Key result
Escitalopram linked to QTc prolongation, Torsade de Pointes, and arrest in structural heart disease.
Why the study?
Evaluating the cardiac safety of escitalopram, the S-enantiomer of citalopram, is important due to concerns about potential cardiac toxicity.
Case Report (n=1)
Alerts clinicians to QTc risk with escitalopram in structural heart disease; leaves open comparative safety versus citalopram.
Previous reviews have focused on the potential cardiac toxicity of the racemic drug citalopram (Celexa(®)). Evaluating the safety of escitalopram (Lexapro(®)) is an important issue to consider, since it is the S-enantiomer of citalopram. Escitalopram has a small effect on the QTc interval. A prolonged QTc was seen in 2% to 14% of escitalopram overdose cases, without serious cardiac sequelae. The QTc prolongation effect of citalopram in beagle dogs has been attributed to the minor metabolite racemic didemethylcitalopram (DDCT). Whether the escitalopram minor metabolite S-DDCT has this effect is not known. Concentrations of S-DDCT are lower than DDCT, but for a broad range of doses of escitalopram and citalopram, the S-DDCT and DDCT concentrations are well below the QTc prolonging concentrations reported in dogs. There is no strong evidence from human and animal studies that the cardiac safety of escitalopram is significantly superior to that of citalopram.
No takes yet. Share an insight, caveat, or question.
Robert H. Howland (2012) conducted a case report in Torsade de Pointes and cardiopulmonary arrest (n=1). Escitalopram was evaluated on Cardiopulmonary arrest secondary to Torsade de Pointes. Escitalopram use was associated with QTc prolongation and Torsade de Pointes leading to cardiopulmonary arrest in a patient with a history of structural heart disease.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: