ArticleCardiology research2020
Paroxysmal Atrial Fibrillation: Insight Into the Intimate Mechanisms of Coagulation.
Article in Cardiology research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04947657 (Correlation Of CoAGulation Biomarkers and Atrial Fibrillation Burden in Patients Post Catheter Ablation), which is not on this map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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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.
Correlation Of CoAGulation Biomarkers and Atrial Fibrillation Burden in Patients Post Catheter Ablation: the COAG-AF Pilot Study
Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Oral anticoagulant therapy for patients with new-onset atrial fibrillation following acute myocardial infarction: A narrative review.Frontiers in cardiovascular medicine · 2022Pooled it
- Factor XI Inhibitors in Atrial Fibrillation: Insights and Implications from Recent Trials.Advances in therapy · 2026Review
- Characterization of Biomarkers of Thrombo-Inflammation in Patients with First-Diagnosed Atrial Fibrillation.International journal of molecular sciences · 2024Article
- Beneficial Effect of Edoxaban on Preventing Atrial Fibrillation and Coagulation by Reducing InflammationFrontiers in pharmacology · 2022Article
- Vascular Endothelial Dysfunction and Immunothrombosis in the Pathogenesis of Atrial Fibrillation.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisArticle
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAtrial fibrillation (AF) is a hypercoagulable state. However, the intimate mechanisms leading to impaired coagulation and the timing of their activation are unclear. The aim of the study was to investigate the factors that initiate the coagulation cascade in the early hours (up to 48 h) of clinical manifestation of paroxysmal atrial fibrillation (PAF).
methodsTissue factor (TF) level, coagulation activity of factor VII (FVIIa), factor XII (FXIIa) and factor XI (FXIa) were measured in plasma of 51 non-anticoagulated patients (26 men and 25 women, aged 59.84 ± 11.42 years) and 52 controls (26 men and 26 women, aged 59.50 ± 10.53 years) by enzyme-linked immunoassays and kinetic assays.
resultsTF was higher in the PAF group (268.63 ± 90.62 pg/mL vs. 170.21 ± 66.19 pg/mL, P < 0.001) as well as FVIIa (170.82±59.39% vs. 95.17±37.90%, P < 0.001), FXIIa (218.31±84.04% vs. 148.41±53.94%, P < 0.001) and FXIa (178.41±55.94% vs. 111.75±37.33%, P < 0.001). Regression analysis showed that in the first 6 h of the disease, increase in time led to increase in FXIIa (r = 0.25, P < 0.05), FXIa (r = 0.75, P < 0.05), TF level (r = 0.25, P < 0.05) and FVIIa (r = 0.25, P < 0.05).
conclusionHemocoagulation changes were observed even < 6 h after the onset of the disease. They suggest that PAF has an early tendency for hypercoagulability, with the involvement of the intrinsic and extrinsic pathways of coagulation.
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