Difference between revisions of "Degenerative Mitral Valve Disease"

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* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) '''Manual of Canine and Feline Cardiology''' ''Saunders''.
 
* Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) '''Manual of Canine and Feline Cardiology''' ''Saunders''.
  
[[Category:Cardiovascular_System_-_Developmental_Pathology]][[Category:to_Do_Katie]]
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[[Category:Cardiovascular_System_-_Developmental_Pathology]][[Category:to_Do_REVIEW]]

Revision as of 20:31, 15 November 2010




Also known as: MVD, 'Mitral Valve Disease', Mitral insufficiency, Mitral endocardiosis, Myxomatous Mitral Valve Disease (MMVD)

  • Common in dogs and cats
  • Rare in other species

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.

Introduction

A congenital malformation or degeneration of the mitral valve leaflets and its supporting structures(chordae tendinae, papillary muscles, valvular leaflets, annulus) results in valvular regurgitation (insufficiency).

Mitral dyplasia. Courtesy of A. Jefferies


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.

Diagnosis

History

  • Exercise Intolerance
  • Cough
  • Dyspnoea
  • Sudden death due to left atrial tear and pulmonary oedema

Clinical Signs

  • Left apical systollic murmur
  • Left sided congestive heart failure
    • Resting Tacchycardia
    • 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

  • Cardiomegaly with dorsal displacement of the trachea
  • Pulmonary Venous Congestion (Enlarged pulmonary Arteries and Veins)
  • Pulmonary Oedema

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

Echocardiography

  • Left Atrial enlargement
  • Left Ventricular Enlargement
  • Increased Fractional Shortening ( The % change in the left venticular diameter during systole used as a measure of systollic function)
  • Malformed Valve leaflets
  • Evidence of the regurgitant jet and turbulent flow using colour doppler

Electrocardiogram (ECG)

  • Enlarged Left Atrium (Wide P Wave)
  • Enlarged Left Ventricle (Tall R wave, wide QRS complex, shift of mean electrical axis to the left)
  • Rhythm disturbances - Sinus Tacchycardia, Atrial Fibrillation, Atrial premature complexes,Atrial Tacchycardia.

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. Treatment is aimed at managing congestive heart failure 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)
  1. 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. Nitropusside
  1. Enhance Systolic function
  • Positive Inotropes to increase cardiac contractility and increase cardiac output.
    • Pimobendan
    • Digoxin
    • Dobutamine
    • Xanthines
  1. Improve Diastolic function
  • Negative Chronotropes to increase the length of diastole (digoxin, atenolol)
  • Calcium channel blockers to improve relaxation (amlodipine)
  1. Control cardiac arrhythmias using anti-arrhythmic drugs

Prognosis

Mitral Valve Dysplasia can remain asymtomatic 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 caridac size, the degree of pulmonary oedema and the size of the left atrium. Caridac size can be measured objectively using the Vertebral Heart Score method. Mean survival of 200-300 days once in overt cardiac failure with stnadard treatment protocols.

Literature Search

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.