Drug-Free Correction of the Tone of the Autonomic Nervous System in the Management of Cardiac Arrhythmia in Coronary Artery Disease

Background: The aim of our study was to examine the possibility of ventricular extrasystole (VES) management in CAD (coronary artery disease) patients by attenuating the sympathetic activity with a course of electrical stimulation of the vagus nerve. Methods: A decrease in sympathetic tone was achieved via vagus nerve electrical stimulation (VNES). VNES was performed in 48 male CAD patients, mean age 53.5±4.1 years. Antiarrhythmic drug therapy was canceled prior to VNES therapy. The effect of VNES on heart rate variability (HRV) and VES were carefully studied. All the patients received a 24-hour ECG monitoring. HRV was calculated for high frequency (HF) and low frequency (LF) bands and the LF/HF index was determined. Results: Immediately following VNES therapy, 30 patients (group 1) reported alleviation of angina signs and the LF/HF index was significantly decreased (p=0.001). Eighteen patients (group 2) showed no change either in health or the LF/HF index. According to ECG and echocardiography, the VES number did not significantly change immediately after VNES therapy. One month after the VNES course, group 1 reported further improvement in health; the LF/HF index approached normal values. In group 2, the LF/HF significantly decreased (p=0.043). However, in the entire study sample, the VES number significantly decreased overall (p=0.025). Conclusion: VNES attenuated the cardiac effects of hypersympathicotonia decreased the ischemic impact on the myocardium, alleviated the cardiac angina signs, and beneficially influenced the VES number in CAD patients

Rhythminotropic Reactions of Human Myocardium in Ischemic and Rheumatic Heart Diseases against the Background of Amiodarone

In human heart failure, Ca2+ homeostasis gets disturbed due to a decrease in the function of the sarcoplasmic reticulum (SR). We studied the differences in the SR function in patients with rheumatic and coronary heart disease, against the background of amiodarone. Cardiac preparations from the atrium of 21 patients with coronary artery disease (CAD) and 14 patients with rheumatic heart disease (RHD) were used in this study. Myocardial strips perfused with oxygenated Krebs-Henzelait solution without and with amiodarone (1 mM/l) at 37°C. The steady state stimulation rate of the muscle strips was 0.5 Hz. The single extraordinary impulse was given as 0.2-1.5 sec after the steady state beat. Then, the first beat after a 4- to 60-sec rest period was evaluated. The extrasystoles of the myocardium in both groups, after long intervals, were decreased after amiodarone treatment. The amplitude of post extrasystoles of amiodarone-treated myocardium showed differences only after long intervals in both groups. Two types of inotropic responses of a failing myocardium after rest periods were observed. Type I post-rest contractions maintained the steady state amplitude after all rests. However, type II was characterized by a reduction in the amplitude of the contractions. Amiodarone treatment of the myocardium showing type I reactions led to an increase in the potentiation after rests, but showed no effect on the reaction of the muscle with the type II response. The results suggested that SR dysfunction was different in CAD and RHD. The realization of the therapeutic effect of amiodarone was found to be dependent on the functional activity of the SR