Cardiology

Research Abstract

C05 - Inotropic and Chronotropic Effects of Sotalol in Healthy Dogs

Thursday, June 14
4:30 PM - 4:45 PM
Location: WSCC 616/617

Sotalol is a class III anti-arrhythmic drug that is commonly prescribed in the treatment of ventricular tachyarrhythmias in dogs. The anti-arrhythmic effects of sotalol are mediated by an increase in action potential duration and prolongation of atrial and ventricular repolarization via antagonism of the delayed rectifier potassium current. These effects have been demonstrated to be independent of sotalol’s ß-blocking properties. However, ß blockade may result in reduced myocardial contractility and also contribute to slowing of the sinus rate. In patients with existing heart disease, a cardiodepressant drug effect may be clinically relevant, yet the inotropic properties of sotalol are not well-characterized in dogs. The aim of this study was to investigate the inotropic and chronotropic effects of sotalol on healthy, awake dogs.


Ten adult, large-breed dogs were recruited from the veterinary community at the Oregon State University College of Veterinary Medicine. Dogs were considered healthy based on history, physical exam, oscillometric blood pressure measurement, transthoracic echocardiography, and a 10-lead electrocardiogram. Each dog also had a baseline 24 hour Holter monitor performed. Sotalol at a dose of 1-2 mg/kg orally q12h was then administered for 12-16 days, followed by a second evaluation including the same diagnostics tests. Physical exam parameters, blood pressure measurements, Holter data, echocardiographic measurements including three-dimensional (3D) left ventricular (LV) volumes and 3D strain were measured at each evaluation. Baseline and post-treatment measurements were assessed for normality, and compared statistically with paired t-tests for normally distributed data and Wilcoxon signed rank tests for non-normally distributed data. 3D data were available for 7/10 dogs. No correction was made for multiple comparisons.


Ten dogs were included in the study, with a mean age of 3.4 years (range, 1.1-6.4 years) and mean weight of 26.1 kg (range, 21-35.8 kg). The mean sotalol dose administered was 1.56 ± 0.23 mg/kg. Heart rate on exam was significantly (p = 0.036) lower post-treatment (81 ± 23 bpm) than pre-treatment (101 ± 26 bpm). Maximum heart rate on Holter monitor was also significantly (p = 0.002) lower on sotalol (195 ± 14 bpm) than at baseline (215 ± 13 bpm). Several echocardiographic indices of systolic function were altered compared to baseline: Fractional shortening (FS) using two-dimensional (2D) and M-mode (MM) measurements was significantly reduced on sotalol (2D 28.9%, interquartile range (IQR) 25.0-30.2; MM 24.9 ± 5.7%) compared to baseline (2D 30.7%, IQR 28.7-33.8; MM 32.5 ± 2.6%) with p = 0.010 and p = 0.004 for 2D and M-mode measurements, respectively. Similarly, ejection fraction (EF) via Simpson’s method of disks (SMOD) was significantly (p = 0.002) lower on sotalol (48 ± 6.8%) than baseline (53.8 ± 4.4%). On sotalol, there was a 12.4 ± 8.2% increase in LV end-systolic dimension on 2D, and a 12.6 ± 12.4% increase on M-mode measurements (p = 0.001, p = 0.010, respectively). There was no significant difference in the 3D left ventricular volumes, nor in global longitudinal or circumferential strain, twist, or torsion.


The results of this study suggest that sotalol has negative inotropic and chronotropic effects in healthy dogs. Standard echocardiographic measurements of systolic function showed a small but statistically significant decrease after sotalol treatment, with a mean reduction in EF (SMOD) of 5.8%. The lack of significance for 3D imaging may reflect the variability in 3D measurements and the small sample size. The effects of sotalol in dogs with structural heart disease should be prospectively assessed to further elucidate the clinical significance of decreased systolic function, and the implications of this reduction in patients at risk for heart failure.

Julia R. Treseder

Cardiology Resident
Oregon State University

Dr. Julia Treseder grew up in the Maryland suburbs of Washington, DC and earned her Bachelor’s degree in biochemistry from Dartmouth College. After college, she studied at the Royal Veterinary College in London for two years. She obtained her veterinary degree from the Virginia-Maryland Regional College of Veterinary Medicine and then completed an internship in small animal medicine and surgery at Louisiana State University. Dr. Treseder began her cardiology training with a one-year specialty internship at Auburn University and is currently completing her cardiology residency at Oregon State University.

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