Isaac E, Cooper SM, Jones SA, Loubani M. Do age-associated changes of voltage-gated sodium channel isoforms expressed in the mammalian heart predispose the elderly to atrial fibrillation? World J Cardiol 2020; 12(4): 123-135 [PMID: 32431783 DOI: 10.4330/wjc.v12.i4.123]
Corresponding Author of This Article
Mahmoud Loubani, BM BCh, FRCS, MD, Consultant Cardiac Surgeon, Professor, Surgeon, Department of Cardiothoracic Surgery, Hull University Teaching Hospitals, Castle Road, Cottingham HU16 5JQ, United Kingdom. mahmoud.loubani@hey.nhs.uk
Research Domain of This Article
Cardiac & Cardiovascular Systems
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Cardiol. Apr 26, 2020; 12(4): 123-135 Published online Apr 26, 2020. doi: 10.4330/wjc.v12.i4.123
Do age-associated changes of voltage-gated sodium channel isoforms expressed in the mammalian heart predispose the elderly to atrial fibrillation?
Emmanuel Isaac, Stephanie M Cooper, Sandra A Jones, Mahmoud Loubani
Emmanuel Isaac, Mahmoud Loubani, Department of Cardiothoracic Surgery, Hull University Teaching Hospitals, Cottingham HU16 5JQ, United Kingdom
Stephanie M Cooper, Sandra A Jones, Department of Biomedical Sciences, University of Hull, Hull HU6 7RX, United Kingdom
Author contributions: All authors contributed to this paper.
Conflict-of-interest statement: No potential conflict of interest. No financial support.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Corresponding author: Mahmoud Loubani, BM BCh, FRCS, MD, Consultant Cardiac Surgeon, Professor, Surgeon, Department of Cardiothoracic Surgery, Hull University Teaching Hospitals, Castle Road, Cottingham HU16 5JQ, United Kingdom. mahmoud.loubani@hey.nhs.uk
Received: October 26, 2019 Peer-review started: October 26, 2019 First decision: November 19, 2019 Revised: January 18, 2020 Accepted: March 12, 2020 Article in press: March 12, 2020 Published online: April 26, 2020 Processing time: 178 Days and 20.3 Hours
Core Tip
Core tip: Nav1.8 has been implicated by multiple studies in producing the late sodium current, predisposing the cardiomyocyte to arrhythmogenic activity. Animal models have demonstrated an enhancement of this aberrant current in aged hearts. Human studies have identified a reduction of Nav1.5 and an increase in Nav1.8 in both heart failure and left ventricular hypertrophy, strongly suggesting that voltage-gated sodium channel expression plays a central role in the development of arrhythmia. Clinically, sodium channel blockade through Ranolazine has proved promising in terminating the arrhythmia. Prevention of atrial fibrillation should focus on lifestyle management, as well as targeting cardiac risk factors. Irbesartan has been demonstrated to slow atrial remodelling, prevent atrial fibrillation in animal models, as well as avert the arrhythmia in human subjects.
