α1-adrenoceptors and takotsubo syndrome: pathophysiologic connotations

I enjoyed reading the contribution by Huanget al.,1 delving into the arrhythmogenesis generated by toxic levels of epinephrine (Epi) in human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), a model for the study of the pathogenesis of takotsubo syndrome (TTS). The authors concentrated on the α1-adrenoceptor stimulation effects of Epi and its blockade on the hiPSC-CMs, studying the responses of their preparation to phentolamine, phenylephrine, clonidine, reactive oxygen species (ROS), H2O2, N-acetyl-I-cysteine, nicotinamide adenine dinucleotide phosphate hydrogen oxidases, and a protein kinase C blocker. Epi prolonged the duration of action potentials and suppressed the velocity of depolarization, inducing arrhythmic events in hiPSC-CMs. The Epi-induced effects, via its α1-adrenoceptors ’ stimulation of hiPSC-CMs led to ion channels’ dysfunction, involving the voltage-dependent Na+ and L-type Ca2+ channels. The authors concluded that α1-adrenoceptor signalling is pathogenetically implicated in arrhythmogenesis encountered in TTS, and that α1-adrenoceptor blockers should be considered in the management of arrhythmias in patients with TTS.
Source: Europace - Category: Cardiology Source Type: research