Horses with a VSD are unlikely to perform at the very highest level; however, many animals are able to perform useful work on the racecourse or in less athletic pursuits. An echocardiographic examination is imperative for accurate prognostication in animals with a VSD, unless clinical signs are already suffisevere to suggest a grave prognosis.
Using 2DE, the size of the VSD should be measured in two different axes, usually the parasternal long and short axes. Occasionally, the largest dimension will be seen in an oblique axis some way between these two conventional views. As a general guide, defects under 2.0-2.5cm in diameter are thought to be restrictive and carry a better prognosis for useful athletic function than larger defects. Sub-pulmonary VSDs and defects in the muscular septum appear to have a worse prognosis. Horses with VSDs associated with other congenital lesions also have a poor outlook. 2DE can also be used to assess the degree of volume overload which results from the shunt. Very similar guidelines apply in this instance to that in animals with mitral regurgitation (MR). In fact, the haemodynamic changes resulting from a VSD are in many ways similar to those associated with MR except that with a VSD there is also pulmonary overcirculation as a result of the left to right shunt. It is important to assess the PA dimension as a dilated PA may precede rupture of this artery and sudden death.
The presence of aortic incompetence due to prolapse of the non-coronary cusp of the aortic valve or the aortic root into the defect is associated with a worsened prognosis compared to animals with a VSD and no aortic incompe
The best way to assess the haemodynamic significance of a VSD is to estimate the pressure gradient across it using DE. If the defect is small and restrictive, only a small amount of blood will be able to flow between the high-pressure LV and the low-pressure RV during systole. Consequently, the pressure in the RV will be almost normal and the pressure gradient between the two chambers results in a high velocity jet of blood through the VSD. If the defect is large, a large quantity of blood may shunt from the LV to the RV, resulting in an increase in the RV pressure. There will also be significant volume overload of the left side, the RV and the pulmonary circulation which may result in pulmonary hypertension, also increasing RV pressure. With a lower-pressure gradient between the LV and the RV than normal, the velocity of the jet of blood will be reduced.
Pulsed-wave Doppler can be useful for detecting the presence of a jet; howbecause the jet is high velocity, even in severe VSDs, aliasing may occur and continuous-wave Doppler is preferable. The pressure gradient is calculated from the estimated jet velocity using the Bernoulli equation (see section 4.2.7). For example, a jet of 4 m/sec would correspond with an estimated pressure gradient of 64 mm Hg. Since the LV systolic pressure is likely to be in the region of 120 mm Hg this means that the RV systolic pressure is 56 mm Hg. Normal RV systolic pressure is up to 40 mm Hg. It is important that the ultrasound beam is parallel with the jet so that the highest velocity is detected, otherwise the severity of the VSD may be exaggerated. If the velocity of the jet is 4.0-4.5 m/ sec or more, the prognosis for future athletic use is good.
Clinical and historical evidence is also pertinent in giving advice on the use of horses with VSDs for athletic work. A recent, normal performance record is supportive evidence for the presence of a relatively insignificant lesion. Owners should be warned of the initial signs of deterioration (reduced exercise tolerance, cough, signs of CHF) and encouraged to allow repeated echocardiographic examination of their animals so that potentially important changes such as increased volume overload or PA dilation can be detected before they present an unacceptable risk to the rider.