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Single right coronary artery (CA) associated with pulmonic stenosis was found in 3 English Bulldogs and a Boxer, suggesting a genetic predisposition for the associated anomalies. The left main coronary branch arose from the single right CA, encircled the pulmonic root over hypoplastic pulmonic valves at the level of the obstruction, and appeared to be the primary cause of underlying pulmonic stenosis. Patch-graft surgery to relieve pulmonic stenosis caused death in 1 dog when the unrecognized anomalous CA was served during the procedure. The anomalous left CA was detectable by use of angiocardiography in all 4 dogs and was recognized before surgery in 2 of them. In 1 dog, a right ventricle-to-pulmonary trunk-bridging conduit was implanted to improve outflow from the right side of the heart.

A 2.5-year-old dog with congenital pulmonary valve dysplasia was treated by percutaneous balloon dilation of the stenotic orifice. Clinical and hemodynamic improvement was apparent immediately and for 9 months after the valvuloplasty procedure.

Using cardiac catheterization, pulmonic stenosis and right-to-left atrial shunt were diagnosed in 3 young dogs that were evaluated because of weakness, cyanosis, and polycythemia. Injection of contrast material into the caudal vena cava or crossing the atrial septal defect with the catheter tip from the right atrium into the left atrium confirmed the diagnosis. Tetralogy of Fallot, with right-to-left shunt through a ventricular septal defect, is a more common congenital malformation associated with the aforementioned clinical signs. Differentiation between the 2 defects is important, because surgical decompression of the right ventricle will lead to reduction of right atrial pressure and diminishment of the shunt.

Congenital supravalvular pulmonic stenosis was diagnosed in a dog. A pulmonary artery-to-pulmonary artery anastomosis of a Dacron arterial conduit restored continuity of blood flow around the obstruction in the main pulmonary artery. By the 6th day after surgery, right ventricular systolic pressure averaged 85 mm of Hg, a decrease of 90 mm from the preoperative value. Angiocardiography confirmed the patency of the conduit. At examination 6 months after surgery, the dog was clinically normal.

Four Collie littermates had multiple cardiac and diaphragmatic anomalies. Ventricular septal defect was found in 3, pulmonic stenosis in 2, atrial septal defect in 1, mitral regurgitaion in 1, and pericardial diaphragmatic hernia in 3. Five additional littermates died within 72 hours of birth but were not necropsied. On the basis of available evidence, it was believed that the defects were congenital but not hereditary.

An Arabian crossbred foal was examined because of a suspected congenital cardiac anomaly. There was a grade V/V crescendo-decresendo holosystolic murmur and thrill in the left 4th intercostal space. The foal was slightly cyanotic and polycythemic. Electrocardiography suggested left ventricular hypertrophy. Angiography and cardiac and vascular pressure recordings led to a diagnosis of pulmonic stenosis. The foal died after cardiac bypass and corrective surgery. Postmortem examination revealed an enlarged right atrium, atresia of the tricuspid orifice, a large, fenestrated patent foramen ovale, eccentric left ventricular hypertrophy, and a large interventricular septal defect. The right ventricle had a small lumen and a relatively thick wall. There was valvular and supravalvular pulmonic stenosis, with poststenotic dilatation of the pulmonary artery. A single coronary artery originated from the anterior sinus of the aorta.

In a retrospective study of 29 dogs with congenital pulmonic stenosis, we evaluated the clinical, radiographic, angiocardiographic, and cardiac catheterization data. Eighteen dogs had no clinical signs of disease and were referred for evaluation of a previously detected cardiac murmur, 5 dogs had congestive right-sided heart failure, and 5 dogs were examined for exercise intolerance or syncope. Dogs with heart failure tended to be older than dogs without clinical signs of heart failure (19.3 months vs 12 months). All dogs had radiographic or electrocardiographic evidence of right ventricular enlargement. Poststenotic dilatation of the main pulmonary artery and apparent pulmonary undercirculation were observed frequently on survey radiographs. Isolated pulmonic valve dysplasia, representing a range of angiographic pulmonic valve abnormalities, was evident in 88% of the available 26 angiographic studies, whereas subvalvular stenosis was uncommon and observed in only 2 dogs. Muscular hypertrophy of the right ventricular infundibulum and supraventricular crest were observed in 96% and 25% of the angiocardiograms, respectively. Poststenotic dilatation of the main pulmonary artery was observed in every dog. A ratio between the width of the main pulmonary artery and the valve annulus was useful in identifying pulmonic stenosis and distinguishing this anomaly from other congenital malformations. The degree of poststenotic dilatation did not appear to be related to the severity of the systolic pressure gradient, which ranged from 20 to 228 mm of Hg (mean, 93 mm of Hg).(ABSTRACT TRUNCATED AT 250 WORDS)

Pulmonic stenosis in 6 dogs were corrected surgically by means of a patch-graft technique, without using cardiac bypass or venous occlusion. Five of the 6 dogs have remained clinically normal for 4 to 40 months following surgery. The stenosis in 1 dog was inadequately repaired. The technique resulted in minimal blood loss, no mortality, and was easily adapted to the minimal size of several of the affected dogs. When performed correctly, the technique relieved the stenosis wherever it occurred (viz, supravalvular, valvular, subvalvular, infundibular, or any combination). The success of the procedure was determined, in part, by pre- and postoperative pressure measurements at the time of surgery, and by periodic physical, radiographic, and electrocardiographic examinations after surgery.