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          "es" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modificaci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en pacientes VHC con presencia y ausencia de placa de ateroma&#46;</p>"
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    "textoCompleto" => "<span class="elsevierStyleSections"><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Introducci&#243;n</span><p id="par0005" class="elsevierStylePara elsevierViewall">La infecci&#243;n cr&#243;nica por el virus de la hepatitis C &#40;VHC&#41; es un problema de salud global&#46; La prevalencia mundial es de aproximadamente 71 millones de personas infectadas&#44; lo que representa 399&#46;000 muertes cada a&#241;o&#46; En Espa&#241;a&#44; el VHC afecta a casi 500&#46;000 personas&#44; aunque esta prevalencia se ha modificado en los &#250;ltimos a&#241;os desde el uso de las nuevas terapias libres de interfer&#243;n<a class="elsevierStyleCrossRefs" href="#bib0155"><span class="elsevierStyleSup">1&#44;2</span></a>&#46;</p><p id="par0010" class="elsevierStylePara elsevierViewall">La infecci&#243;n por VHC es una de las principales causas de enfermedad hep&#225;tica cr&#243;nica y de carcinoma hepatocelular&#44; pero tambi&#233;n se asocia a manifestaciones extrahep&#225;ticas e importantes alteraciones metab&#243;licas<a class="elsevierStyleCrossRefs" href="#bib0165"><span class="elsevierStyleSup">3&#44;4</span></a>&#46; Recientemente se ha informado del aumento de ateromatosis subcl&#237;nica y de una mayor incidencia de eventos cardiovasculares en pacientes con VHC<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">5&#44;6</span></a>&#46; Algunos estudios muestran que la infecci&#243;n cr&#243;nica por VHC es un factor de riesgo independiente para la ateromatosis carot&#237;dea&#44; enfermedad coronaria y accidente cerebrovascular&#59; sin embargo&#44; los resultados de los diferentes trabajos son poco concluyentes<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">7-11</span></a>&#46;</p><p id="par0015" class="elsevierStylePara elsevierViewall">La infecci&#243;n por VHC aumenta la secreci&#243;n de citoquinas proinflamatorias y modifica la actividad del sistema inmunol&#243;gico&#46; Este estado inflamatorio sostenido puede promover la aterog&#233;nesis en pacientes infectados<a class="elsevierStyleCrossRef" href="#bib0210"><span class="elsevierStyleSup">12</span></a>&#46; Adem&#225;s&#44; es conocido que el VHC y la enfermedad hep&#225;tica provocan una modificaci&#243;n de los l&#237;pidos y de las lipoprote&#237;nas&#44; sobre todo de la apolipoprote&#237;na B&#44; utiliz&#225;ndolos como hu&#233;sped para su replicaci&#243;n y difusi&#243;n&#46; El VHC circula unido a las lipoprote&#237;nas de baja densidad &#40;LDL&#41; y a las lipoprote&#237;nas de muy baja densidad &#40;VLDL&#41;&#44; e interacciona con los receptores celulares de las LDL atravesando la pared de las arterias<a class="elsevierStyleCrossRef" href="#bib0215"><span class="elsevierStyleSup">13</span></a>&#46; Estudios in vivo demuestran ARN del VHC colonizando y reproduci&#233;ndose en las placas de ateroma ricas en colesterol<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">14&#44;15</span></a>&#46; Este riesgo cardiovascular puede verse incrementado por otros trastornos asociados al VHC&#44; como son la hiperhomocisteinemia&#44; la hipoadiponectinemia y sobre todo la resistencia a la insulina&#46; A pesar de la falta de consenso en ciertos aspectos sobre la relaci&#243;n entre la infecci&#243;n por el VHC y la formaci&#243;n de placas de ateroma&#44; la enfermedad cardiovascular es un problema emergente en los pacientes infectados por este virus<a class="elsevierStyleCrossRefs" href="#bib0230"><span class="elsevierStyleSup">16-20</span></a>&#46; Por lo tanto&#44; aunque actualmente existen tratamientos antivirales efectivos para curar la infecci&#243;n viral&#44; es necesario comprender mejor c&#243;mo la infecci&#243;n por VHC influye en el riesgo cardiovascular&#46; En este estudio&#44; se ha investigado si el VHC es un factor de riesgo independiente de ateromatosis subcl&#237;nica&#44; si existen diferencias en el perfil lip&#237;dico de los pacientes infectados con o sin placas de ateroma&#44; as&#237; como su asociaci&#243;n con la carga viral y la progresi&#243;n de la enfermedad hep&#225;tica medida por el grado de fibrosis&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">Pacientes y m&#233;todos</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Dise&#241;o del estudio y pacientes</span><p id="par0020" class="elsevierStylePara elsevierViewall">En este estudio observacional y transversal se incluyeron pacientes ambulatorios con infecci&#243;n cr&#243;nica por VHC &#40;VHC-positivos&#41; y pacientes sin infecci&#243;n &#8212;grupo control&#8212; &#40;VHC-negativos&#41; seguidos en 2 hospitales universitarios entre marzo de 2015 y junio de 2016&#46; El grupo con VHC-positivo estaba formado por pacientes con infecci&#243;n cr&#243;nica por VHC serol&#243;gicamente confirmada &#40;es decir&#44; positivo para anticuerpos anti-VHC y carga viral detectable&#41; de cualquier genotipo y grado de fibrosis hep&#225;tica&#46; Estos pacientes fueron reclutados en las Unidades de Hepatolog&#237;a de los hospitales universitarios Arnau de Vilanova y Santa Mar&#237;a de Lleida&#59; y entraron en el estudio antes de iniciar tratamiento con antivirales de acci&#243;n directa &#40;AAD&#41;&#46; El grupo control incluy&#243; pacientes con VHC negativos y riesgo cardiovascular moderado-bajo &#40;&#237;ndice SCORE<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>5&#37;&#44; tablas SCORE European Low Risk Chart&#41;<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a>&#44; procedentes de una unidad de riesgo cardiovascular donde se realiza ecograf&#237;a arterial para el diagn&#243;stico de ateromatosis subcl&#237;nica &#40;Unidad de Detecci&#243;n y Tratamiento de Enfermedades Aterotromb&#243;ticas &#91;UDETMA&#93; del Hospital Universitario Arnau de Vilanova de Lleida&#41;&#46; Los criterios de exclusi&#243;n para ambos grupos incluyeron&#58; <span class="elsevierStyleItalic">1&#41;</span> edad &#60;<span class="elsevierStyleHsp" style=""></span>30 o &#62;<span class="elsevierStyleHsp" style=""></span>75 a&#241;os&#59; <span class="elsevierStyleItalic">2&#41;</span> cirrosis descompensada&#59; <span class="elsevierStyleItalic">3&#41;</span> presencia de carcinoma hepatocelular u otros tumores&#59; <span class="elsevierStyleItalic">4&#41;</span> enfermedad hep&#225;tica cr&#243;nica no VHC &#40;por alcohol&#44; virus hepatitis B&#44; patolog&#237;a autoinmune o por dep&#243;sito de hierro&#41;&#59; <span class="elsevierStyleItalic">5&#41;</span> infecci&#243;n por VIH&#59; <span class="elsevierStyleItalic">6&#41;</span> enfermedad inflamatoria o infecciosa aguda o cr&#243;nica&#59; <span class="elsevierStyleItalic">7&#41;</span> antecedentes de eventos cardiovasculares previos seg&#250;n la Clasificaci&#243;n Internacional de Enfermedades&#44; 10&#46;<span class="elsevierStyleSup">a</span> revisi&#243;n &#40;ICD10-CM&#41; &#91;a&#41; enfermedad cerebrovascular&#58; ataque isqu&#233;mico transitorio y&#47;o accidente cerebrovascular estable&#59; b&#41; enfermedad card&#237;aca isqu&#233;mica&#58; infarto agudo de miocardio&#44; angina de pecho inestable&#44; arritmias y&#47;o insuficiencia card&#237;aca congestiva&#59; c&#41; enfermedad arterial perif&#233;rica de las extremidades inferiores o aneurisma a&#243;rtico&#93;&#59; <span class="elsevierStyleItalic">8&#41;</span> insuficiencia renal cr&#243;nica &#40;ecuaci&#243;n CKD-EPI<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>60<span class="elsevierStyleHsp" style=""></span>ml&#47;min&#47;1&#44;73 m<span class="elsevierStyleSup">2</span>&#41;&#59; <span class="elsevierStyleItalic">9&#41;</span> diagn&#243;stico de diabetes mellitus&#59; <span class="elsevierStyleItalic">10&#41;</span> pacientes con dislipidemia tratados con hipolipemiantes&#59; <span class="elsevierStyleItalic">11&#41;</span> antecedentes de hipertensi&#243;n arterial &#40;HTA&#41; en tratamiento&#46;</p><p