<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0003-3170</journal-id>
<journal-title><![CDATA[Angiología]]></journal-title>
<abbrev-journal-title><![CDATA[Angiología]]></abbrev-journal-title>
<issn>0003-3170</issn>
<publisher>
<publisher-name><![CDATA[Arán Ediciones S.L.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0003-31702023000600002</article-id>
<article-id pub-id-type="doi">10.20960/angiologia.00494</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Influencia del estrés oxidativo en la evolución de la aterosclerosis carotídea]]></article-title>
<article-title xml:lang="en"><![CDATA[Impact of oxidative stress on the progression of carotid atherosclerosis]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Río-Solá]]></surname>
<given-names><![CDATA[Mª Lourdes del]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Losa-Rodríguez]]></surname>
<given-names><![CDATA[Rita]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Aguirre-Gervás]]></surname>
<given-names><![CDATA[Beatriz]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Gonzalo-Benito]]></surname>
<given-names><![CDATA[Hugo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital Clínico Universitario de Valladolid Servicio de Angiología, Cirugía Vascular y Endovascular ]]></institution>
<addr-line><![CDATA[Valladolid ]]></addr-line>
<country>España</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Hospital Santiago Apóstol Servicio de Análisis Clínicos ]]></institution>
<addr-line><![CDATA[Burgos ]]></addr-line>
<country>España</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Hospital Clínico Universitario de Valladolid Servicio de Análisis Clínicos ]]></institution>
<addr-line><![CDATA[Valladolid ]]></addr-line>
<country>España</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Instituto de Ciencias de la Salud de Castilla y León  ]]></institution>
<addr-line><![CDATA[Valladolid ]]></addr-line>
<country>España</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2023</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2023</year>
</pub-date>
<volume>75</volume>
<numero>6</numero>
<fpage>349</fpage>
<lpage>361</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_arttext&amp;pid=S0003-31702023000600002&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_abstract&amp;pid=S0003-31702023000600002&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://scielo.isciii.es/scielo.php?script=sci_pdf&amp;pid=S0003-31702023000600002&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción y objetivo: el estrés oxidativo (EO) ha demostrado una clara influencia en el desarrollo de las placas de ateroma por los daños provocados en el endotelio vascular. El objetivo de este trabajo es realizar un estudio de los principales marcadores de estrés oxidativo en pacientes con enfermedad aterosclerótica de la arteria carótida como signo de vulnerabilidad, analizar la implicación de la situación redox y el estado metabólico mitocondrial en la patología aterosclerótica de la arteria carótida y su relación con la clínica neurológica.  Pacientes y métodos: se estudiaron las placas de ateroma obtenidas de pacientes intervenidos de endarectomía carotídea (asintomáticos y sintomáticos) en el Servicio de Angiología, Cirugía Vascular y Endovascular del Hospital Clínico Universitario de Valladolid en el año 2020. Se recogieron variables clínicas y demográficas y la existencia de sintomatología neurológica. Las características anatómicas y hemodinámicas se estudiaron mediante estudio eco Doppler y angiografía mediante tomografía computarizada (CTA) en el preoperatorio. Se analizaron las placas de ateroma como estimadores del grado de peroxidación lipídica que reflejaron el estado redox. Se ha estimado un tamaño muestral de 45 muestras en cada grupo, con una tasa de pérdidas de seguimiento del 5 %. Se estudiaron las diferencias entre los grupos mediante &#967;2 y la t de Student para determinar la relación entre el potencial redox con las características morfológicas de la placa de ateroma. Se utilizó el programa estadístico SPSS 27.0, aceptando como significativo un valor p &lt; 0,05.  