Treat Canis Heart: mitral valve degenerative disease

ISSN 2398-2969

Heart: mitral valve degenerative disease

i canis

Contributor(s):

Serena Brownlie

Mark Rishniw

Ruth Willis

Mark Oyama

Pedro Oliveira

Amara Estrada

Synonym(s): Degenerative mitral valve disease (DMVD), mitral valve disease, endocardiosis, chronic valvular disease, myxomatous mitral valve degeneration (MMVD)

Introduction

Myxomatous mitral valve degeneration (MMVD) is the most common acquired disease in dogs.
MMVD causes mitral regurgitation, heart enlargement, and can lead to left-sided congestive heart failure (CHF).
Cause: inherited predisposition in some breeds, ie Cavalier King Charles Spaniel, and Dachshunds. Toy and miniature Poodles, miniature Schnauzers, Pomeranians, Chihuahuas, Cocker Spaniels, Pekingese, Fox Terriers, Maltese and Boston Terriers are predisposed to MMVD. Cavalier King Charles Spaniels (CKCS) have the highest reported incidence of DVD with 56% over 4 years of age and 100% over 10 years of age affected in a US study.
Signs: left apical systolic murmur.
Diagnosis: presumptive: detection of the characteristic murmur in an adult small-breed dog; definitive: echocardiograph.
Treatment: for dogs who meet EPIC Stage B2 criteria (pimobendan) and Stage C or D (CHF).
Prognosis: the median time to development of CHF once a MMVD dog progresses to a Stage B2 is 1228 days (95% CI: 856-NA because stopped early). Patients typically remain asymptomatic during this time period. The median time from the first CHF episode to the first intensification of CHF treatment is 98 days (range 3-885 days). Median survival time after diagnosis of CHF is 281 days (range 3-885 days). Survival times tend to be shorter in large breed dogs and dogs with myocardial failure.
Print off the owner factsheet on Mitral valve disease in dogs Mitral valve disease in dogs to give to your client.

Pathogenesis

Etiology

MMVD has been studied for a long time and while the underlying cause of it remains unknown, the pathology of the disease has been well described. Histologic changes in this disease show accumulation of the mucopolysaccharides hyaluronic acid and chondroitin sulfate.
Fibroblastic proliferation results in swirls and nodules in the expanded mucopolysaccharide matrix. The fibrosa layer degenerates with swelling, hyalinizination, and disintegration of the collagen bundles.
Gross lesions become more severe with time. The lesions begin as small discrete nodules at the margins of the valve leaflets. At this stage, the valve is typically competent. When the nodules enlarge they also start to coalesce, forming irregular opacities at the tips of the leaflets. These lesions enlarge further and tend to bulge up on the atrial surface. Calcification and hemorrhage can be seen in the body of the valve.
With these changes, the valve becomes grossly distorted by coalescing grayish-white nodules and plaques and becomes incompetent and leaks across the incompetent valve start to occur. The valve edges are contracted and appear rolled up.
Chordae tendineae also become thickened, irregular, and may be ruptured. As these changes continue to progress, so does the functional incompetence of the valve. Other structures comprising the mitral valve apparatus are primarily or secondarily affected.
- The valve annulus becomes dilated secondary to atrial and ventricular dilation.
- The left atrium becomes dilated due to an increase in left atrial pressure.
- Jet lesions of the atrial endocardium occur due to the turbulent jet of MR disrupting the endothelium and leading to fibrosis.
- The left ventricle becomes eccentrically hypertrophied due to volume overload.

Pathophysiology

During the initial stages of MMVD, although there is gross thickening of the mitral valve, the valve is competent and there are no hemodynamic changes. The leaflets may begin to prolapse, or bow backward, into the left atrium in systole; however, they remain competent.
As the degeneration progresses, the mitral valve and chordae tendineae continue to thicken, so that the leaflets no longer coapt properly. This leads to insufficiency across the valve, most commonly called mitral regurgitation (MR) when some of the blood from the left ventricle is pumped backwards into the left atrium instead of into the aorta in systole.
As MMVD progresses, the MR will progress and so the compensatory cardiac changes will attempt to maintain normal cardiac output. There will be progressive left atrial dilation and eccentric hypertrophy of the left ventricle and as long as the metabolic demands of the body are met, there will be no signs of heart failure.
Over time, while the cardiac compensation may maintain cardiac output at rest, it may be unable to do so with activity or stress. There will be inadequate perfusion to meet the increased metabolic demands of the body and the systemic compensatory mechanisms will become activated to maintain blood pressure. This likely begins to occur when the MR has become moderate to severe. The sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) will be activated and lead to increases in preload and afterload.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Kittleson M & Kienle R (1998 ) Myxomatous atrioventricular valve degeneration. In: Small Animal Cardiovascular Medicine. 1st edition. Eds: M Kittleson and R Kienle. Mosby, St Louis pp 297-318.

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RELATED SOUNDS

Heart sound: mitral incompetence

Heart sound: mitral insufficiency

Heart: mitral valve degenerative disease

Introduction