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Front. Physiol. | doi: 10.3389/fphys.2019.00135

The Association between Diabetes Mellitus and Atrial Fibrillation: Clinical and Mechanistic Insights

 Anne M. Gillis1*,  Loryn J. Bohne1, Dustin Johnson1,  Robert A. Rose1 and Stephen B. Wilton1
  • 1Cardiac Sciences, University of Calgary, Canada

A number of clinical studies have reported that diabetes mellitus (DM) is an independent risk factor for AF. After adjustment for other known risk factors including age, sex and cardiovascular risk factors, DM remains a significant if modest risk factor for development of AF. The mechanisms underlying the increased susceptibility to AF in DM are incompletely understood, but are thought to involve both electrical and structural remodeling in the atria. Electrical remodeling in DM may involve alterations in gap junction function that affect atrial conduction velocity due to changes in expression or localization of connexins. Electrical remodeling can also occur due to changes in atrial action potential morphology in association with changes in ionic currents, such as sodium or potassium currents, that can affect conduction velocity or susceptibility to triggered activity. Structural remodeling in DM results in atrial fibrosis, which can alter conduction patterns and susceptibility to re-entry in the atria. In addition, increases in atrial adipose tissue, especially in Type II DM, can lead to disruptions in atrial conduction velocity or conduction patterns that may affect arrhythmogenesis. Whether the insulin resistance in type II DM activates unique intracellular signaling pathways independent of obesity requires further investigation. In addition, the relationship between incident AF and glycemic control requires further study.

Keywords: Atrial Fibrillation, Diabetes Mellitus, Risk factors, mechanisms, ATRIAL REMODELING

Received: 30 Apr 2018; Accepted: 04 Feb 2019.

Edited by:

Jichao Zhao, The University of Auckland, New Zealand

Reviewed by:

Martin Stiles, The University of Auckland, New Zealand
Ghassen Cheniti, Centre Hospitalier Universitaire (CHU) de Bordeaux, France  

Copyright: © 2019 Gillis, Bohne, Johnson, Rose and Wilton. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: MD. Anne M. Gillis, University of Calgary, Cardiac Sciences, Calgary, T2N 4Z6, AB, Canada, amgillis@ucalgary.ca