Why the study?
Does intravenous molar sodium lactate terminate propafenone-induced malignant ventricular tachycardia in a child with junctional automatic tachycardia?
Does intravenous molar sodium lactate terminate propafenone-induced malignant ventricular tachycardia in a child with junctional automatic tachycardia?
Intravenous molar sodium lactate may be an effective treatment for terminating propafenone-induced malignant ventricular tachycardia.
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May support MSL rescue in propafenone-induced pediatric VT; hypothesis-generating and requires prospective validation.
Propafenone may aggravate the preexisting arrhythmia or induce another one. Usually, such proarrhythmic effects occur in patients with spontaneous ventricular arrhythmias and/or coronary heart disease with poor left ventricular function. We report the case of a 5-year-old girl with junctional automatic tachycardia and no structural heart disease, in whom malignant ventricular tachycardia occurring during propafenone treatment could be terminated by molar sodium lactate (MSL) infusion. The serum propafenone level obtained before MSL infusion was within the therapeutic range. Two hypothesis could explain the beneficial effects of MSL in our patient: (1) alkalinization facilitates the cell membrane hyperpolarization and thus can decrease the voltage-dependent effect of Class Ic drugs, (2) alkalinization could displace propafenone from its tissue receptor sites by an increase in the nonionized fraction.
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Scanu et al. (1991) studied this question.
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