Long-chain acylcarnitine 18:1 acutely increases human atrial myocardial contractility and arrhythmia susceptibility

Author:

Aitken-Buck Hamish M.1ORCID,Krause Julia23,van Hout Isabelle1,Davis Philip J.4,Bunton Richard W.4,Parry Dominic J.4,Williams Michael J. A.5ORCID,Coffey Sean5ORCID,Zeller Tanja23,Jones Peter P.1,Lamberts Regis R.1ORCID

Affiliation:

1. Department of Physiology, HeartOtago, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand

2. University Heart and Vascular Centre, University Medical Centre Hamburg-Eppendorf, Hamburg, Germany

3. DZHK (German Centre for Cardiovascular Research), Partner Site Hamburg/Kiel/Lübeck, Hamburg, Germany

4. Department of Cardiothoracic Surgery, Otago Medical School—Dunedin Campus, Dunedin Hospital, Dunedin, New Zealand

5. Department of Medicine, Heart Otago, Otago Medical School—Dunedin Campus, University of Otago, Dunedin, New Zealand

Abstract

For the first time, the fatty acid metabolite, long-chain acylcarnitine 18:1, is shown to acutely increase the arrhythmia susceptibility and contractility of human atrial myocardium. In vitro, this was linked to an influx of Ca2+ and an enhanced propensity for spontaneous RyR2-mediated Ca2+ release.

Funder

Manatu Hauora | Health Research Council of New Zealand

National Heart Foundation of New Zealand

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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