PDA, Aortic and Pulmonic Stenosis - Update on Common Congenital Heart Diseases
World Small Animal Veterinary Association Congress Proceedings, 2016
Viktor Szatmári, DVM, PhD, DECVIM-CA (Cardiology)
Department of Clinical Sciences of Companion Animals, Faculty of Veterinary Medicine, Utrecht University, Utrecht, The Netherlands

During the presentation the diagnostic process, prognosis and the therapy of the three most common congenital cardiac anomalies in dogs will be reviewed.

Patent ductus arteriosus (PDA), aortic stenosis and pulmonic stenosis are the three most common congenital cardiac anomalies in dogs. In cats, all these three anomalies are very rare.

Screening for congenital cardiac anomalies is performed by cardiac auscultation at the first and subsequent veterinary health checks, usually together with the first vaccination at about 6 weeks of age. The earlier a congenital cardiac anomaly is diagnosed, the better the long-term prognosis is, provided that the anomaly can and will be treated successfully. Selling puppies with a congenital cardiac anomaly to a new owner with a label of "just an innocent murmur" should be prevented.

Patent ductus arteriosus (PDA) with a left-to-right shunting results in a continuous murmur with the point of maximal intensity at the left cardiac base. The murmur of a PDA should be present at the first veterinary health check. Small PDAs may not cause a murmur and are detected as coincidental findings during a Doppler echocardiographic examination. Diagnosing a PDA can be done with a stethoscope in most dogs, based on the characteristic murmur. Occluding the PDA is recommended if the murmur is louder than 2 out of 6 in an asymptomatic puppy because PDA leads to cardiogenic pulmonary edema and subsequently to death in the majority of dogs in a young age. Performing a Doppler echocardiographic examination is however recommended before surgery so as 1) to look for coinciding cardiac anomalies, 2) to assess the size of the left atrium and left ventricle (both in systole and diastole) and 3) to see which technique (such as Amplatz, coil or surgical ligation) would be the most suitable for that individual dog. The best long-term result can be reached when the PDA is occluded in an asymptomatic puppy. When atrial fibrillation, congestive heart failure or severe pulmonary hypertension develop, the long-term prognosis after ductal closure is much less favorable.

Aortic stenosis is in most dogs caused by a subvalvular fibrous ring. Dogs with a mild and moderate stenosis do not usually show clinical signs and they often have a normal life expectancy. However, dogs with a severe stenosis may experience exercise intolerance, syncope and sudden death. Middle-aged to elderly dogs with aortic stenosis may develop infective endocarditis with various clinical signs, such as lameness, fever, central neurologic symptoms, petechial bleedings, brady- or tachy-arrhythmias. Several attempts have been done to try to find an effective therapy for severe subaortic stenosis, without any success so far. Open heart surgery and balloon valvuloplasty failed to improve survival time, despite successfully reducing the pressure gradient. A recent study has shown that administration of atenolol has not resulted in improved survival either. The same study pointed out that dogs with a Doppler-derived pressure gradient of less than 130 mm Hg have a much longer survival time (median 8.3 years) than dogs with a pressure gradient of above 130 mm Hg (median survival of 2.8 years). A Doppler echocardiographic examination is essential not only to diagnose and grade aortic stenosis, but also to establish its etiology. If the aortic stenosis is dynamic and it is caused by systolic anterior motion of the septal mitral valve (SAM) as a result of a mitral valve dysplasia, the stenosis and the secondary left ventricular concentric hypertrophy may be reversible with daily lifelong atenolol therapy.

Pulmonic stenosis is in most dogs valvular, and similarly to the aortic stenosis, it can be mild, moderate and severe, based on the Doppler-derived pressure gradient. Similarly to the aortic stenosis, the definitive diagnosis of pulmonic stenosis (including the severity and etiology) is made by Doppler echocardiography, as auscultation findings of aortic and pulmonic stenosis are identical. Severe stenosis (Doppler-derived pressure gradient of 80 mm Hg and higher) is an indication for balloon valvuloplasty. Dogs with a valvular stenosis without annulus hypoplasia are the best candidates for this minimal invasive catheter intervention. The procedure has the best outcome if performed in asymptomatic young dogs. If a severe pulmonic stenosis is left untreated, exercise intolerance, syncope, sudden death and ascites and/or pleural effusion can develop usually in adult age. Balloon valvuloplasty might be considered on an individual basis in dogs with 1) annulus hypoplasia, 2) an abnormal coronary artery (often English bulldogs), 3) supravalvular or pulmonic branch stenosis, and 4) a double-chambered right ventricle.

Cardiac biomarkers (such as plasma NT proBNP) have become a widespread used test for diagnosing and staging of common acquired cardiac diseases in dogs. Unfortunately, NT proBNP plasma levels are not elevated in asymptomatic dogs with pulmonic stenosis, even if the stenosis is severe. Therefore, plasma NT proBNP measurement is not a suitable screening test in asymptomatic puppies with a cardiac murmur.

References

1.  Saunders AB, Gordon SG, Boggess MM, Miller MW. Long-term outcome in dogs with patent ductus arteriosus: 520 cases (1994–2009). J Vet Intern Med. 2014;28:401–410.

2.  Eason BD, Fine DM, Leeder D, Stauthammer C, Lamb K, Tobias AH. Influence of beta blockers on survival in dogs with severe subaortic stenosis. J Vet Intern Med. 2014;28:857–862.

3.  Connolly DJ, Boswood A. Dynamic obstruction of the left ventricular outflow tract in four young dogs. J Small Anim Pract. 2003;44:319–325.

4.  Kobayashi K, Hori Y, Chimura S. Plasma N-terminal pro B-type natriuretic peptide concentrations in dogs with pulmonic stenosis. J Vet Med Sci. 2014;76:827–831.

  

Speaker Information
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Viktor Szatmári, DVM, PhD, DECVIM-CA (Cardiology)
Clinical Sciences of Companion Animals
Faculty of Veterinary Medicine, Utrecht University
Utrecht, The Netherlands


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