Abstract
AimsAtrial 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.Methods and ResultsA 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.ConclusionsThis study provides novel insights into understanding atrial electro-mechanics illustrating that AFER impairs atrial contraction due to reduced intracellular Ca2+ transients.
Highlights
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia [1,2] and has an increase in incidence and prevalence with each decade of adult life [3,4]
This study provides novel insights into understanding atrial electro-mechanics illustrating that atrial fibrillation-induced electrical remodeling (AFER) impairs atrial contraction due to reduced intracellular Ca2+ transients
Using the multi-scale models we investigated the functional impact of AFER on atrial electrical and mechanical activities in order to elucidate the mechanism underlying atrial stunning
Summary
Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia [1,2] and has an increase in incidence and prevalence with each decade of adult life [3,4]. Atrial stunning is the loss of mechanical atrial contraction following a successful cardioversion, which is maximal immediately after cardioversion and can take up to 6 weeks for normal atrial contraction to re-establish [6]. Atrial stunning occurs rarely following spontaneous cardioversion in paroxysmal arrhythmias. Previous studies have shown that factors delaying return of normal atrial mechanical function include duration of atrial fibrillation, presence of structural heart disease, atrial pressures and atrial size [6,7,8]. The exact mechanisms causing impaired atrial mechanics, as occurs in atrial stunning are unknown. Some postulated mechanisms include tachycardia induced atrial cardiomyopathy, accumulation of cytosolic calcium and atrial hibernation [6,7,8]
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