Mitral valve dysplasia in cats (Left AV valve disorder)

© Norsworthy et al (1998) The Feline Patient. Lippincott, Williams and Wilkins., Philadelphia, USA

Mitral valve dysplasia (MVD) is a common congenital cardiac anomaly of the cat. A wide spectrum of lesions has been observed, including abnormal papillary muscle structure and dysplasia of chordae tendineae and mitral valve leaflets. MVD may be seen in conjunction with other congenital abnormalities, such as ventricular septal defects (VSD). The typical lesion is one of valvular incompetence that results in mitral regurgitation of blood into the left atrium. There may also be a component of valvular stenosis.

Physical examination typically reveals a prominent (grade I to VI) holosystolic regurgitant murmur over the mitral valve area. The cardiac impulse may also be displaced as a result of significant cardiomegaly in association with ventricular volume overload.

Cats may be evaluated for a murmur during routine examination or may have signs of left-sided congestive heart failure (tachypnoea, dyspnoea). Weight loss may occur. Most affected cats exhibit a degree of fatigue during exertion.

Diagnosis

Many cats present within the first 2 years of life, although when the lesion is mild, it is not unusual for cats to survive for years without clinical signs.

In radiography, prominent left atrial enlargement appears with variable left ventricular enlargement. There may be enlargement of the pulmonary veins, venous congestion, and pulmonary oedema, Pleural effusion is uncommon. This needs to be differentiated from a similar radiographic appearance that is seen with feline heartworm disease.

With ultrasound (echocardiography), severe left atrial enlargement is typical. Dysplasia of the mitral valve leaflets (shortened, malformed leaflets) and chordae tendineae are evident. There is variable left ventricular enlargement. Contractility is usually within normal limits or slightly increased. Doppler echocardiography may demonstrate significant mitral regurgitation. The extent of the regurgitation jet, rather than the velocity, correlates well with severity.

ECGs may show evidence of left ventricular enlargement (tall and wide R waves) and left atrial enlargement (widened P waves) may be seen. Atrial arrhythmias (atrial premature complexes) may also occur.

Treatment

Take all measures to minimise any stress to cats exhibiting respiratory distress (e.g. delay radiographs and catheter placement).  To facilitate breathing, thoracentesis should be performed when pleural effusion is suspected (muffled heart sounds). Furosemide should be administered when pulmonary oedema is present. In the crisis setting, give 2-4 mg/kg IV initially, then 1-2 mg/kg IV or IM q 4-6 hrs until the oedema has resolved. Furosemide is often continued as needed (6.25-12.5 mg OID to BID) to control oedema formation. A quarter inch of nitroglycerin should be applied to a hairless area every 4-6 hours until the oedema has resolved. Renal function will need to be monitored regularly, specifically blood urea, creatinine, and urine protein:creatinine ratios.

Oxygen is administered by face mask, if tolerated, or by oxygen cage or tent (50% oxygen).

ACE inhibitors, either enalapril or benazepril should also be administered once the patient is stabilised to reduce blood pressure and therefore after-load on the heart. If contractility is reduced, digoxin may be administered (one-quarter of a 0.125 mg tablet q 24-48hrs).

Aspirin may reduce the chance of thrombus formation, given at an oral dose of 5 mg/kg daily. Thoracocentesis or abdominocentesis may be needed periodically to remove excess fluid accumulation in the chest or abdomen respectively.

Surgical correction of MVD has had limited success in the cat and is associated with high morbidity and cost.

Prognosis

The prognosis for cats with MVD depends on the severity of the valvular incompetence and degree of ventricular volume overloading. Cats with mild lesions usually remain asymptomatic and have a good prognosis. Cats with significant lesions and evidence of moderate to severe volume overload early in life have a guarded to poor prognosis and usually develop congestive heart failure.