11th Edition

World Heart Congress

THEME: "Empowering Hearts, Empowering Lives: Shaping the Future of Cardiovascular Health"

img2 12-13 Oct 2026
img2 Bali, Indonesia
Mariann Gyöngyösi

Mariann Gyöngyösi

Medical University of Vienna, Austria

Title: Increased levels of circulating oxidative stress biomarkers in patients with Long COVID syndrome

Biography

Mariann Gyöngyösi is Professor of Internal Medicine and Cardiology at the Department of Cardiology, Medical University of Vienna (MUW), Austria, and holds an honorary doctorate (Honoris Causa) from Semmelweis University, Budapest, Hungary. Born in Hungary, she has held Austrian citizenship since 2002.

She completed her medical education and specialist training in internal medicine and cardiology at Albert Szent-Györgyi Medical University in Szeged, Hungary, and earned her Ph.D. in 1995. She obtained her habilitation at the Medical University of Vienna in 2002 and has been a Fellow of the European Society of Cardiology since 2006.

Her postdoctoral training includes fellowships at Goethe University Frankfurt (formerly JWG University), supported by prestigious programs such as the Eötvös Fellowship, Tempus Individual Mobility Grant, Pfeiffer Fellowship, INSERM Fellowship (France), and the European Society of Cardiology Training and Research Fellowship.

Professor Gyöngyösi has received numerous honors, including awards from the Austrian Society of Cardiology, the Billroth Prize, the Best Manuscript Award from Circulation Research, and the Paul Dudley White International Scholar Award of the American Heart Association (2023 and 2024).

She has been the recipient of six European Union grants, along with numerous unrestricted research grants. Her research and clinical interests focus on interventional cardiology, cell- and gene-based therapies, and long COVID.

She has authored 285 original research articles and 11 book chapters, with an h-index of 53 and more than 9,500 citations.

Abstract

Background: Multiorgan involvement in long COVID has been linked to chronic stress conditions and redox imbalance, characterized by increased oxidative stress, which may help explain the wide range of symptoms.

Methods: Patients with long COVID syndrome (defined according to the Delhi Consensus 2021) (n = 126) from the POSTCOV Registry (EC 1008/2021 and 1758/2022; NCT05398952) were prospectively included in this biomarker study. Circulating blood levels of six oxidative stress biomarkers—total oxidant capacity (TOC), total antioxidant capacity (TAC), peroxidase activity (EPA), polyphenols (PPm), autoantibodies against oxidized LDL (oLAB), and serotonin—were compared with those of age- and sex-matched healthy controls (n = 42) who were anti-spike protein pan-negative (i.e., no prior COVID-19 vaccination or SARS-CoV-2 infection). TOC, TAC, EPA, PPm, and oLAB were measured using commercially available microtiter plate assays, while serotonin levels were determined by ELISA.

Results: Long COVID patients were divided into three subgroups (n = 42 each) based on their dominant clinical manifestations: cardiovascular (CV), pulmonary (PU), or neuropsychiatric (NEU). Among the redox parameters, TAC was significantly decreased in long COVID patients compared with controls (1.65 ± 0.51 vs 1.91 ± 0.56 mmol/L) and was similarly reduced across all subgroups (CV: 1.63 ± 0.43, PU: 1.72 ± 0.51, NEU: 1.60 ± 0.56 mmol/L). A trend toward higher TOC levels was observed in long COVID patients compared with controls (0.068 ± 0.057 vs 0.063 ± 0.046 mmol/L), although this did not reach statistical significance. oLAB levels were higher in long COVID patients (821 ± 621 vs 641 ± 593 mU/mL), with a significant increase observed in the PU subgroup (917 ± 613 mU/mL). Trend toward increased EPA was noted across all long COVID subgroups but did not reach significance. A non-significant decrease in serotonin levels was observed in long COVID patients and across all subgroups compared to controls.

Conclusions: This study reveals, for the first time, a complex dysregulation of oxidative homeostasis in patients with long COVID. This imbalance may impair mitochondrial function and energy metabolism, potentially contributing to persistent, multisystem symptoms and long-term disease.