ArticleLife (Basel, Switzerland)2024
A Blood Supply Pathophysiological Microcirculatory Mechanism for Long COVID.
Article in Life (Basel, Switzerland), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Microvascular Dynamics: Insights and Applications.Life (Basel, Switzerland) · 2026Article
- Persistent Redox Imbalance in Post-COVID-19 Syndrome: Lipid Peroxidation, Antioxidant Enzyme Depletion, and Reduced Nitric Oxide Availability in an Amazonian Population.Antioxidants (Basel, Switzerland) · 2026Article
- Unraveling the cardiovascular burden of long COVID: symptom profiles, underlying mechanisms, and clinical management insights.Frontiers in cardiovascular medicine · 2026Review
- Analysis of Cytological Markers of Cellular Senescence in High-Risk Cardiovascular Patients After COVID-19.BioMed research international · 2026Article
- Lessons from irritable bowel syndrome: potential for understanding and managing post-COVID.Frontiers in immunology · 2026Review
- Long COVID Mechanisms, Microvascular Effects, and Evaluation Based on Incidence.Life (Basel, Switzerland) · 2025Review
- Automated Foveal Avascular Zone Segmentation in Optical Coherence Tomography Angiography Across Multiple Eye Diseases Using Knowledge Distillation.Bioengineering (Basel, Switzerland) · 2025Article
- A Coupled Model of the Cardiovascular and Immune Systems to Analyze the Effects of COVID-19 Infection.Biotech (Basel (Switzerland)) · 2025Article
- Overview of Inflammatory and Coagulation Markers in Elderly Patients with COVID-19: Retrospective Analysis of Laboratory Results.Life (Basel, Switzerland) · 2025Article
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1 author.
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Abstract
backgroundThe term "Long COVID" is commonly used to describe persisting symptoms after acute COVID-19. Until now, proposed mechanisms for the explanation of Long COVID have not related quantitative measurements to basic laws. In this work, a common framework for the Long COVID pathophysiological mechanism is presented, based on the blood supply deprivation and the flow diffusion equation.
methodsCase-control studies with statistically significant differences between cases (post-COVID patients) and controls, from multiple tissues and geographical areas, were gathered and tabulated. Microvascular loss (ML) was quantified by vessel density reduction (VDR), foveal avascular zone enlargement (FAZE), capillary density reduction (CDR), and percentage of perfused vessel reduction (PPVR). Both ML and hemodynamic decrease (HD) were incorporated in the tissue blood supply reduction (SR) estimation.
resultsML data were found from 763 post-COVID patients with an average VDR, FAZE, CDR, and PPVR of 16%, 31%, 14%, and 21%, respectively. The average HD from 72 post-COVID patients was 37%. The estimated SR for multiple tissues with data from 634 post-COVID patients reached a sizeable 47%. This large SR creates conditions of lower mass diffusion rates, hypoxia, and undernutrition, which at a multi-tissue level, for a long time, can explain the wide variety of the Long COVID symptoms.
conclusionsDisruption of peripheral tissue blood supply by the contribution of both ML and HD is proposed here to be the principal cause of the mechanism leading to Long COVID symptoms.
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