ArticlePloS one2020
Controlling the thickness of the atherosclerotic plaque by statin medication.
Article in PloS one, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 12 citations in OpenAlex.
- Oncometabolites and Hypoxia-Regulated Exosomes Shape HIF-Driven Macrophage Programs Across Type 2 Diabetes, Atherosclerosis, and Cancer.International journal of molecular sciences · 2026Review
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- Ectopic lipid deposition in kidney diseases: mechanisms in specific cell types and therapeutic strategies.Frontiers in endocrinology · 2026Review
- Analysis of carotid atherosclerotic plaque characteristics using optical coherence tomography.Neurosurgical review · 2025Article
- The Interplay Between Carotid Intima-Media Thickness and Selected Serum Biomarkers in Various Stages of Chronic Kidney Disease.Biomedicines · 2025Article
- The association between basilar artery wall thickness and posterior circulation ischemic stroke: insights from high-resolution vascular wall imaging in subclinical atherosclerosis.Frontiers in neurology · 2025Article
- Effect of Lipid Composition on the Atheroprotective Properties of HDL-Mimicking Micelles.Pharmaceutics · 2022Article
- The Mutual Contribution of 3-NT, IL-18, Albumin, and Phosphate Foreshadows Death of Hemodialyzed Patients in a 2-Year Follow-Up.Antioxidants (Basel, Switzerland) · 2022Article
- A biomathematical model of atherosclerosis in mice.PloS one · 2022Article
- Recognized and Potentially New Biomarkers-Their Role in Diagnosis and Prognosis of Cardiovascular Disease.Medicina (Kaunas, Lithuania) · 2021Review
- Management of High-Risk Atherosclerotic Patients by Statins May Be Supported by Logistic Model of Intima-Media Thickening.Journal of clinical medicine · 2021Article
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atherosclerosis, a chronic inflammatory disorder of the arterial wall, is a complex process whose dynamics are affected by multiple factors. The disease control consists of restraining it by administering statins. Slowing down or halting the plaque growth depends on the patient age at which the statin treatment begins and on the thickness of the intima-media (IMT) at that time. In this paper, we propose a mathematical model to estimate the sets of atherosclerosis states, from which the use of statins can restrain the disease. Our model is control-theoretic, and the estimated sets are the viability kernels, in the parlance of viability theory. To our best knowledge, this way of modelling the atherosclerosis progression is original. We compute two viability kernels, each for a different statin-treatment dose. Each kernel is composed of the vector [age, IMT] from which the disease can be restrained. By extension, the disease can't be restrained from the kernel complements, this being mainly because of the disease and patient-age advancement. The kernels visualise tradeoffs between early and late treatments, which helps the clinician to decide when to start the statin treatment and which statin dose may be sufficient.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.