Vagal nerve stimulation improves myocardial recovery after STEMI: a randomized trial

Background ST-segment elevation myocardial infarction (STEMI) occurs due to an acute blockage of blood flow in a coronary artery supplying the heart. This blockage causes ischemia and necrosis, leading to complications like arrhythmias, heart failure, and death. Timely diagnosis and treatment are crucial to reduce myocardial damage and improve patient outcomes. Recent studies have underscored the therapeutic potential of vagus nerve stimulation (VNS) in cardiovascular diseases, given its critical role in regulating heart rate and blood pressure, as well as in inhibiting pro-inflammatory processes. While invasive VNS necessitates surgical implantation, Transcutaneous VNS (tVNS) provides an accessible, safer alternative by stimulating the auricular branch of the vagus nerve at the outer ear. Purpose This study aims to assess the therapeutic effects of tVNS on early myocardial damage in patients with STEMI following primary percutaneous coronary intervention (PCI) by evaluating left ventricular ejection fraction (LVEF), wall motion abnormalities, and troponin levels. Methods Sixty patients with acute STEMI were admitted and given guideline-directed therapy. They were randomized 1:1 into active or sham groups in a sham-controlled trial. During hospitalization, immediately following catheterization and angioplasty, the active group received tVNS for 60 minutes, while the sham group received low-intensity stimulation. Echocardiography was performed 48 hours post-stimulation to assess the wall motion score index (WMSI) and LVEF. Blood samples for inflammatory markers and Troponin levels were taken at baseline and at 24 and 48 hours. Primary endpoints included changes in myocardial damage assessed via echocardiography, LVEF, and biomarkers. A t-test was used to determine significance at p < 0.05. Results The tVNS group demonstrated a significantly higher LVEF (45.9%) than the sham stimulation (43.5%, F(1,53) = 7.97, p = 0.007). Additionally, the tVNS group exhibited a significantly lower wall motion abnormalities (1.36) than the controls (1.39; F(1,53) = 4.58, p < 0.05). Furthermore, the tVNS group experienced a significantly greater decline in troponin from 24 to 48 hours (1205.5) compared to the controls (387.5; F(1,48) = 4.08, p < 0.05). Conclusions These preliminary results support existing literature on the potential role of VNS. Moreover, this research marks the first pioneering trial conducted on human subjects. Although derived from a relatively small cohort, the results consistently point in the same direction, underscoring a coherent trend across all measured outcomes. The early findings provide a promising foundation for using tVNS as an adjunctive therapy for myocardial recovery in STEMI patients. Further research with a larger cohort and long-term follow-up is necessary to assess the durability of these benefits and explore the full potential of tVNS as a non-invasive therapeutic strategy in the management of STEMI.