tricuspid dysplasia in dogs

4 downloads 12 Views 469KB Size Report
Mar 18, 2013 - Seven dogs presented no clinical symptoms to date. ... which rarely occurs in dogs and cats (16, 18-20). It is ... ascites (four dogs), and hydrothorax (three dogs). Two .... Differential diagnosis includes myocarditis, tricuspid ...

Bull Vet Inst Pulawy 57, 123-126, 2013 DOI: 10.2478/bvip-2013-0023

TRICUSPID DYSPLASIA IN DOGS URSZULA PASŁAWSKA, AGNIESZKA NOSZCZYK-NOWAK, ADRIAN JANISZEWSKI,, AND JÓZEF NICPOŃ Department of Internal Medicine and Clinic of Diseases of Horses, Dogs and Cats, Faculty of Veterinary Medicine, University of Environmental and Life Science, 50-366 Wroclaw, Poland [email protected] Received: 25 October, 2012

Accepted: February 13, 2013

Abstract The aim of the study was to estimate prevalence of tricuspid dysplasia (TD) in dogs with respect to breed, age, sex, clinical signs, and echocardiographic findings and to compare this data with literature. TD was found in 15 dogs (6.5% of congenital cardiac disease) of 215 dogs with congenital heart defects. All dogs had right heart enlargement on thoracic radiographs, echocardiography, and electrocardiography. Doppler echocardiography revealed tricuspid valve regurgitation. Seven dogs presented no clinical symptoms to date. TD took the form of Ebstein anomaly in all Labrador Retrievers, one Boxer, and one German Shepherd dog. TD predominated in males (11 males vs. three females). The body weight of the affected dogs, with the exception of the Miniature Schnauzer, exceeded 20 kg. Two dogs (Boxer and Bull Terrier) had additional congenital cardiac lesions in the form of mitral valve dysplasia. The most affected breeds in the study were the Labrador Retriever and Boxer.

Key words: dog, tricuspid dysplasia, congenital heart defect. Tricuspid dysplasia (TD) represents a complex abnormal position or thickened valve leaflets, pathologically short or long chordae tendineae or papillary muscles. TD is a congenital heart disease, which rarely occurs in dogs and cats (16, 18-20). It is most commonly observed in large-breed dogs – over 20 kg of body weight, and is especially noted in Labrador Retrievers, Boxers, and German Shepherds, less frequently in Old English Sheepdogs, Great Danes, Weimaraners, and Irish Setters (6, 14). A retrospective study by Chetboul et al. (6) showed increased risk of TD in the Labrador Retriever by 35 and 7 times compared to other breeds and mongrels, respectively. A genetic study of Labrador Retriever suggested that TD is related to a single recessive gene susceptibility locus on CFA9 (1, 10). Small-breed dogs e.g. Yorkshire Terrier, Beagle, English Cocker Spaniel, French Bulldog, and Poodle may also be affected (11). The majority of affected dogs are of pure breed. The aim of the study was to estimate prevalence of TD in Poland with respect to breed, age, sex, clinical signs, and echocardiographic findings and to compare this data with literature.

Material and Methods Two hundred and fifteen dogs with congenital heart defects were patients of the Department. The dogs were presented for examination mostly at 8 months of age with loud heart murmur (14 dogs), exercise intolerance (eight dogs), respiratory distress (five dogs), ascites (four dogs), and hydrothorax (three dogs). Two

dogs (Boxer and Bull Terrier) had additional congenital cardiac lesions in the form of mitral valve dysplasia. The dogs were referred for cardiologic examination to the Clinic, where thoracic radiographs (lateral and dorsoventral), echocardiography using Aloka 4000+ (M- and B-Mode, colour, PW and CV Doppler) and electrocardiography were performed in accordance with acceptable standards. The diagnostic procedures were done without the pharmacological sedation of animals.

Results Tricuspid dysplasia was found in 15 dogs: three Boxers, three Labrador Retrievers, two Golden Retrievers, and one Bull Terrier, Doberman Pincher, Great Dane, German Shepherd dog, Polish Lowland Sheepdog, Miniature Schnauzer, as well as Yorkshire Terrier. All dogs had right heart enlargement on thoracic radiographs, echocardiography, and electrocardiography. Doppler echocardiography revealed tricuspid valve regurgitation. Seven dogs showed no clinical symptoms to date. TD in the form of Ebstein’s anomaly was diagnosed in all Labrador Retrievers, in one Boxer, and in one German Shepherd dog (Fig. 1). TD predominated in males (11 males vs. three females). With the exception of one Miniature Schnauzer, all affected dogs had a moderate to large body weight exceeding 20 kg.

