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Updated: Oct 21, 2025

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Changes in left atrial structure and function over a decade in the general population
Flemming Javier Olsen1,2, Niklas Dyrby Johansen1,2, Kristoffer Grundtvig Skaarup1,2
1The Copenhagen City Heart Study, Bispebjerg and Frederiksberg Hospital, Frederiksberg, Denmark.
Aims:
Assessing left atrial (LA) size and function is an important part of the echocardiographic examination. We sought to assess how LA size and function develop over time, and which clinical characteristics promote atrial remodelling.
Methods And Results:
We examined longitudinal changes of the LA between two visits in the Copenhagen City Heart Study (n = 1065). The median time between the examinations was 10.4 years. LA measurements included: maximal LA volume (LAVmax), minimal LA volume (LAVmin), and LA emptying fraction (LAEF). Clinical and echocardiographic accelerators were determined from linear regression. The value of LA remodelling for predicting incident atrial fibrillation (AF) and heart failure (HF) was examined by Cox proportional hazards regressions. During follow-up, LAVmax and LAVmin significantly increased by 8.3 and 3.5 mL/m2, respectively. LAEF did not change. Age and AF were the most impactful clinical accelerators of LA remodelling with standardized beta-coefficients of 0.17 and 0.28 for changes in LAVmax, and 0.18 and 0.38 for changes in LAVmin, respectively. Left ventricular (LV) systolic function, diameter, and mass were also significant accelerators of LA remodelling. Changes in both LAVmax and LAVmin were significantly associated with incident AF [n = 46, ΔLAVmax: HR = 1.06 (1.03-1.09), P < 0.001 and ΔLAVmin: HR = 1.14 (1.10-1.18), P < 0.001, per 1 mL/m2 increase] and HF [n = 27, ΔLAVmax: HR = 1.08 (1.04-1.12), P < 0.001 and ΔLAVmin: HR = 1.13 (1.09-1.18), P < 0.001, per 1 mL/m2 increase].
Conclusion:
Both maximal and minimal LA volume increase over time. Clinical accelerators included age and AF. LV structure and systolic function also accelerate LA remodelling. LA remodelling poses an increased risk of clinical outcomes.
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