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

Sergey V. Popov, PhD, ScD, Sergey A. Afanasiev, PhD, ScD*, Igor O. Kurlov, PhD, Anna V. Pisklova, PhD.

Federal State Budgetary Institution “Research Institute for Cardiology” of Siberian Branch of the  RAMS, Tomsk, Russian Federation

*Corresponding author: Professor Sergey A. Afanasiev, PhD, ScD. FSBI “RI Cardiology” SB RAMS. 111a Kievskaya Street, Tomsk, 634012, Russia. Phone: +7 3822 440511. E-mail: tursky@cardio-tomsk.ru

Published: June 25, 2013

Abstract: 

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.

Keywords: 
coronary artery disease; angina pectoris; electric vagus nerve stimulation; sympathetic nervous system; ECG Holter monitoring.
References: 

1.Olshansky B, Sabbah HN, Hauptman PJ, Colucci WS. Parasympathetic nervous system and heart failure: pathophysiology and potential implications for therapy. Circulation 2008; 118(8):863-71.

2.Singh RB, Kartik C, Otsuka K, Pella D, Pella J. Brain-heart connection and the risk of heart attack. Biomed Pharmacother 2002; 6 Suppl 2:257-65.

3. Packer M. The neurohormonal hypothesis: a theory to explain the mechanism of disease progression in heart failure. J Am Coll Cardiol 1992; 20(1):248-54.

4. Akutsu Y, Kaneko K, Kodama Y, Li H-L, Kawamura M, Asano T,et al. . J Nucl Med 2009; 50(1):61-7.

5. Brunner-La Rocca HP, Esler MD, Jennings GL, Kaye DM. Effect of cardiac sympathetic nervous activity on mode of death in congestive heart failure. Eur Heart J 2001; 22(13):1136-43.

6. Algra A, Tijssen JG, Roelandt J R, Pool J, Lubsen J. Heart rate variability from 24-hour electrocardiography and the 2-year risk of sudden death. Circulation 1993; 88(1):180-5.

7. Seely AJE, Macklem PT. Complex systems and the technology of variability analysis. Crit Care 2004; 8(6):R367-84.

8. Floras JS. Sympathetic nervous system activation in human heart failure: clinical implications of an updated model. J Am Coll Cardiol 2009; 54(5):375-85.

9. Watson AMD, Hood SG, Ramchandra R, McAllen RM, May CN. Increased cardiac sympathetic nerve activity in heart failure is not due to desensitization of the arterial baroreflex. Am J Physiol Heart Circ Physiol 2007; 293(1):H798-804.

10. Notarius CF, Floras JS.Limitations of the use of spectral analysis of heart rate variability for the estimation of cardiac sympathetic activity in heart failure. Europace 2001; 3(1):29-38.

11. Van de Berne P, Montano N, Pagani M, Oren R, Somers VK. Absence of low-frequency variability of sympathetic nerve activity in severe heart failure. Circulation 1997; 95(6):1449-54.

12. Dibner-Dunlap ME, Thames MD. Control of sympathetic nerve activity by vagal mechanoreflexes is blunted in heart failure. Circulation 1992; 86(6):1929-34.

13. Rosen VM, Taylor DC, Parekh H, Pandya A, Thompson D, Kuznik A,et al. Cost effectiveness of intensive lipid-lowering treatment for patients with congestive heart failure and coronary heart disease in the US. Pharmacoeconomics 2010; 28(1):47-60.

14. Francis GS, Tang WH. Pathophysiology of congestive heart failure. Rev Cardiovasc Med 2003; 4 Suppl 2:S14-20.

15. Girgis I, Chakko SC, de Marchena E, Jara C, Diaz P, Castellanos A, et al. Effect of clonidine on heart rate variability in congestive heart failure. Am J Cardiol 1998; 82(3):335-7.

16. Lang CC, Rayos GH, Chomsky DB, Wood AJ, Wilson JR. of on in with . Circulation 1997; 96(1):238-45.

17. You-hua Z, You-cheng S, Jun Z, Xian-qi Y. Sympathetic inhibition with clonidine improves autonomic balance in congestive heart failure. Int J Cardiol 1997; 59(2):139-44.

18. Sabbah HN. Electrical vagus nerve stimulation for the treatment of chronic heart failure. Cleve Clin J Med 2011; 78 Suppl 1:S24-9.

19. Zhang Y, Popovic ZB, Bibevski S, Fakhry I, Sica DA, Van Wagoner DR, et al. Chronic vagus nerve stimulation improves autonomic control and attenuates systemic inflammation and heart failure progression in a canine high rate pacing model. Circ Heart Fail 2009; 2(6):692–9.

20. Zamotrinsky A, Afanasiev S, Karpov RS, Cherniavsky A. of of the in with . Coronary Artery Disease 1997; 8 (8-9):551-7.

21. Malik M, Camm AJ. of --what they really and what we really . Am J Cardiol 1993; 72(11):821-2.

22. Bigger JT Jr, Fleiss JL, Steinman RC, Rolnitzky LM, Kleiger RE, Rottman JN. of and . Circulation 1992; 85(1):164-71.

23. Khlopov NA, Sharafislamov FS, Rubakova LC. Topographic-Anatomical Basis of Acupuncture. Moscow: Nauka,1988. [ Book in Russian].

24. Zamotrinsky AV, Kondratiev B, de Jong JW. Vagal neurostimulation in patients with coronary artery disease. Auton Neurosci 2001; 88(1-2):109-16.

25. Belkina LM, Matsievskii DD, Saltykova VA, Radzievskii SA, Korchazhkina NB. Electroacupuncture effect on the systemic hemodynamics in animals with postinfarct cardiosclerosis. Biull Eksp Biol Med 1999; 127(1):29-34. [Article in Russian].

26. Schwartz PJ, Pagani M, Lombardi F, Malliani A, Brown AM. A cardiocardiac sympathovagal reflex in the cat. Circ Res 1973; 32(2):215-20.

27. Сhen SW. A wavelet-based heart rate variability analysis for the study of nonsustained ventricular tachycardia. IEEE Trans Biomed Eng 2002; 49(7):736-42.

28. Ciaccio EJ. Localization of the slow conduction zone during reentrant ventricular tachycardia. Circulation 2000; 102(4):464-9.

29. Horvath G, Racker DK, Goldberger JJ, Johnson D, Jain S, Kadish AH. Electrophysiological and anatomic heterogeneity in evolving canine myocardial infarction. Pacing Clin Electrophysiol 2000; 23(7):1068-79.

30. Zhang Y, Yamada H, Bibevski S, Zhuang S, Mowrey KA, Wallick DW, et al. Chronic atrioventricular nodal vagal stimulation: first evidence for long-term ventricular rate control in canine atrial fibrillation model. Circulation 2005; 112(19):2904-11.

31. Li M, Zheng C, Sato T, Kawada T, Sugimachi M, Sunagawa K. in . Circulation 2004; 109(1):120-4.

32. Nakayama Y, Miyano H, Shishido T, Inagaki M, Kawada T, Sugimachi M, et al. - on of the various of . Circulation 2001; 104(19):2277-9.

The fully formatted PDF version is available.

Download Article

Int J Biomed. 2013; 3(2):74-77. © 2013 International Medical Research and Development Corporation. All rights reserved.