Abstract
Ventricular septal defects (VSDs) were diagnosed in 27 horses; in 26 affected horses systolic murmurs were detected over both sides of the chest. Holodiastolic decrescendo murmurs were also detected in 5 horses. Standardbreds and Arabian horses were over-represented, while Thoroughbred horses were under-represented, when compared to the hospital population (P < 0.0001). Five horses had previously raced successfully, one 2-year-old was training successfully and close to racing, and 4 horses had competed successfully in other types of competition. Eleven horses had a history of exercise intolerance or poor performance, 5 horses were stunted and 3 horses were in congestive heart failure at the time of presentation. The VSD murmur was detected as an incidental finding in 14 horses. Membranous VSD were most commonly detected (in 23/27 affected horses) and were typically found underneath the septal leaflet of the tricuspid valve and the right and/or noncoronary leaflet of the aortic valve. Muscular VSDs were much less common and were located in any portion of the muscular septum. The VSDs ranged in size from 1-4.6 cm (maximal diameter) in affected horses. A left to right shunt through the VSD was detected in 26/27 affected horses with Doppler echocardiography. The peak velocity of shunt flow detected through the VSD was 0-5.8 m/s. The interventricular pressure gradients estimated from the peak shunt velocity obtained with Doppler echocardiography were 0-135 mmHg. Right ventricular pressures estimated with Doppler echocardiography were 15-84 mmHg, similar to invasively obtained measurements of right ventricular pressure in 80% of horses in which right sided cardiac catheterisation was performed (n = 5). Left ventricular and left atrial volume overload was detected in the majority (23/27) of horses. Right atrial and right ventricular volume overload was severe in 3 horses with muscular VSDs, mild in 1 horse with a perimembranous VSD, and mild in 2 horses with membranous VSDs. Concurrent left ventricular dysfunction was detected in 2 horses. Aortic valve prolapse was seen in 7 horses associated with the membranous location of the VSD; 6 of these horses had very mild (1+) or mild (2+) aortic regurgitation. Severe (4+) aortic regurgitation was present in one horse, severe mitral regurgitation in 2 horses, severe tricuspid regurgitation in 3 horses, and severe pulmonary regurgitation was detected in 2 horses. Mitral valve prolapse, tricuspid valve dysplasia, a flail aortic valve leaflet, and a bicuspid pulmonary valve were additional findings detected in one horse each. Post mortem examinations were performed in 8 horses which confirmed the echocardiographic findings. Sixteen out of 27 horses had a history of racing or competing successfully either before or after the diagnosis of the VSD. Two horses were useful pleasure horses, 3 horses presented in congestive heart failure, 1 horse developed signs of congestive heart failure, 2 horses were lost to follow-up and 2 are still alive but are small and stunted. The successful racehorses usually had a membranous VSD that measured < or = 2.5 cm in its largest diameter and a peak velocity of shunt flow through the VSD of > or = 4 m/s. Two-dimensional (2-D) and Doppler echocardiography is useful in assessing the haemodynamic significance of VSDs in horses and can be used to help formulate a prognosis for life and performance.
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