Balloon dilation of congenital subaortic stenosis in the dog.

Balloon dilation during cardiac catheterization was evaluated for the treatment of congenital subaortic stenosis (SAS) in nine dogs. Under general anesthesia, bilateral cardiac catheterization was performed through the right jugular vein and carotid artery. Thermodilution cardiac output, and left ventricular and aortic root pressures and angiograms were obtained before and after balloon dilation. Balloons measuring 18-20 mm in diameter and 30-40 mm in length were positioned across the stenosis and three inflations 4-5 minutes apart were performed. There was no significant change in cardiac output, aortic pressure, or degree of aortic regurgitation after balloon dilation. For the entire group balloon dilation resulted in significant decreases in left ventricular systolic pressure (-61.2 +/- 37.2 mm Hg [mean change +/- SD], range -14 to -123), mean systolic pressure gradient (-39.6 +/- 24.4 mm Hg, range -8.4 to -72.2), and peak systolic pressure gradient (-64.3 +/- 46.5 mm Hg, range -17 to -143). Calculated left ventricular outflow cross-sectional area increased significantly (+.4 +/- .5 cm2, range -.06 to + 1.30). Clinical signs improved in the five symptomatic dogs. Individual hemodynamic responses varied widely, but the magnitude of improvement correlated with the severity of obstruction. Three dogs showed a decrease of 60% or greater (> or = 100 mm Hg), and six dogs showed a decrease of 25-50% (17-71 mm Hg) in peak systolic gradient after balloon dilation. Complications were frequent but most were transient and manageable. These preliminary results suggest that balloon dilation can acutely decrease outflow resistance in dogs with SAS and may be effective therapy for some affected dogs.

Increased serum growth hormone concentration in feline hypertrophic cardiomyopathy.

Serum growth hormone concentration was measured by radioimmunoassay in 31 cats with hypertrophic cardiomyopathy, 38 normal cats, and 35 cats with other cardiac disease. Cats with hypertrophic cardiomyopathy had a significantly increased serum growth hormone concentration when compared with normal cats and cats with other cardiac disease. The serum growth hormone concentration in cats with hypertrophic cardiomyopathy was less than that previously reported in cats with growth hormone secreting pituitary tumors. Pituitary tumors were not identified in eight of the cats with hypertrophic cardiomyopathy examined at necropsy. An increased serum growth hormone concentration may be measured in cats with hypertrophic cardiomyopathy but it is unclear if the increased serum growth hormone concentration is a cause or effect of hypertrophic cardiomyopathy.

Response of cats with dilated cardiomyopathy to taurine supplementation.

Between October 1986 and September 1988, 37 cats with moderate to severe idiopathic myocardial failure (dilated cardiomyopathy) were evaluated. Clinical management of these cats was similar to that described in the literature, except that it also included administration of 500 or 1,000 mg of the sulfur amino acid, taurine per day. Early death (death within the first 30 days of treatment) occurred in 14 (38%) cats. One cat was lost to follow-up evaluation. Twenty-two cats (59%) had marked clinical and echocardiographic improvement and survived longer than 240 days. In all but 1 cat, the observed improvement in echocardiographic measurements persisted. Hypothermia and thromboembolism were positively associated with an increased risk of early death. Administration of digoxin did not significantly affect survival. All 22 cats that survived greater than 30 days remained clinically stable despite withdrawal of all medications except taurine. Administration of taurine was eventually discontinued in 20 of the 22 cats and adequate taurine intake was thereafter provided for in the food. The clinical response and 1-year survival rate of 58% (21 of 36 cats with a known outcome) in the taurine-treated group represents a marked improvement, compared with a 1-year survival rate of 13% (4 of 31 cats with a known outcome) in a retrospectively evaluated population of 33 cats with dilated cardiomyopathy.

Permanent transvenous pacemaker implantation in forty dogs.

Permanent transvenous cardiac pacemakers were implanted in 40 dogs. Electrocardiographic diagnoses included persistent atrial standstill (3 dogs), sick sinus syndrome (8 dogs), and high-grade second-degree or third-degree atrioventricular (AV) block (29 dogs). Thirteen dogs were alive and well 4 to 42 months after pacemaker implantation (mean, 16.9 months). The mean and median survival times of the 26 dogs that died or were euthanatized during the study were 17.9 months and 13 months, respectively. Most of these dogs succumbed to problems unrelated to the arrhythmia and pacemaker implant. One dog was lost to follow-up. Complications associated with permanent transvenous pacemaker implantation included lead dislodgement, infection, hematoma formation, skeletal muscle stimulation, ventricular arrhythmia, migration of the pulse generator, and skin erosion. Lead dislodgement was the most common complication, occurring in 7 of 9 dogs paced using untined electrode leads and in 6 of 30 dogs paced using tined leads. Lead dislodgement did not occur in the only dog paced using an actively fixed endocardial lead. It was concluded that permanent transvenous cardiac pacing is a feasible, less traumatic alternative to epimyocardial pacing in dogs, but that successful use of this technique requires careful implantation technique and anticipation of the potential complications.