title: Effects of Persistent Atrial Fibrillation-Induced Electrical Remodeling on Atrial Electro-Mechanics - Insights from a 3D Model of the Human Atria.
abstract: OBJECTIVE
  Atrial stunning, a loss of atrial mechanical contraction, can occur following a successful cardioversion. It is hypothesized that persistent atrial fibrillation-induced electrical remodeling (AFER) on atrial electrophysiology may be responsible for such impaired atrial mechanics. This simulation study aimed to investigate the effects of AFER on atrial electro-mechanics.
  
  
  RESULTS
  A 3D electromechanical model of the human atria was developed to investigate the effects of AFER on atrial electro-mechanics. Simulations were carried out in 3 conditions for 4 states: (i) the control condition, representing the normal tissue (state 1) and the tissue 2-3 months after cardioversion (state 2) when the atrial tissue recovers its electrophysiological properties after completion of reverse electrophysiological remodelling; (ii) AFER-SR condition for AF-remodeled tissue with normal sinus rhythm (SR) (state 3); and (iii) AFER-AF condition for AF-remodeled tissue with re-entrant excitation waves (state 4). Our results indicate that at the cellular level, AFER (states 3 & 4) abbreviated action potentials and reduced the Ca2+ content in the sarcoplasmic reticulum, resulting in a reduced amplitude of the intracellular Ca2+ transient leading to decreased cell active force and cell shortening as compared to the control condition (states 1 & 2). Consequently at the whole organ level, atrial contraction in AFER-SR condition (state 3) was dramatically reduced. In the AFER-AF condition (state 4) atrial contraction was almost abolished.
  
  
  CONCLUSIONS
  This study provides novel insights into understanding atrial electro-mechanics illustrating that AFER impairs atrial contraction due to reduced intracellular Ca2+ transients.
authors.affiliation: Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.
authors.forename: Ismail
authors.initials: I
authors.lastname: Adeniran
authors.affiliation: Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.|Taunton & Somerset Hospital, Somerset, United Kingdom.
authors.forename: David H
authors.initials: DH
authors.lastname: MacIver
authors.affiliation: Manchester Heart Centre, Manchester Royal Infirmary, Manchester, United Kingdom.
authors.forename: Clifford J
authors.initials: CJ
authors.lastname: Garratt
authors.affiliation: Department of Engineering, Lancaster University, Lancaster, United Kingdom.
authors.forename: Jianqiao
authors.initials: J
authors.lastname: Ye
authors.affiliation: Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.|School of Physiology and Pharmacology, and Cardiovascular Research Laboratories, University of Bristol, Bristol, United Kingdom.
authors.forename: Jules C
authors.initials: JC
authors.lastname: Hancox
authors.affiliation: Biological Physics Group, School of Physics and Astronomy, University of Manchester, Manchester, United Kingdom.
authors.forename: Henggui
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000200:Action Potentials / Q000502:physiology; D001281:Atrial Fibrillation / Q000473:pathology / Q000503:physiopathology*; D016275:Atrial Function / Q000502:physiology*; D064752:Atrial Remodeling; D002118:Calcium / Q000378:metabolism; D003198:Computer Simulation; D006325:Heart Atria / Q000033:anatomy & histology; D006329:Heart Conduction System / Q000033:anatomy & histology / Q000502:physiology* / Q000503:physiopathology; D006801:Humans; D008955:Models, Cardiovascular; D009200:Myocardial Contraction / Q000502:physiology; D032383:Myocytes, Cardiac / Q000166:cytology / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000502:physiology
chemical_list: D002118:Calcium