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Dysplasia and Stenosis of Atrioventricular Valves in Animals

BySandra P. Tou, DVM, DACVIM-Cardiology, DACVIM-SAIM, Department of Clinical Sciences, College of Veterinary Medicine, North Carolina State University
Reviewed/Revised May 2025

Tricuspid Valve Dysplasia in Animals

Tricuspid valve dysplasia is a congenital malformation of the tricuspid valve leaflets or any other component of the tricuspid valve complex.

Congenital malformation of the tricuspid valve complex occurs in dogs and cats. Breeds predisposed are Labrador Retrievers and German Shepherd Dogs.

Tricuspid dysplasia results in tricuspid insufficiency and systolic regurgitation of blood into the right atrium. Rarely, tricuspid valve stenosis can be noted. Chordae tendineae are commonly shortened or absent, and tricuspid valve leaflets may be thickened or adhered to the ventricular or interventricular septal wall (see tricuspid valve dysplasia image).

Other concurrent congenital anomalies, such as mitral valve dysplasia, septal defects, subaortic stenosis, or pulmonic stenosis, may be present. In Ebstein anomaly, another defect affecting the tricuspid valve, some leaflets of the tricuspid valve are displaced toward the cardiac apex.

Pathophysiology of Tricuspid Valve Dysplasia

Malformation of the tricuspid valve results in varying degrees of valvular insufficiency. Substantial tricuspid regurgitation leads to volume overload of the right heart, dilating the right atrium and ventricle. Pulmonary blood flow may be decreased, resulting in fatigue and tachypnea. As the pressure in the right atrium increases, venous return is impaired, causing signs of right-sided heart failure (ascites, jugular venous distention, and possibly pleural effusion).

Clinical Findings of Tricuspid Valve Dysplasia

Clinical signs of tricuspid valve dysplasia correlate with the severity of the defect.

Affected animals may display signs of right-sided CHF (ascites, jugular venous distension).

There may be no audible murmur or a holosystolic murmur of tricuspid regurgitation that is prominent at the right cardiac apex. Atrial arrhythmias, especially paroxysmal supraventricular tachycardia, can occur.

Diagnosis of Tricuspid Valve Dysplasia

Echocardiography demonstrates malformation of the tricuspid valve and varying degrees of right atrial and ventricular dilatation. Doppler echocardiography demonstrates tricuspid regurgitation. The caudal vena cava may be appreciably enlarged.

Electrocardiography and radiography typically demonstrate right atrial (wide P waves in lead II) and right ventricular (deep S waves in lead II) enlargement. Splintered R waves may be observed on electrocardiography.

Treatment of Tricuspid Valve Dysplasia

For dogs with right-sided heart failure, CHF therapy and periodic abdominocentesis may be needed to control peritoneal effusion.

The prognosis for animals with clinical signs is highly dependent on disease severity and the degree of tricuspid regurgitation.

Mitral Valve Dysplasia in Animals

Mitral valve dysplasia is a congenital malformation of the mitral valve leaflets or any other component of the mitral valve complex (valve leaflets, chordae tendineae, papillary muscles). Often more than one component is defective.

Mitral valve dysplasia is a condition of the atrioventricular valves, as are tricuspid valve dysplasia and mitral valve stenosis. It results in mitral insufficiency and systolic regurgitation of blood into the left atrium.

Mitral valve dysplasia is a common congenital cardiac defect in cats. Predisposed dog breeds are Bull Terriers, German Shepherd Dogs, and Great Danes.

Pathophysiology of Mitral Valve Dysplasia

Malformation of the mitral valve complex results in a varying degree of valvular insufficiency. Substantial mitral regurgitation leads to volume overload of the left heart, which results in dilatation of the left atrium and ventricle.

The severity of mitral regurgitation determines the degree of left heart enlargement and the risk of left-sided CHF. Severe mitral regurgitation can subsequently result in pulmonary venous congestion and pulmonary edema.

