ArticleEuropean heart journal open2021
Vitamin K antagonist use induces calcification and atherosclerotic plaque progression resulting in increased hypercoagulability.
Article in European heart journal open, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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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
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- The Role of Micronutrients in Atherosclerosis: Mechanisms and Clinical Application.Journal of cellular and molecular medicine · 2025Review
- Protease-activated receptors in vascular smooth muscle cells: a bridge between thrombo-inflammation and vascular remodelling.Cell communication and signaling : CCS · 2025Review
- Platelet biology and function: plaque erosion vs. rupture.European heart journal · 2024Review
- Direct Oral Anticoagulants as the First Choice of Anticoagulation for Patients with Peripheral Artery Disease to Prevent Adverse Vascular Events: A Systematic Review and Meta-Analysis.Journal of cardiovascular development and disease · 2023Review
Corrections and comments
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Authors and funding
11 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aims: Vascular calcification is a hallmark of atherosclerotic burden and can predict the cardiovascular outcome. Vitamin K antagonists (VKA) are widely used anticoagulant drugs to treat patients at risk of arterial and venous thrombosis but are also associated with increase vascular calcification progression. We aim to unravel the paradox that VKA suppresses plasma coagulation but promotes vascular calcification and subsequent atherosclerosis-dependent coagulability of the vessel wall. Methods and results: Conclusions: Oral anticoagulation with VKA aggravates vascular calcification and atherosclerosis. VSMC phenotype differentiation impacts coagulation potential in a TF-dependent manner. VKA-induced vascular calcification increases hypercoagulability and could thereby potentially positively affect atherothrombosis.
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Registered trials
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