id="par0025" class="elsevierStylePara elsevierViewall">Todos los pacientes firmaron un consentimiento informado antes de entrar en el estudio&#44; que fue aprobado por el comit&#233; de &#233;tica de los 2 hospitales involucrados&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Datos cl&#237;nicos y anal&#237;ticos</span><p id="par0030" class="elsevierStylePara elsevierViewall">Los datos cl&#237;nicos fueron recogidos en una entrevista estandarizada en la visita de seguimiento de consultas&#46; Se utilizaron muestras de sangre en ayunas para medir los siguientes par&#225;metros s&#233;ricos&#58; glucosa&#44; colesterol total &#40;CT&#41;&#44; colesterol LDL y HDL&#44; triglic&#233;ridos &#40;TG&#41;&#44; creatinina y prote&#237;na C reactiva &#40;PCR&#41;&#46; Se calcularon los coeficientes lip&#237;dicos&#58; colesterol no HDL &#40;colesterol total<span class="elsevierStyleHsp" style=""></span>&#8722;<span class="elsevierStyleHsp" style=""></span>colesterol HDL&#41;&#44; TG&#47;HDL colesterol &#40;indicador de resistencia a la insulina&#41; y CT&#47;HDL colesterol &#40;&#237;ndice aterog&#233;nico&#41;&#44; realizando todas las determinaciones en el mismo laboratorio&#46; Las mediciones antropom&#233;tricas &#40;peso y altura&#41; para el c&#225;lculo del &#237;ndice de masa corporal &#40;IMC&#41; y la presi&#243;n arterial se registraron en la UDETMA antes de realizar la ecograf&#237;a arterial&#46; La presi&#243;n arterial sist&#243;lica y diast&#243;lica se midi&#243; en 3 ocasiones en posici&#243;n sedestaci&#243;n&#44; y tras 10<span class="elsevierStyleHsp" style=""></span>min de reposo&#44; utilizando un oscil&#243;metro autom&#225;tico &#40;OMRON HEM-705 CP<span class="elsevierStyleSup">&#174;</span>&#41;&#46; Se registr&#243; la media de las 2 &#250;ltimas mediciones&#46; Los pacientes tambi&#233;n fueron clasificados de acuerdo con su historial de tabaquismo como fumadores&#44; exfumadores o no fumadores&#46; El riesgo cardiovascular se calcul&#243; utilizando las tablas de riesgo SCORE<a class="elsevierStyleCrossRef" href="#bib0255"><span class="elsevierStyleSup">21</span></a>&#46; En el grupo de pacientes con hepatitis cr&#243;nica&#44; la carga viral de ARN del VHC se analiz&#243; mediante transcripci&#243;n inversa-reacci&#243;n en cadena de la polimerasa &#40;RT-PCR&#41;&#44; con un l&#237;mite de detecci&#243;n de 12<span class="elsevierStyleHsp" style=""></span>UI&#47;ml&#46; Se realiz&#243; elastograf&#237;a de transici&#243;n hep&#225;tica &#40;Fibroscan<span class="elsevierStyleSup">&#174;</span> &#91;FS&#93;&#44; Echosens&#44; Par&#237;s&#44; Francia&#41; para valorar el grado de fibrosis hep&#225;tica clasific&#225;ndolo as&#237;&#58; menor de 7&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; no fibrosis &#40;F0-1&#41;&#59; de 7&#44;6-9&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; fibrosis moderada &#40;F2&#41;&#59; de 9&#44;6-12&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; fibrosis significativa &#40;F3&#41;&#59; y mayor de 12&#44;5<span class="elsevierStyleHsp" style=""></span>KPas&#44; cirrosis hep&#225;tica &#40;F4&#41;&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Evaluaci&#243;n de la ateromatosis arterial subcl&#237;nica</span><p id="par0035" class="elsevierStylePara elsevierViewall">La presencia de placas de ateroma en territorios carot&#237;deo y femoral se determin&#243; usando un ec&#243;grafo General Electric &#40;modelo Vivid-I<span class="elsevierStyleSup">&#174;</span>&#41; con una sonda vascular 12L-RS siguiendo un m&#233;todo estandarizado descrito previamente<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a>&#46; Todas las im&#225;genes fueron capturadas y le&#237;das por un &#250;nico equipo&#44; formado por profesionales previamente acreditados&#46; El coeficiente de kappa para la confiabilidad intraobservador se estableci&#243; en 1&#46; La placa de ateroma se defini&#243; como una estructura focal que sobresale en la luz vascular&#44; o un grosor &#237;ntima-media &#40;GIMc&#41; &#62;<span class="elsevierStyleHsp" style=""></span>1&#44;5<span class="elsevierStyleHsp" style=""></span>mm&#44; de acuerdo con el consenso de Mannheim<a class="elsevierStyleCrossRef" href="#bib0265"><span class="elsevierStyleSup">23</span></a>&#46; Se analizaron 12 territorios vasculares para diagnosticar presencia de placa de ateroma&#58; se exploraron arterias car&#243;tidas &#40;com&#250;n&#44; bifurcaci&#243;n&#44; interna y externa&#41; y arterias femorales &#40;comunes y superficiales&#41; de forma bilateral&#44; utilizando un plano axial y longitudinal&#44; con ultrasonograf&#237;a eco-Doppler en modo B y eco-color&#46; Se defini&#243; ateromatosis subcl&#237;nica como la presencia de una o m&#225;s placas en cualquiera de los territorios estudiados&#46; Se midi&#243; el GIM carot&#237;deo&#44; en el segmento distal de la arteria siendo el valor final la media del territorio carot&#237;deo&#44; en los pacientes sin placas de ateroma&#46;</p></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">An&#225;lisis estad&#237;stico</span><p id="par0040" class="elsevierStylePara elsevierViewall">Las variables categ&#243;ricas se describieron como frecuencia y porcentaje y se compararon usando la prueba de Chi-cuadrado de Pearson&#46; Las variables cuantitativas se describieron como la mediana y el intervalo intercuartil &#40;IQR&#41;&#44; o la media y desviaci&#243;n est&#225;ndar &#40;DE&#41; seg&#250;n su distribuci&#243;n&#46; Las variables distribuidas normalmente se compararon mediante la prueba t de Student&#44; mientras que la prueba no param&#233;trica de Mann-Whitney se utiliz&#243; para comparar variables no normalmente distribuidas&#46; Las variables que muestran diferencias significativas entre los pacientes con y sin placas de ateroma se incluyeron en una regresi&#243;n log&#237;stica m&#250;ltiple condicional por pasos hacia atr&#225;s para predecir la presencia de placas de ateroma&#46; Se utiliz&#243; un an&#225;lisis de las caracter&#237;sticas del operador receptor &#40;ROC&#41; para establecer un l&#237;mite para edad&#44; y se calcul&#243; la presencia de placa seg&#250;n la edad de la poblaci&#243;n a estudio&#44; transformando la variable cuantitativa en variable dicot&#243;mica de acuerdo con los valores de corte obtenidos&#46;</p><p id="par0045" class="elsevierStylePara elsevierViewall">Se estudi&#243; la asociaci&#243;n de las modificaciones del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica por ANOVA y la existencia de correlaci&#243;n entre la carga viral y los l&#237;pidos por R de Spearman&#46; La significaci&#243;n estad&#237;stica se estableci&#243; en un valor &#945; bilateral &#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#44; y todos los an&#225;lisis se realizaron utilizando el software SPSS &#40;IBM Statistics for Windows&#44; versi&#243;n 20&#46;0&#44; Armonk&#44; NY&#58; IBM Corp&#46;&#41;&#46;</p></span></span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Resultados</span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Caracter&#237;sticas de la poblaci&#243;n estudiada</span><p id="par0050" class="elsevierStylePara elsevierViewall">La muestra del estudio incluy&#243; 204 pacientes&#58; 102 en el grupo con VHC positivo y 102 en el grupo control&#46; La <a class="elsevierStyleCrossRef" href="#tbl0005">tabla 1</a> describe los datos cl&#237;nicos y de laboratorio relativos a ambas poblaciones&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0055" class="elsevierStylePara elsevierViewall">Los grupos estudiados no presentaron diferencias estad&#237;sticamente significativas en cuanto a sexo&#44; edad ni historia de tabaquismo&#46; El grupo control present&#243; valores significativamente m&#225;s altos en la mayor&#237;a de los factores de riesgo cardiovasculares tradicionales&#44; incluyendo el IMC&#44; la presi&#243;n arterial sist&#243;lica y diast&#243;lica&#44; y el perfil de l&#237;pidos s&#233;ricos&#46; No se observaron diferencias significativas en cuanto a las cifras de glucosa&#44; triglic&#233;ridos&#44; ni en el coeficiente TG&#47;HDL o indicador de resistencia a la insulina&#44; aunque