Case Studies In Small Animal
This dog had severe pulmonic stenosis. You should note that the chest radiographs from this dog were not very helpful. This was primarily because of this dog's chest configuration. Bulldog chests are always difficult to interpret.
The ECG from this dog was typical of severe right ventricular enlargement. There were deep S waves in leads I, II, and aVF. There was also a very deep S wave in lead V4. You should have also noted in lead II that the P waves were too wide (0.05 seconds) and were notched. These are typical findings for a dog with left atrial enlargement. Of course, this dog did not have left atrial enlargement so this is a false positive finding. The P wave will also become wider when the intraatrial conduction system is disrupted. This may explain this finding in this dog.
The echocardiogram from this dog showed that the pulmonic stenosis had at least an annular component since the annulus of the pulmonic valve was markedly reduced in size. Upon careful examination of the pulmonic valve cusps, a valvular component could also be appreciated (this was not shown).
In many English bulldogs, pulmonic stenosis is of the subvalvular type and is either associated with or caused by a particular type of coronary anomaly called an R2A coronary artery anomaly (shown below).
In this type of anomaly, there is only one coronary artery ostium that originates from the right coronary artery sinus (RAS). The right coronary artery courses normally back along the top of the right ventricle in the atrioventricular groove. The left coronary artery, instead of originating from the left coronary ostium also originates from the right coronary ostium. To get to the left ventricle it courses cranially over the front of the junction of the right ventricular outflow tract and pulmonary artery, right at or just below the pulmonic valve region. Immediately in this region is where the stenosis occurs. In "Daisy" the coronary ostium appeared to be similarly placed as in the above diagram. However, it appeared to course between the pulmonary artery and the aorta.
In the past, we have observed sudden death when we tried to do balloon valvuloplasty on English bulldogs with an R2A type of coronary artery anomaly. At postmortem exam, we found that the left coronary artery had been avulsed off of its origin resulting in acute loss of blood supply to the left ventricle. In daisy's case we were as concerned with that happening although we were not 100% sure that we could correctly determine the course of the coronary arteries. However, even if the left coronary artery went between the pulmonary artery and the aorta, we presumed that inflation of a balloon in this region would cause cessation of coronary flow during the time of balloon inflation. This could also result in catastrophic complications. Consequently, it was decided not to perform balloon valvuloplasty.
The owners primary complaint was the syncopal events the dog was experiencing. The usual rule-outs in this type of dog with this type of disease are a tachyarrhythmia, a bradyarrhythmia, and vasodilation. The tachyarrhythmia could be a supraventricular or a ventricular tachycardia due to the dog's cardiac disease. A bradyarrhythmia could occur secondary to right ventricular mechanoreceptor stimulation and reflex stimulation of vagal efferents to the heart during excitement or with exercise when the right ventricular pressure increased further as the right heart tried to pump more blood. Similarly, mechanoreceptor stimulation could produce a reflex increase in vagal tone to the systemic arterioles resulting in acute vasodilation leading to systemic hypotension. The event recorder showed no arrhythmia during a syncopal episode and so an arrhythmia was ruled out. Consequently, it could be assumed that Daisy was having vasodepressor syncope in which she had acute vasodilation resulting in severe hypotension leading to syncope. The only problem with this theory is that her events were not precipitated by exercise or excitement.
No treatment was initially prescribed and Daisy was sent home. I talked to the owner again about 6 weeks after her hospitalization. During that time, Daisy had only two more syncopal events. The first one occurred when she was outside in the back yard on a hill where she passed out. The owner said she literally rolled over 3 or 4 times down the hill on to the deck. She wasn't unconscious very long and recovered quickly. The last one, however, was a different story. That time he was talking to his neighbor in the house when she suddenly fell over. Again, she was white. Her eyes were open but she did not respond. She urinated and defecated during the event. He estimated that the event lasted 3 to 5 minutes. Owners tend to exaggerate this time since it seems so long to them. However, this was at least the fourth event this owner had witnessed and regardless of its true length, it was clearly much longer than the previous events. After this episode, Daisy did not bounce right back. He had to carry her for a while and she did not seem right for a couple of days afterward. He took her in to his veterinarian who noted that the heart rhythm was normal on auscultation. The other observation the owner had was that the other three episodes were preceded by a "gagging" sound and this one was not. This observation brought one more rule-out into the picture - stimulation of vagal afferents in the pharynx. Consequently, I decided to have a surgeon examine her pharynx to see if there were any particular problems that might be surgically correctable before attempting to treat her medically.
Daisy was examined by our soft tissue surgeons and found to have an elongated soft palate, stenotic nares, and everted saccules. She underwent surgery to correct these abnormalities. Only one everted saccule was surgically corrected. At the time of the last update (four months following the procedure) she was doing very well and had not had another syncopal event.
©Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.