier King Charles Spaniel. http://www.thecavalierclub.co.uk/health/hearts/french.html. accessed 19.10.2011
Gough A and Thomas A (2010) Breed predispositions to disease in dogs and cats 2nd edition. Wiley-Blackwell, Chichester, UK pp 175
Griffiths LG, Orton EC and Boon JA (2004) Evaluation of techniques and outcomes of mitral valve repair in dogs. Journal of the American Veterinary Medical Association 224: 1941-1945
Gordon S (2004) Chronic Valvular Disease: Pharmacotherapy, Current and Future Directions. 1st International Canine Valvular Disease Symposium, Paris, October 30-31, 2004. http://www.vin.com/Members/CMS/Misc/default.aspx?id=8890. accessed 19.10.2011
Häggström J (2004a) Aetiology and Pathophysiology of Myxomatous Mitral Valve Disease in Dogs. World Small Animal Association Conference Proceedings 4-6th Oct 2004, Rhodes, Greece. Available from VIN Associate. http://www.vin.com/Members/Proceedings/Proceedings.plx?CID=wsava2004&PID=pr08584&O=VIN accessed 18.10.2011
Häggström J (2004b) Is the Cavalier King Charles Spaniel a Useful Model for Myxomatous Mitral Valve Disease in Other Dogs? 1st International Canine Valvular Disease Symposium, Paris, October 30-31, 2004. http://www.vin.com/Members/CMS/Misc/default.aspx?id=8403. accessed 19.10.2011
Häggström J, Höglund K and Borgarelli M (2009) An update on treatment and prognostic indicators in canine myxomatous mitral valve disease. Journal of Small Animal Practice 50(1): 25-33
Häggström J, Pedersen HD and Kvart C (2004) New insights into degenerative mitral valve disease in dogs. Veterinary Clinics of North America: Small Animal Practice 3: 1209-1226
Kittleson M and Kienle R (1998) Myxomatous atrioventricular valve degeneration. In: Kittleson M and Kienle R. Small Animal Cardiovascular Medicine. 1st edition. Mosby: St Louis, USA pp 297-318
Lewis T, Swift S, Woolliams J and Blott S (2010) Heritability of premature mitral valve disease in Cavalier King Charles spaniels. The Veterinary Journal 188: 73-6
Lundin T and Kvart C (2010) Evaluation of the Swedish breeding program for cavalier King Charles spaniels. Acta Veterinaria Scandinavica 52: 54
MacDonald KA, Kittleson MD, Munro C and Kass P (2003) Brain Natriuretic Peptide Concentration in Dogs with Heart Disease and Congestive Heart Failure. Journal of Veterinary Internal Medicine 17: 172–177
Merck (2009) Degenerative Valve Disease. http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/11213.htm accessed 19.10.2011
Olsen LH, Fredholm M and Pedersen HD (1999) Epidemiology and inheritance of mitral valve prolapse in Dachshunds. Journal of Veterinary Internal Medicine 13: 448-456
Orton EC (2004) Mitral Valve Surgery: Current Veterinary Practice. 1st International Canine Valvular Disease Symposium Paris, October 30-31, 2004. http://www.vin.com/Members/CMS/Misc/default.aspx?id=8892. accessed 19.10.2011
Orton EC, Hackett TB, Mama K and Boon JA (2005) Technique and outcome of mitral valve replacement in dogs. Journal of the American Veterinary Medical Association 226: 1508-1511
Prošek R (2007) Degenerative Valve Disease. Client leaflet. Available from VIN Associate. http://www.vin.com/Members/SearchDB/vp/vpa02515.htm. accessed 19.10.2011.
Rishniw M (2005) Myxomatous Mitral Valve Degeneration (MMVD). Available from VIN Associate. http://www.vin.com/Members/Associate/Associate.plx?DiseaseId=1328&FindingList=374958,374961 Accessed 18.10.2011
Swenson L, Häggström J, Kvart C and Juneja K (1996) Relationship between parental cardiac status in Cavalier King Charles Spaniels and prevalence and severity of chronic valvular disease in offspring. Journal of the American Veterinary Medical Association 208: 2009-2012
Williams JL, Toyoda Y, Ota T, Gutkin D, Katz W, Zenati M and Schwartzman D (2008) Feasibility of Myxomatous Mitral Valve Repair Using Direct Leaflet and Chordal Radiofrequency Ablation. Journal of Internal Cardiology 21: 547–554
http://www.eurolupa.org accessed 19.10.2011
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