ArticleResearch and practice in thrombosis and haemostasis2024
Challenging the current hypothesis that thrombosis is responsible for the post-COVID-19 condition.
Article in Research and practice in thrombosis and haemostasis, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- COVID-19 as a Modifier of Genetically Determined Coagulation Phenotype: Implications for Precision Risk Stratification After Infection.Biochemical genetics · 2026Observational
- Cardiovascular sequelae of Long COVID: immune dysregulation inflammation as central drivers.Frontiers in immunology · 2026Review
- Applicability and adaptation of cognitive behavior therapy for long COVID neuropsychiatric symptoms: a review with insights from ME/CFS.BMC infectious diseases · 2025Review
- Reported particles are not blood clots, so anticoagulant drugs are not a plausible treatment.Research and practice in thrombosis and haemostasis · 2024Article
- Fibrinaloid microclots in long COVID: assessing the actual evidence properly.Research and practice in thrombosis and haemostasis · 2024Article
- Superficial Vein Thrombosis in an Asymptomatic Case of Cholangiocarcinoma with Recent History of COVID-19.Life (Basel, Switzerland) · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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Abstract
People with the post-COVID-19 condition suffer symptoms that persist beyond 12 weeks following acute COVID-19 infection. Fatigue, shortness of breath, and cognitive dysfunction ("brain fog") are common. Scientists, clinicians, and patients debate the pathophysiology. One pathophysiological hypothesis is that prothrombotic changes associated with acute COVID-19 persist, causing clots that lead to symptoms. This theory, arising from a research team in South Africa and supported by a paper in Nature Medicine, has been widely disseminated on social media and entered the public narrative as a cause of the post-COVID-19 condition. We describe the development of this theory, examine the findings of a Cochrane review that critically appraises the "microclot" beliefs, and critically appraise the influential study relating clotting biomarkers to cognitive deficits. We conclude the inferences for the hypothesis are not based on evidence, unlicensed use of antithrombotic medication is not justified, and apheresis should not be considered outside of a well-designed clinical trial.
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