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The pathophysiology of heart failure (HF) is complex and involves reduced myocyte contractility, extracellular matrix deposition, and electrophysiological remodeling that collectively impair ventricular function and increase the risk for lethal arrhythmias. 1 Despite the myriad processes involved, a key feature of HF is elevated sympathetic activity and parasympathetic withdrawal, leading to autonomic imbalance. 2 Indeed, beta blocker therapy remains one of the few effective pharmacological treatments for HF. However, in addition to decreasing sympathetic input to the heart, increasing parasympathetic activity may also be beneficial for restoring autonomic balance.

From drugs to devices and back again: chemical vagal nerve stimulation for the treatment of heart failure