los niveles fueron en todos los casos superiores en los pacientes control &#40;96&#44;5 vs&#46; 94&#44;2<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;888&#59; 121&#44;5 vs&#46; 102&#44;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;070&#59; y 2&#44;3 vs&#46; 2&#44;1&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;449&#41;&#46; Adem&#225;s&#44; los pacientes control presentaron niveles significativamente superiores de creatinina s&#233;rica&#44; de PCR y de &#237;ndice de riesgo cardiovascular &#40;SCORE&#41;&#44; aunque el riesgo era bajo-moderado en ambos grupos&#46; En los pacientes con infecci&#243;n cr&#243;nica por VHC&#44; casi un 55&#37; presentaba enfermedad hep&#225;tica avanzada &#40;de ellos&#44; el 29&#44;4&#37; cirrosis o fibrosis grado 4 por elastograf&#237;a hep&#225;tica&#41;&#46; Un 67&#44;2&#37; eran genotipo 1&#44; un 6&#44;7&#37; genotipo 2&#44; un 9&#44;7&#37; genotipo 3 y el 16&#44;4&#37; genotipo 4&#46;</p><p id="par0060" class="elsevierStylePara elsevierViewall">El porcentaje de pacientes con ateromatosis fue significativamente mayor en el grupo con VHC positivo que en el grupo control &#40;58&#44;8 vs&#46; 28&#44;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; sin observarse diferencias significativas en el GIM carot&#237;deo medido en los pacientes sin ateromatosis &#40;0&#44;76 vs&#46; 0&#44;89<span class="elsevierStyleHsp" style=""></span>mm&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;18&#41; aunque fue superior en los pacientes infectados&#46; En el grupo control las placas se distribuyeron un 35&#37; en territorio carot&#237;deo&#44; un 23&#44;9&#37; en territorio femoral y un 41&#44;1&#37; en ambos territorios&#44; mientras que en los pacientes infectados con VHC un 45&#44;3&#37; de placas de ateroma se detectaron en car&#243;tidas&#44; un 19&#44;8&#37; en femorales y un 34&#44;9&#37; en ambas &#225;reas vasculares&#46; El n&#250;mero medio de placas de ateroma fue de 2&#44;95 &#40;1-10&#41; en pacientes infectados frente a 2&#44;44 &#40;1-8&#41; en los pacientes no infectados&#46; No se observaron diferencias significativas entre las poblaciones ni por territorio vascular afecto &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;710&#41; ni por el n&#250;mero de placas medio detectado &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;420&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0005">fig&#46; 1</a>&#41;&#46;</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0065" class="elsevierStylePara elsevierViewall">En la <a class="elsevierStyleCrossRef" href="#tbl0010">tabla 2</a> se analizan los factores asociados a la presencia de placa de ateroma en cada una de las poblaciones estudiadas&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><p id="par0070" class="elsevierStylePara elsevierViewall">La presencia de placa de ateroma en ambos grupos &#40;con y sin infecci&#243;n por VHC&#41; se asoci&#243; de forma estad&#237;sticamente significativa al sexo masculino&#44; a cifras superiores de presi&#243;n arterial&#44; a niveles elevados de triglic&#233;ridos&#44; y a un mayor riesgo cardiovascular seg&#250;n las tablas &#40;SCORE&#41;&#46; Respecto a la edad&#44; no se observ&#243; asociaci&#243;n con la presencia de placa de ateroma en los pacientes infectados&#44; mientras que s&#237; que se identific&#243; en el grupo control&#44; de manera que la presencia de placa se asoci&#243; a mayor edad &#40;51&#44;8 a&#241;os en pacientes control sin ateromatosis vs&#46; 67&#44;3 a&#241;os en pacientes control con ateromatosis&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; Respecto al h&#225;bito tab&#225;quico&#44; se detect&#243; asociaci&#243;n en los pacientes con VHC &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;003&#41; siendo m&#225;s frecuente la placa en los pacientes fumadores y&#47;o exfumadores &#40;81&#44;6&#37;&#41;&#59; pero no en los controles &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;499&#41;&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">En cuanto al perfil lip&#237;dico&#44; los pacientes VHC con placa presentaban menores cifras de colesterol HDL &#40;57&#44;6 vs&#46; 50&#44;9<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;023&#41; y mayores niveles de triglic&#233;ridos &#40;89&#44;3 vs&#46; 112&#44;6<span class="elsevierStyleHsp" style=""></span>mg&#47;dl&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;029&#41;&#44; coeficiente TG&#47;HDL &#40;1&#44;7 vs&#46; 2&#44;3&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;026&#41; y coeficiente CT&#47;HDL &#40;3 vs&#46; 3&#44;4&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;035&#41; que los pacientes infectados sin placa&#46; No se ha observado significaci&#243;n de estos factores lip&#237;dicos entre los pacientes controles sin o con presencia de placa de ateroma&#46;</p><p id="par0080" class="elsevierStylePara elsevierViewall">Respecto a los factores virales en los pacientes infectados por VHC&#44; no se detect&#243; asociaci&#243;n entre la presencia de placa y la carga viral cuantificada por ARN &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;936&#41;&#44; pero s&#237; se encontraron diferencias significativas con el grado de fibrosis hep&#225;tica&#44; siendo m&#225;s frecuente la presencia de placa en los pacientes con fibrosis avanzada &#40;F4 sin ateroma 23&#44;8&#37; vs&#46; F4 con ateromatosis 33&#44;3&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;016&#41;&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">Se analiz&#243; la edad&#44; seg&#250;n el an&#225;lisis de la ROC&#44; y la edad superior a 54 a&#241;os fue el mejor valor de corte para predecir la presencia de placas de ateroma &#40;AUC<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;682&#44; error est&#225;ndar<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;039 &#91;IC 95&#37;&#58; 0&#44;6-0&#44;7&#93;&#44; 67&#37; de sensibilidad y 60&#37; de especificidad&#41;&#46; Por debajo de este punto de corte &#40;&#60;<span class="elsevierStyleHsp" style=""></span>54 a&#241;os&#41;&#44; el porcentaje de pacientes con placas de ateroma fue del 57&#37; en el grupo VHC positivo y del 4&#37; en el grupo control &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; En los pacientes con edad mayor o igual a 54 a&#241;os&#44; la ateromatosis aument&#243; hasta un 61&#37; en el grupo con VHC positivo y hasta el 50&#37; en el grupo control&#44; sin observarse diferencias significativas en este tramo de edad entre poblaciones &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;252&#41;&#46; En el grupo con edad menor de 54 a&#241;os&#44; los pacientes con VHC positivo ten&#237;an mucha m&#225;s probabilidad de ateromatosis que el grupo control &#40;OR &#61; 30&#59; IC95&#37;&#58; 6&#44;58-136&#44;67&#59; p &#60; 0&#44;001&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0010">fig&#46; 2</a>&#41;&#46;</p><elsevierMultimedia ident="fig0010"></elsevierMultimedia></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0115">Factores asociados con ateromatosis subcl&#237;nica</span><p id="par0090" class="elsevierStylePara elsevierViewall">La <a class="elsevierStyleCrossRef" href="#tbl0015">tabla 3</a> muestra las caracter&#237;sticas cl&#237;nicas de los pacientes con y sin ateromatosis subcl&#237;nica&#46; La infecci&#243;n cr&#243;nica por VHC se asoci&#243; significativamente a la presencia de ateromatosis subcl&#237;nica&#44; al igual que los factores de riesgo cardiovascular tradicionales como el sexo masculino&#44; la edad avanzada&#44; la presi&#243;n arterial sist&#243;lica&#44; puntuaciones elevadas en el SCORE&#44; los niveles s&#233;ricos bajos de colesterol HDL y m&#225;s elevados de triglic&#233;ridos&#46; Tambi&#233;n se asoci&#243; con valores incrementados del cociente TG&#47;HDL&#46; La presencia de placas de ateroma no se asoci&#243; con el IMC&#44; los niveles de glucosa ni los valores de PCR&#46; Tampoco se observ&#243; asociaci&#243;n con el perfil lip&#237;dico formado por colesterol total&#44; LDL y colesterol no HDL&#44; ni con el &#237;ndice aterog&#233;nico &#40;CT&#47;HDL&#41;&#46;</p><elsevierMultimedia