# Does hemolysis matter after pulsed field ablation for atrial fibrillation? Insights from the Best Ablate Registry

**Authors:** Alireza Sepehri Shamloo, Robert Hättasch, Claudius Sebastian Baldauf, Philipp Formum, Toshinori Chiba, Philipp Attanasio, Felix Hohendanner, Nikolaos Dagres, Gerhard Hindricks, Verena Tscholl

PMC · DOI: 10.1016/j.hroo.2025.11.010 · Heart Rhythm O2 · 2025-11-21

## TL;DR

This study investigates whether hemolysis occurs after pulsed field ablation for atrial fibrillation and its potential impact on kidney function.

## Contribution

The study provides new insights into hemolysis and renal outcomes following PFA, using biomarker analysis in a clinical registry.

## Key findings

- PFA caused significant changes in hemolysis biomarkers like LDH and haptoglobin.
- No cases of clinically significant hemolysis or acute kidney injury were observed.
- Myocardial injury and lesion burden were linked to hemolysis biomarker changes.

## Abstract

Pulsed field ablation (PFA) has emerged as a novel nonthermal modality for atrial fibrillation (AF) ablation, offering tissue selectivity and procedural safety. However, emerging data have raised concerns about hemolysis-related biomarker shifts and potential renal failure after PFA.

This study aimed to evaluate biomarker-defined hemolysis and the incidence of acute renal injury after PFA in patients undergoing AF.

In this prospective observational study, 84 patients with paroxysmal or persistent AF undergoing PFA using either the Affera or PulseSelect system were enrolled. Paired venous blood samples were obtained before and 24 hours after the procedure. Biomarkers of hemolysis (lactate dehydrogenase [LDH], haptoglobin, hemoglobin, and bilirubin), renal function parameters (serum creatinine, urea, and electrolytes), and cardiac enzymes (high-sensitivity cardiac troponin, N-terminal pro-B-type natriuretic peptide) were systematically analyzed. Clinically significant hemolysis was defined as a postprocedural haptoglobin concentration of <0.04 g/L or a combination of indirect bilirubin of >1.5 times baseline and LDH more than twice baseline. Multivariable linear regression and mediation analyses were performed to identify procedural predictors of biomarker changes and explore the potential mediating role of myocardial injury.

Significant postprocedural changes were observed in biomarkers of hemolysis, including a reduction in haptoglobin (−0.17 ± 0.21 g/L; P < .001), an increase in LDH (+43.32 ± 79.98 U/L; P < .001), and bilirubin concentrations (P < .001). No patient met the predefined criteria for clinically significant hemolysis. Acute kidney injury stage 1, without oliguria, was observed in 3 patients (3.6%). Cardiac biomarker analysis revealed a substantial rise in high-sensitivity troponin (+1151.7 ± 750.8 ng/L; P < .001), whereas N-terminal pro-B-type natriuretic peptide decreased significantly after ablation (P < .001). The total number of PFA applications independently predicted changes in both LDH and haptoglobin.

In our study, PFA for AF was associated with an increase in hemolytic parameters, without significant short-term renal impact or occurrence of clinically significant hemolysis. Hemolysis seems to be influenced by both lesion burden and myocardial injury, highlighting the need for further investigation into the long-term clinical relevance of biomarker-defined hemolysis in PFA-treated patients.

## Linked entities

- **Proteins:** HB1 (hemoglobin 1)
- **Diseases:** atrial fibrillation (MONDO:0004981), acute kidney injury (MONDO:0002492)

## Full-text entities

- **Genes:** HAVCR1 (hepatitis A virus cellular receptor 1) [NCBI Gene 26762] {aka CD365, HAVCR, HAVCR-1, KIM-1, KIM1, TIM}, HP (haptoglobin) [NCBI Gene 3240] {aka HP2ALPHA2, HPA1S}, LCN2 (lipocalin 2) [NCBI Gene 3934] {aka 24p3, MSFI, NGAL, p25}
- **Diseases:** left (MESH:D018487), ischemic attack (MESH:D002546), Kidney Disease (MESH:D007674), hemolytic anemia (MESH:D000743), myocardial and hemolytic injury (MESH:D009202), thromboembolic (MESH:D013923), stroke (MESH:D020521), coronary artery disease (MESH:D003324), AKI (MESH:D058186), Cardiac injury (MESH:D006331), pericardial effusion (MESH:D010490), mitral regurgitation (MESH:D008944), pericardial tamponade (MESH:D002305), Hemolysis (MESH:D006461), Complications (MESH:D008107), atrial appendage thrombus (MESH:D013927), hypertension (MESH:D006973), Chronic kidney disease stage 2 or 3 (MESH:D015451), renal failure (MESH:D051437), oliguria (MESH:D009846), AF (MESH:D001281), end-stage renal disease (MESH:D007676), femoral vein pseudoaneurysms (MESH:D017541), diabetes mellitus (MESH:D003920), tubular injury (MESH:D000230), LDH (MESH:C538133)
- **Chemicals:** fentanyl (MESH:D005283), piritramide (MESH:D010892), propofol (MESH:D015742), heparin (MESH:D006493), creatinine (MESH:D003404), Cardiac enzymes (-), potassium (MESH:D011188), sodium (MESH:D012964), bilirubin (MESH:D001663), urea (MESH:D014508)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12925781/full.md

## References

15 references — full list in the complete paper: https://tomesphere.com/paper/PMC12925781/full.md

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Source: https://tomesphere.com/paper/PMC12925781