Featuring Original Pure Breed English Bulldogs, History & Description

the Original Pure Breed Bulldog Image

English Bulldogs History & Description from the Early Breed Development to 1893, Essential Graphic Description of English Bulldog's Features of that time

Images of White Pure Breed Bulldogs

Animals in the World English Bulldogs


British Bulldog Photos

British Bulldog Photos

Champion Bulldog Puppies Pics, English Bulldog Bloodlines Pics


Photo Ambient English Bulldogs


Photo Ambience English Bulldogs

Congenital cardiac anomalies in an English bulldog

Marina J. McConkey

Abstract

A 4-year-old male castrated English bulldog was referred to the Atlantic Veterinary College for evaluation of exercise intolerance, multiple syncopal episodes, and a grade IV/VI heart murmur. The dog was shown to have 3 congenital cardiac anomalies: atrial septal defect, mitral valve dysplasia, and subaortic stenosis. Medical management consisted of exercise restriction, atenolol, pimobendan, and taurine.

Résumé

Anomalies cardiaques congénitales chez un Bouledogue anglais. Un Bouledogue anglais castré âgé de 4 ans a été dirigé vers l’Atlantic Veterinary College pour l’évaluation d’une intolérance à l’exercice, d’épisodes syncopaux multiples et d’un souffle cardiaque de degré IV/VI. On a constaté que le chien avait 3 anomalies cardiaques congénitales : communication interauriculaire, dysplasie de la valvule mitrale et sténose sous-aortique. La gestion médicale comportait une restriction de l’exercice, et l’administration d’aténolol, de pimobendan et de taurine.

(Traduit par Isabelle Vallières)

A 4-year-old male castrated English bulldog was referred to the Cardiology Service at the Atlantic Veterinary College (AVC) for further evaluation of exercise intolerance, multiple syncopal episodes and a grade IV/VI heart murmur. The heart murmur was first diagnosed when the current owner adopted the dog at about 14 months of age. At that time the dog was free of clinical signs. The dog then suffered approximately 5 syncopal episodes over the following 2.5 y, being all episodes associated with overheating or exercise. A perceived decline in well-being over the 2 to 3 wk prior to presentation prompted the owner to seek veterinary medical attention for the dog. The results of bloodwork (VetTest, LaserCyte; IDEXX Laboratories, Markham, Ontario) ordered by the referring veterinarian were within normal limits except for a mild decrease in total protein [46 g/L; reference range (RR): 52 to 82 g/L]. The referring veterinarian also reported an elevated blood pressure and poor femoral pulses.

On physical examination at AVC the dog was bright and alert. A grade III/VI heart murmur was heard with maximum intensity over the cranial sternum. The femoral pulse occurred conspicuously later than the palpable heartbeat, and was appreciably weaker than the apex beat, suggesting pulsus parvus et tardus. The dog’s breathing was mildly stertorous when excited but appeared otherwise normal. The dog also had mild dental tartar and mild bilateral entropion. Flea dirt was noted upon dermal examination. The findings from the physical examination were otherwise normal.

An electrocardiogram demonstrated a normal sinus rhythm with mild ST segment depression. Echocardiography was also performed. 2D/M-mode measurements were as follows: interventricular septal thickness 10.4 mm at end-diastole, 13.3 mm at end-systole; left ventricular chamber dimension at end-diastole 65.1 mm, left ventricular chamber dimension at end-systole 55.3 mm; left ventricular free wall thickness at end-diastole 12.7 mm, left ventricular free wall thickness at end-systole 13.3 mm. Fractional shortening was 15% (RR: 25% to 45%). A discrete band of echogenic tissue was observed proximal to the aortic annulus causing severe narrowing of the left ventricular outflow tract (Figure 1). A post-stenotic dilation of the ascending aorta was also noted. The left atrium was markedly enlarged; the left atrium:aorta ratio was 2.44:1 [reference value (RV): < 1.6]. The chamber measurements for both the right atrium and the right ventricle were within normal limits. A left to right shunting atrial septal defect was noted. No masses or effusions associated with the heart were noted and the heart displayed a regular rhythm.

Echocardiographic still image showing discrete echogenic tissue causing a severe narrowing of the left ventricular outflow tract (arrows on left) and the post-stenotic dilation of the ascending aorta (arrows on right). The ECG in the lower left corner ...

Spectral Doppler measurements were performed to examine blood flow. The right ventricular outflow tract had laminar blood flow with a peak velocity across the pulmonic valve of 0.73 m/s (RV: < 1.2 m/s). The left ventricular outflow tract had turbulent blood flow with a peak velocity across the aortic valve of 4.33 m/s (RV: < 1.5 m/s). The pressure gradient was 75 mmHg. The mitral valve was abnormal with restricted movement of the septal leaflet resulting in a stenotic valvular orifice in diastole and incomplete coaptation in systole causing mitral regurgitation. Mitral valve inflow velocity at E point was 1.6 m/s (RV: < 1.0 m/s). Mitral valve inflow velocity at A point was not visualized. The pressure half-time was 78 ms (RV: < 52 ms). The only other diagnostic test performed was a quantification of plasma taurine level (Amino Acid Analysis Laboratory, University of California at Davis School of Veterinary Medicine, Davis, California, USA). The level was 169 nmol/L (heparinized sample; RR: 200 to 350 nmol/mL; no known risk for taurine deficiency > 150 nmol/mL).

