The effect of cardiovascular abnormalities on performance (Proceedings)

The normal horse's heart rate varies with exercise up to a maximum of 200 - 240 beats/ minute. The exercising horse should have a sinus tachycardia with a heart rate of 70-120 beats/minute trotting, 120-150 beats/minute cantering, 150-180 beats/minute at the hand gallop, and 180-240 at the gallop. The horse's heart rate should recover quickly if the horse is fit, dropping below 100 beats/minute in the first 5 minutes following maximal exercise and returning to baseline within 30-45 minutes following exercise. Cardiac arrhythmias are the most common cardiovascular cause of poor performance.

Cardiac Arrhythmias

Arrhythmias are frequently detected in the normal horse at rest and immediately post exercise. Exercising electrocardiography needs to be performed to determine the significance of cardiac arrhythmias on performance.

Atrial Fibrillation

Atrial fibrillation is the cardiac arrhythmia most frequently associated with poor performance. The degree of exercise intolerance is dependant upon the presence, type and severity of the horse's underlying cardiac disease and on the individual's resting vagal tone. Although horses with atrial fibrillation usually have normal resting heart rates, they have higher than normal heart rates during exercise, usually 40-60 beats/minute higher for each exercise level. The cardiac output of exercising horses decreases significantly at high work loads due to marked increases of heart rate resulting in shortened ventricular filling time and the lack of the atrial contribution to ventricular filling. Thus atrial fibrillation causes a marked drop in performance, resulting in race times that decrease by 15-30 seconds or more. Conversion from atrial fibrillation to sinus rhythm usually results in the return of the horse to its previous level of performance.

The large atrial myocardial size and high vagal tone of the normal horse are two criteria necessary for the development of atrial fibrillation. In most instances it is suspected that an atrial premature contraction initiates the arrhythmia. Potassium depletion also predisposes horses to the development of atrial fibrillation and can occur associated with furosemide administration, bicarbonate administration and/or excessive sweating. Horses with atrial fibrillation often have a decrease in resting systolic left ventricular function that is manifested echocardiographically as a decrease in fractional shortening. This usually returns to normal within several days of conversion to sinus rhythm. Persistent left ventricular dysfunction following conversion also suggests the presence of underlying myocardial disease.

Ventricular and Supraventricular Premature Depolarizations

Occasional premature depolarizations may be detected post exercise and are clinically insignificant if infrequent. Ventricular premature depolarizations and paroxysms of ventricular tachycardia have been observed in horses quitting or fatiguing while exercising on the treadmill. Supraventricular extrasystoles are observed less frequently during an exercising ECG. Paroxysmal ventricular tachycardia detected at peak exercise, or as the horse is tiring, indicates an exercise-induced myocardial problem. Exercising ventricular arrhythmias have been associated with arterial hypoxemia in horses with upper respiratory dysfunction, particularly those with severe upper respiratory tract obstruction. Problems with myocardial perfusion or a pre-existing myocarditis or cardiomyopathy must also be considered. Exercise-induced electrolyte and metabolic disturbances may also be involved in the pathogenesis of some of these arrhythmias. The premature depolarizations may decrease race times by 2-3 seconds for horses with occasional exercising premature depolarizations to 20-30 seconds or more for horses with sustained ventricular tachycardia. Sustained ventricular tachycardia has also been associated with collapse and sudden death. The detection of frequent ventricular or supraventricular premature depolarizations during peak exercise or in the immediate post exercise period should prompt further cardiac evaluation.

Advanced Second-degree A-V Block

Severe bradyarrhythmias are uncommon and associated with severe exercise intolerance and/or collapse. Advanced second degree atrio-ventricular block or third degree heart block are usually associated with an inflammatory focus and may respond to aggressive treatment with large doses of corticosteroids. If no response to the steroids is seen, there are probably degenerative changes in the A-V node and the horse's prognosis is poor to grave.

Myocarditis/Cardiomyopathy

Echocardiography is the technique of choice for evaluating horses with suspected myocardial dysfunction. Exercise-induced myocardial dysfunction can be diagnosed with stress echocardiography. Stress echocardiography is very useful in assessing the cardiovascular component of poor performance in horses with normal resting left ventricular function or borderline myocardial dysfunction at rest and a vague history of exercise intolerance. Global assessments of left ventricular function should be made pre and post exercise to evaluate the myocardial response to peak exercise. No change or a decrease in systolic thickening of the left ventricular free wall and interventricular septum following strenuous exercise is abnormal.