ident="tbl0015"></elsevierMultimedia><p id="par0095" class="elsevierStylePara elsevierViewall">El an&#225;lisis multivariado revel&#243; una probabilidad muy superior de ateromatosis en pacientes con VHC positivo en comparaci&#243;n con el grupo control &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37 &#91;5&#44;5-37&#44;5&#93;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41; &#40;<a class="elsevierStyleCrossRef" href="#tbl0015">tabla 3</a>&#41;&#46; Otros factores de riesgo independientes de ateromatosis subcl&#237;nica incluyeron el sexo masculino&#44; la edad avanzada y el mayor coeficiente TG&#47;HDL o indicador indirecto de resistencia a la insulina&#46; Ni la presi&#243;n arterial sist&#243;lica&#44; ni el perfil lip&#237;dico contribuyeron al modelo predictivo para la presencia de placas de ateroma&#46;</p></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0120">Descripci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en los pacientes con VHC en relaci&#243;n con la presencia de placa de ateroma</span><p id="par0100" class="elsevierStylePara elsevierViewall">Analizamos el perfil lip&#237;dico en los pacientes VHC con y sin enfermedad ateromatosa&#44; teniendo en cuenta el grado de fibrosis hep&#225;tica medida mediante elastograf&#237;a&#46;</p><p id="par0105" class="elsevierStylePara elsevierViewall">En los pacientes VHC sin enfermedad ateromatosa&#44; no observamos diferencias significativas en ninguno de los valores del perfil lip&#237;dico tradicional&#44; ni en los coeficientes indicativos de resistencia a la insulina &#40;TG&#47;HDL&#41; ni en el factor aterog&#233;nico &#40;CT&#47;HDL&#41; &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>a y b&#41;&#46;</p><elsevierMultimedia ident="fig0015"></elsevierMultimedia><p id="par0110" class="elsevierStylePara elsevierViewall">En los pacientes VHC con enfermedad ateromatosa &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>c y d&#41;&#44; se observaron diferencias significativas en las cifras de colesterol total &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;018&#41;&#44; en los niveles de colesterol no HDL &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;002&#41; y de colesterol LDL &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;002&#41;&#44; as&#237; como en el &#237;ndice aterog&#233;nico &#40;CT&#47;HDL&#41; &#40;p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; con tendencia a aumentar a medida que progresa la fibrosis hep&#225;tica&#44; y disminuyendo significativamente en presencia de cirrosis&#46; No se observaron cambios en los niveles de colesterol HDL&#44; triglic&#233;ridos ni en el coeficiente TG&#47;HDL y los grados de fibrosis en presencia de placa de ateroma&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Al analizar la correlaci&#243;n entre la carga viral y el perfil lip&#237;dico&#44; tan solo se detect&#243; una leve asociaci&#243;n entre el ARN del VHC y los niveles de colesterol no HDL &#40;r<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;219&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;04&#41;&#44; sin detectarse asociaci&#243;n con ning&#250;n otro par&#225;metro anal&#237;tico&#46;</p></span></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0125">Discusi&#243;n</span><p id="par0120" class="elsevierStylePara elsevierViewall">Este estudio observacional analiza la presencia de enfermedad ateromatosa en sujetos con y sin infecci&#243;n cr&#243;nica por VHC&#44; encontrando que los pacientes infectados tienen mayor presencia de ateromatosis subcl&#237;nica y en edades m&#225;s precoces que los controles&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Nuestros resultados concuerdan con lo publicado recientemente en 2 metaan&#225;lisis que describen una mayor presencia de ateromatosis en poblaciones infectadas por VHC &#40;entre un 38 y un 65&#37;&#41;<a class="elsevierStyleCrossRefs" href="#bib0175"><span class="elsevierStyleSup">5&#44;6</span></a>&#46; En estos estudios&#44; las placas de ateroma se identificaron por ecograf&#237;a Doppler vascular&#44; y el diagn&#243;stico se estableci&#243; con un valor de GIMc<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1&#44;3<span class="elsevierStyleHsp" style=""></span>mm<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a>&#46; En nuestro trabajo se siguieron los criterios de Manheim para el diagn&#243;stico de ateromatosis&#44; definiendo la placa como un GIMc<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>1&#44;5<span class="elsevierStyleHsp" style=""></span>mm&#46; Una de las posibles razones de nuestra tasa m&#225;s elevada es la ampliaci&#243;n del estudio femoral&#44; que aumenta la probabilidad de detectar ateromatosis&#46; Se ha publicado la existencia de enfermedad ateromatosa en territorio femoral en ausencia de placas carot&#237;deas en poblaci&#243;n general<a class="elsevierStyleCrossRef" href="#bib0270"><span class="elsevierStyleSup">24</span></a>&#46; Adem&#225;s&#44; nosotros tambi&#233;n analizamos diferentes genotipos virales&#44; que no han sido evaluados en estudios previamente publicados<a class="elsevierStyleCrossRef" href="#bib0250"><span class="elsevierStyleSup">20</span></a>&#44; aunque es conocido que el genotipo 3 produce m&#225;s alteraciones metab&#243;licas que el resto<a class="elsevierStyleCrossRefs" href="#bib0305"><span class="elsevierStyleSup">25&#44;26</span></a>&#46; Aunque la presencia de placa fue mayor en los pacientes infectados&#44; estos presentaban un bajo &#237;ndice de riesgo cardiovascular seg&#250;n las tablas SCORE European Risk Chart&#46; Varios estudios poblacionales han demostrado asociaci&#243;n entre la presencia de placas en arterias perif&#233;ricas e incidencia de eventos cardiovasculares&#44; incluso en sujetos sin eventos previos &#40;1&#44;8 veces el aumento del riesgo de eventos coronarios y 4&#44;1 veces el aumento del riesgo de eventos cardiovasculares&#41;<a class="elsevierStyleCrossRefs" href="#bib0315"><span class="elsevierStyleSup">27&#44;28</span></a>&#46; En l&#237;nea con estas publicaciones&#44; la presencia de placas de ateroma en nuestra poblaci&#243;n no se asoci&#243; con factores de riesgo cardiovascular tradicionales como el IMC&#44; la glucemia o la dislipidemia&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">Nuestro estudio involucra la primera cohorte espa&#241;ola de pacientes monoinfectados con VHC cr&#243;nica&#44; aunque cuenta con las limitaciones intr&#237;nsecas de un dise&#241;o transversal y del sesgo de selecci&#243;n en los pacientes controles&#44; ya que pertenecen a un grupo de pacientes de una consulta de riesgo cardiovascular&#46; Para minimizar este sesgo&#44; limitamos los criterios de selecci&#243;n a sujetos con riesgo bajo a moderado &#40;probabilidad &#60;<span class="elsevierStyleHsp" style=""></span>5&#37; de experimentar eventos cardiovasculares a los 10 a&#241;os&#41; sin presencia de enfermedad cardiovascular previa ni toma de f&#225;rmacos para hipertensi&#243;n ni dislipidemia&#46; Excluimos los pacientes con diabetes y enfermedad renal cr&#243;nica para evitar factores de confusi&#243;n&#46; Algunas publicaciones identifican que el virus VHC promueve el desarrollo de diabetes e insuficiencia renal cr&#243;nica&#44; lo que predispone a la presencia de lesiones ateromatosas<a class="elsevierStyleCrossRef" href="#bib0230"><span class="elsevierStyleSup">16</span></a>&#46; Tambi&#233;n podr&#237;a crear confusi&#243;n el hecho de observar una mayor presencia de exfumadores o fumadores activos entre aquellos con placa VHC&#43;&#44; as&#237; como las diferencias entre el grado de fibrosis hep&#225;tica en los sujetos con y sin placa&#59; pero tal como demuestra el an&#225;lisis multivariante&#44; ni el tabaquismo ni la fibrosis influ&#237;an en el desarrollo de las placas de ateroma&#44; mientras que s&#237; se observ&#243; una asociaci&#243;n elevada &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37&#41; del VHC <span class="elsevierStyleItalic">per se</span>&#46;</p><p id="par0135" class="elsevierStylePara elsevierViewall">Ante estos resultados&#44; identificamos como factor independiente de ateromatosis la