Vagus nerve stimulation (VNS) has been found to exert anti-inflammatory effects in different clinical settings and has been associated with improvement of clinical outcomes. However, evidence on the mechanistic link between the potential association of inflammatory status with clinical outcomes following VNS is scarce. This review aims to summarize the existing knowledge linking VNS with inflammation and its potential link with major outcomes in cardiovascular diseases, in both preclinical and clinical studies. Existing data show that in the setting of myocardial ischemia and reperfusion, VNS seems to reduce inflammation resulting in reduced infarct size and reduced incidence of ventricular arrhythmias during reperfusion. Furthermore, VNS has a protective role in vascular function following myocardial ischemia and reperfusion. Atrial fibrillation burden has also been reduced by VNS, whereas suppression of inflammation may be a potential mechanism for this effect. In the setting of heart failure, VNS was found to improve systolic function and reverse cardiac remodeling. In summary, existing experimental data show a reduction in inflammatory markers by VNS, which may cause improved clinical outcomes in cardiovascular diseases. However, more data are needed to evaluate the association between the inflammatory status with the clinical outcomes following VNS.
Keywords: arrhythmias; cardiovascular disease; heart failure; inflammation; myocardial ischemia; tragus; vagus nerve stimulation.