Mitral regurgitation (MR) is the commonest cause of heart failure in horses however a murmur of MR is often detected as an incidental finding during a clinical examination. 

• Although rare in yearling Thoroughbreds it is present in up to 21% of 2-year-old Thoroughbreds in race training, suggesting that it may develop in response to the training induced eccentric hypertrophy and increased blood volume. In these cases the degree of regurgitation is usually mild, the murmur is localised and low grade, 1-3/6 and may be crescendo in nature suggestive of mitral prolapse. On echocardiographic and post mortem examination the mitral valve appears grossly normal. This type of condition does not progress and the murmur may disappear if the horse retires from active work. If the regurgitant fraction is small, the heart compensates for the abnormal flow and athletic performance is not significantly affected. 

• Mitral regurgitation can also occur in response to thickening and fibrosis of the valve leaflets. This is thought to be a progressive condition albeit the progression is often very slow. In these cases, as the regurgitant fraction increases, the left atrium will dilate to accommodate the abnormal flow. Although this will allow a normal pressure gradient to be maintained, this will predispose the horse to atrial fibrillation. Ultimately as the valvular regurgitation increases further, forward flow will be compromised and left atrial pressures will start to rise. There will be progressive dilatation of the left ventricle and left atrium and stretching of the mitral annulus further disrupting the competence of the valve. Ultimately the increased left atrial pressures will result in pulmonary hypertension with pressure overload of the right ventricle. Dilatation of the right ventricle as a result of this increased pressure will cause stretching of the tricuspid annulus and the development of tricuspid regurgitation. These horses will ultimately present in biventricular failure. 

• Mitral regurgitation will also develop as a result of rupture of one or more chordae tendinea. Most commonly the rupture is of a minor chorda of one of the commissural cusps. In these cases the murmur is usually pansystolic grade 5- 6/6 and the course of events is as described above for more severe valvular disease. Occasionally there is rupture of a number of chordae of one of the major valve leaflets. When this occurs the volume of regurgitant flow is suddenly very large and there is little time for atrial dilatation to occur. Left atrial pressures rise abruptly and the horse presents with acute left sided failure often in severe respiratory distress. 

• Mitral regurgitation will occur secondary to any other condition that causes dilation of the valve annulus e.g. secondary to dilated cardiomyopathy, aortic insufficiency and ventricular septal defects. The progression and severity will depend on the degree of regurgitation and the progression of the underlying condition. 

• Mitral regurgitation may also occur as a result of congenital dysplasia of any part of the mitral valve apparatus. The clinical signs and progression in cases with congenital abnormalities depend on the severity of the abnormality and associated regurgitation. It must be remembered that these horses may first present as mature animals if the heart has not been auscultated previously and performance has not been affected. 

• Infective endocarditis 

• occurs rarely. There is no pathognomonic sign of endocarditis and therefore diagnosis is difficult. The symptoms will relate to the damage to the heart, the intermittent bacteraemia and the involvement of other organ systems. Cardiac failure may occur secondary to severe valvular dysfunction, or myocardial involvement. Arrhythmias may occur due to extension of infection into the myocardium (myocarditis). Other clinical signs relate to the effects of immune complexes and thromboembili on other organ systems e.g. spleen, kidney etc. Shifting lameness is often reported due to immune mediated synovitis, or infection of joints or epiphyses.

  Early aggressive treatment is required to minimise the damage to the valves. Owners should be advised that therapy will be prolonged with no guarantee of the outcome. Cardiac failure may occur secondary to valvular dysfunction despite successful treatment of the initial infection. Animals should be initially treated with antimicrobials for a minimum of three weeks (ideally 4-6 weeks), based on the results of sensitivity testing. Where sensitivity results are not available broad spectrum antibiotic cover should be given (e.g. Penicillin/Gentamycin, Trimethorprim/Sulphadoxine, Enrofloxacin. The prognosis in all cases, especially those involving the left heart valves is poor. In a recent survey of 10 cases all but one were ultimately euthanased or died. 

Considerations during the pre-purchase examination with a horse with mitral regurg  

Further diagnostic tests (echocardiography) are often carried out if the murmur is clearly audible and present throughout systole to further evaluate the cause of the regurgitation before advising on the suitability of the horse. This often gives the client baseline information against which future progression can be assessed. This can be of value if the client is likely to want to sell the horse at a later date. This horse would likely be excluded from loss of use insurance policies as MR may cause atrial enlargement, predispose to atrial fibrillation or may progress to cause cardiac failure. Mitral regurgitation would not increase the risk of sudden cardiac death and so this should not be an exclusion criterion. 

TRICUSPID REGURGITATION. 

Very common in National Hunt horses (16.4 % Patteson and Cripps, 47 % Young and Wood). Is not associated with thickening of the valve leaflets tends not to progress and if mild/moderate will not affect racing performance. Tricuspid regurgitation does not normally result in cardiac failure although very occasionally primary right sided cardiac failure can occur. Tricuspid regurgitation will develop as a result of pulmonary hypertension caused by left ventricular failure. More rarely tricuspid regurgitation may develop as a result of a ruptured chorda or congenital dysplasia of any part of the tricuspid valve apparatus. 

