Mitral/Tricuspid Regurgitation, Acquired
Basic Information 
Definition
• Mitral valve regurgitation is the most important valvular condition affecting athletic performance in horses. It may be caused by dysfunction of any part of the mitral valve apparatus, including the valve annulus, leaflets, chordae tendineae, or papillary muscles.
• The etiology remains unclear. Degenerative myxomatous changes as well as cellular infiltration with lymphocytes, histiocytes, and fibroblasts in the valves leading to general or nodular thickening are often reported. In addition, physical training may result in regurgitation because of training-induced myocardial hypertrophy. This may expand the valvular annulus, leading to valvular incompetence, but in these cases, the valves may also be affected pathologically.
• Whereas mitral regurgitation may affect athletic performance, tricuspid valve regurgitation rarely gives rise to clinical signs in horses.
Clinical Presentation
Physical Exam Findings
• A systolic cardiac murmur will be heard at the apical area of the left hemi-thorax (mitral regurgitation) or right hemi-thorax (tricuspid regurgitation). The intensity of the murmur is not always an accurate guide to the severity of the disease. However, in general, loud murmurs occurring throughout systole are more often associated with significant disease than quiet murmurs of shorter duration, particularly if a palpable thrill accompanies the loud murmur.
• Depending on the severity of the regurgitation, one or more of the following signs may be observed:
Etiology and Pathophysiology
• Initiating factors leading to degenerative changes of the valvular apparatus are unknown.
• An insidious onset of mitral regurgitation can generally be completely compensated for years without clinical signs.
• Compensatory mechanisms include atrial and ventricular dilatation; eccentric hypertrophy; and increased resting HR, contractility of the ventricles, and lymphatic drainage.
• For a minor proportion of horses with mitral regurgitation, the valvular regurgitation can no longer be compensated, leading to signs of left-sided heart failure with pulmonary edema. Initially, this may only manifest during high demand such as more strenuous exercise, but as the disease progresses, compensatory mechanisms fail, and tachycardia, coughing, and frothy fluid at the nostrils are observed when the horse is at rest. Eventually, signs of right-sided heart failure may appear, including edema and distension of the jugular veins.
• Rarely, acute mitral regurgitation develops (eg, secondary to rupture of major chorda tendineae), and in these situations, pulmonary pressures increase abruptly with development of pulmonary edema. Shortly thereafter, signs of right-sided heart failure develop with dependent edema and distension of the jugular veins.
• Severe mitral regurgitation is the most common cause of heart failure in horses.
• The mitral valve and the aortic valve are the most common locations for bacterial endocarditis (see “Endocarditis, Infective” in this section); however, the disease is not commonly encountered.
• Tricuspid regurgitation rarely causes clinical signs. If the regurgitation is severe, signs of right-sided heart failure may develop with jugular distension, jugular pulsation, and dependent edema.
• Murmurs of tricuspid, mitral, and aortic regurgitation are often detected in Standardbred and Thoroughbred racehorses. They may develop in response to training, and the prevalence may increase with age and training. However, the regurgitations are generally mild and remain constant over time, with no negative effect on racing performance documented.
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