infecci&#243;n cr&#243;nica por VHC sin influencia de otros factores cardiovasculares tradicionalmente conocidos&#44; lo que sugiere un papel directo del VHC en el desarrollo de las lesiones ateromatosas&#46; Estudios recientes han demostrado la presencia de ARN del VHC en la placa carot&#237;dea<a class="elsevierStyleCrossRefs" href="#bib0220"><span class="elsevierStyleSup">14&#44;15</span></a> y por el entorno proinflamatorio que induce el virus<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">4-12</span></a>&#46; En nuestro estudio&#44; los niveles de PCR marcador de riesgo cardiovascular e inflamaci&#243;n sist&#233;mica&#44; ampliamente aceptado para la poblaci&#243;n<a class="elsevierStyleCrossRef" href="#bib0260"><span class="elsevierStyleSup">22</span></a>&#44; no mostraron diferencias significativas entre ambos grupos&#44; si bien las prote&#237;nas de s&#237;ntesis hep&#225;ticas como PCR pueden estar alteradas en pacientes con enfermedad hep&#225;tica cr&#243;nica&#46; Adem&#225;s&#44; detectamos que la presencia de ateromatosis en la poblaci&#243;n VHC se desarrolla en edades mucho m&#225;s tempranas que en el grupo sin infecci&#243;n&#46; Tal y como se observa en la <a class="elsevierStyleCrossRef" href="#fig0010">figura 2</a>&#44; hemos encontrado que por debajo de 54 a&#241;os existen diferencias significativas de presencia de placa en los pacientes infectados frente a los controles&#46; Este hallazgo sugiere que los pacientes con infecci&#243;n por VHC presentan ateromatosis acelerada o envejecimiento vascular prematuro&#44; de forma similar a lo observado en otras enfermedades cr&#243;nicas inflamatorias y autoinmunes<a class="elsevierStyleCrossRef" href="#bib0325"><span class="elsevierStyleSup">29</span></a>&#46; Adem&#225;s de la edad y la infecci&#243;n por VHC&#44; el sexo masculino y el coeficiente TG&#47;HDL &#40;marcador indirecto de insulinorresistencia&#41; fueron los &#250;nicos factores significativamente asociados con la presencia de ateromatosis&#46; Este coeficiente es un &#237;ndice predictivo pron&#243;stico de enfermedad cardiovascular&#44; utilizado como marcador de aterog&#233;nesis en poblaci&#243;n general&#44; y aunque hay pocos datos&#44; su valor predictivo en cardiopat&#237;a es alto<a class="elsevierStyleCrossRef" href="#bib0300"><span class="elsevierStyleSup">30</span></a>&#46; Adem&#225;s&#44; es un buen marcador de aterog&#233;nesis en la poblaci&#243;n infectada&#44; ya que no se modifica significativamente con la progresi&#243;n de la enfermedad hep&#225;tica ni con la carga viral&#46;</p><p id="par0140" class="elsevierStylePara elsevierViewall">En este trabajo&#44; analizamos la modificaci&#243;n del perfil lip&#237;dico en diferentes estadios de progresi&#243;n de enfermedad hep&#225;tica medida por elastograf&#237;a &#40;<a class="elsevierStyleCrossRef" href="#fig0015">fig&#46; 3</a>&#41;&#44; detectando que en los pacientes infectados sin placa de ateroma no existen diferencias en cuanto a los niveles de l&#237;pidos s&#233;ricos y la fibrosis hep&#225;tica&#46; Pero en los pacientes VHC con ateromatosis&#44; las part&#237;culas m&#225;s aterog&#233;nicas &#40;formadas por LDL y VLDL&#41;&#44; que son el transportador principal del VHC en plasma&#44; aumentan conforme progresa la fibrosis&#44; y descienden significativamente al establecerse la cirrosis hep&#225;tica&#46; Estas part&#237;culas m&#225;s aterog&#233;nicas se correlacionan d&#233;bilmente con la carga viral&#44; sin observar asociaci&#243;n con el desarrollo de placa de ateroma&#44; lo que podr&#237;a deberse a la fluctuaci&#243;n en el tiempo de la viremia o a que estos valores dependen de la progresi&#243;n de la fibrosis hep&#225;tica&#44; descendiendo en estadios de cirrosis&#46;</p><p id="par0145" class="elsevierStylePara elsevierViewall">En resumen&#44; nuestros resultados muestran que los pacientes con infecci&#243;n cr&#243;nica por VHC tienen una mayor prevalencia de ateromatosis subcl&#237;nica que la poblaci&#243;n no infectada&#44; con inicio en edades precoces &#40;ateromatosis acelerada&#41;&#46; El perfil metab&#243;lico y la valoraci&#243;n del riesgo cardiovascular mediante el uso de las tablas tradicionales no son buenos predictores&#44; ya que la mayor&#237;a de estos pacientes presentan SCORES de bajo riesgo y un perfil lip&#237;dico tambi&#233;n de &#171;bajo riesgo&#187; &#40;menores cifras de colesterol no HDL y de colesterol LDL&#41;&#46; Esto apoya la necesidad de pruebas cardiovasculares no invasivas adicionales de uso rutinario&#44; como la ecograf&#237;a arterial&#44; que podr&#237;a mejorar la estratificaci&#243;n del riesgo en esta poblaci&#243;n&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0130">Conflicto de intereses</span><p id="par0150" class="elsevierStylePara elsevierViewall">Los autores declaran no tener ning&#250;n conflicto de intereses&#46;</p></span></span>"
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            1 => array:2 [
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          "titulo" => "Abstract"
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            0 => array:2 [
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              "titulo" => "Background"
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            1 => array:2 [
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            3 => array:2 [
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              "titulo" => "Dise&#241;o del estudio y pacientes"
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              "titulo" => "Datos cl&#237;nicos y anal&#237;ticos"
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              "titulo" => "Evaluaci&#243;n de la ateromatosis arterial subcl&#237;nica"
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              "titulo" => "An&#225;lisis estad&#237;stico"
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              "titulo" => "Caracter&#237;sticas de la poblaci&#243;n estudiada"
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              "titulo" => "Factores asociados con ateromatosis subcl&#237;nica"
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              "identificador" => "sec0050"
              "titulo" => "Descripci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en los pacientes con VHC en relaci&#243;n con la presencia de placa de ateroma"
            ]
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          "titulo" => "Agradecimientos"
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    "fechaRecibido" => "2018-07-06"
    "fechaAceptado" => "2018-12-04"
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          "titulo" => "Palabras clave"
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            0 => "Virus de la hepatitis C &#40;VHC&#41;"
            1 => "Placa de ateroma"
            2 => "Arteriosclerosis subcl&#237;nica"
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          "clase" => "keyword"
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            0 => "Hepatitis C virus &#40;HCV&#41;"
            1 => "Atheromatous plaque"
            2 => "Subclinical atherosclerosis"
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        "titulo" => "Resumen"
