The vagus nerve in myocardial infarction

Myocardial infarction can result from and leads to sympathetic activation, whereas vagal engagement provides a counter-regulatory influence that can limit ischaemic injury. This article reviews the organization of vagal sensory and efferent pathways, their transmitters and receptors, and their targets within the myocardium, coronary and systemic vasculature, and other organs including the intestine and spleen. Atrial mechanosensitive afferents mediate the Bainbridge reflex, resulting in tachycardia, whereas activation of ventricular mechano- and chemosensitive afferents trigger the Bezold-Jarisch reflex, eliciting bradycardia and hypotension during coronary occlusion and reperfusion, with probable cardioprotective significance. Vagal pathways contribute to remote ischaemic conditioning, linking peripheral sensory stimulation to vagal activation and the release of circulating protective factors. In experimental models, vagal stimulation reduces infarct size, arrhythmogenesis, and limits inflammation. Smaller clinical studies reported reduced infarct size and improved clinical outcome with remote ischaemic conditioning and electrical auricular vagus stimulation. However, the efficacy of remote ischaemic conditioning in recruiting cardioprotective vagal activity in patients with ischaemic heart disease remains to be definitively established.