Estrés oxidativo en la aterosclerosis carotídea y biomarcadores pronósticos relacionados en el desarrollo de ictus
A direct consequence of atherosclerotic disease is the development of stroke. However, the natural evolution of atherosclerotic lesions with the same degree of stenosis is completely different in symptomatic patients (with a greater risk of recurrence) than in asymptomatic patients. This implies the...
| Autor: | |
|---|---|
| Tipo de recurso: | tesis doctoral |
| Estado: | Versión publicada |
| Fecha de publicación: | 2024 |
| País: | España |
| Institución: | Universidad de Valladolid |
| Repositorio: | UVaDOC. Repositorio Documental de la Universidad de Valladolid |
| OAI Identifier: | oai:uvadoc.uva.es:10324/67803 |
| Acceso en línea: | https://doi.org/10.35376/10324/67803 https://uvadoc.uva.es/handle/10324/67803 |
| Access Level: | acceso abierto |
| Palabra clave: | Cardiovascular, aparato Enfermedades Atherosclerosis Aterosclerosis Oxidative Stress Estrés oxidativo Vulnerable plaque Placa vulnerable 3207.04 Patología Cardiovascular |
| Sumario: | A direct consequence of atherosclerotic disease is the development of stroke. However, the natural evolution of atherosclerotic lesions with the same degree of stenosis is completely different in symptomatic patients (with a greater risk of recurrence) than in asymptomatic patients. This implies the existence of two types of carotid disease: a stable form (unlikely to produce stroke) and an unstable form (not necessarily more stenotic) with a high risk of producing symptoms. Oxidative stress has shown a clear influence on the development of atheromatous plaques through damage to the vascular endothelium. The aim of this work is to analyze the implication of the redox situation in atherosclerotic pathology, its relationship with plaque vulnerability and the presence of neurological symptoms. For this purpose, a prospective observational study was carried out in which samples of patients who underwent carotid thromboendarterectomy in the Angiology and Vascular Surgery Department of the Hospital Clínico Universitario de Valladolid who met NASCET criteria in 2020 were analyzed. Methodologically, a descriptive analysis of the clinical-demographic characteristics and the presence of neurological symptoms was performed. An ultrasound study and computed tomography angiography were performed to determine the anatomical and hemodynamic characteristics of the atheromatous plaque preoperatively to establish the degree of carotid stenosis. Related serum biomarkers were determined, including lipid profile parameters, uric acid, markers of inflammation and tissue hypoperfusion. In conjunction, oxidative stress markers were measured in atheroma plaque for the assessment of antioxidant capacity (FRAP, ABTS and uric acid), antioxidant defenses (superoxide dismutase and catalase), oxidative damage (lipid peroxidation and DNA damage) and mitochondrial energy dysfunction (lactate). Analysis of serum biomarkers reveals differences in uric acid determination, finding significantly higher levels in patients with non-calcified and vulnerable plaques. The analysis of oxidative stress markers in atheroma plaque reveals that calcified atheroma plaques have greater antioxidant capacity in the ABTS parameter (p=0.007) and FRAP, while uric acid levels behave inversely; greater antioxidant defense in the measurement of superoxide dismutase activity (p=0.049) and catalase activity; less oxidative damage in DNA damage and lipid peroxidation, and less oxidative damage in DNA damage and lipid peroxidation. Our study provides insight into the underlying oxidative stress state of carotid atheroma plaque, providing complete information on the stroke risk of a patient with carotid stenosis regardless of the degree of stenosis. The results explain why non-calcified atheroma plaques are highly vulnerable and more likely to develop neurological complications. This is the first study to demonstrate a relationship between the involvement of oxidative stress, with a large number of biomarkers in atheroma plaque, and the development of stroke in atherosclerotic patients. |
|---|