Unauthenticated | 156.17.187.72 Download Date | 3/18/13 12:10 PM

124

A

B RA

RV

LV

RA

LA RV

Fig. 1. Dysplastic tricuspid valve – Ebstein’s anomaly in a 7 month Labrador Retriever. A. Echocardiography –apical four chamber view, with large right atrium and small right ventricle. LV - left ventricle, LA – left atrium. B. Autopsy in the same dog, enlarged right atrium (RA) and small right ventricle (RV) B

A

RV

RV

LV

TR RA LA

LV

RA LA

Fig. 2 TD - Abnormal papillary muscle in enlarged right ventricle causing tricuspidal regurgitation (TR) in 4-monthold Yorkshire Terrier. Right parasternal long axis view. RV – right ventricle, RA – right atrium, LV-left ventricle, LA – left atrium

A

B

Fig. 3. Necropsy of the dysplastic tricuspid valve in two dogs (A and B) with a lack of cordae tendineae between tricuspid valve and papillary muscle (arrows). The right figure (B) shows chaotic arrangement of chordate tendineae within the right ventricle

Unauthenticated | 156.17.187.72 Download Date | 3/18/13 12:10 PM

125

Discussion Congenital and secondary tricuspid malformation are rare disorders in dogs. Secondary tricuspid insufficiency as a result of tricuspid endocardiosis, pulmonary hypertension, and right ventricular dilatation was occasionally observed in dogs, whereas in humans these cases are more common (14). The occurrence of tricuspid dysplasia ranges from 7.0% to 7.5% of all congenital heart defects (20). However, prevalence and breed associations may exhibit geographical variations. In the study, TD made up 6.5% of congenital cardiac diseases. The disease can occur as a solitary anomaly or complex problem. The association of TD with mitral deformation is often observed because TD is a result of a developmental abnormality of the right ventricle, which can occur simultaneously with left ventricle developmental abnormalities (5, 7). In addition, TD has occasionally occurred simultaneously with ventricular septum defects, pulmonic stenosis, aortic stenosis, atrial septal defects, and persistent left cranial vena cava (8, 15). In the study, TD occurred with mitral dysplasia in 14% of TD cases. Tricuspid dysplasia leads to right heart enlargement and signs of right heart failure: abdominal distension due to ascites, weakness, lethargy, jugular vein distension and pulsation, hepatomegaly, splenomegaly, and sometimes subcutaneous oedema. ECG examination may suggest right atrium and ventricular enlargement and may show arrhythmias. Echocardiography is the gold standard for TD diagnosis. The echocardiographic examination allows the assessment of mild, moderate, or severe TD. The classification is based on the degree of tricuspid leaflet deformation, regurgitation, and the size of right ventricle (7). TD may result in valvular insufficiency, stenosis, or both. All dogs examined in the study had severe tricuspid insufficiency (Fig. 2). TD involved the leaflets and chordae tendinae and often papillary muscles (Fig. 3). One of the forms of TD is Ebstein’s anomaly, which occured in 1/3 of the dogs in the study. Similar frequency of TD and Ebstein’s anomaly was observed by Chetboul et al. (6). Ebstain’s anomaly is characterised by apical displacement of the septal and posterior tricuspid valve leaflets, leading to atrialisation of the right ventricle. Surgery with artificial valve implantation is the only possibility that allows for full recovery. Successful surgery for TD in human medicine was described in 1962, while in animals this procedure is rarely performed because of the necessity to use extracorporeal circulation, as well as the technical challenges, high costs, and long reconvalescence (4). Nowadays, the surgical correction of TD described in human medicine is unfavourable in veterinary patients (9). Pharmacological treatment is focused on maintaining the patient in the asymptomatic period for as long as possible. In rare cases in humans, the length of life exceeds 70 years (3). Survival of dogs with TD depends on the extent to which the normal function of

the valves is compromised. Surprisingly, many dogs with severe TD exhibit no symptoms during a relatively long period – until they are in congestive heart failure. It is reasonable to use diuretics (furosemide, spironolactone), ACE inhibitors (enalapril, benazepril, imidapril), and, in some cases, positive inotropic- drugs (digoxin, pimobendan) in different combinations. Positive ionotriopic drugs are given to improve glomerular filtration or to support left ventricular function during the end stage of the disease, when left sided heart failure develops (13). Antiarrhythmic drugs may become necessary in cases of arrhythmias. Supraventricular tachyarrhythmias are common but most dogs and cats do not develop any rhythm disturbances (12, 14, 17). Pharmacological treatment enables a short term improvement of clinical status. A well balanced diet with sufficient energy and low sodium is recommended e.g. Cardiac support diet, HD diet. In cases of deterioration oxygen therapy and evacuation of ascetic or/and pleural fluid may be needed. Differential diagnosis includes myocarditis, tricuspid valve endocarditis, tricuspid endocardiosis, tricuspid valve prolaps, right ventricular dysplasia, right ventricular enlargement with tricuspidal regurgitation as a result of pulmonary insufficiency, and arrhythmogenic right ventricular cardiomyopathy (2). To conclude, tricuspidal dysplasia was observed in 6.5 % of the dogs with congenital heart disease. The most affected breeds in the study were Labrador Retrievers and Boxers. Tricuspid dysplasia occurs 3 times more often in males than females.