Clinical signs of myocarditis/cardiomyopathy vary but most horses present with exercise intolerance or signs of congestive heart failure. Arrhythmias and/or murmurs of mitral and tricuspid regurgitation are often detected. Atrial and ventricular premature depolarizations are common in less severely affected horses. Murmurs of valvular regurgitation are usually associated with clinically insignificant, mild or moderate atrioventricular valvular regurgitation. The echocardiogram is normal or a mild decrease in shortening fraction (20-30%) is detected, occasionally with segmental wall abnormalities. These horses have a fair to good prognosis for recovery and return to performance with rest and/or corticosteroid therapy.

Heart Murmurs

Physiological flow murmurs occur frequently in horses and may be difficult to distinguish from murmurs associated with underlying cardiac disease. Valvular regurgitation and ventricular septal defects (VSDs) occur frequently and may impair performance, result in the horse's premature demise or have no apparent effect on life expectancy or performance capabilities. The echocardiographic findings that are used to formulate a prognosis for longevity and performance in horses with valvular regurgitation include the abnormalities detected on the valve leaflets, degree of cardiac chamber enlargement, severity of the resultant volume overload, size of the regurgitant jet, and relative relationship of jet size to chamber size.

Mitral Insufficiency

The valvular insufficiency most likely to cause clinical signs is mitral regurgitation. Most horses with clinically insignificant to mild mitral regurgitation are able to perform successfully at all levels of athletic endeavor. Significant mitral regurgitation causes increased left atrial pressure and pulmonary hypertension. This leads to the development of performance related clinical signs; increased respiratory rate and effort during exercise, prolonged recovery time after exercise, coughing, exercise induced pulmonary hemorrhage, exercise intolerance and/or atrial fibrillation. Acute signs of left sided congestive heart failure are unusual unless acute severe mitral regurgitation is present. With acute severe mitral regurgitation pulmonary edema develops and the horse presents with a foamy nasal discharge and/or coughing and expelling copious quantities of foamy fluid from the lungs. Horses with ruptured mitral chordae tendineae may also have a sudden onset of poor performance or die suddenly with no prior clinical signs. Horses with severe chronic mitral regurgitation are more likely to present with clinical signs of right sided congestive heart failure, including ventral edema, generalized venous distention and jugular pulses. Once the mitral regurgitation becomes hemodynamically significant, it is likely to affect performance.

Horses with mitral valve prolapse or degenerative mitral valve disease, clinically insignificant or mild mitral regurgitation, no significant left atrial or left ventricular enlargement, and normal myocardial function have a good to excellent prognosis for performance. The mitral regurgitation in horses with degenerative valve disease, moderate mitral regurgitation, moderate enlargement of the left atrium and left ventricle, and normal myocardial function will probably progress slowly over several years. If severe mitral regurgitation is detected with Doppler echocardiography and only mild to moderate left atrial and left ventricular enlargement are present, the regurgitation is likely to deteriorate rapidly and the horse should be re-examined more frequently. Horses with a major ruptured chorda tendineae, flail mitral valve leaflet or bacterial endocarditis must be given a guarded to poor prognosis for performance and life, as rapid deterioration is also likely in these horses. Horses with pulmonary artery dilatation should be given a guarded to grave prognosis and not be used because of the risk of pulmonary artery rupture and sudden death.

Tricuspid Insufficiency

Most horses are able to perform successfully at all levels of athletic endeavor with clinically insignificant to moderate tricuspid regurgitation. Severe tricuspid regurgitation is most common secondary to chronic pulmonary hypertension associated with mitral regurgitation and/or other left heart disease. Atrial fibrillation, generalized venous distention, systolic jugular pulsations, peripheral edema, pleural effusion, hepatic congestion and rarely, ascites, may develop if the tricuspid insufficiency is severe.

Horses with tricuspid valve prolapse or degenerative tricuspid valve disease, clinically insignificant to moderate tricuspid regurgitation, minimal to moderate right atrial and ventricular enlargement, and normal myocardial function also have an excellent prognosis for performance. Horses with a major ruptured chorda tendineae, flail tricuspid valve leaflet, bacterial endocarditis, or pulmonary hypertension from severe left sided heart disease must be given a guarded to poor prognosis as more rapid deterioration is likely. Once tricuspid regurgitation is severe, it is likely to affect performance, particularly for the most rigorous types of athletic endeavor. However, the progression to congestive heart failure and death is slow.

Aortic Insufficiency

Most horses are able to perform successfully at all levels of athletic endeavor with clinically insignificant to severe aortic regurgitation, until mitral regurgitation also develops. Bounding arterial pulses indicate the presence of hemodynamically significant aortic regurgitation. Horses with aortic regurgitation rarely develop clinical signs of congestive heart failure but may have exercise intolerance with severe aortic regurgitation. Concurrent atrial fibrillation and/or ventricular premature depolarizations may complicate any performance problems present.