        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Introducci&#243;n</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Se desconoce la asociaci&#243;n entre ateromatosis subcl&#237;nica e infecci&#243;n cr&#243;nica por el virus de la hepatitis C &#40;VHC&#41;&#44; relevante ahora que los antivirales mejoran la supervivencia en los pacientes infectados&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Objetivos</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Conocer si el VHC es factor de riesgo independiente de ateromatosis subcl&#237;nica y analizar las modificaciones del perfil lip&#237;dico seg&#250;n niveles de ARN viral y fibrosis hep&#225;tica&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">Pacientes y m&#233;todos</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Estudio observacional y transversal&#59; incluye 102 pacientes VHC positivos y 102 sujetos VHC negativos con paridad de sexo y edad&#44; sin antecedentes de enfermedad cardiovascular&#44; renal ni diabetes&#46; La ateromatosis &#40;presencia de placas de ateroma&#41; y el grosor &#237;ntima-media carot&#237;deo &#40;GIMc&#41; se evalu&#243; mediante ecograf&#237;a de arterias car&#243;tidas y femorales&#46;</p></span> <span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Resultados</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La presencia de ateromatosis en cualquier territorio vascular fue mayor en pacientes VHC que en sujetos no infectados &#40;58&#44;8&#37; frente a 28&#44;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#46; En el an&#225;lisis multivariante&#44; los factores significativamente asociados con ateromatosis incluyeron infecci&#243;n por VHC &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44;37 &#91;5&#44;5-37&#44;3&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; edad &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>1&#44;12 &#91;1&#44;1-1&#44;2&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41;&#44; sexo masculino &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>4&#44;32 &#91;1&#44;9-9&#44;5&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;001&#41; y el coeficiente triglic&#233;ridos&#47;colesterol HDL &#40;TG&#47;HDL-indicador indirecto de insulinorresistencia&#41; &#40;OR<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>1&#44;34 &#91;1&#44;1-1&#44;6&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>0&#44;007&#41;&#46; Los pacientes VHC con placas de ateroma presentaban mayor coeficiente TG&#47;HDL&#44; sin diferencias significativas en cuanto a la carga viral ni grado de fibrosis hep&#225;tica con un perfil lip&#237;dico de &#171;bajo riesgo&#187;&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Conclusiones</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">La infecci&#243;n VHC es factor de riesgo independiente de ateromatosis subcl&#237;nica&#46; La ecograf&#237;a arterial sist&#233;mica en esta poblaci&#243;n mejora la evaluaci&#243;n del riesgo cardiovascular m&#225;s all&#225; de las alteraciones del perfil lip&#237;dico y del c&#225;lculo de riesgo por tablas SCORE&#46;</p></span>"
        "secciones" => array:5 [
          0 => array:2 [
            "identificador" => "abst0005"
            "titulo" => "Introducci&#243;n"
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          1 => array:2 [
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            "titulo" => "Objetivos"
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          2 => array:2 [
            "identificador" => "abst0015"
            "titulo" => "Pacientes y m&#233;todos"
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          3 => array:2 [
            "identificador" => "abst0020"
            "titulo" => "Resultados"
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          4 => array:2 [
            "identificador" => "abst0025"
            "titulo" => "Conclusiones"
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      "en" => array:3 [
        "titulo" => "Abstract"
        "resumen" => "<span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0040">Background</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">The association between subclinical atheromatosis and chronic hepatitis C virus &#40;HCV&#41; infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection&#46;</p></span> <span id="abst0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0045">Objectives</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis&#46;</p></span> <span id="abst0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Patients and methods</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">We conducted an observational&#44; cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age&#44; with no history of cardiovascular or kidney disease or diabetes&#46; Atheromatosis &#40;the presence of atheromatous plaques&#41; and the carotid intima-media thickness &#40;CIMT&#41; were assessed using ultrasonography of the carotid and femoral arteries&#46;</p></span> <span id="abst0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Results</span><p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection &#40;58&#46;8&#37; vs&#46; 28&#46;4&#37;&#44; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;0001&#41;&#46; In the multivariate analysis&#44; the factors significantly associated with atheromatosis included HCV infection &#40;OR&#44; 14&#46;37 &#91;5&#46;5-37&#46;3&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41;&#44; age &#40;OR&#44; 1&#46;12 &#91;1&#46;1-1&#46;2&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41;&#44; male sex &#40;OR&#44; 4&#46;32 &#91;1&#46;9-9&#46;5&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>&#46;001&#41; and the triglyceride&#47;HDL cholesterol coefficient &#40;TG&#47;HDL-indirect indicator of insulin resistance&#41; &#40;OR&#44; 1&#46;34 &#91;1&#46;1-1&#46;6&#93;&#59; p<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>&#46;007&#41;&#46; The HCV-positive patients with atheromatous plaques had a higher TG&#47;HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a &#8216;low risk&#8217; lipid profile&#46;</p></span> <span id="abst0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Conclusions</span><p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">HCV infection is an independent risk factor for subclinical atheromatosis&#46; Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables&#46;</p></span>"
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            "titulo" => "Objectives"
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            "titulo" => "Patients and methods"
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            "titulo" => "Results"
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            "titulo" => "Conclusions"
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          "es" => "<p id="spar0065" class="elsevierStyleSimplePara elsevierViewall">Modificaci&#243;n del perfil lip&#237;dico seg&#250;n el grado de fibrosis hep&#225;tica en pacientes VHC con presencia y ausencia de placa de ateroma&#46;</p>"
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                  \t\t\t\t"><span class="elsevierStyleItalic">HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">1 &#40;1&#44;6&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">60 &#40;58&#44;8&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAS &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">PAD &#40;mmHg&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Glucemia &#40;g&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Creatinina &#40;g&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Colesterol total &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">No HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">LDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t ; entry_with_role_rowhead " align="left" valign="\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">HDL colesterol &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t"><span class="elsevierStyleItalic">Triglic&#233;ridos &#40;mg&#47;dl&#41;</span>&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t\ttable-entry\n
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                  \t\t\t\t">159 &#40;134&#44;2&#41;&nbsp;\t\t\t\t\t\t\n
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                  \t\t\t\t">0&#44;047&nbsp;\t\t\t\t\t\t\n
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                  """
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Vol. 219. Núm. 6.
Páginas 293-302 (agosto - septiembre 2019)
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Vol. 219. Núm. 6.
Páginas 293-302 (agosto - septiembre 2019)
Original
Infección crónica por el virus de la hepatitis C: un factor de riesgo independiente para la ateromatosis subclínica
Chronic hepatitis C infection: An independent risk factor for subclinical atheromatosis
Visitas
72
T. Revuelto Artigasa,b,c,d,
Autor para correspondencia
tamararevuelto@gmail.com