The physical examination and diagnostic test findings in this bulldog were consistent with concurrent congenital cardiac abnormalities: severe subaortic stenosis, mitral valve dysplasia resulting in mitral stenosis and regurgitation with secondary left atrial enlargement, and an atrial septal defect. The left atrial enlargement detected on echocardiography coupled with multiple syncopal episodes in this dog was indicative of progressive disease. A guarded prognosis for long-term survival was given with a warning that the onset of left-sided congestive heart failure was unpredictable (weeks to months or more). Medical management was initiated and consisted of exercise restriction, atenolol (PMS Atenolol; Pharmascience, Montreal, Quebec) 6.25 mg, PO, q24h for 3 d, then 6.25 mg, PO, q12h thereafter; pimobendan (Vetmedin; Boehringer Ingelheim, Burlington, Ontario), 1.25 mg, PO, q12h, and taurine (generic) 500 mg, PO, q12h.

Discussion

Syncope is a sudden, transient loss of consciousness with spontaneous recovery. The 4 major pathophysiologic causes of syncope are cardiogenic dysfunction, hypotensive disorders, alterations in blood constituents, and neurologic causes (1). In this dog the cause of syncope is clearly cardiogenic dysfunction. The combination of congenital cardiac abnormalities in this case resulted in reduced cardiac output. Evidence for this is provided by the reduced left ventricular contractility demonstrated by the decreased calculated fractional shortening. The pulsus parvus et tardus is further evidence of a small stroke volume and is often noted in dogs with marked subaortic stenosis (1). Because cardiac output is one of the direct determinants of blood pressure, a drop in cardiac output will result in a drop in mean arterial pressure. Severe hypotension can result in decreased cerebral perfusion and subsequent syncope. During exercise, sympathetic adrenergic stimulation results in regional changes to peripheral resistance such that working muscles, the skin and lungs have greater blood flow while the splanchnic vasculature and non-working muscles receive less blood flow. Cardiac output should normally increase during exercise such that the overall decrease in peripheral resistance does not result in hypotension (2). Cardiac output is the product of heart rate multiplied by stroke volume. In this patient, although heart rate may increase during exercise, stroke volume is already compromised at rest and does not increase appropriately with exercise. A decreased cardiac output during exercise is the ultimate result with subsequent severe hypotension causing syncope.

Exercise intolerance and syncope, however, are merely clinical signs of the grave cardiac anomalies present in this dog. It is uncommon for dogs to have 3 concurrent congenital cardiac anomalies (atrial septal defect, mitral valve dysplasia, and subaortic stenosis) (3–5), but this particular trilogy of defects has been reported (5,6). Two studies reported that atrial septal defects were rare in dogs, accounting for approximately 1% to 3% of canine cardiac defects (3,4). However, 1 retrospective study found that the incidence of atrial septal defects in dogs was much higher than previously thought, representing the second most commonly diagnosed congenital heart defect after mitral valve dysplasia in the population examined (6). Approximately 30% of animals with an atrial septal defect also had 1 or more other congenital heart defects, including mitral valve dysplasia and subaortic stenosis (6). Mitral valve dysplasia and subaortic stenosis have been associated in other reports as well (7–9). Subaortic stenosis is one of the most common congenital cardiac anomalies in dogs (3,4,10). English bulldogs do not appear to have a predisposition to any of these particular cardiac anomalies (3,4,6) although this breed does appear to be predisposed to pulmonic stenosis (3).

The most hemodynamically significant lesions present in this dog are mitral valve dysplasia and subaortic stenosis. Open heart mitral valve repair or replacement in dogs has a high surgical risk with poor outcomes (11), but advancements are being made (12). Furthermore, the prohibitive cost of this procedure limits its availability to many clients (12). Likewise, open surgical correction of subaortic stenosis has not been shown to improve survival in dogs (13), with a report of sudden death occurring even after apparently successful surgery (14). When comparing balloon valvuloplasty to atenolol for treatment of subaortic stenosis, there was no evidence of surgical benefit over medical management (15).

The prognosis for dogs with subaortic stenosis declines as the severity of the stenosis worsens. A study of 195 untreated dogs with subaortic stenosis showed that dogs with severe stenosis (left ventricular — aortic pressure gradient > 80 mmHg) were 16 times more likely to die suddenly than dogs with moderate or mild subaortic stenosis (9). Furthermore, sudden death was most likely to occur within the first 3 y of life (9). With a pressure gradient of 75 mmHg coupled with poor left ventricular systolic function, this English bulldog falls into the moderate-to-severe category. Interestingly, dogs with less severe lesions are more likely to develop left heart failure or infective endocarditis, presumably because they live long enough to develop late major complications of subaortic stenosis (9).

