ArticleHeliyon2024
Association of lipopolysaccharide with new-onset atrial fibrillation in ST-segment elevation myocardial infarction.
Article in Heliyon, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- Gut-heart axis disruption and LPS translocation: driving atrial fibrillation through inflammatory storm and fibrotic mechanisms.Frontiers in endocrinology · 2026Review
- Impact of gut microbiome on atrial fibrillation: Mechanistic insights and future directions in individualized medicine.World journal of cardiology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Lipopolysaccharide (LPS) is related to various cardiovascular diseases. However, the relationship between LPS and new-onset atrial fibrillation (NOAF) after ST-segment elevation myocardial infarction (STEMI) has yet to be elucidated. This study aimed to evaluate the impact of LPS on NOAF in STEMI patients. Methods: This was a single-center retrospective observational study including 806 patients diagnosed with STEMI. LPS levels were determined using a commercial ELISA kit. NOAF was characterized by postadmission AF with the absence of any prior history of AF. Results: A total of 806 participants were enrolled, with 752 individuals in the non-AF group (93.3%) and 54 individuals in the AF group (6.7%). Multivariable analysis showed that LPS (OR = 1.047; 95% CI: 1.029-1.065, P < 0.001) was an independent risk marker for NOAF. The analysis of the ROC demonstrated that LPS had an AUC of 0.717 in predicting NOAF. When LPS was added to the conventional model, the ability of the risk model to discriminate and reclassify NOAF was improved significantly (IDI 0.053, P = 0.001; NRI 0.510, P < 0.001). Conclusion: Elevated LPS is associated with an increased risk of NOAF in STEMI patients. The integration of LPS can improve the ability to predict NOAF in STEMI patients.
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.