Vagal neurostimulation in patients with coronary artery disease

Abstract We tested the hypotheses that (1) progression of coronary artery disease (CAD) increases sympathetic inflow to the heart, thus impairing cardiac blood supply, and (2) reduced sympathetic tone improves cardiac microcirculation and ameliorates severity of anginal symptoms. Electrical irritation of the nerve auricularis—a sensitive ramus of the vagus nerve—provides a central sympatholytic action. Using this technique, we studied the effects of vagal neurostimulation (VNS) on hemodynamics, the content of atrial noradrenergic nerves and the microcirculatory bed of CAD patients. VNS was performed in the preoperative period of CAD patients with severe angina pectoris. The comparison groups consisted of untreated patients with CAD or Wolff–Parkinson–White syndrome. Atrial tissue of patients with this syndrome ( n =6); with effort angina ( n =14); with angina at rest ( n =10); and with severe angina treated with VNS ( n =8) contained the following volume percentages of noradrenergic nerves: 1.7±0.1%, 1.3±0.3%, 0.5±0.1% ( p p p E i ) to late ( A i ) waves increased from 1.07±0.12 to 1.65±0.17 after VNS ( p p