open access

Vol 25, No 6 (2018)
Original articles — Clinical cardiology
Published online: 2017-12-28
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Vagal stimulation after acute coronary occlusion: The heart rate matters

Waheed Manati, Julien Pineau, Rosa Doñate Puertas, Elodie Morel, Timour Quadiri, Bernard Bui-Xuan, Philippe Chevalier
DOI: 10.5603/CJ.a2017.0156
·
Pubmed: 29297176
·
Cardiol J 2018;25(6):709-713.

open access

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

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.

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.

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Keywords

vagal stimulation, myocardial ischemia, sudden death, myocardial infarction, ventricular fibrillation, heart rate

About this article
Title

Vagal stimulation after acute coronary occlusion: The heart rate matters

Journal

Cardiology Journal

Issue

Vol 25, No 6 (2018)

Pages

709-713

Published online

2017-12-28

DOI

10.5603/CJ.a2017.0156

Pubmed

29297176

Bibliographic record

Cardiol J 2018;25(6):709-713.

Keywords

vagal stimulation
myocardial ischemia
sudden death
myocardial infarction
ventricular fibrillation
heart rate

Authors

Waheed Manati
Julien Pineau
Rosa Doñate Puertas
Elodie Morel
Timour Quadiri
Bernard Bui-Xuan
Philippe Chevalier

References (20)
  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.

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