Rapid Fire Abstracts
Julia Treiber, MD
senior physician
Kerckhoff Klinik, Germany
Jan Sebastian Wolter
physician
Kerckhoff-Klinik, Germany
Sören Backhaus, MD
Consultant Cardiologist
Department of Cardiology, Heart Centre, Kerckhoff-Clinic Bad Nauheim, Germany
Thomas Neumann, MD
senior physician
kerckhoff clinik Bad Nauheim, Germany
Malte Kuniss, MD
senior physician
kerckhoff clinic Bad Nauheim, Germany
Jörg Yogarajah, MD
physician
kerckhoff clinic Bad Nauheim, Germany
Till Keller, MD
physician
Kerckhoff-Klinik, Germany
Samuel Sossalla, MD
chief medical officer
Kerckhoff Klinik, Germany
Andreas Rolf, MD
Senior Cardiologist
Kerckhoff Klinikum Bad Nauheim, Germany
Andreas Rolf, MD
Senior Cardiologist
Kerckhoff Klinikum Bad Nauheim, Germany
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 function. Yet 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.
Purpose: To compare tissue characteristics of LV fibrosis by CMR in patients with and without AF in a large single center all comer cohort.
Methods:
Patients from a large single center CMR registry were divided into no AF and AF patients. Presence of AF was adjudicated by two doctors blinded to the imaging results. Native T1 and extracellular volume (ECV) as markers of LV fibrosis as well as T2 as indicator of myocardial inflammation were measured on a 3.0T Siemens Skyra scanner. Volumetric and tissue parameters were compared between groups. Means were controlled for baseline differences in EF, endsystolic volume (ESVi) and LGE mass (% myocardium).
Results:
From April 2017 to May 2023 2879 patients were enrolled in the registry and completed one-year follow-up. Of those 590 had a history of paroxysmal AF. AF patients had lower EF, higher ESVi and more LGE mass ( EF 52 ± 15 vs 48 ± 16, p = 0.001; ESVi 46 ± 31 vs 50 ± 31, p = 0.007; LGE mass 4 ± 6 vs 5 ± 8, p = 0.001). Controlled for baseline differences in EF, ESVi and LGE mass AF patients had significantly higher native T1, T2 and ECV. (T1 1130 ± 65 vs 1138 ± 128, p =0.006; ECV 0.262 ± 0.1 vs. 0.272 ± 0.2, p < 0.001; T2 38.7 ± 3.6 vs 39.3 ± 7.2, p = 0.01).
Conclusion:
Our data suggest that fibrosis and inflammation may play an active role in AF induced heart failure. Future prospective observation studies are warranted to confirm these results.
