Most valvular diseases of horses are regurgitant, rather than stenotic. Valvular regurgitation can be secondary to infection (eg endocarditis), wear and tear (degeneration), cardiac dilation (stretching of valve annulus, eg cardiomyopathy), or trauma (eg ruptured chord). With more and more horses undergoing echocardiography, clinically insignificant and otherwise undetectable regurgitation of all 4 valves is being diagnosed more frequently.
Tricuspid valve stenosis is extremely rare. Mild tricuspid valve regurgitation is often detected as an incidental finding during cardiac ultrasonography in horses showing no clinical signs of right sided heart disease.
Clinically significant tricuspid regurgitation can occur secondarily to bacterial endocarditis, cardiomyopathy, myocarditis, pulmonary hypertension (most often caused by chronic left heart failure), a ruptured chord, or secondarily to other diseases that cause right heart enlargement and stretching of the valve annulus.
Clinically significant tricuspid valve regurgitation results in right atrial enlargement (seen on ultrasound) and a jugular pulse. Classically, it causes a band-shaped systolic murmur, heard best on the right side of the chest. Right heart failure results in distended peripheral veins, peripheral edema, ascites, and liver dysfunction. Cardiac ultrasound evidence of impending right heart failure includes demonstration of an enlarged right heart.
Clinically significant pulmonic valve disease is even more rare than tricuspid valve disease in the horse. Primary pulmonic valve regurgitation has been reported in a few horses with pulmonic valve rupture or bacterial endocarditis. Significant pulmonic valve regurgitation occurs most commonly secondarily to severe left heart failure and pulmonary hypertension. Mild, incidental pulmonic valve regurgitation is not uncommonly seen with color flow doppler in asymptomatic horses.
Mitral valve insufficiency is the most likely valvular problem when a band-shaped systolic murmur is heard on the left side of the chest with point of maximal intensity over the mitral valve region or heart apex. Other than flow murmurs, it is probably the most common systolic murmur heard in adult horses.
Mitral valve insufficiency may or may not be clinically significant. Cardiac ultrasound exam is essential to determine the degree of insufficiency and the likelihood of clinical significance. Mitral valve stenosis is extremely rare.
As with the tricuspid valve, mild mitral valve regurgitation is sometimes detected in clinically normal horses by color flow or pulsed wave doppler echocardiography. This regurgitation is probably clinically insignificant if there are no secondary cardiac changes (described below). Approximately 10-15% of horses have some mitral valve changes visible with echocardiography, including thickening of the valve cusps or thickening of the chordae tendinae.
As the degree of mitral regurgitation increases, the left atrium and left ventricle dilate. At first, the left ventricle may be hyper-contractile (increased fractional shortening) to compensate for the backward flow into the left atrium. As the heart begins to fail, fractional shortening returns to normal or is decreased, the left ventricle and left atrium are dilated, and the horse exhibits exercise intolerance.
Horses with mitral regurgitation and even with mild cardiac changes often can continue to compete successfully. However, it is impossible to predict how long it will take the heart to fail, or even if it will fail. This needs to be stressed to owners, especially on prepurchase exams. Ideally, horses with mitral regurgitation should have cardiac ultrasound performed yearly.
Since this is not economically palatable for many owners, they should at least have their veterinarian auscult the horse's heart yearly or semi-yearly (eg when vaccines are being given) and re-ultrasound if the character of the murmur changes, if resting heart rate increases, or if the horse shows any evidence of decreased exercise performance.
In horses with mitral valve regurgitation, the left side of the heart initially expands slightly. An early indication of left ventricular enlargement is rounding of the heart apex (seen during cardiac ultrasound exam). As enlargement continues, the chamber volumes increase and the wall thicknesses decrease.
In the average 450-500 kg horse, the left atrium can be considered to be enlarged if the two-dimensional diameter is >13.5 cm, if it is significantly larger than the right atrium, or if the left atrial appendage in systole is greater than the diameter of the aortic root. The left ventricle is enlarged if its diastolic diameter is >130 mm. The severity of mitral valve regurgitation can also be estimated by the size of the regurgitant jet measured by pulsed wave or color flow Doppler.
If Doppler indicates that the regurgitation is only along the valve or extends no more than a third of the way back into the atrium, the lesion is likely to be clinically insignificant. The amount of regurgitation is considered to be severe if the jet extends back into the atrium 2/3 or more of its depth. If the amount of regurgitation is considered to be moderate at the time of examination, it is impossible to predict how long the horse will continue to remain stable vs when the heart might begin to fail.
Contractility (measured by determining left ventricular fractional shortening) may actually be slightly increased initially in horses with mitral regurgitation, to compensate for the amount of blood going backwards through the valve during systole. Eventually, as the amount of regurgitation becomes more significant, the left heart enlarges further and fractional shortening returns to normal.
As the horse progresses into heart failure, the left atrium becomes more dilated, contractility decreases, pulmonary hypertension develops, and the right heart begins to undergo secondary enlargement and eventually failure. The enlarged atria can lead to atrial fibrillation. Dilatation of the pulmonary artery (diameter greater than that of the aorta) is an indication of severe left heart failure. These horse are at risk of rupturing their pulmonary arteries, resulting in sudden death.
