Vol 25, No 6 (2018)
Original articles — Clinical cardiology
Published online: 2017-12-28

open access

Page views 2516
Article views/downloads 934
Get Citation

Connect on Social Media

Connect on Social Media

Vagal stimulation after acute coronary occlusion: The heart rate matters

Waheed Manati1, Julien Pineau2, Rosa Doñate Puertas1, Elodie Morel2, Timour Quadiri3, Bernard Bui-Xuan3, Philippe Chevalier21
Pubmed: 29297176
Cardiol J 2018;25(6):709-713.

Abstract

Background: There is a well documented causal link between autonomic imbalance and cardiac elec­trical instability. However, the mechanisms underlying the antiarrhythmic effect of vagal stimulation are poorly understood. The vagal antiarrhythmic effect might be modulated by a decrease in heart rate.

Methods: The proximal anterior interventricular artery was occluded in 16 pigs by clamping under general anaesthesia. Group 1: heart rates remained spontaneous (n = 6; 12 occlusions); Group 2: heart rates were fixed at 190 bpm with atrial electrical stimulation (n = 10; 20 occlusions). Each pig received two occlusions, 30 min apart, one without and one with vagal stimulation (10 Hz, 2 ms, 5–20 mA). The antiarrhythmic effect of vagal activation was defined as the time to the appearance of ventricular fibrillation (VF) after occlusion.

Results: In Group 1, vagal stimulation triggered a significant decrease in basal heart rate (132 ± 4 vs. 110 ± 17 bpm, p < 0.05), and delayed the time to VF after coronary occlusion (1102 ± 85 vs. 925 ± ± 41 s, p < 0.05). In Group 2, vagal stimulation did not modify the time to VF (103 ± 39 vs. 91 ± 20 s). Analyses revealed that heart rate and the time to VF were positively linearly related.

Conclusions: Maintaining a constant heart rate with atrial electrical stimulation in pigs prevented vagal stimulation from modifying the time to VF after acute coronary occlusion.

Article available in PDF format

View PDF Download PDF file

References

  1. Priori SG, Aliot E, Blomstrom-Lundqvist C, et al. Task Force on Sudden Cardiac Death, European Society of Cardiology. Europace. 2002; 4(1): 3–18.
  2. Kent KM, Smith ER, Redwood DR, et al. Electrical stability of acutely ischemic myocardium. Influences of heart rate and vagal stimulation. Circulation. 1973; 47(2): 291–298.
  3. Myers RW, Pearlman AS, Hyman RM, et al. Beneficial effects of vagal stimulation and bradycardia during experimental acute myocardial ischemia. Circulation. 1974; 49(5): 943–947.
  4. Ando M, Katare RG, Kakinuma Y, et al. Efferent vagal nerve stimulation protects heart against ischemia-induced arrhythmias by preserving connexin43 protein. Circulation. 2005; 112(2): 164–170.
  5. Corr PB, Gillis RA. Role of the vagus nerves in the cardiovascular changes induced by coronary occlusion. Circulation. 1974; 49(1): 86–97.
  6. Rosenshtraukh L, Danilo P, Anyukhovsky EP, et al. Mechanisms for vagal modulation of ventricular repolarization and of coronary occlusion-induced lethal arrhythmias in cats. Circ Res. 1994; 75(4): 722–732.
  7. De Ferrari GM, Vanoli E, Stramba-Badiale M, et al. Vagal stimulation and prevention of sudden death in conscious dogs with a healed myocardial infarction. Circ Res. 1991; 68(5): 1471–1481.
  8. De Ferrari GM, Vanoli E, Curcuruto P, et al. Prevention of life-threatening arrhythmias by pharmacologic stimulation of the muscarinic receptors with oxotremorine. Am Heart J. 1992; 124(4): 883–890.
  9. Chevalier P, Ruffy F, Danilo P, et al. Interaction between alpha-1 adrenergic and vagal effects on cardiac rate and repolarization. J Pharmacol Exp Ther. 1998; 284(3): 832–837.
  10. Kawada T, Yamazaki T, Akiyama T, et al. Differential acetylcholine release mechanisms in the ischemic and non-ischemic myocardium. J Mol Cell Cardiol. 2000; 32(3): 405–414.
  11. Aupetit JF, Frassati D, Bui-Xuan B, et al. Efficacy of a beta-adrenergic receptor antagonist, propranolol, in preventing ischaemic ventricular fibrillation: dependence on heart rate and ischaemia duration. Cardiovasc Res. 1998; 37(3): 646–655.
  12. Aupetit JF, Bui-Xuan B, Kioueh I, et al. Opposite change with ischaemia in the antifibrillatory effects of class I and class IV antiarrhythmic drugs resulting from the alteration in ion transmembrane exchanges related to depolarization. Can J Physiol Pharmacol. 2000; 78(3): 208–216.
  13. Vaillant FGP, Descotes J, Tabib A, et al. Protective effect of ivabradine against ventricular fibrillation in pigs during acute myocardial ischemia [abstract]. Eur Heart J. ; 2007: P2687.
  14. Van Winkle DM, Feigl EO. Acetylcholine causes coronary vasodilation in dogs and baboons. Circ Res. 1989; 65(6): 1580–1593.
  15. Kovach JA, Gottdiener JS, Verrier RL. Vagal modulation of epicardial coronary artery size in dogs. A two-dimensional intravascular ultrasound study. Circulation. 1995; 92(8): 2291–2298.
  16. Meesmann M, Karagueuzian HS, Ino T, et al. The role of enhanced vagal activity on ischemic ventricular tachycardia: pharmacologic basis of inefficiency. Am Heart J. 1991; 121(6 Pt 1): 1703–1713.
  17. Inagaki M, Kawada T, Lie M, et al. Intravascular parasympathetic cardiac nerve stimulation prevents ventricular arrhythmias during acute myocardial ischemia. Conf Proc IEEE Eng Med Biol Soc. 2005; 7: 7076–7079.
  18. Maxwell MP, Hearse DJ, Yellon DM. Species variation in the coronary collateral circulation during regional myocardial ischaemia: a critical determinant of the rate of evolution and extent of myocardial infarction. Cardiovasc Res. 1987; 21(10): 737–746.
  19. Armour J. Myocardial ischaemia and the cardiac nervous system. Cardiovascular Research. 1999; 41(1): 41–54.
  20. Feliciano L, Henning RJ. Vagal nerve stimulation releases vasoactive intestinal peptide which significantly increases coronary artery blood flow. Cardiovasc Res. 1998; 40(1): 45–55.