Aortic regurgitation is usually very well tolerated by horses with normal left ventricular function, in the absence of mitral regurgitation. Horses with aortic valve prolapse or degenerative aortic valve disease, clinically insignificant to moderate aortic regurgitation, minimal to moderate left ventricular and aortic root enlargement, normal myocardial function and a jet area consistent with the degree of left ventricular enlargement have an excellent prognosis for performance. The aortic regurgitation is likely to progress slowly throughout the horse's life. Horses with fenestrations, small tears of the free edge of the valve leaflet, flail valve leaflets and bacterial endocarditis should initially be given a more guarded prognosis, as these valvular insufficiencies could progress more rapidly. Horses with moderate to severe aortic regurgitation and normal left ventricular function can exercise as well as normal individuals. The regurgitation usually progresses slowly over many years in these horses and is well tolerated. Even horses with severe aortic regurgitation and severe left ventricular dilatation continue to perform successfully for 2 ½ - 3 years, if they have normal myocardial function, before developing signs of congestive heart failure and/or sudden death. Once horses with severe aortic regurgitation develop significant mitral regurgitation, they rapidly develop severe pulmonary hypertension and signs of left-sided heart failure.

Ventricular Septal Defect

The echocardiographic findings that are used to formulate a prognosis for horses with VSDs are the number, size and location of the defect(s), degree of left ventricular volume overload, maximal velocity and direction of shunt flow through the defect and the presence and severity of concurrent aortic regurgitation. Horses with a perimembranous VSD measuring 2.5 cm or smaller in 2 mutually perpendicular planes, with a peak shunt velocity of > 4 m/sec, little or no prolapse of the aortic valve into the VSD with little or no aortic regurgitation have a good prognosis for performance and a normal life expectancy. Many of these horses are able to compete successfully as racehorses or upper level performance horses. The size of the VSD is related to the performance ability of the horse and longevity; horses with VSDs > 2.5 cm but < 3.5 cm usually do not have normal exercise tolerance at maximal levels of athletic performance but may be able to be successful pleasure horses or lower level performance horses. Most horses with VSDs > 3.5 cm in diameter are likely to have a shortened life expectancy and develop congestive heart failure.

Sinus of Valsalva Aneurysm and Aortic Root Rupture

Sinus of Valsalva aneurysms are congenital defects in the media of the wall of the aorta in the right sinus of Valsalva that are asymptomatic until associated with aortic root rupture later in life. Most horses with sinus of Valsalva aneurysms that rupture are male and at least 10 years old. A ruptured sinus of Valsalva aneurysm should be considered in the differential diagnosis for a stallion or gelding > 10 years old with tachycardia and colic without any detectable primary gastrointestinal problem. When the aortic sinus of Valsalva aneurysm ruptures into the right atrium, right ventricle, through the tricuspid valve, or dissects down into the interventricular septum, an aortic cardiac fistula is created. These subendocardial dissections can subsequently rupture into the right or left ventricle. Aortic root rupture at the right sinus of Valsalva can also occur without a pre-existing aneurysm. In these horses a defect is imaged in the wall of the aorta at the right sinus of Valsalva, with no other pre-existing aortic root abnormalities. The rupture of a sinus of Valsalva aneurysm or the aortic root is life threatening. The prognosis is guarded to grave with most affected horses living < 6 months following rupture. The affected animals should not be used for performance, as the risk of sudden death is high.

Vascular Disease

Aortoiliac Thrombosis

Aortoiliac thrombosis occurs infrequently, but can be associated with exercise-associated unilateral hind limb lameness, ataxia, collapse or breeding failure in stallions. Physical examination of an affected horse at rest may reveal weak metatarsal arterial pulses or delayed saphenous refill in the affected limb. Marked hyperpnea, other signs of respiratory distress and profuse, generalized sweating are often present post exercise with trembling of the affected limb. Rectal examination may reveal fremitus, a weak or absent pulse, or aneurismal dilatation of the affected artery or arteries. A hypoechoic to echogenic mass partially occluding the arterial lumen is imaged with transrectal ultrasonography. Horses with aortoiliac thrombosis have a guarded prognosis for performance at best.

Jugular vein thrombosis

Jugular vein thrombophlebitis is a common problem in performance horses and may result in complete occlusion of the affected vein. Complete fibrous occlusion or a severe stricture of the jugular vein may impede venous return from the head such that, if adequate collateral circulation does not develop, impaired venous drainage of the upper airways may limit performance. In most horses, however, the prognosis for jugular vein thrombophlebitis is good and the vein recannalizes after thrombophlebitis.