https://doi.org/10.1007/s00392-025-02625-4
1Kerckhoff Klinik GmbH Abteilung für Kardiologie Bad Nauheim, Deutschland; 2Justus-Liebig-Universität Giessen Medizinische Klinik I, Kardiologie Bad Nauheim, Deutschland; 3Universitätsklinikum Gießen und Marburg GmbH Medizinische Klinik I - Kardiologie und Angiologie Gießen, Deutschland
Background and aims: It is well known that atrial fibrillation (AF) can affect left ventricular (LV) function not only in heart failure (HF) patients but also in patients with previously normal cardiac function. However, the mechanism underlying this effect is not fully understood. While there is a huge body of evidence supporting AF-induced fibrosis in the left atrium (LA), data on LV fibrosis and inflammation are sparse and contradictory. This study was designed to compare tissue characteristics of LV fibrosis and inflammation by cardiac magnetic resonance imaging (CMR) in patients with and without AF in a large, all-comers cohort.
Methods: Patients enrolled in a single-center CMR registry were divided into those with AF and those without. The presence of AF was adjudicated by two investigators blinded to the imaging results. Native T1 and extracellular volume (ECV), as markers of LV fibrosis, and T2, as an indicator of myocardial inflammation, were measured on a 3.0 T scanner. Volumetric and tissue parameters were compared between groups. Means were controlled for baseline differences in LV ejection fraction (LV-EF), LV end-systolic volume (LV-ESVi), and late gadolinium enhancement (LGE) mass (% myocardium). The presence of AF and CMR parameters were checked for their prognostic significance regarding the combined primary endpoint of all-cause mortality and hospitalization for HF after one year by multivariate cox regression analysis.
Results: From April 2017 to May 2023, 2.879 patients were enrolled in the registry and completed the one-year follow-up. Of those, 590 had a history of AF. AF patients had a lower LV-EF and a higher LV-ESVi and LGE mass. When controlled for baseline differences in LV-EF, LV-ESVi, and LGE mass, AF patients had significantly higher native T1 (p=0.006), T2 (p=0.01), and ECV (p<0,001). 85 patients reached the primary endpoint. In a multivariable model with functional parameters and variables for tissue characterization only T1 remained a significant prognosticator.
Conclusions: Our data suggest that ventricular fibrosis and inflammation is associated with AF-induced left ventricular dysfunction. Future prospective observational studies are warranted to confirm these results.