Subaortic stenosis has been medically managed with beta-adrenergic blocking drugs, such as atenolol (9). This drug is a negative chronotrope and inotrope and is thought to decrease myocardial oxygen demand while increasing time for ventricular and coronary filling (9). Pimobendan has both inotropic and vasodilatory properties and is typically contraindicated for use with obstructive lesions such as subaortic stenosis (16). However, in the case of this English bulldog left ventricular systolic dysfunction was evident. Pimobendan can improve forward flow of blood via its positive inotropic properties (16). In this unique situation, pimobendan may have beneficial cardiac effects similar to those when used for degenerative mitral valve disease (16).

This report describes a trilogy of congenital cardiac anomalies in an English bulldog, resulting in severe cardiac dysfunction necessitating an unusual treatment approach. Despite medical therapy, the prognosis remains poor.

Acknowledgments I thank Dr. Étienne Côté for his encouragement and feedback in writing this paper. Dr. Côté and his resident, Dr. Erin Trageser, were the principle clinicians on this case. It was a pleasure to work with, and learn from, these fine veterinarians. CVJ

Footnotes Use of this article is limited to a single copy for personal study. Anyone interested in obtaining reprints should contact the CVMA office (hbroughton/at/cvma-acmv.org) for additional copies or permission to use this material elsewhere. Go to: References 1. Fox PR, Sisson D, Moise NS. Textbook of Canine and Feline Cardiology: Principles and Clinical Practice. 2nd ed. Philadelphia, Pennsylvania: Saunders; 1999. pp. 446–454.

2. Reece WO. Duke’s Physiology of Domestic Animals. 12 ed. Ithaca, New York: Comstock Publishing; 2004. pp. 356–378.

3. Silva J, Vannini S, Bussadori R, Bussadori C. Retrospective review of congenital heart disease in 976 dogs. J Vet Intern Med. 2011 Mar 21;

4. Tidholm A. Retrospective study of congenital heart defects in 151 dogs. J Small Anim Pract. 1997;38:94–98.

5. Chetboul V, Trolle JM, Nicolle JM, et al. Congenital heart diseases in the boxer dog: A retrospective study of 105 cases (1998–2005) J Vet Med A Physiol Pathol Clin Med. 2006;53:346–351.

6. Chetboul V, Charles V, Nicolle A, et al. Retrospective study of 156 atrial septal defects in dogs and cats (2001–2005) J Vet Med A Physiol Pathol Clin Med. 2006;53:179–184.

7. White RN, Boswood A, Garden OA, Hammond RA. Surgical management of subvalvular aortic stenosis and mitral dysplasia in a golden retriever. J Small Anim Pract. 1997;38:251–255.

8. Fernandez del Palacio MJ, Bayon A, Bernal LJ, Ceron JJ, Navarro JA. Clinical and pathological findings of a severe subvalvular aortic stenosis and mitral dysplasia in a rottweiler puppy. J Small Anim Pract. 1998;39:481–485.

9. Kienle RD, Thomas WP, Pion PD. The natural clinical history of canine congenital subaortic stenosis. J Vet Intern Med. 1994;8:423–431.

10. O’Grady MR, Holmberg DL, Miller CW, Cockshutt JR. Canine congenital aortic stenosis: A review of the literature and commentary. Can Vet J. 1989;30:811–815.

11. Griffiths LG, Orton EC, Boon JA. Evaluation of techniques and outcomes of mitral valve repair in dogs. J Am Vet Med Assoc. 2004;224:1941–1945.

12. Behr L, Chetboul V, Sampedrano CC, et al. Beating heart mitral valve replacement with a bovine pericardial bioprosthesis for treatment of mitral valve dysplasia in a bull terrier. Vet Surg. 2007;36:190–198.

13. Orton EC, Herndon GD, Boon JA, Gaynor JS, Hackett TB, Monnet E. Influence of open surgical correction on intermediate-term outcome in dogs with subvalvular aortic stenosis: 44 cases (1991–1998) J Am Vet Med Assoc. 2000;216:364–367.

14. Hirao H, Hoshi K, Kobayashi M, et al. Surgical correction of subvalvular aortic stenosis using cardiopulmonary bypass in a dog. J Vet Med Sci. 2004;66:559–562.

15. Meurs KM, Lehmkuhl LB, Bonagura JD. Survival times in dogs with severe subvalvular aortic stenosis treated with balloon valvuloplasty or atenolol. J Am Vet Med Assoc. 2005;227:420–424.

16. Boswood A. Current use of pimobendan in canine patients with heart disease. Vet Clin North Am Small Anim Pract. 2010;40:571–580.