Display options
Share it on

Cardiovasc Res. 2021 Jul 27;117(9):2083-2091. doi: 10.1093/cvr/cvaa253.

Mechanism of ventricular premature beats elicited by left stellate ganglion stimulation during acute ischaemia of the anterior left ventricle.

Cardiovascular research

Bastiaan J D Boukens, Michael Dacey, Veronique M F Meijborg, Michiel J Janse, Joseph Hadaya, Peter Hanna, M Amer Swid, Tobias Opthof, Jeffrey L Ardell, Kalyanam Shivkumar, Ruben Coronel

Affiliations

  1. Department of Medical Biology, Amsterdam UMC, University of Amsterdam, Heart Center, Meibergdreef 9, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands.
  2. Department of Experimental Cardiology, Amsterdam UMC, University of Amsterdam, Heart Center, Meibergdreef 9, P.O. Box 22660, 1100 DD Amsterdam, The Netherlands.
  3. UCLA Cardiac Arrhythmia Center, Los Angeles, CA, USA.
  4. L'Institut de RYtmologie et de Modelisation Cardiaque (LIRYC), Universite de Bordeaux, Bordeaux, France.

PMID: 32853334 PMCID: PMC8318107 DOI: 10.1093/cvr/cvaa253

Abstract

AIMS: Enhanced sympathetic activity during acute ischaemia is arrhythmogenic, but the underlying mechanism is unknown. During ischaemia, a diastolic current flows from the ischaemic to the non-ischaemic myocardium. This 'injury' current can cause ventricular premature beats (VPBs) originating in the non-ischaemic myocardium, especially during a deeply negative T wave in the ischaemic zone. We reasoned that shortening of repolarization in myocardium adjacent to ischaemic myocardium increases the 'injury' current and causes earlier deeply negative T waves in the ischaemic zone, and re-excitation of the normal myocardium. We tested this hypothesis by activation and repolarization mapping during stimulation of the left stellate ganglion (LSG) during left anterior descending coronary artery (LAD) occlusion.

METHODS AND RESULTS: In nine pigs, five subsequent episodes of acute ischaemia, separated by 20 min of reperfusion, were produced by occlusion of the LAD and 121 epicardial local unipolar electrograms were recorded. During the third occlusion, left stellate ganglion stimulation (LSGS) was initiated after 3 min for a 30-s period, causing a shortening of repolarization in the normal myocardium by about 100 ms. This resulted in more negative T waves in the ischaemic zone and more VPBs than during the second, control, occlusion. Following the decentralization of the LSG (including removal of the right stellate ganglion and bilateral cervical vagotomy), fewer VPBs occurred during ischaemia without LSGS. During LSGS, the number of VPBs was similar to that recorded before decentralization.

CONCLUSION: LSGS, by virtue of shortening of repolarization in the non-ischaemic myocardium by about 100 ms, causes deeply negative T waves in the ischaemic tissue and VPBs originating from the normal tissue adjacent to the ischaemic border.

© The Author(s) 2020. Published by Oxford University Press on behalf of the European Society of Cardiology.

Keywords: Arrhythmias; Autonomic nervous system; Injury current; Ischaemia; Repolarization

References

  1. J Mol Cell Cardiol. 1986 Apr;18(4):339-55 - PubMed
  2. Heart Rhythm. 2020 May;17(5 Pt A):795-803 - PubMed
  3. Circ Res. 1978 May;42(5):603-13 - PubMed
  4. JACC Clin Electrophysiol. 2019 Aug;5(8):881-896 - PubMed
  5. Comput Methods Programs Biomed. 2002 Nov;69(3):225-36 - PubMed
  6. Circulation. 1985 Oct;72(4):922-32 - PubMed
  7. Circ Res. 1991 May;68(5):1241-9 - PubMed
  8. Circulation. 1985 Sep;72(3):585-95 - PubMed
  9. Circ Res. 1980 Aug;47(2):151-65 - PubMed
  10. Expert Rev Cardiovasc Ther. 2012 Aug;10(8):947-9 - PubMed
  11. Circ Res. 1979 Dec;45(6):764-70 - PubMed
  12. J Am Coll Cardiol. 2017 Jun 27;69(25):3070-3080 - PubMed
  13. Nat Rev Cardiol. 2014 Jun;11(6):346-53 - PubMed
  14. Circ Res. 1981 Sep;49(3):792-806 - PubMed

Publication Types

Grant support