Key result
Both intravenous and local TMAO administration significantly increased LSG function and activity, shortened effective refractory period, and aggravated ischemia-induced ventricular arrhythmia.
Why the study?
TMAO was previously shown to activate the atrial autonomic ganglion plexus and promote atrial arrhythmia, but whether it activates the cardiac sympathetic nervous system to modulate ventricular arrhythmia was unknown.
The gut microbe-derived metabolite TMAO aggravates ischemia-induced ventricular arrhythmias by activating the cardiac sympathetic nervous system through both direct and central autonomic pathways.
No takes yet. Share an insight, caveat, or question.
TMAO may aggravate ischemic ventricular arrhythmias via sympathetic activation in animals; leaves open human translation and microbiota-targeted therapies.
Meng et al. (2019) studied Ischemia-induced ventricular arrhythmia. Trimethylamine N-oxide (TMAO) vs. Control was evaluated on Left stellate ganglion (LSG) function and activity, effective refractory period, and ischemia-induced ventricular arrhythmia. Both intravenous and local TMAO administration significantly increased LSG function and activity, shortened effective refractory period, and aggravated ischemia-induced ventricular arrhythmia.
Synapse has enriched one closely related paper. Consider it for comparative context: