Arrhythmias
Luuk H.G.A Hopman
PhD Student
Department of Cardiology, Amsterdam UMC
Amsterdam, Noord-Holland, Netherlands
Luuk H.G.A Hopman
PhD Student
Department of Cardiology, Amsterdam UMC
Amsterdam, Noord-Holland, Netherlands
Irene M. Frenaij, MD
Cardiologist
Amsterdam University Medical Centers- Location VUmc, Netherlands
Jose Alonso Solis-Lemus, PhD
Post-doctoral Research Associate
King's College London
London, England, United Kingdom
Sulayman El Mathari, MD
MD
Amsterdam University Medical Centers - Location Amc, Netherlands
Mark J. Mulder, MD
MD
Amsterdam UMC, Netherlands
Pranav Bhagirath, MD, PhD
Clinical research fellow
Guy's and St Thomas' NHS Foundation Trust, United Kingdom
Steven A. Niederer, PhD
Professor
King's College London, United Kingdom
Cornelis P. Allaart, MD, PhD
Professor
Amsterdam UMC
Amsterdam, Noord-Holland, Netherlands
Marco J. Götte, MD, PhD
MD, PhD
Department of Cardiology, Amsterdam UMC, Vrije Universiteit Amsterdam, Amsterdam Cardiovascular Sciences, De Boelelaan 1118, 1081 HV Amsterdam, The Netherlands
Amsterdam, Noord-Holland, Netherlands
Left atrial (LA) fibrosis is considered to be a key driver to the initiation and perpetuation of atrial fibrillation (AF). In histological studies evaluating atrial fibrosis, LA appendage (LAA) tissue is often used as a surrogate marker to research structural remodeling in the entire LA. However, it is unclear whether the fibrosis content assessed in LAA samples accurately represents fibrosis content of the LA-body.
In recent years, late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) imaging has matured as a clinical applicable, non-invasive tool to identify the degree of atrial fibrosis and therefore can be used to evaluate LAA and LA-body fibrosis separately.
The objective of this study was to evaluate the relation between LAA and LA-body fibrosis content using 3D LGE-CMR.
Methods:
Data from 47 AF patients scheduled for a first pulmonary vein isolation (PVI) procedure were retrospectively analyzed. Prior to PVI, all patients underwent a CMR scan including an ECG gated free-breathing 3D contrast-enhanced MR angiogram (CE-MRA) and inversion recovery prepared gradient echo pulse sequence to acquire high resolution 3D LGE images. Using CEMRG software (King’s College, London, UK), the LA including LAA was semi-automatically segmented on the 3D CE-MRA, which provides a high contrast for identifying the LA and LAA endocardium. Subsequently, the 3D CE-MRA was co-registered with the 3D LGE images. A 3D reconstruction was generated (Figure panel A) allowing to calculate separately the volume (ml) and fibrosis extent (%) of the entire LA (‘LA-body’) and LAA, respectively. LA-body fibrosis extent was compared to LAA fibrosis extent using a paired samples T-test and Pearson correlation.
Results:
Mean LA-body fibrosis extent was significantly higher than LAA fibrosis extent (29.80 ± 14.15% vs. 21.62 ± 12.08%, p< 0.001) (Figure panel B). The correlation between LA-body fibrosis extent and LAA fibrosis extent was high (r=0.74, p< 0.001) (Figure panel C). Volume of the LA-body segmentation was 107.21 ± 28.96ml and volume of the LAA segmentation was 6.89 ± 4.34ml. For both the LA-body volume and LAA volume, no relation with the extent of fibrosis was found (r=-0.02, p=0.90 and r=-0.26, p=0.08, respectively).
Conclusion:
The strong correlation between LA-body and LAA fibrosis as assessed by 3D LGE-CMR supports that in histological studies, LAA fibrosis could be used as a clinical useful surrogate to investigate LA tissue characteristics in AF patients. However, histological analysis of the LAA may still misrepresent AF disease state, as the amount of LAA fibrosis was found to be on average one third lower than the amount of LA-body fibrosis. More research combining non-invasive CMR-based tissue characterization, invasive mapping techniques, and atrial appendage histology is required to determine whether the LAA is a decent surrogate for the assessment of LA structural remodeling in patients suffering from AF.