Myxomatous Mitral Valve Disease in Dogs: Inheritance and Breeding Schemes
World Small Animal Veterinary Association Congress Proceedings, 2017
L.H. Olsen
Department of Veterinary and Animal Sciences, University of Copenhagen, Frederiksberg, Denmark

Myxomatous mitral valve disease (MMVD) is the most common heart disease in dogs. The disease is seen as relative benign condition because many dogs with MMVD do not develop clinical signs of congestive heart failure (CHF);1 however, it can be challenging to identify MMVD dogs at high risk of developing CHF and cardiac mortality early in life.

The prevalence of MMVD increases with advancing age and the disease is most common seen in small to medium-size dog breeds including Cavalier King Charles Spaniels (CKCS). The mitral valve becomes thickened and/or enlarged leading to mitral valve prolapse (MVP) and mitral regurgitation. The tricuspid valve may also be affected. Lesions in aortic and pulmonary valves are uncommon.

Early signs of MMVD including MVP and/or thickening of the mitral valve, combined with no or minimal mitral regurgitation. With advancing age, presence of mild to severe mitral regurgitation can become evident, and some dogs develop CHF. The time from recognition of a heart murmur to onset of CHF is estimated to 3 to 5 years. Dogs with CHF receiving cardiac medical therapy live in average for 1 year. Research aimed reducing the prevalence of MMVD in dogs using breeding schemes and studies on genetic background and disease progression have been published the recent years.

Genetic Background

A genetic background of MMVD in dogs has been suggested for long time since a higher prevalence of the MMVD appears in certain dog breeds. Studies have reported strong genetic background with polygenic inheritance. In CKCS, a positive association between parental heart status and mitral regurgitation murmur intensity in 5-year-old offspring has been reported.2 Moreover, a positive association between the degree of MVP in parents and offspring has been shown in Dachshunds.3 A high heritability for MMVD in CKCS has been estimated from data obtained in a United Kingdom (UK) breeding scheme.4 The heritability of having a mitral regurgitation murmur and of the grade of murmur intensity were estimated to 0.33 and 0.67, respectively. Genome-wide association studies have been performed. Interestingly, two gene loci on chromosomes 13 and 14 were found to differ between CKCS with early and late onset of MMVD.5 However, another similar genome-wide association study, including a lower number of CKCS, did not find any association between gene loci and MMVD disease severity.6 In Whippet dogs, another dog breed predisposed to MMVD, chromosome 15 was reported to be associated with MMVD.7 Inconsistency between genome wide association studies in dogs with MMVD may be due to differences between dog breeds and/or dog populations.

Breeding Schemes and Recommendations

Breeding restrictions or recommendations aimed at decreasing the prevalence of MMVD in CKCS have been developed in breeding clubs in different countries. The high heritability of the disease indicates that selection against the disease could be successful.4 Differences between ongoing breeding schemes exist. Some breeding schemes are mandatory, where others are voluntary, and the schemes include cardiac auscultation or a combination of cardiac auscultation and echocardiography. Parent cardiac information is included in some breeding schemes. Moreover, examination intervals differ between breeding schemes. Some schemes include annual cardiac examinations where as others are based on a more limited number of cardiac examinations during the dog’s lifetime. In some breeding clubs, the cardiac examination results are open to the public, in others the results are only known by the dog owner. It is still unknown how much the above mentioned factors influence the efficacy of a breeding scheme aimed at reducing the prevalence of MMVD.

The British voluntary breeding scheme based on auscultation reported an effect in a subgroup of dogs auscultated by general practitioners but only a trend was reported when the dogs were auscultated by a veterinary cardiologist.8 A mandatory breeding scheme in Sweden including annual cardiac auscultation and parent information did not result in significant effect of the scheme; however, the follow-up period was relative short (from 2007 to 2009).9 A mandatory Danish breeding scheme based on auscultation and echocardiography recently reported a decreased risk of having a heart murmur due to MMVD in CKCS over an 8- to 10-year time period.10 In the Danish breeding scheme, the degree of mitral regurgitation was evaluated using auscultation (grade 1–6) and degree of MVP was evaluated by echocardiography (grade 0–3). Risk of having a mitral regurgitation murmur or MVP>1 in 2010–2011 compared with 2002–2003 was evaluated. Included dogs were divided into two groups: Dogs that were products of the breeding scheme (defined as dogs with both parents approved by the breeding scheme before breeding) and non-products of the breeding scheme (defined as dogs with at least 1 parent with unknown cardiac status before breeding). In 2010–2011, the odds of having mitral regurgitation murmur were 0.27 if dogs were a product of the breeding scheme, reflecting a 73% decreased risk over an 8- to 10-year time period. No significant risk reduction was found for the dogs that were non-products of the breeding scheme. These findings indicate that it is possible to reduce the risk of having a heart murmur due to MMVD in CKCS over an 8- to 10-year period by a mandatory breeding scheme based on auscultation and echocardiography.

Conclusions and Perspectives

New knowledge regarding the genetic background and MMVD in dogs has been published. Breeding schemes can reduce the risk of having heart murmurs due to MMVD in CKCS. Further studies are needed to identify factors with the most significant influence on the efficacy of breeding schemes aimed at reducing the prevalence of MMVD.


1.  Borgarelli M et al. J Vet Intern Med. 2012;26(1):69.

2.  Swenson L et al. J Am Vet Med Assoc. 1996;208(12):2009.

3.  OIsen LH et al. J Vet Intern Med. 1999;13(5:)448.

4.  Lewis T et al. Vet J. 2011;188(1):73.

5.  Madsen MB et al. J Hered. 2011;102(suppl 1):S62.

6.  French et al. Vet J. 2012;193(1):283.

7.  Stern et al. PLoS One. 2015;10(10:)e0141234.

8.  Swift S et al. J Vet Intern Med. 2017;31(1):9.

9.  Lundin et al. Acta Vet Scand. 2010;52:54.

10.  Birkegard et al. J Vet Intern Med. 2016;30(1):63.


Speaker Information
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L.H. Olsen
Department of Veterinary and Animal Sciences
University of Copenhagen
Frederiksberg C, Denmark

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