Degenerative Mitral Valve Disease

Also known as: MVD — Mitral Valve Disease — Mitral Insufficiency — Mitral Endocardiosis — Myxomatous Mitral Valve Disease (MMVD) — Endocardiosis — Mitral Regurgitation — Chronic Valvular Disease

Introduction

Endocardiosis is a valvular insufficiency. The most commonly affected site is the mitral valve. The condition results in slowly developing heart failure as the valves become swollen and shortened/misshapen, so the heart cannot pump blood effectively from the left ventricle to the circulation.

Blood passes back into the left atrium, compromising the filling from the pulmonary vein, which leads to back pressure on the pulmonary capillaries. Resultant oedema forms in the lungs, and can be heard as moist sounds on auscultation. This reduces the oxygenation of blood leading to exercise intolerance. Failure of the left side eventually compromises the function of the right side. In right sided heart failure there is a pooling of blood in the venous system i.e. in the liver. In some cases a jet lesion can occur, where a small stream of blood passes back into the left atrium and contacts the atrial wall.

Signalment

Endocardiosis tends to affect middle-aged and older dogs, with males being predisposed. Breeds with particular predisposition to the disease include smaller breeds such as Chihuahuas, Boston Terriers, Poodles, Pomeranians, Cavalier King Charles Spaniels and larger breeds such as the German Shepherd. It is the most common heart condition in dogs. In dogs over 9 years old 97% show lesions, of which approximately 40% are clinically significant. The condition is often found at post mortem as an incidental age related change. The disease is rare in cats.

Clinical Signs

Signs depend on stage of disease, but may include coughing, syncope, weight loss, pale or cyanotic mucus membranes and prolonged capillary refill time. If left sided heart failure is present then signs will also include exercise intolerance, weakness, dyspnoea, inappetance and lethargy. If right sided heart failure is present then signs including hepatomegaly, jugular pulses & distension, pleural effusion, ascites and peripheral oedema will occur.

Diagnosis

Clinical signs plus signalment of the dog are indicative of the disease. Upon physical examination a murmur over the left heart apex may be heard. Snaps, crackles, pops will also be heard if pulmonary edema is present. Muffled heart sounds in the presence of pleural/pericardial fluid will be auscultated.

Upon radiography there will be visible signs of left sided heart enlargement. There will possibly be none, some or all of the following radiographic signs - left atrial enlargement (DV view appears at 2-3 o'clock position), left ventricular enlargement, dorsal displacement of trachea, bronchial compression, pulmonary venous congestion and/or edema and right-sided signs (distended caudal vena cava, ascites, pleural effusion, hepatomegaly).

Electrocardiography (ECG) may show a left atrial enlargement pattern, left ventricular enlargement pattern and rhythm disturbances (supraventricular arrhythmias: atrial premature complexes, atrial tachycardia, and ventricular rhythm disturbances).

Echocardiography may detail irregularities of the valves affected (e.g. thickening, shortening, and/or prolapse of the valve leaflets), abnormal valve movements & valve regurgitation, left atrial enlargement (wide P wave) and left ventricular dilation (tall R wave, wide QRS complex). Dopper will demonstrate the presence of regurgitative flow. On M wave echography there may be a normal to increased fractional shortening of the myocardium in early stages of the disease and a decreased fractional shortening of the myocardium in later stages of the disease.

Treatment

If animal is presented in left or right sided heart failure treatment is given at the onset of clinical signs. Such treatments include ACE inhibitors and diuretics.

If the disease is detected but the animal is not yet in heart failure then no treatment is required. Exercise must also be restricted and special formulated sodium reduced cardiac diets recommended.

Symptomatic treatments are also given if clinical signs persist while the animal is on heart failure medications.

Prognosis

Asymptomatic patients may live for many years. Once heart failure occurs, life expectancy is usually around one year although some patients remain stable for years on heart failure medications.

Test yourself with the Endocardial Pathology Flashcards

Endocardial Pathology Flashcards

References

Ettinger, S.J. and Feldman, E. C. (2000) Textbook of Veterinary Internal Medicine Diseases of the Dog and Cat Volume 2 (Fifth Edition), W.B. Saunders Company

Ettinger, S.J, Feldman, E.C. (2005) Textbook of Veterinary Internal Medicine (6th edition, volume 2), W.B. Saunders Company

Fossum, T. W. et. al. (2007) Small Animal Surgery (Third Edition), Mosby Elsevier

Introduction

Mitral dyplasia. Courtesy of A. Jefferies

Mitral valve dysplasia is a congenital malformation or degeneration of the mitral valve leaflets and its supporting structures (chordae tendinae, papillary muscles, valvular leaflets, annulus) resulting in valvular regurgitation (insufficiency). It is common in dogs and cats and rare in other species.

Chronic mitral regurgitation leads to volume overload of the left heart, which results in dilatation (eccentric hypertrophy) of the left ventricle and atrium. When mitral regurgitation is severe, cardiac output decreases, which results in signs of left sided cardiac failure (LCHF) and pulmonary venous congestion. Dilatation of the left-sided chambers predisposes affected animals to arrhythmias. In some cases, malformation of the mitral valve complex causes a degree of valvular stenosis as well as insufficiency.

In advanced cases, signs of right sided congestive heart failure may follow due to an increased pressure load on the right ventricle as a result of long standing pulmonary congestion.

Signalment

Typically in middle aged to older small breed dogs. Genetically predisposed breeds include Cavalier King Charles Spaniel, Bull Terriers, German Shepherds, and Great Danes.

