Why the study?
Information is limited regarding whether beta-blockade augments or attenuates the onset of torsade de pointes in patients with IKr inhibitor-induced labile repolarization.
Does pharmacological beta-blockade augment the torsadogenic action of IKr inhibitors in chronic atrioventricular block dogs?
Does pharmacological beta-blockade augment the torsadogenic action of IKr inhibitors in chronic atrioventricular block dogs?
Pharmacological beta-blockade can augment the torsadogenic action of IKr inhibitors, as demonstrated by the higher incidence of torsade de pointes with dl-sotalol compared to d-sotalol in a canine model.
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Pharmacological beta-blockade may augment torsadogenicity of IKr inhibitors in this model; leaves open translation to clinical sotalol safety.
Information is still limited whether β-blockade may augment or attenuate the onset of torsade de pointes in patients with I Kr inhibitor-induced labile repolarization process. We compared the proarrhythmic effects of d -sotalol with those of dl -sotalol using the chronic atrioventricular block dogs, since d - and l -isomers share a similar blocking action on I Kr but β-blocking activity resides only in l -isomer. dl -Sotalol (3 mg/kg, p.o.) induced torsade de pointes in 3 out of 4 animals, whereas d -sotalol (3 mg/kg, p.o.) induced it in only 1 out of 4 animals. Thus, β-blockade can augment torsadogenic action of I Kr inhibitor.
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Goto et al. (2019) studied this question.
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