RT info:eu-repo/semantics/article
T1 Redox imbalance and metabolic stress in carotid atherosclerosis: Associations with symptomatology and plaque calcification
A1 Río Sola, María Lourdes del
A1 Pérez Fernández, Sandra
A1 Gonzalo Benito, Hugo
A1 Losa Rodríguez, Rita
K1 Carotid atherosclerosis
K1 Oxidative stress
K1 Antioxidant defenses
K1 Lipid peroxidation
K1 Mitochondrial metabolism
K1 Stroke
K1 Plaque vulnerability
K1 3213 Cirugía
AB Background and aims: Oxidative stress (OS) is a central driver of atherosclerosis, yet its role in carotid plaquevulnerability and neurological symptoms remains insufficiently defined. This study aimed to comprehensivelycharacterize the redox and metabolic profiles of carotid plaques and evaluate their associations with plaquecalcification and clinical symptomatology in patients undergoing carotid endarterectomy.Methods and results: Ninety-two patients were prospectively enrolled. Patients were classified as symptomatic orasymptomatic according to recent neurological events, and plaques were categorized as calcified or non-calcifiedbased on preoperative angio-CT. Excised tissue was analyzed for total antioxidant capacity (FRAP, ABTS),enzymatic defenses (catalase, superoxide dismutase [SOD]), oxidative damage markers (8-hydroxy-2′-deoxy-guanosine [8-OHdG], malondialdehyde + 4-hydroxy-2-nonenal [MDA + HNE]), uric acid, and lactate. Non-calcified plaques exhibited reduced antioxidant activity (ABTS: 2635.08 vs. 2803.28 μM, p = 0.007), lowerSOD activity (1.11 vs. 1.49 U/mL, p = 0.049), and higher lactate levels (11.45 vs. 8.57 mg/dL, p = 0.001),indicating metabolic instability. Symptomatic patients showed higher uric acid (p = 0.001), reduced SOD (p =0.009), and increased lipid peroxidation, while FRAP and ABTS did not differ significantly. The two analyticalaxes did not fully overlap, as 75 % of non-calcified and 60 % of calcified plaques derived from symptomaticpatients (p = 0.235).Conclusion: Carotid plaques associated with symptoms and lacking calcification displayed redox imbalance andmetabolic dysfunction, suggesting a more biologically active and rupture-prone phenotype. Importantly, thesefindings support the integration of tissue oxidative biomarkers with clinical and imaging data to refine stroke riskstratification, guide secondary prevention, and improve postoperative surveillance strategies.
PB Elsevier
SN 0939-4753
YR 2025
FD 2025
LK https://uvadoc.uva.es/handle/10324/80084
UL https://uvadoc.uva.es/handle/10324/80084
LA eng
NO Nutrition, Metabolism and Cardiovascular Diseases, 2025, p. 104423
NO Producción Científica
DS UVaDOC
RD 01-dic-2025