# The Relationship Between Blood Parameters and Gastrointestinal Bleeding in Atrial Fibrillation Patients Receiving Oral Anticoagulants

## TL;DR

This study explores how blood markers can predict gastrointestinal bleeding in patients with atrial fibrillation who take blood thinners.

## Contribution

The study identifies specific inflammatory markers that may help predict gastrointestinal bleeding in patients on different types of anticoagulants.

## Key findings

- Inflammatory indices like NLR and PLR are elevated in patients on NOACs who experience GI bleeding.
- Hypoalbuminemia and elevated urea are linked to bleeding in patients on warfarin.
- HAS-BLED scores are higher in patients who experience GI bleeding, unlike CHA2DS2-VASc scores.

## Abstract

Background/Objectives: Atrial fibrillation (AF) is a prevalent cardiac arrhythmia associated with significant morbidity, including stroke, heart failure, and increased mortality, necessitating oral anticoagulant (OAC) therapy to reduce thromboembolic risk. However, OACs, including warfarin and non-vitamin K antagonist oral anticoagulants (NOACs), increase the risk of gastrointestinal (GI) bleeding, a serious complication requiring precise risk stratification in the emergency department (ED). Methods: This retrospective cohort study was conducted in the Emergency Department of Balikesir University Hospital in Turkey between 2019 and 2023 and evaluates systemic inflammatory markers as predictors of GI bleeding in AF patients receiving OACs. A total of 155 patients were divided into case (GI bleeding) and control (no GI bleeding) groups, comparing demographics, comorbidities, CHA2DS2-VASc and HAS-BLED scores, and inflammatory indices (uric acid/albumin ratio, neutrophil-to-lymphocyte ratio [NLR], platelet-to-lymphocyte ratio [PLR], systemic immune inflammation index [SII]). Results: For patients receiving NOACs, the case group exhibited significantly higher uric acid/albumin ratio, NLR, PLR, and SII (p < 0.05). For patients receiving warfarin, only the uric acid/albumin ratio was significantly elevated (p < 0.001). Hypolipidemia and elevated uric acid were associated with bleeding risk in patients receiving NOACs, while hypoalbuminemia and elevated urea predicted bleeding in patients receiving warfarin. HAS-BLED scores were significantly higher in bleeding groups, unlike CHA2DS2-VASc scores. Conclusions: These findings suggest that inflammatory indices, particularly in patients taking NOACs, are associated with GI bleeding risk stratification. Integrating these biomarkers into clinical practice could optimize personalized anticoagulation strategies, reducing morbidity and mortality in AF patients.