Atomoxetine resulting in Takotsubo syndrome: Is the locally-released norepinephrine from the autonomic sympathetic cardiac nerves or the blood-borne catecholamines the cause?

摘要

The case report by Yamaguchi et al. published on line ahead of print on November 14, 2013 in the Journal [5] about an 11-year-old boy with attention-deficit/hyperactivity disorder (ADHD) treated for 2 years with atomoxetine, who suffered Takotsubo syndrome (TTS), implicating this drug, is of interest to clinicians managing patients with ADHD and for a possible TTS pathophysiological connotation. Atomoxetine, as the authors state, is a noncentral nerve-stimulating agent blocking reuptake of noradrenalin, and, as such, it can lead to cardiac responses similar to the ones resulting from intense efferent autonomic cardiac sympathetic nerve stimulation [2]. The pathophysiology of TTS is still elusive, but the currently prevailing theory implicates high catecholamines (both epi-nephrine and norepinephrine) as mediators for the resulting cardiomyocyte toxicity/injury [1,3,4].