search.noResults

search.searching

saml.title
dataCollection.invalidEmail
note.createNoteMessage

search.noResults

search.searching

orderForm.title

orderForm.productCode
orderForm.description
orderForm.quantity
orderForm.itemPrice
orderForm.price
orderForm.totalPrice
orderForm.deliveryDetails.billingAddress
orderForm.deliveryDetails.deliveryAddress
orderForm.noItems
Received: 26 June 2024 | Accepted: 9 July 2024 DOI: 10.1111/eve.14034


C L INI C A L COMMENTA RY Congenital valvular dysplasia in the horse


Todd Sumerfield | Carl Toborowsky College of Veterinary Medicine, Veterinary Clinical Medicine , University of Illinois at Urbana- Champaign , Urbana , Illinois , USA


Correspondence: Todd Sumerfield Email: tsmrfld@illinois.edu


In the case report described in this issue, Bell et al. ( 2024 ) describe a previously unreported occurrence of aortic, mitral and tricuspid valve dysplasia (TVD) in a 7- month- old, Warmblood- cross colt. The prevalence of congenital heart disease (CHD) in the horse is lim- ited to historical studies that suggest a prevalence of 0.03%–0.2% (Buergelt, 2003 ; Michaëlsson & Ho, 2000 ). Valvular dysplasia appears to make up an even smaller group of CHD in horses, and was identified in only 8/18 foals in one report (Hall et al., 2010 ). The reported numbers likely underestimate total occurrence, as the true numbers include foals with severe cardiac malformations who die during or shortly after birth, as well as clinically silent defects that go undetected. Despite the suspectedly low occurrence of congen- ital valvular disease, the equine practitioner must still be aware of these conditions and be familiar with the clinical presentation and available diagnostics for detection and management of congenital valvular dysplasia. The horse in this report had changes consistent with congen-


ital dysplasia of the aortic, mitral and tricuspid valves. Individual case reports of dysplasia of the mitral valve (Marr & Bowen, 2010 ; McGurrin et al., 2003 ; Schober et al., 2000 ) and mitral and tricuspid valves (Duz et al., 2013 ) in horses have been published. Anecdotal observation of TVD as an isolated congenital defect has also been previously reported by the authors. Most congenital abnormalities of the tricuspid valve in horses are forms of atresia (Hall et al., 2010 ; Krüger et al., 2016 ; Meurs et al., 1997 ), with some investigators suggesting it is among the most common form of equine CHD (Hall et al., 2010 ). Atrioventricular valvular dysplasia can also be a component of complex CHD (Bayly et al., 1982 ; Kohnken et al., 2018 ; van der Luer & van der Linde- Sipman, 1978 ). Dysplasia of the aortic valve has been described as an isolated abnormality (Clark et al., 1987 ; Taylor et al., 2007 ), as well as in combination with other CHD (Michlik et al., 2014 ). The clinical signs of valvular dysplasia tend to manifest early


in life, particularly when disease is severe. The clinical presenta- tion of horses with CHD varies greatly based on disease severity.


Most foals diagnosed with one or more forms of valvular dyspla- sia present with lethargy, exercise intolerance, failure to thrive, dyspnoea, cyanosis or syncope within the first days to weeks of life (Scansen, 2019 ). Clinical signs are often nonspecific, which can complicate diagnosis and delay management. Recognition of disease requires that the practitioner consider CHD as a differ- ential. Abnormal cardiac auscultation is often the first diagnostic that triggers suspicion of CHD, as most forms of valvular dyspla- sia are associated with a loud heart murmur. The heart sounds in foals are usually readily auscultatable, as their chest walls are thin and the heart abuts the thoracic wall. Physiological mur- murs are commonly heard from turbulent blood flow through a patent ductus arteriosus in the neonate up to 4 days of age. These murmurs may be systolic, though continuous murmurs are also auscultated. Continuous murmurs will typically cease to be heard within 24 h after birth and are considered abnormal if detected beyond 4 days of age (Reef, 1985 ). Tachycardia can also be suggestive of CHD, as many affected


foals present with inappropriate tachyarrhythmias. The heart rate in normal Thoroughbred foals during the first 5 min after birth ranges from 30 to 90 beats/min, with a gradual change of the rate to 72– 133 beats/min by 10 h of age (Rossdale, 1967 ). While tachycardia is a nonspecific finding, it should elicit consideration of CHD as a differential. Cases of mitral valve dysplasia (MVD) may result in mitral regur-


gitation (MR) and/or stenosis; however, mitral stenosis (MS) is not commonly reported. The murmur of mitral valve regurgitation is often loud (grade IV/VI or greater), heard best over the left hemi- thorax towards the apex of the heart and should occur during the systolic phase of the cardiac cycle. In cases of MS, there may also be a soft, diastolic murmur heard in the same location. Patients with severe MVD are often presented with signs of left- sided congestive heart failure (CHF). These signs include tachypnoea, weakness and frank pulmonary oedema. Physical examination findings on presen- tation often include tachycardia with weak pulses, and auscultation


This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. © 2024 The Author(s). Equine Veterinary Education published by John Wiley & Sons Ltd on behalf of EVJ Ltd.


568 | aaep.org/wiley-redirect Equine Vet Educ. 2024;36:568–570.


Page 1  |  Page 2  |  Page 3  |  Page 4  |  Page 5  |  Page 6  |  Page 7  |  Page 8  |  Page 9  |  Page 10  |  Page 11  |  Page 12  |  Page 13  |  Page 14  |  Page 15  |  Page 16  |  Page 17  |  Page 18  |  Page 19  |  Page 20  |  Page 21  |  Page 22  |  Page 23  |  Page 24  |  Page 25  |  Page 26  |  Page 27  |  Page 28  |  Page 29  |  Page 30  |  Page 31  |  Page 32  |  Page 33  |  Page 34  |  Page 35  |  Page 36  |  Page 37  |  Page 38  |  Page 39  |  Page 40  |  Page 41  |  Page 42  |  Page 43  |  Page 44  |  Page 45  |  Page 46  |  Page 47  |  Page 48  |  Page 49  |  Page 50  |  Page 51  |  Page 52  |  Page 53  |  Page 54  |  Page 55  |  Page 56  |  Page 57  |  Page 58  |  Page 59  |  Page 60  |  Page 61  |  Page 62  |  Page 63  |  Page 64  |  Page 65  |  Page 66  |  Page 67  |  Page 68  |  Page 69  |  Page 70  |  Page 71  |  Page 72  |  Page 73  |  Page 74  |  Page 75  |  Page 76  |  Page 77  |  Page 78  |  Page 79  |  Page 80  |  Page 81  |  Page 82  |  Page 83  |  Page 84  |  Page 85  |  Page 86  |  Page 87  |  Page 88  |  Page 89  |  Page 90  |  Page 91  |  Page 92