ArticleJournal of thrombosis and thrombolysis2024
Elevated plasma protein carbonylation increases the risk of ischemic cerebrovascular events in patients with atrial fibrillation: association with a prothrombotic state.
Article in Journal of thrombosis and thrombolysis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Protein carbonylation as a modulator of fibrin clot properties in thyroid disorders: impact of therapy.Journal of thrombosis and thrombolysis · 2026Article
- Fibrinogen Oxidation and Thrombosis: Shaping Structure and Function.Antioxidants (Basel, Switzerland) · 2025Review
- The Interplay Between Carotid Intima-Media Thickness and Selected Serum Biomarkers in Various Stages of Chronic Kidney Disease.Biomedicines · 2025Article
- Letter to the editor to ''Elevated plasma protein carbonylation increases the risk of ischemic cerebrovascular events in patients with atrial fibrillation: association with a prothrombotic state''.Journal of thrombosis and thrombolysis · 2025Article
- Post-translational modifications of fibrinogen: implications for clotting, fibrin structure and degradation.Molecular biomedicine · 2024Review
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Authors and funding
5 authors.
Funding
Abstract
introductionPlasma protein carbonylation that reflects oxidative stress has been demonstrated to be associated with the prothrombotic fibrin clot phenotype. However, the role of protein carbonyls (PC) in predicting ischemic stroke in atrial fibrillation (AF) is largely unknown. This study aimed to investigate whether PC increase the risk of stroke in anticoagulated AF patients during follow-up.
methodsIn 243 AF patients on anticoagulation (median age 69 years; median CHA
resultsPlasma PC levels (median, 3.16 [2.54-3.99] nM/mg protein) at baseline showed positive associations with age (P < 0.001), CHA
conclusionOur findings suggest that in patients with AF enhanced protein carbonylation is associated with increased "residual" risk of stroke despite anticoagulation, which is at least in part due to unfavorably altered fibrin clot phenotype.
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Registered trials
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