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Updated: Aug 16, 2025

Estimating Bilateral Atrial Function by Cardiovascular Magnetic Resonance Feature Tracking in Patients with Paroxysmal Atrial Fibrillation
Published on: July 20, 2022
Cardiovascular Magnetic Resonance Imaging-Based Right Atrial Strain Analysis of Cardiac Amyloidosis
Jan Eckstein1, Vanessa Sciacca2, Hermann Körperich1
1Institute for Radiology, Nuclear Medicine and Molecular Imaging, Heart and Diabetes Center North Rhine Westphalia, University of Bochum, 32545 Bad Oeynhausen, Germany.
Insights
Magnetic resonance imaging (MRI) can quantify right atrial strain (RAS) and strain rate (RASR) to help differentiate cardiac amyloidosis (CA) from hypertrophic cardiomyopathy (HCM). These MRI measures show impaired right atrial function in CA patients, aiding diagnosis.
Area of Science:
- Cardiology
- Medical Imaging
- Cardiac Physiology
Background:
- Cardiac amyloidosis (CA) presents as a hypertrophic phenotype, mimicking hypertrophic cardiomyopathy (HCM), which complicates diagnosis and delays treatment.
- The diagnostic utility of magnetic resonance imaging (MRI) in quantifying right atrial strain (RAS) and strain rate (RASR) for differentiating CA and HCM is not well-established.
Purpose of the Study:
- To assess diagnostic differences in longitudinal RAS and RASR between CA, HCM, and control subjects (CTRL).
- To investigate the impact of atrial fibrillation (AF) on right atrial function in CA patients.
- To evaluate the potential for diagnostic overlap using RAS and RASR in tricuspid regurgitation (TR) patients.
Main Methods:
- Quantification of RAS and RASR using MRI feature-tracking in biopsy-confirmed CA patients (including subtypes), CTRL, HCM, and TR patients.
- Comparison of strain parameters between groups.
- Post hoc analysis to identify intergroup differences and assess diagnostic performance (AUC).
Main Results:
- Significant differentiation (p < 0.001) in reservoir, conduit, and booster RAS and RASRs was observed between CA and HCM, and between CA and CTRL.
- Booster and reservoir RAS and RASRs demonstrated reliable diagnostic performance (AUC > 0.8).
- CA patients with AF showed significantly impaired reservoir and booster RAS/RASR compared to those in sinus rhythm. Discriminative power for CA vs. TR was insufficient (p = 0.069). Differentiation between CA subtypes was not achievable.
Conclusions:
- MRI-derived RAS and RASR are impaired in CA patients.
- These parameters may support noninvasive differentiation between CA, HCM, and CTRL.
- Atrial function assessment via RAS/RASR in CA is affected by atrial fibrillation.
Abstract:
Background: Cardiac amyloidosis (CA) manifests in a hypertrophic phenotype with a poor prognosis, making differentiation from hypertrophic cardiomyopathy (HCM) challenging and delaying early treatment. The extent to which magnetic resonance imaging (MRI) quantifies the right atrial strain (RAS) and strain rate (RASR), providing valuable diagnostic information, is not yet clinically established. Aims: This study assesses diagnostic differences in the longitudinal RAS and RASR between CA and HCM patients, control subjects (CTRL) and CA subtypes in addition to the impact of atrial fibrillation (AF) on the right atrial function in CA patients. The RAS and RASR of tricuspid regurgitation (TR) patients are used to assess the potential for diagnostic overlap. Methods: RAS and RASR quantification was conducted via MRI feature-tracking for biopsy-confirmed CA patients with subtypes identified. Strain parameters were compared for CTRL, HCM and TR patients. Post hoc testing identified intergroup differences. Results: In total, 41 CA patients were compared to 47 CTRL, 20 HCM and 31 TR patients. Reservoir (R), conduit and booster RAS and RASRs allow for significant differentiation (p < 0.001) between CA and HCM patients (R: 10.6 ± 14.3% vs. R: 33.5 ± 16.3%) and CTRL (R: 44.6 ± 15.7%). Booster and reservoir RAS and RASRs qualified as reliable diagnostic tests (AUC > 0.8). CA patients with AF, in contrast to sinus rhythm, demonstrated a significantly impaired reservoir RAS and RASR and booster RASR. The discriminative power of RAS for CA vs. TR was insufficient (R: 10.6% ± 14.3% vs. 7.0% ± 6.0%, p = 0.069). Differentiation between 21 transthyretin and 20 light-chain amyloidosis subtypes was not achievable (R: 0.7% ± 1.0% vs. 0.7% ± 1.0%, p = 0.827). Conclusion: The MRI-derived RAS and RASR are impaired in CA patients and may support noninvasive differentiation between CA, HCM and CTRL.
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