Transvenous vagal nerve stimulation (VNS) in acute myocardial infarction (AMI) markedly reduces the infarction size and improves chronic cardiac function (LB670)

Background: Although VNS is known to have a powerful anti‐infarct effect, the technical difficulty associated with VNS precludes its application under emergent settings of AMI. We developed a novel technique where we stimulate the vagal system transvenously and evaluated how the VNS affects the infarction size and cardiac function in the long term. Method: We ligated a left anterior descending coronary artery for 3 hours, then reperfused. For transvenous VNS, we performed the field electrical stimulation by pacing catheter in the superior vena cava. VNS reduced mean heart rate about 20‐30% during I/R. One month after ischemia‐reperfusion, we compared the infarct size, hemodynamics and load insensitive cardiac function, i.e., end‐systolic elastance (Ees) (Millar pressure and sonomicrometric volumetry) with or without VNS treatment. Results: In comparison with no VNS, transvenous VNS significantly decreased the infarction size more than 80% (1.1±1.2 vs. 7.8±1.2cm2, p<0.05), doubled left ventricular Ees (6.5±1.7 vs. 13.2±0.6 mmHg/ml, p<0.05), and decreased NT‐pro BNP (3667±1637 vs. 843±256 pmol/ml, p<0.05). Conclusion: Transvenous VNS in AMI markedly reduces the infarct size and improves cardiac function in the chronic phase (4 weeks after AMI). Transvenous VNS would be a novel therapy of AMI to prevent heart failure in the long term.