# Rhythm control in persistent atrial fibrillation improves endothelial function without uniform anti-inflammatory effects: A 9-month prospective cohort study

**Authors:** Maximilian Seidel, David Bogdahn, Felix S. Seibert, Moritz Anft, Sarah Skrzypczyk, Ulrik Stervbo, Eva Kohut, Kamil Rosiewicz, Benjamin Sasko, Christian Ukena, Nina Babel, Timm H. Westhoff

PMC · DOI: 10.1016/j.ijcha.2026.101879 · International Journal of Cardiology. Heart & Vasculature · 2026-01-23

## TL;DR

Controlling heart rhythm in patients with persistent atrial fibrillation improves blood vessel function, but does not consistently reduce inflammation.

## Contribution

This study shows that endothelial function improves after rhythm control in atrial fibrillation without uniform anti-inflammatory effects.

## Key findings

- Endothelial function, measured by FMD, improved significantly after successful rhythm control therapy.
- Inflammatory markers showed mixed responses, with some decreasing and others increasing over time.
- Hemodynamic normalization appears to be the main driver of vascular health improvement.

## Abstract

•Rhythm control in atrial fibrillation improves endothelial function.•Endothelial recovery occurs without consistent anti-inflammatory effects.•Inflammatory cytokines show heterogeneous patterns after rhythm control therapy.•Improvement in vascular health appears driven by hemodynamic normalization.

Rhythm control in atrial fibrillation improves endothelial function.

Endothelial recovery occurs without consistent anti-inflammatory effects.

Inflammatory cytokines show heterogeneous patterns after rhythm control therapy.

Improvement in vascular health appears driven by hemodynamic normalization.

Atrial fibrillation (AF) is associated with systemic inflammation, endothelial dysfunction, and adverse cardiovascular outcomes. While there is robust evidence, that inflammation contributes to AF pathogenesis, the existence of a reverse relation – whether AF contributes to inflammation − remains elusive. This study therefore evaluates the impact of rhythm control on systemic inflammation and endothelial function.

In this prospective observational study, 124 patients with persistent AF undergoing successful rhythm control therapy (electrical cardioversion or catheter ablation) were followed for nine months. Various Cytokines, high-sensitivity C-reactive protein (hsCRP), flow-mediated dilation (FMD) and additional inflammatory biomarkers were measured at baseline, 1 week, 1 month, 3 months, and 9 months. FMD was assessed by high-resolution brachial artery ultrasound. Patients with AF recurrence throughout the follow-up period were excluded from primary analysis.

In patients without AF recurrence, FMD improved significantly from 6.3 % (4.6–8.3) to 7.6 % (5.1–8.8) (p < 0.001). HsCRP, IL-8 and fibrinogen declined modestly (p = 0.002, p < 0.001 and p < 0.001, respectively), whereas IL-2, IP-10, IL-12p70, MCP-1 and TNF-α increased significantly over time (all p < 0.001). Elevated pre-treatment hsCRP was weakly associated with AF recurrence (r = 0.20, p = 0.023; AUC = 0.61). IL-6 showed temporal variation but no sustained change from baseline.

Rhythm control therapy in persistent AF is associated with an improvement of endothelial function but not with a homogeneous improvement of systemic inflammatory serological profiles. Thus, the improvement in FMD appears to be mediated primarily by hemodynamic restoration rather than anti-inflammatory effects.

## Linked entities

- **Proteins:** CXCL8 (C-X-C motif chemokine ligand 8), IL2 (interleukin 2), CXCL10 (C-X-C motif chemokine ligand 10), CCL2 (C-C motif chemokine ligand 2), TNF (tumor necrosis factor), IL6 (interleukin 6)
- **Diseases:** atrial fibrillation (MONDO:0004981)

## Full-text entities

- **Genes:** FGB (fibrinogen beta chain) [NCBI Gene 2244] {aka HEL-S-78p}, CRP (C-reactive protein) [NCBI Gene 1401] {aka PTX1}, IL2 (interleukin 2) [NCBI Gene 3558] {aka IL-2, TCGF, lymphokine}, IL6 (interleukin 6) [NCBI Gene 3569] {aka BSF-2, BSF2, CDF, HGF, HSF, IFN-beta-2}, CXCL10 (C-X-C motif chemokine ligand 10) [NCBI Gene 3627] {aka C7, IFI10, INP10, IP-10, SCYB10, crg-2}, CCL2 (C-C motif chemokine ligand 2) [NCBI Gene 6347] {aka GDCF-2, HC11, HSMCR30, MCAF, MCP-1, MCP1}, TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, CXCL8 (C-X-C motif chemokine ligand 8) [NCBI Gene 3576] {aka GCP-1, GCP1, IL8, LECT, LUCT, LYNAP}
- **Diseases:** AF (MESH:D001281), inflammation (MESH:D007249), endothelial dysfunction (MESH:D014652)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

35 references — full list in the complete paper: https://tomesphere.com/paper/PMC12860693/full.md

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Source: https://tomesphere.com/paper/PMC12860693