Dilatation of the left-sided chambers predisposes affected animals to arrhythmias.

When mitral regurgitation is severe, cardiac output decreases, and clinical signs of poor cardiac output may occur (weakness, syncope).

In some cases, malformation of the mitral valve complex causes a degree of valvular stenosis in addition to insufficiency.

Clinical Findings of Mitral Valve Dysplasia

Clinical signs correlate with the severity of the defect. Affected animals may display signs of left-sided CHF.

A holosystolic murmur of mitral regurgitation is prominent at the left cardiac apex. A soft diastolic murmur is possible if concurrent stenosis is present. Affected animals may have a precordial thrill over the left cardiac apex.

Diagnosis of Mitral Valve Dysplasia

Echocardiography demonstrates malformation of the mitral valve complex (fused chordae tendineae and thickened, immobile valve leaflets, abnormal appearance of the papillary muscles) and left atrial and ventricular dilatation. Doppler echocardiography demonstrates severe mitral regurgitation. Evidence of mitral stenosis also may be identified on echocardiography.

Electrocardiography may demonstrate atrial arrhythmias (atrial premature complexes, atrial fibrillation), especially in animals with severe left atrial dilatation. Evidence of both left atrial (widened P waves in lead II) and left ventricular (tall R waves in lead II) enlargement may also be present.

Thoracic radiographs may demonstrate severe left atrial enlargement. Other findings may include left ventricular enlargement, pulmonary venous congestion, and pulmonary edema.

Treatment of Mitral Valve Dysplasia

Animals with CHF should be treated medically. Open heart surgery can be considered on an individual patient basis. For treatment of progressive left-sided CHF, see management of heart failure.

The prognosis for animals with clinical signs and severe mitral valve dysplasia is poor. Mildly affected animals may remain free of clinical signs for several years.

Mitral Valve Stenosis in Animals

Mitral valve stenosis is a narrowing of the mitral valve orifice caused by abnormalities of the mitral valve, resulting in obstruction to left ventricular inflow. This congenital abnormality is rare in dogs and cats and can occur together with other congenital defects such as subaortic stenosis, mitral valve dysplasia, and pulmonic stenosis.

Pathophysiology of Mitral Valve Stenosis

Mitral valve stenosis results in increased resistance to left atrial outflow, creating a pressure gradient between the left atrium and left ventricle. This leads to left atrial enlargement and increases in pulmonary venous and capillary wedge pressures. Pulmonary edema can develop as a consequence, and syncope occurs in some cases.

Clinical Findings of Mitral Valve Stenosis

Mitral stenosis can result in a diastolic heart murmur that is typically low-grade (I-II/VI). If concurrent mitral valve dysplasia is present, a systolic murmur with maximum intensity at the left cardiac apex may be heard.

Diagnosis of Mitral Valve Stenosis

Echocardiography provides a definitive diagnosis of mitral valve stenosis. Doming of the mitral valve leaflets toward the left ventricle during diastole, left atrial enlargement, and thickening of the mitral valve leaflets can be noted. Doppler echocardiography demonstrates turbulent diastolic flow across the mitral valve, beginning at the mitral valve and extending into the left ventricle. A pressure gradient is documented between the left atrium and left ventricle in early diastole.

Radiographs demonstrate varying degrees of left atrial enlargement and pulmonary edema in animals with left-sided CHF.

Electrocardiography may demonstrate widened P waves (indicating left atrial enlargement) and supraventricular arrhythmias.

Treatment of Mitral Valve Stenosis

Medical management of animals with mitral valve stenosis involves use of diuretics and dietary sodium restriction. Excessive diuresis should be avoided because it can decrease cardiac output severely.

Surgical or interventional therapy options include closed commissurotomy (disruption of the stenosis without the use of bypass), open commissurotomy, mitral valve replacement, and balloon valvuloplasty.

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