Bradyarrhythmias and pacemaker therapy in dogs with Chagas disease.

BACKGROUND: Chagas disease (Trypanosomiasis) is a cause of myocarditis in the southern United States causing cardiac conduction abnormalities, arrhythmias, and heart failure. OBJECTIVES: To report clinical findings and outcome in Chagas positive (CP) dogs requiring pacemaker implantation for bradyarrhythmias. ANIMALS: One hundred and forty-four client-owned dogs requiring pacemaker implantation. METHODS: Retrospective case series. Information regarding history, physical exam, laboratory and diagnostic imaging findings, treatment, and survival were obtained from medical records, with additional follow-up information obtained by contacting referring veterinarians and owners. RESULTS: Of the 144 dogs requiring pacemaker implantation from January 2001 to May 2010, 83 (57.6%) had a Chagas titer performed and 9 (10%) were CP. Concurrent ventricular arrhythmias (odds ratio 1.61, P = .005) or atrioventricular (AV) block (odds ratio 4.18, P < .001) increased the likelihood that a Chagas titer was submitted. Median age for CP dogs was 6.2 years (range, 0.3-10); 7 were male. Bradyarrhythmias included high-grade 2nd or 3rd degree AV block (n = 8) and sinus bradycardia with 1st degree AV block (n = 1); 5 had concurrent ventricular arrhythmias. A positive Chagas titer had a negative impact on survival (hazard ratio 4.04; 95% CI 1.36-12.1, P = .012) with a reported median survival time of 365 days (interquartile range, 84-973 days). CONCLUSIONS AND CLINICAL IMPORTANCE: Bradyarrhythmias can result in clinical signs requiring pacemaker implantation in CP dogs, and although the diagnosis negatively impacts survival, pacemaker therapy is a viable treatment option.

Rescue administration of a helper-dependent adenovirus vector with long-term efficacy in dogs with glycogen storage disease type Ia.

Glycogen storage disease type Ia (GSD-Ia) stems from glucose-6-phosphatase (G6Pase) deficiency and causes hypoglycemia, hepatomegaly, hypercholesterolemia and lactic acidemia. Three dogs with GSD-Ia were initially treated with a helper-dependent adenovirus encoding a human G6Pase transgene (HDAd-cG6Pase serotype 5) on postnatal day 3. Unlike untreated dogs with GSD-Ia, all three dogs initially maintained normal blood glucose levels. After 6-22 months, vector-treated dogs developed hypoglycemia, anorexia and lethargy, suggesting that the HDAd-cG6Pase serotype 5 vector had lost efficacy. Liver biopsies collected at this time revealed significantly elevated hepatic G6Pase activity and reduced glycogen content, when compared with affected dogs treated only by frequent feeding. Subsequently, the HDAd-cG6Pase serotype 2 vector was administered to two dogs, and hypoglycemia was reversed; however, renal dysfunction and recurrent hypoglycemia complicated their management. Administration of a serotype 2 HDAd vector prolonged survival in one GSD-Ia dog to 12 months of age and 36 months of age in the other, but the persistence of long-term complications limited HDAd vectors in the canine model for GSD-Ia.