Editor, – Reference is made to the article 'Inside the isomers: the tale of chiral switches' (Aust Prescr 2004;27:109-13). In this article it is asserted that &aos;in overdose, there is a concern about the potential for sudden death, possibly related to QT prolongation due to a secondary metabolite formed from (R)-citalopram. (S)-citalopram (escitalopram) was therefore developed with the aim of a better harm: benefit ratio compared to (R)-citalopram'.
Significantly, the authors of this article have not referenced any of the statements in this paragraph. I would like to advise that the statement regarding the propensity of a metabolite of the (R)-enantiomer of citalopram to cause sudden death as a result of QT prolongation is completely unfounded.
A survey has investigated the effects of citalopram, at therapeutic doses, on ECG parameters.1 The authors concluded that citalopram has no significant effects on PQ, QRS or QTc intervals, during short-or long-term treatment. Nor were there any deaths or clinically significant arrhythmias reported among all pure citalopram intoxications (n=108 with doses up to 5.2 g) over a two-year period in Sweden.2
Since there is absolutely no basis to the assertion that a metabolite of (R)-citalopram is associated with sudden death as a result of QT prolongation, the reason given for the development of (S)-citalopram is also purely speculative and quite simply, untrue.
Debbie Pelser
Medical Department Manager
Lundbeck Australia
Baulkham Hills, NSW