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Risk Factors in Cardiovascular Health: Focusing on Environmental Contaminants
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Risk Factors in Cardiovascular Health: Focusing on Environmental Contaminants

A special issue of Journal of Cardiovascular Development and Disease (ISSN 2308-3425). This special issue belongs to the section "Epidemiology, Lifestyle, and Cardiovascular Health".

Deadline for manuscript submissions: 30 August 2026 | Viewed by 368

Special Issue Editor

Prof. Dr. Ewa Konduracka

E-Mail Website
Guest Editor
Department of Coronary Disease and Heart Failure, Jagiellonian University Medical College, John Paul II Hospital, 31-202 Krakow, Poland
Interests: impact of environmental pollution on human health; cardio-oncology; heart failure; diabetes; atherosclerosis and its complications; cardiogenic shock and intensive care

Special Issue Information

Dear Colleagues,

Despite significant advances in pharmacotherapy, interventional techniques, and the growing public awareness of preventive measures, cardiovascular diseases remain the leading cause of mortality worldwide. Among the numerous cardiovascular risk factors, increasing attention is being directed toward the substantial impact of environmental pollution on cardiovascular health. Environmental contaminants often contribute to the onset and progression of cardiovascular disorders by modifying and accelerating classical risk factors.

We invite authors to submit original research articles, review papers, and experimental studies that explore the relationship between exposure to environmental pollutants—both organic and inorganic chemical substances—as well as noise pollution and cardiovascular diseases. Submissions addressing mechanistic pathways, epidemiological evidence, preventive strategies, and public health implications are particularly encouraged.

Topics of Interest Include (but are not limited to):

  1. Cardiovascular effects of air, food, water, and soil pollution
  2. Exposure to organic and inorganic chemicals
  3. Noise pollution and its impact on cardiovascular risk
  4. Environmental stressors, oxidative stress, and endothelial dysfunction, coagulation disturbances
  5. Links between environmental exposure and hypertension, atherosclerosis, stroke, arrhythmias, and heart failure
  6. Preventive cardiology and public health strategies in the context of environmental risk

Prof. Dr. Ewa Konduracka
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Cardiovascular Development and Disease is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cardiovascular complications
  • environmental contaminants
  • oxidative stress
  • endothelial dysfunction
  • coagulation disturbances

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (1 paper)

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Research

14 pages, 7744 KB  
Article
Effect of Perfluorooctanesulfonic Acid on Fibrin Clot Properties and Thrombin Generation: Linking Environmental Pollution with Cardiovascular Diseases
by Jakub Kuciński, Krzysztof Krawczyk, Konrad Kieca, Aleksander Siniarski, Michał Ząbczyk and Ewa Konduracka
J. Cardiovasc. Dev. Dis. 2026, 13(5), 209; https://doi.org/10.3390/jcdd13050209 - 13 May 2026
Viewed by 188
Abstract
Perfluorooctanesulfonic acid (PFOS) is a persistent organic pollutant linked in epidemiological studies to increased coronary artery disease (CAD) risk, higher LDL-cholesterol, hypertension, and other adverse outcomes. However, the mechanisms by which PFOS affects cardiovascular physiology, particularly coagulation, remain insufficiently understood. We evaluated the [...] Read more.
Perfluorooctanesulfonic acid (PFOS) is a persistent organic pollutant linked in epidemiological studies to increased coronary artery disease (CAD) risk, higher LDL-cholesterol, hypertension, and other adverse outcomes. However, the mechanisms by which PFOS affects cardiovascular physiology, particularly coagulation, remain insufficiently understood. We evaluated the ex vivo effects of PFOS on fibrin clot structure and thrombin generation in platelet-poor plasma (PPP) and citrated whole blood from ten healthy volunteers (five women, aged 27–32 years; mean serum PFOS: 2.63 ± 0.85 μg/L). PPP samples were incubated with PFOS at 50, 200, and 400 μg/L. Assays included calibrated automated thrombogram, clot permeability (Ks), clot lysis time (CLT), thromboelastography (400 μg/L), and scanning electron microscopy (SEM). PFOS did not significantly modify endogenous thrombin potential or peak thrombin. In contrast, it reduced Ks and prolonged CLT at 200 and 400 μg/L, indicating impaired fibrinolysis. SEM images confirmed the formation of thinner, tightly packed fibrin fibers with reduced pore size at higher PFOS concentrations. These findings were consistent across dilution models, with only minimal changes observed in low-dilution protocols. Overall, PFOS appears to disrupt fibrin polymerization, generating denser and more fibrinolysis-resistant clots without major effects on thrombin generation. Such alterations may promote a prothrombotic state and predispose exposed individuals to clinically relevant thrombotic events, including myocardial infarction and stroke. Further studies are required to define the clinical consequences of PFOS-related coagulation abnormalities in exposed populations. Full article
(This article belongs to the Special Issue Risk Factors in Cardiovascular Health: Focusing on Environmental Contaminants)
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