VALVULAR DYSPLASIA IN THE HORSE may also reveal coarse bronchovesicular sounds and crackles
bilaterally if the horse is in active CHF (Schober et al., 2000 ). Tricuspid valve dysplasia will also result in a systolic murmur
secondary to tricuspid regurgitation, though this murmur is often quieter than that of MR and is heard loudest over the right hemi- thorax. This murmur is not to be confused with the loud, right- sided systolic heart murmur associated with a ventricular septal defect (VSD), which is the most commonly reported congenital heart defect in foals (Hall et al., 2010 ). Other clinical findings such as oedema, hydrothorax, ascites, hydropericardium and enlarge- ment of the liver may be observed if the horse is in right- sided CHF. Aortic dysplasia may be accompanied by systolic or diastolic
murmurs depending on the presence or absence of left ventricular outflow tract obstruction or aortic insufficiency (AI), respectively. Not all patients with aortic valve dysplasia will have an audible murmur (Taylor et al., 2007 ). This case report from Bell et al. ( 2024 ) describes a grade IV/VI, bilateral, continuous murmur. Together with the findings of the echocardiogram and post- mortem exam- ination, it can be inferred that the diastolic component of the mur- mur was likely due to AI. Systolic and diastolic murmurs may also be described as a ‘to- and- fro’ murmur, rather than a true contin- uous murmur. The murmur of AI may have a musical decrescendo quality, and is sometimes described as having a ‘creaking’ sound. Although murmur grade has a strong positive correlation to AI severity, arterial pulse quality serves as the best clinical guide. Diastolic runoff caused by AI results in low diastolic pressure, with severely affected horses having diastolic arterial pressures below 50 mmHg. This diastolic runoff leads to a pulse pressure greater than 60 mmHg, which confers to the peripheral pulse palpable hyperkinesis. The eventual result of severe AI is left ventricular volume over-
load and subsequent left- sided CHF. Horses with severe AI may present with the same signs of left- sided heart disease as a horse with MR. Clinical signs in animals with CHD may be difficult to dis- cern from other, acquired noncardiac disease, such as pneumonia, dysmaturity, sepsis, parasitic disease, toxaemia, uraemia, drugs, al- lergic reactions or nutritional deficiencies such as white muscle dis- ease (Reef, 1985 ). Differentiation of congenital valvular disease from other dif-
ferentials can be difficult in the ante- mortem period. Thoracic ra- diographs can identify generalised cardiomegaly and cardiogenic pulmonary oedema, particularly in foals. As radiography cannot reli- ably determine chamber size, intracardiac shunts or cardiac function, patients with suspected cardiac disease will benefit from an echo- cardiogram. Even with an echocardiogram, however, determining the aetiology of changes to the valve leaflets (i.e. congenital malfor- mation vs acquired disease) may prove difficult. Echocardiography may demonstrate specific chamber enlargement depending on which valves are affected. Colour- flow Doppler may reveal a jet of turbulent regurgitant blood flow at the atrioventricular valves. There are other considerations for complete assessment of cardiac func- tion; however, these are beyond the scope of this commentary.
| 569 Ultimately, the long- term prognosis for equine patients with con-
genital valvular dysplasia depends on the severity of the underlying pathology and resultant regurgitation. In mild cases, some level of athletic performance may be achievable. In severe cases that result in cardiac decompensation and CHF, however, the prognosis is gen- erally poor to grave. While treatment of CHF may not be considered in all cases, medical management can be attempted with diuretics, positive inotropes and anti- arrhythmic medications as indicated. Definitive diagnosis of valvular dysplasia in equine patients often
occurs in the post- mortem period. Necropsy findings in affected foals may include marked enlargement of the affected chambers of the heart, and valves often display fused and/or malformed leaflets with shortened chordae tendineae (Marr & Bowen, 2010 ). If avail- able, histopathological evaluation of valve leaflets is recommended for confirmation of suspected congenital valvular dysplasia. Clinically significant congenital valvular dysplasia, while rare in
foals, is an important differential for the equine practitioner and should be considered when evaluating young horses presented with vague clinical signs.
AUTHOR CONTRIBUTIONS Todd Sumerfield: Writing – original draft. Carl Toborowsky: Writing – review and editing.
FUNDING INFORMATION There are no funders to report for this commentary.
CONFLICT OF INTEREST STATEMENT No conflicts of interest have been declared.
ETHICS STATEMENT Not required for this commentary.
ORCID Todd Sumerfield
https://orcid.org/0009-0002-6273-8599 Carl Toborowsky
https://orcid.org/0009-0005-1700-9452
REFERENCES
Bayly , W.M. , Reed , S.M. , Leathers , C.W. , Brown , C.M. , Traub , J.L. , Paradis , M.R. et al.
( 1982 ) Multiple congenital heart anomalies
in five Arabian foals . Journal of the American Veterinary Medical Association , 181 ( 7 ), 684 – 689 .
Bell , J. , Shearer , P. , Hale , J. & Hughes , K.J. ( 2024 ) Aortic, mitral and tri- cuspid valvular dysplasia in a 7- month- old colt . Equine Veterinary Education , 36 ( 11 ), e288 – e294 . Available from: https:// doi. org/ 10. 1111/ eve. 13979
Buergelt , C.D. ( 2003 ) Equine cardiovascular pathology: an overview . Animal Health Research Reviews , 4 ( 2 ), 109 – 129 . Available from: https:// doi. org/ 10. 1079/ ahr20 0353
Clark , E.S. , Reef , V.B. , Sweeney , C.R. & Lichtensteiger , C. ( 1987 ) Aortic valve insufficiency in a one- year- old colt . Journal of the American Veterinary Medical Association , 191 ( 7 ), 841 – 844 .
Duz , M. , Philbey , A.W. & Hughes , K.J. ( 2013 ) Mitral valve and tricuspid valve dysplasia in a 9- week- old standardbred colt . Equine Veterinary Education , 25 , 339 – 344 . Available from: https:// doi. org/ 10. 1111/j. 2042- 3292. 2012. 00392. x
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