Resultados: las placas de ateroma calcificadas mostraron mayor capacidad antioxidante con respecto a las placas de ateroma no calcificadas en el parámetro ABTS: 2,2-ácino-bis(ácido 3-etilbenzotiazolina-6-sulfónico) (2635,08 frente a 2803,28). La relación es estadísticamente significativa (p = 0,007). También mostraron mayor defensa antioxidante tanto cuando se analizó la actividad de la catalasa (160,73 frente a 175,13) y la actividad SOD (1,11 frente a 1,49; p = 0,049). En el estudio del metabolismo energético de las placas carotídeas de ateroma objetivamos que los niveles de lactato fueron mayores en las placas no calcificadas (11,45 frente a 8,57; p = 0,001). Los niveles plasmáticos de ácido úrico (1,48 frente a 2,33) y la actividad de la catalasa (146,79 frente a 176,81) fueron significativamente más elevados en los pacientes con sintomatología neurológica (p = 0,001 y 0,025, respectivamente).  Conclusiones: las placas homogéneas de ateroma y calcificadas de la arteria carótida presentan mayor capacidad y defensa antioxidante que las placas de ateroma no calcificadas y heterogéneas. Los pacientes con sintomatología neurológica presentaron placas de ateroma con menor capacidad y defensas antioxidantes que los pacientes asintomáticos neurológicos.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction and objective: oxidative Stress (OS) has proven to have a clear impact on the development of atherosclerotic plaques due to the damage it causes to vascular endothelium. The aim of this study is to conduct a research on key oxidative stress markers in patients with carotid artery atherosclerotic disease as a sign of vulnerability, analyze the implications of the redox status and mitochondrial metabolic state in carotid artery atherosclerotic disease, and its relationship with neurological clinical presentation.  Patients and methods: atherosclerotic plaques obtained from carotid endarterectomy patients (both asymptomatic and symptomatic) performed the Department of Angiology, Vascular and Endovascular Surgery of Hospital Clínico Universitario de Valladolid, Spain in 2020 will be examined. The clinical-demographic variables and the presence of neurological symptoms will be recorded. Anatomical and hemodynamic characteristics will be studied using Doppler ultrasound and coronary computed tomography angiography (CCTA) preoperatively. Atherosclerotic plaques will be analyzed as estimators of the degree of lipid peroxidation showing the redox state. A sample size of 45 speciments from each group has been estimated with a loss to follow-up rate of 5 %. Inter-group differences will be studied using the chi-square and Student&#8217;s t tests to establish the relationship between redox potential and morphological characteristics of the atheromatous plaque. SPSS 27.0 statistical software will be used, with a significance level set at p &lt; 0.05.  Results: calcified atherosclerotic plaques showed higher antioxidant capacity compared to non-calcified plaques in the ABTS parameter (2,2-azino-bis(3-ethylbenzthioziozline-6-sulfonic)) (2635.08 vs 2803.28), with statistically significant relationship (p = 0.007). They also exhibited greater antioxidant defense when analyzing catalase activity (160.73 vs 175.13) and SOD activity (1.11 vs 1.49) (p = 0.049). In the study of the energy metabolism of carotid atherosclerotic plaques, it was observed that lactate levels were higher in non-calcified plaques (11.45 vs 8.57) (p = 0.001). Plasma levels of uric acid (1.48 vs. 2.33) and catalase activity (146.79 vs 176.81) were significantly higher in patients with neurological symptoms (p = 0.001 and p = 0.025, respectively).  Conclusions: homogeneous and calcified carotid artery atherosclerotic plaques exhibit higher antioxidant capacity and defense compared to non-calcified and heterogeneous plaques. Patients with neurological symptoms showed atherosclerotic plaques with lower antioxidant capacity and defenses compared to asymptomatic neurological patients.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Estrés oxidativo]]></kwd>
<kwd lng="es"><![CDATA[Carótida]]></kwd>
<kwd lng="es"><![CDATA[Ictus]]></kwd>
<kwd lng="es"><![CDATA[Aterosclerosis]]></kwd>
<kwd lng="en"><![CDATA[Oxidative stress]]></kwd>
<kwd lng="en"><![CDATA[Carotid]]></kwd>
<kwd lng="en"><![CDATA[Stroke]]></kwd>
<kwd lng="en"><![CDATA[Atherosclerosis]]></kwd>
</kwd-group>
</article-meta>
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