Autor para correspondencia.
, N. Zaragoza Velascob,c,d, X. Gómez Arbonesd,e, T. Vidal Ballesterc, C. Piñol Felisd,e, J.M. Reñe Espinetb,d,e, A. Betriu Barsc,d
a Servicio de Aparato Digestivo, Hospital Universitario Santa María, Lleida, España
b Servicio de Aparato Digestivo, Hospital Universitario Arnau de Vilanova, Lleida, España
c Unidad de Detección y Tratamiento de Enfermedades Aterotrombóticas (UDETMA), Hospital Universitario Arnau de Vilanova (Grupo de Investigación Translacional Vascular y Renal, IRBLleida), Lleida, España
d Instituto de Investigación Biomédica, Lleida, España
e Universidad de Lleida (UdL), Lleida, España
Contenido relacionado
Rev Clin Esp. 2019;219:322-310.1016/j.rce.2019.01.012
V. Estrada, I. Sagastagoitia
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Estadísticas
Figuras (3)
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Tablas (3)
Tabla 1. Características de los pacientes a estudio, agrupados por infección por VHC
Tabla 2. Factores asociados a la presencia de placa de ateroma en las poblaciones estudiadas
Tabla 3. Características de los pacientes estudiados, agrupados por la presencia de placa de ateroma. Comparación bivariante y análisis multivariante (regresión logística condicional por pasos atrás)
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Resumen
Introducción