References 1.

2. 3.

4. 5.

6.

7.

8.

Andelfinger G., Wright K.N., Lee H.J., Siemens L.M., Benson D.W.: Canine tricuspid valve malformation, a model of human Ebstein anomaly, maps to dog chromosome 9. J Med Genet 2003, 40, 320-324. Ammash N.M., Warnes C.A., Connolly H.M., Danielson G.K., Seward J.B.: Mimics of Ebstein’s anomaly. Am Heart J 1997, 134, 508-513. Attie F., Rosas M., Rijlaarsdam M., Buendia A., Zabal C., Kuri J., Granados N.: The adult patients with Ebstein’s anomaly: Outcome in 72 unoperated patients. Medicine 2000, 79, 63-69. Bernard C.N., Schrire V.: Surgical correction of Ebstein’s malformation with prosthetic tricuspid valve. Surgery 1963, 54, 302-308. Bialostozky D., Medrano G., Muňoz-Castellanos L., Contreras R.: Vectorcardiographic study and anatomic observations in 21 cases of Ebstein’s malformation of the tricuspid valve. Am J Cardiol 1972, 30, 354-361. Chetboul V., Tran D., Carlos C., Tessier D., Pouchelon I.L.: Congenital malformations of the tricuspid valve in domestic carnivores: A retrospective study of 50 cases. Schweiz Arch Tierheilkd 2004, 146, 265-275. Correa-Villasenor A., Ferencz C., Neil C.A., Wilson P.D., Boughman J.A.: Ebstein’s malformation of the tricuspid valve: genetic and environmental factors. Teratology 1994, 50, 137-147. Diana A., Guglielmini C., Acocella F., Valerio F., Cipone M.: Chylothorax associated with tricuspid dysplasia and atrial septal defect in a bullmastiff. J Am Anim Hosp Assoc 2009, 45, 78-83.

Unauthenticated | 156.17.187.72 Download Date | 3/18/13 12:10 PM

126 9.

10.

11.

12. 13.

14.

Eyster G.E., Anderson L., Evans A.T., Chaffe A., Bender G., Johnston J., Muir W., Blanchard G.: Ebstein’s anomaly: a raport of 3 cases in the dog. J Am Vet Med Assoc 1977, 170, 709-713. Famula T.R., Siemens L.M., Davidson A.P., Packard M.: Evaluation of the genetic basis of tricuspidal valve dyplasia in Labrador retrievers. Am J Vet Res 2002, 63, 816-820. Gregori T., Gomez Ochoa P., Quintavalla F., Mavropoulou A., Quintavalla C.: Congenital heart defects in dogs: a double retrospective study on cases from University of Parma and University of Zaragoza. Ann Fac Med Vet Parma 2008, 28, 79-90. Hoffmann G., Amberger C.N., Seiler G., Lombard C.W.: Tricuspid valve dysplasia in fifteen dogs. Schweiz Arch Tiercheilkd 2000, 142, 268-77. Jost Ch.H.A., Connolly H.M., O’Leary P.W., Warnes C.A., Tajik A.J., Seward J.B.: Left heart lesions in patients with Ebstein anomaly. Mayo Clin Proc 2005, 80, 361-368. Kornreich B.G., Moise N.S.: Right atrioventricular valve malformation in dogs and cats: an electrocardiographic

15. 16. 17.

18.

19.

20.

survey with emphasis on splintered QRS complexes. J Vet Int Med 1997, 11, 226-230. Lisowska A., Sobkowicz B., Musiał W.J., Skibińska E.: Congenital tricuspid valve dysplasia in a patient with advanced heart failure. Kardiol Pol 2006, 63, 201-203. Liu S.K., Tilley L.P.: Dysplasia of the tricuspid valve in the dog and cat. J Am Vet Med Assoc 1976, 169, 623630. de Madron E., Kadish A., Spear J.F., Knight D.H.: Incessant atrial tachycardias in a dog with tricuspid dysplasia. Clinical management and electrophysiology. J Vet Int Med 1987, 1, 163-169. Riesen S.C., Kovacevic A., Lombard C.W., Amberger C.: Echocardiographic screening of purebred cats: an overview from 2002 to 2005. Schweiz Arch Tierheilkd 2007, 149, 73-76. Sousa M.G., Gerardi D.G., Alves R.O., Camacho A.A.: Tricuspid valve dysplasia and Ebstein’s anomaly in dogs: case report. Arq Bras Med Vet Zootec 2006, 58, 762-767. Tidholm A.: Retrospective study of congenital heart defects in 151 dogs. J Small Anim Pract 1997, 38, 94-98.

Unauthenticated | 156.17.187.72 Download Date | 3/18/13 12:10 PM