Chronic mitral valve or tricuspid valve endocardiosis is a disease in dogs characterized by progressive myxomatous degeneration of the atrio-ventricular (AV) valves. It is estimated that this disease accounts for 50% of canine cardiac disease. This disease process is also seen in humans, horses, and pigs. Mitral valve endocardiosis is seen in all dog breeds, but the prevalence of the disease varies greatly, with small-to medium-size breeds most commonly affected.
Progression of this disease begins with a small regurgitant fraction from the ventricle into the atrium that the atrium can easily accept and the forward stroke volume is maintained. As the disease progresses over time, the regurgitant fraction of the total left ventricular stroke volume increases. Forward stroke volume is maintained until a certain point when vascular, renal, and neurohormonal compensatory mechanisms are overwhelmed. The left ventricle then compensates by increasing the end diastolic volume (preload) and by increasing heart rate over time. This increase in preload leads to an increase in force of contraction of the left ventricle. The regurgitant fraction is ejected into the left atrium at low pressure before enough pressure is generated to open the aortic valve and cause forward flow into the aorta.
The systolic function is well preserved because little work is required by the left ventricle to allow ejection of the regurgitant fraction into the low pressure left atrium. Over time, the left ventricle will eccentrically hypertrophy due to volume overload and the atrial regurgitant volume will lead to atrial enlargement. This leads to increased pressure within the left atrium and can result in pulmonary congestion and edema. This same scenario can also occur with tricuspid valve endocardiosis in the right ventricle and right atrium. Eventually increased pressure in the right atrium can lead to right-sided heart failure seen as ascites and/or pleural effusion. A left-sided apical systolic murmur can be heard most commonly with mitral valve disease or a right-sided apical systolic murmur with tricuspid valve disease. Arrhythmias from the enlarged atria or ventricles may also be seen.
Clinical signs of AV valve endocardiosis are usually not observed by the owner until the animal is in congestive heart failure secondary to preload overload from mitral or tricuspid valve regurgitation. Left sided heart failure is the most commonly seen as the left side of the heart is most commonly affected. Clinical signs of left heart failure may be subtle such as increased respiratory rate at rest to mild decreases in activity or exercise intolerance. Other clinical signs may include coughing, not sleeping through the night, coughing more at night or decreased appetite. Signs may progress to coughing up pink-tinted foam to fulminant respiratory distress. Clinical signs of right heart failure secondary may include weight gain, abdominal distension, inappetance, difficulty breathing, exercise intolerance and increased lethargy.
A way for owners to monitor to their pet at home for early signs of congestive heart failure is to count the resting respiratory rate. This can be done when the pet is sound asleep and the number of breathes per 15 seconds is counted. This number is then multiplied by 4. If this number is consistently above 40 when the pet is sound asleep, this may be an early sign of congestive heart failure and the veterinarian should be contacted.
Other signs of AV valve endocardiosis may be syncope or sudden death due to atrial or ventricular arrhythmias.
Treatment for this disease varies amongst clinicians. A general treatment protocol is the institution of a loop diuretic such as furosemide and an angiotensin converting enzyme (ACE) inhibitor when these patients present in heart failure. Some clinicians will institute ACE inhibitors prior to heart failure, although there is no scientific evidence that starting these medications before heart failure improves prognosis.
In severe or recurrent cases of heart failure, diuretics with effects in the distal nephron, positive inotropes, and other afterload reducers may be added for treatment. Digoxin, a cardiac glyocoside, may also be advocated for its effects on contractility, vagal tone, and baroreceptor activity. Finally, β-blockers or calcium channel blockers may be added in cases of tachycardia refractory to digoxin.
Animals diagnosed with congestive heart failure secondary to AV valve endocardiosis should have thoracic radiographs, echocardiograms and ECG recordings performed every 4-6 months. Holter monitor, 24-hour ECG monitoring may be recommended in animals with arrhythmias noted from other diagnostic tests. Patients that are asymptomatic and have not been in congestive heart failure should be seen every 6-12 months for thoracic radiographs and echocardiograms.