Se desconoce la asociación entre ateromatosis subclínica e infección crónica por el virus de la hepatitis C (VHC), relevante ahora que los antivirales mejoran la supervivencia en los pacientes infectados.

Objetivos

Conocer si el VHC es factor de riesgo independiente de ateromatosis subclínica y analizar las modificaciones del perfil lipídico según niveles de ARN viral y fibrosis hepática.

Pacientes y métodos

Estudio observacional y transversal; incluye 102 pacientes VHC positivos y 102 sujetos VHC negativos con paridad de sexo y edad, sin antecedentes de enfermedad cardiovascular, renal ni diabetes. La ateromatosis (presencia de placas de ateroma) y el grosor íntima-media carotídeo (GIMc) se evaluó mediante ecografía de arterias carótidas y femorales.

Resultados

La presencia de ateromatosis en cualquier territorio vascular fue mayor en pacientes VHC que en sujetos no infectados (58,8% frente a 28,4%, p<0,001). En el análisis multivariante, los factores significativamente asociados con ateromatosis incluyeron infección por VHC (OR=14,37 [5,5-37,3]; p<0,001), edad (OR=1,12 [1,1-1,2]; p<0,001), sexo masculino (OR=4,32 [1,9-9,5]; p<0,001) y el coeficiente triglicéridos/colesterol HDL (TG/HDL-indicador indirecto de insulinorresistencia) (OR=1,34 [1,1-1,6]; p=0,007). Los pacientes VHC con placas de ateroma presentaban mayor coeficiente TG/HDL, sin diferencias significativas en cuanto a la carga viral ni grado de fibrosis hepática con un perfil lipídico de «bajo riesgo».

Conclusiones

La infección VHC es factor de riesgo independiente de ateromatosis subclínica. La ecografía arterial sistémica en esta población mejora la evaluación del riesgo cardiovascular más allá de las alteraciones del perfil lipídico y del cálculo de riesgo por tablas SCORE.

Palabras clave:
Virus de la hepatitis C (VHC)
Placa de ateroma
Arteriosclerosis subclínica
Abstract
Background

The association between subclinical atheromatosis and chronic hepatitis C virus (HCV) infection is unknown but is relevant now that antivirals are improving the survival of patients with the infection.

Objectives

To determine whether HCV is an independent risk factor for subclinical atheromatosis and to analyse the changes in lipid profiles according to viral RNA levels and hepatic fibrosis.

Patients and methods

We conducted an observational, cross-sectional study that included 102 HCV-positive patients and 102 HCV-negative patients with parity in terms of sex and age, with no history of cardiovascular or kidney disease or diabetes. Atheromatosis (the presence of atheromatous plaques) and the carotid intima-media thickness (CIMT) were assessed using ultrasonography of the carotid and femoral arteries.

Results

There was a greater presence of atheromatosis in any vascular territory in HCV-positive patients than in the patients without infection (58.8% vs. 28.4%, p<.0001). In the multivariate analysis, the factors significantly associated with atheromatosis included HCV infection (OR, 14.37 [5.5-37.3]; p<.001), age (OR, 1.12 [1.1-1.2]; p<.001), male sex (OR, 4.32 [1.9-9.5]; p<.001) and the triglyceride/HDL cholesterol coefficient (TG/HDL-indirect indicator of insulin resistance) (OR, 1.34 [1.1-1.6]; p=.007). The HCV-positive patients with atheromatous plaques had a higher TG/HDL coefficient but no significant differences in terms of the viral load or degree of hepatic fibrosis and with a ‘low risk’ lipid profile.

Conclusions

HCV infection is an independent risk factor for subclinical atheromatosis. Systemic arterial ultrasonography for this population improves the cardiovascular risk assessment beyond lipid profile abnormalities and the risk calculation using SCORE tables.

Keywords:
Hepatitis C virus (HCV)
Atheromatous plaque
Subclinical atherosclerosis

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