Abstract
We evaluated proarrhythmic risk of intravenous oseltamivir with chronic atrioventricular block canine model (n = 4) and action-potential assay on guinea-pig right ventricle (n = 5). Oseltamivir in doses of 3–30 mg/kg, i.v. did not induce torsade de pointes in the canine model, whereas that in concentrations of 30–300 μM decreased maximum rate of phase 0 depolarization, shortened action potential duration at 30%, 60% and 90% repolarization levels, but prolonged difference in action-potential duration between 30% and 90% repolarization levels in a concentration-related manner. These results indicate that oseltamivir will not induce torsade de pointes clinically, since it inhibits both inward and outward currents.
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