In horses with acute onset of mitral regurgitation that are exhibiting signs of heart failure, rupture of a chorda tendina is likely. In these cases, the heart may not have had time to enlarge, and the size of the heart does not correlate to the severity of clinical signs. The ruptured chord or a prolapsing valve leaflet may be seen on ultrasound exam.
Treatment of horses with mitral regurgitation depends on the severity of the disease. Horses with moderate to severe regurgitation may benefit from the use of angiotensin converting enzyme inhibitors (eg quinapril, 120 mg PO per day). Horses exhibiting signs of heart failure should be treated symptomatically:
Furosemide-0.5 - 3.0 mg/kg q 12 h, PO IV or IM (Oral absorption may be variable, and parenteral administration is preferred)
Digoxin-0.011 - 0.018 mg/kg q 12 h, PO (tablets). (Loading dose 2X this) Peak serum concentrations of digoxin should not exceed 2.5 ng/ml.
Aortic valve insufficiency is the most common cause of diastolic murmurs, particularly those detected in older horses. The most common cause of aortic regurgitation is valve degeneration. Although the murmur can be loud and dramatic, horses often can continue to function athletically. Occasionally a valve cusp can tear resulting in acute severe aortic regurgitation, and these horses show signs of cardiac compromise.
With time, however, the valve edge can smooth out and even some of these horses can return to some level of function. Aortic regurgitation usually progresses slowly, and since horses are often already older when it is first detected, it rarely causes exercise intolerance or heart failure, unless there is concurrent mitral valve regurgitation or myocardial disease.
Aortic regurgitation causes a holodiastolic, decrescendo murmur, heard best on the left side of the chest over the aortic valve area. The murmur can also be musical or honking. The intensity of the murmur does not correlate well with the degree of regurgitation.
Peripheral arterial pulses are strong, and sometimes described as bounding. This is because diastolic pressures are low, making the difference between systolic and diastolic pressures great. An extremely strong, or “water-hammer” pulse is indicative of left ventricular volume overload and more severe aortic regurgitation.
Aortic valve thickening or cusp prolapse may be seen with cardiac ultrasonography. The size of the regurgitant jet can be demonstrated with pulsed wave or color flow Doppler. The degree of aortic regurgitation is considered to be severe if the jet extends beyond the septal leaflet of the mitral valve, or 2/3 or the way back into the left ventricle. Aortic regurgitation is also considered to be more significant when the jet is wider at its origin.
A short or elevated pressure half-time (steep slope of the down side of the continuous wave Doppler trace) also indicates a more significant degree of aortic regurgitation. Sometimes a small regurgitant diastolic plume can be seen with color flow in horses that have no detectable murmur. It is likely that these horses will develop a diastolic murmur with time; it would be interesting to follow their progress.
High frequency vibrations of the septal leaflet of the mitral valve or the interventricular septum can also be seen in horses with aortic regurgitation; these are caused by turbulence in the left ventricular outflow tract. As with mitral regurgitation, severity of aortic regurgitation can be judged by the degree of left heart enlargement.
Left ventricular dilatation is judged by size of the left ventricular dimension in diastole, septal and free wall thinning, and increase e-point septal separation. As for mitral regurgitation, contractility is increased initially, becoming decreased if the horse goes into heart failure. Enlargement of the aortic root does not seem to predispose to rupture, unless there is a pre-existing aneurysm in the sinus of Valsalva.
Horses with aortic valve regurgitation are at greater risk for ventricular arrhythmia. As long as heart rhythm is normal, horses with aortic regurgitation often can continue to compete, and rarely go into heart failure, as long as the mitral valve remains intact.
As for mitral valve insufficiency, periodic cardiac ultrasound examinations are recommended to detect progression of left ventricular dilation and development of mitral valve insufficiency. Progression of disease is usually slow. Administration of angiotensin converting enzyme inhibitors may prolong athletic function, but currently there is no data in the horse to support this. However, they can do no harm, except perhaps to the pocket book.
Aortic valve rupture occurs sporadically in horses. These horses appear to have a congenital weakness in the sinus of Valsalva which can develop into an aneurysm. If the aneurysm ruptures into the chest, the horse bleeds out and dies acutely. However, sometimes when the aneurysm ruptures it ruptures into the right atrium or dissects down the interventricular septum and empties into the right or left ventricle. This causes an aortic-cardiac fistula.
Most commonly, the horse experiences acute volume/pressure overload, particularly if the aorta ruptures into the right heart. However, some of these horse can be stabilized. Horses with aortic-cardiac fistulas most commonly have a continuous murmur heard best on the right side of the chest, and a systolic murmur on the left side of the chest. They may be tachycardic and/or arrhythmic.
Treatment / management of horses with subclinical valvular disease
Horses that have murmurs with no clinical signs of cardiac compromise do not require specific treatment. We usually recommend that they be monitored closely for any change in exercise tolerance. Angiotensin converting enzyme inhibitors decrease afterload and work of the heart, and have been advocated to slow progression of disease in cases of mitral or aortic valve regurgitation in people and dogs. There is no published evidence to show a beneficial effect of these drugs in horses, although one could expect them to be helpful in this species as well.
The problem in the past has been poor oral bioavailability of available drugs. There is a recent abstract in the literature that suggests there may be a beneficial effect of giving 120mg of quinapril orally per 1000-1100 pound horse orally once daily. A recent study performed by colleagues at NCSU suggests that sufficient quinapril is absorbed at this dose to inhibit angiotensin converting enzyme.