Diagnosis

History

Animals may remain asymptomatic for years. Typical reported signs include exercise intolerance and dyspnoea as a result of reduced cardiac output and a ventilation perfusion mismatch due to pulmonary oedema. A progressive cough often during rest or recumbency is frequently seen and needs to be distinguished from primary respiratory disease. Sudden death is possible due to a left atrial tear or advanced pulmonary oedema.

Clinical Signs

• Left apical systolic murmur
• Left sided congestive heart failure
  • Resting Tachycardia
  • Pale Mucous membranes
  • Prolonged Capillary refill time (CRT)
  • Prolonged Jugular filling time
  • Pulmonary crackles / evidence of pulmonary oedema
  • Cool extremities
  • Loss of sinus arrhythmia
  • Cardiac arrhythmias e.g. Atrial fibrillation, Atrial premature complexes

Diagnostic imaging

Radiography

Left lateral, right lateral and ventrodorsal views of the thorax are needed. The key radiographic signs associated with mitral valve dysplasia and resulting left sided congestive heart failure are cardiomegaly, pulmonary venous congestion (enlarged pulmonary arteries and veins) and pulmonary oedema. Cardiomegaly may lead to dorsal displacement of the trachea.

Evidence of right sided congestive heart failure maybe evident in severe cases e.g. distended caudal vena cava, hepatomegaly, ascites, pleural effusions.

Echocardiography

Evidence of left atrial and left ventricular enlargement is visible on echocardiography. The 'fractional shortening' is also increased which is measured as the percentage change in the left ventricular diameter during systole and is used as a measure of systolic function. It is also possible to see structural changes in the valve leaflets in some cases. The regurgitant jet of blood can be detected using colour doppler and evidence of turbulent flow.

Electrocardiogram (ECG)

A resting ECG trace may show evidence of an enlarge left atrium (wide P wave), an enlarged left ventricle (tall R wave, wide QRS complex, shift of mean electrical axis to the left) and rhythm disturbances such as sinus tachycardia, atrial fibrillation, atrial premature complexes and atrial tachycardia.

Laboratory Tests

Pro-brain natriuretic peptide (N-BNP) is a newly described cardiac hormone considered to be an effective marker of severity and prognosis of acute coronary syndromes and congestive heart failure. Circulating levels of the hormone increase in peripheral blood with increased myocardial stress. Commercial assays are not currently available.

Treatment

No treatment is recommended prior to the onset of heart failure. Once there is evidence of congestive heart failure, treatment is aimed at its management through a combination of drugs.

The aims of treatment are to:

1. Reduce Preload

Diuretics to reduce circulating fluid volume (Frusemide, Benzofluazide, Spironolactone, Amiloride)

Vasodilators to reduce venous return (Nitrates, ACE inhibitors, Alpha antagonists)

2. Reduce Afterload

Vasodilators to decrease systemic vascular resistance

ACE inhibitors e.g. Enalapril, Benzapril, Imidopril

Pimobendan

Calcium channel blockers e.g. Amlodipine

Nitrates e.g. Nitroprusside

3. Enhance Systolic function

Positive inotropes to increase cardiac contractility and increase cardiac output (Pimobendan, Digoxin, Dobutamine, Xanthines)

4. Improve Diastolic function

Negative chronotropes to increase the length of diastole (Digoxin, Atenolol)

Calcium channel blockers to improve relaxation (Amlodipine)

5. Control cardiac arrhythmias using anti-arrhythmic drugs

Prognosis

Mitral Valve Dysplasia can remain asymptomatic for many years (average 4 years). Once congestive heart failure has developed, the progression of the diseae can be monitored by the severity of the clinical signs (cough, exercise intolerance) and radiographically looking at cardiac size, the degree of pulmonary oedema and the size of the left atrium. Cardiac size can be measured objectively using the Vertebral Heart Score method. Mean survival is 200-300 days once in overt cardiac failure with standard treatment protocols.

Literature Search

Use these links to find recent scientific publications via CAB Abstracts (log in required unless accessing from a subscribing organisation).


Mitral Valve Dysplasia publications

Myxomatous degenerative mitral valve disease: an update. Disatian, S.; Faculty of Veterinary Science, Chulalongkorn University, Bangkok, Thailand, Thai Journal of Veterinary Medicine, 2010, 40, 2, pp 151-157, many ref. - Full Text Article

Latest information about canine mitral valve disease: results of the QUEST trial. Häggström, J.; The North American Veterinary Conference, Gainesville, USA, Small animal and exotics. Proceedings of the North American Veterinary Conference, Orlando, Florida, USA, 17-21 January, 2009, 2009, pp 188-191, 10 ref. - Full Text Article

Treatment of mitral valve disease in dogs. French, A.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 107-108 - Full Text Article

Prognostic variables in canine mitral valve disease. Häggstrom, J.; Gething, M.; Jones, B.; Australian Small Animal Veterinary Association, Bondi, Australia, 33rd World Small Animal Veterinary Association Congress, Dublin, Ireland, 20-24 August 2008, 2008, pp 112-113, 7 ref. - Full Text Article

Other MDV Full Text Articles

References

• Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
• Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.
• Tilley, L.P. and Smith, F.W.K.(2004) The 5-minute Veterinary Consult (Third edition) Lippincott, Williams & Wilkins.
• Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) Manual of Canine and Feline Cardiology Saunders.