Case Studies In Small Animal
This dog's radiographs were diagnostic for left atrial enlargement. This combined with her loud left apical systolic heart murmur was suggestive of primary mitral regurgitation. The echocardiographic findings confirmed this diagnosis and identified the lesion as severe. This dog's M-mode echocardiogram was typical of a large dog with severe mitral regurgitation. She had a very large left ventricle with evidence of moderate myocardial failure (reduced myocardial contractility). The moderate myocardial failure was diagnosed because of the moderate increase in end-systolic diameter. Note that the shortening fraction was within normal range yet myocardial contractility was at least moderately reduced. This is another good example where shortening fraction does not accurately reflect myocardial function.
Please note that in this dog with severe left ventricular hypertrophy, there was no evidence of this on the ECG (false negative finding).
Because myocardial function was decreased, a positive inotropic agent such as digoxin may be indicated to treat this type of patient. This was considered in this patient. However, the patient also had ventricular arrhythmias. There is always the potential to make a ventricular arrhythmia worse with digoxin, especially if digoxin toxicity occurs. Although it would be valid to try this dog on digoxin, the clinician treating this case decided not to use it. Since it is unusual to see an even moderate inotropic response to digoxin in this type of case, I cannot argue with his decision.
This dog had clear evidence of severe mitral regurgitation. The most common cause of mitral regurgitation in an older dog is myxomatous degeneration of the valve leaflets and chordae tendineae. The fact that this dog had evidence of a chordal rupture may make one lean toward this diagnosis. However, this dog had evidence of a heart murmur since it was at least 4 years of age. Since there was no evidence of another cardiovascular abnormality it is logical to assume that this murmur was caused by a leaky mitral valve. The only breed known to have myxomatous degeneration commonly as early as 4 years of age is the cavalier King Charles spaniel. Since this dog was clearly not that breed, myxomatous degeneration at that age was unlikely. Consequently, it is much more likely that this dog was born with an abnormally formed (dysplastic) mitral valve. The fact that the leaflets were not thickened also makes this diagnosis more likely. Consequently, it is most likely that this dog had mild to moderate mitral valve dysplasia all of its life and that this lesion did not produce severe problems until the dog was ten years of age.
This dog had a ventricular arrhythmia (premature ventricular complexes). This is unusual in dogs with mitral valve disease. It is unknown why they occurred in this dog. Although these complexes were frequent, it was decided not to treat these premature complexes in this dog for several reasons. First, the dog did not have a disease that commonly predisposes her to sudden death. By far the two most common diseases that predispose to sudden death are dilated cardiomyopathy and subaortic stenosis. Second, the ectopic focus did not fire at a very fast rate. The rate the focus fired was well under 200 beats/minute and so well away from the previous t wave (R on T phenomenon) which generally places it in a benign category. Third, the arrhythmia did not appear to adversely affect hemodynamics. Lastly, we primarily use sotalol and beta blockers to attempt to prevent sudden death in dogs with ventricular arrhythmias. Both can decrease myocardial contractility and this dog's myocardial function was already compromised. Sotalol is expensive. We could have tried amiodarone but this drug has many side effects which may be more likely to adversely affect the dog than the arrhythmia. We could have also tried mexiletine but it also is expensive. For all of these reasons, it was decided not to place this dog on antiarrhythmic therapy.
Three Month Follow-Up
In a telephone conversation three months after Manny was last examined, the owner indicated that he thought Manny was doing well overall. She was still on Lasix, but at 125 mg (4 mg/kg) q12 hours, and on lisinopril at 15 mg once a day. The owner reported that he increased the dose of Lasix up to 150 mg on some days when he noticed her coughing and that this promptly took care of the problem. He was not monitoring respiratory rate at rest so he was told to count Manny's respiratory rate by counting the number of times she breathed in 15 seconds and multiplying it times four, but to do this only when she was sleeping or resting quietly. Respiratory rate when resting or asleep in a dog should be less than 30 breaths/minute. He was also told that he could increase the dose of Lasix to 150 mg q12 hours if the respiratory rate was in the 40s but to call back and discuss the situation with us if it was higher than that. He also told me that Manny was having episodes of stumbling on her front legs and falling on her chin over the last week. Because she had a ventricular tachydysrhythmia on her last examination, he was told that this could be due to an abnormal heart rhythm and that she could die suddenly during one of these events. He was told that he should come back in for another examination to see if we could figure out the cause of this problem. He indicated that he would do that. At the time of this last update, this had not yet been done.
©Mark D. Kittleson, D.V.M., Ph.D. All rights reserved.