Considerations during the pre-purchase examination for tricuspid regurg 

If the murmur is not associated with thickening of the tricuspid leaflets it is unlikely to progress and is unlikely to affect performance. If however a horse has a high grade band, shaped murmur the very rare possibility of primary valvular disease could not be ruled out by auscultation and therefore further diagnostic tests (echocardiography) may be necessary to confirm normal valve structure before advising on the suitability of the horse. The presence of a murmur may affect resale value. This horse would likely be excluded from loss of use insurance policies as theoretically this may cause atrial enlargement and predispose to atrial fibrillation. However this seems to occur more commonly with MR. Tricuspid regurgitation would not increase the risk of sudden cardiac death and so this should not be an exclusion criterion. 

Progressive disease associated with thickening and fibrosis of the aortic valve leaflets. More common in horses over 10 years of age. Tends to progress very slowly and in older horses rarely affects performance. Aortic insufficiency causes volume overload of the left ventricle resulting in dilatation. This occurs gradually over years and may ultimately lead to mitral regurgitation, due to dilatation of the mitral orifice. MR may then result in cardiac failure. When severe aortic insufficiency is present in a young horse this is likely to be due to dilatation of the aortic root or another cause of early degeneration e.g. congenital abnormality of the valve, or association with a ventricular septal defect. These cases may progress more rapidly and ventricular function should be monitored. Although pleasure horses usually continue to perform adequately (even with severe aortic insufficiency and marked volume overload) gross dilatation of the ventricle will increase afterload and increase oxygen consumption. The aortic insufficiency also causes decreased coronary perfusion due to reduced diastolic aortic pressure and oxygen delivery to the myocardium is compromised. Increased oxygen demand and reduced coronary reserve increases susceptibility to ventricular arrhythmias that can result in sudden death. Affected horses must be monitored regularly so they can be retired from work before severe ventricular dilatation develops. 

Considerations during the pre-purchase examination for aortic insufficiency 

The progression of this condition is difficult to predict in young horses and therefore in most cases these animals cannot be considered suitable for ridden work. Horses with dilated ventricles are at increased risk of sudden cardiac death. Horses will require regular expensive monitoring if they are to be kept in work. Insurance companies are likely to exclude the heart from both loss of use and sudden death policies. In old horses progression is usually slow; therefore horses with very low grade localized murmurs could be considered to be suitable for purchase in some cases, although old horses are thought to have an increased risk of sudden death, unrelated to aortic valve disease. NB As these murmurs are often musical it is often difficult to determine the severity of the disease and therefore further tests are often necessary before advise on the suitability of the horse can be given. 

The most common congenital abnormality in large animals. The significance of the condition very much depends on the size of the defect. If the defect is small, and is restrictive to blood flow, animals will grow and perform normally. If the defect is large, left ventricular volume overload and cardiac failure will occur. Small restrictive defects will not affect performance. Large defects are not compatible with life. Although congenital abnormalities are usually diagnosed in young animals; as minor defects may not affect performance they may only become apparent in later life e.g. during pre purchase examinations. Animals with clinically significant defects often appear normal at birth, but then fail to grow or develop signs of cardiac failure. 

• In horses, septal defects are usually located in the membranous septum below the aortic and tricuspid valves. They are most commonly found in Shetland and Welsh Mountain ponies although other breeds may be affected. In some cases, small defects in the membranous septum (which may or may not be patent) can cause distortion of the aortic valve leaflets and result in aortic insufficiency. 

• Less commonly defects are located in the muscular part of the septum. Defects in this position can be large and most often occur in Arabian or TB breeds. When defects are large the pressure in the right ventricle approaches or equals that of the left ventricle. In these cases there may be little flow across the defect and no audible murmur. However the animal will have murmurs of tricuspid and mitral regurgitation which occur secondary to dilation of the tricuspid and mitral valve annulus and clinical signs of cardiac failure. 

• Defects are rarely located beneath the pulmonary valve in the infundibular septum. Unlike the other septal defects the murmur will be heard over the left hemithorax at the level of the pulmonary valve and will be similar to that of pulmonary stenosis.

•   Echocardiography is valuable for determining the likely significance of a ventricular septal defect. Murmur loudness is not necessarily associated with a poor prognosis. Affected animals should not be used for breeding. 

0. Considerations during the pre-purchase examination 

0. The severity of the defect cannot be assessed by the intensity or radiation of the cardiac murmur therefore further tests (echocardiography) are required before advise can be given on the suitability of the horse for purchase. Valid insurance exclusions include any liability from atrial fibrillation and congestive heart failure, but should not include sudden cardiac death 

0. 5) OTHER CONGENITAL DEFECTS. 

0. Sporadically any other developmental abnormality may occur (e.g. endocardial cushion defects, mitral, aortic, tricuspid dysplasia, Fenestration of cardiac valves, pulmonic atresia, single ventricle, etc.) including complex congenital deformities (e.g. tetralogy of fallot). Arabian and Thoroughbred horses appear to have a higher incidence of complex congenital disorders compared to other breeds. Diagnosis is based on auscultation (use basic principles to attempt to identify the component abnormalities), clinical signs e.g. cyanosis, and ultimately confirmed by two dimensional echocardiography.