Why the study?
Does intravenous oseltamivir induce torsade de pointes in preclinical models?
Does intravenous oseltamivir induce torsade de pointes in preclinical models?
Preclinical evidence suggests that intravenous oseltamivir does not carry a proarrhythmic risk for torsade de pointes, likely due to its inhibition of both inward and outward currents.
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Does not raise TdP concerns in canine model; leaves open clinical translation for intravenous oseltamivir.
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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Nakamura et al. (2016) studied this question.
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