array:23 [ "pii" => "S1889183704714439" "issn" => "18891837" "doi" => "10.1016/S1889-1837(04)71443-9" "estado" => "S300" "fechaPublicacion" => "2004-01-01" "aid" => "71443" "copyright" => "Sociedad Española de Hipertension-Liga Española para la Lucha de la Hipertensión Arterial (SEH-LELHA)" "copyrightAnyo" => "2004" "documento" => "article" "crossmark" => 0 "subdocumento" => "fla" "cita" => "Hipertens Riesgo Vasc. 2004;21:4-10" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 2516 "formatos" => array:3 [ "EPUB" => 7 "HTML" => 2270 "PDF" => 239 ] ] "itemSiguiente" => array:18 [ "pii" => "S1889183704714440" "issn" => "18891837" "doi" => "10.1016/S1889-1837(04)71444-0" "estado" => "S300" "fechaPublicacion" => "2004-01-01" "aid" => "71444" "copyright" => "Sociedad Española de Hipertension-Liga Española para la Lucha de la Hipertensión Arterial (SEH-LELHA)" "documento" => "article" "crossmark" => 0 "subdocumento" => "fla" "cita" => "Hipertens Riesgo Vasc. 2004;21:11-22" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 2914 "formatos" => array:3 [ "EPUB" => 10 "HTML" => 2535 "PDF" => 369 ] ] "es" => array:10 [ "idiomaDefecto" => true "titulo" => "Metaplasia del epitelio parietal glomerular en ratas espontáneamente hipertensas" "tienePdf" => "es" "tieneTextoCompleto" => 0 "tieneResumen" => array:2 [ 0 => "es" 1 => "en" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "11" "paginaFinal" => "22" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Metaplasia of glomerular parietal epithelial cells (GPEC) in spontaneously hypertensive rats" ] ] "contieneResumen" => array:2 [ "es" => true "en" => true ] "contienePdf" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "J.M. Rojo Ortegaa, J.M. Rojo Manauteb" "autores" => array:2 [ 0 => array:2 [ "nombre" => "J.M." "apellidos" => "Rojo Ortegaa" ] 1 => array:2 [ "nombre" => "J.M." "apellidos" => "Rojo Manauteb" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1889183704714440?idApp=UINPBA00004N" "url" => "/18891837/0000002100000001/v1_201307261555/S1889183704714440/v1_201307261555/es/main.assets" ] "itemAnterior" => array:18 [ "pii" => "S1889183704714427" "issn" => "18891837" "doi" => "10.1016/S1889-1837(04)71442-7" "estado" => "S300" "fechaPublicacion" => "2004-01-01" "aid" => "71442" "copyright" => "Sociedad Española de Hipertension-Liga Española para la Lucha de la Hipertensión Arterial (SEH-LELHA)" "documento" => "simple-article" "crossmark" => 0 "subdocumento" => "edi" "cita" => "Hipertens Riesgo Vasc. 2004;21:1-3" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 1809 "formatos" => array:3 [ "EPUB" => 10 "HTML" => 1508 "PDF" => 291 ] ] "es" => array:7 [ "idiomaDefecto" => true "titulo" => "Lesiones de sustancia blanca e hipertensión arterial" "tienePdf" => "es" "tieneTextoCompleto" => 0 "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "1" "paginaFinal" => "3" ] ] "contienePdf" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "P. Armario" "autores" => array:1 [ 0 => array:2 [ "nombre" => "P." "apellidos" => "Armario" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S1889183704714427?idApp=UINPBA00004N" "url" => "/18891837/0000002100000001/v1_201307261555/S1889183704714427/v1_201307261555/es/main.assets" ] "es" => array:11 [ "idiomaDefecto" => true "titulo" => "Factores relacionados con la presencia de lesiones silentes de sustancia blanca cerebral en la hipertensión arterial" "tieneTextoCompleto" => 0 "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "4" "paginaFinal" => "10" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "C. Sierra Benito, A. de la Sierra Iserte, E. Gómez-Angelats, A. Coca Payeras" "autores" => array:4 [ 0 => array:4 [ "nombre" => "C." "apellidos" => "Sierra Benito" "email" => array:1 [ 0 => "csierra@clinic.ub.es" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">1</span>" "identificador" => "cor0005" ] ] ] 1 => array:2 [ "nombre" => "A." "apellidos" => "de la Sierra Iserte" ] 2 => array:2 [ "nombre" => "E." "apellidos" => "Gómez-Angelats" ] 3 => array:2 [ "nombre" => "A." "apellidos" => "Coca Payeras" ] ] "afiliaciones" => array:1 [ 0 => array:1 [ "entidad" => "Unidad de Hipertensión Arterial. Servicio de Medicina Interna. IDIBAPS (Institut d’Investigacions Biomèdiques August Pi i Sunyer). Hospital Clínic. Universidad de Barcelona. Barcelona. España" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "1" "correspondencia" => "Correspondencia: Unidad de Hipertensión. Hospital Clínic. Villarroel, 170. 08036 Barcelona. España." ] ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "es" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec218779" "palabras" => array:4 [ 0 => "lesiones de sustancia blanca cerebral" 1 => "presión arterial" 2 => "hipertrofia ventricular izquierda" 3 => "gen de la enzima de conversión de la angiotensina" ] ] ] "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Key words" "identificador" => "xpalclavsec218778" "palabras" => array:4 [ 0 => "cerebral white matter lesions" 1 => "blood pressure" 2 => "left ventricular hypertrophy" 3 => "angiotensin converting enzyme gene" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "es" => array:1 [ "resumen" => "<span class="elsevierStyleSectionTitle">Introducción</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">El significado clínico y la patogénesis de las lesiones cerebrales de sustancia blanca (LSB) no están aclarados. La mayoría de los estudios sugieren que la edad y la hipertensión arterial son los factores más importantes relacionados con la presencia de LSB. También se ha sugerido la existencia de factores genéticos en la susceptibilidad de desarrollar LSB. El objetivo del presente trabajo ha sido evaluar posibles factores clínicos, biológicos y genéticos relacionados con la presencia de LSB en pacientes de mediana edad afectos de hipertensión arterial esencial.</p> <span class="elsevierStyleSectionTitle">Material y métodos</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Se han incluido 71 pacientes hipertensos esenciales de ambos sexos, de edades comprendidas entre 50- 60 años, nunca tratados, y sin evidencia de enfermedad cardiovascular. Se realizaron las siguientes exploraciones: monitorización ambulatoria de la presión arterial (MAPA) de 24 horas, ecocardiograma y estudio de los polimorfismos genéticos del sistema renina-angiotensina mediante reacción en cadena de la polimerasa. A todos los pacientes se les realizó una resonancia magnética cerebral para valorar la presencia o ausencia de LSB.</p> <span class="elsevierStyleSectionTitle">Resultados</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">Veintiocho (39,4 %) de los pacientes hipertensos mostraban LSB en la resonancia. Los pacientes con LSB tenían unas cifras de presión arterial (PA) sistólica, diastólica y presión de pulso significativamente mayores que los pacientes hipertensos sin LSB, tanto en la clínica como en la MAPA. No se objetivó una asociación entre el perfil circadiano y las LSB, así como tampoco con la variabilidad de la PA. La presencia de una hipertrofia del ventrículo izquierdo (HVI) concéntrica era significativamente mayor (p = 0,002) en pacientes con LSB (54 %) que en hipertensos sin LSB (11%). En referencia al estudio genético se objetivó que los pacientes con LSB presentaban una mayor frecuencia del genotipo DD del gen de la enzima de conversión de la angiotensina (ECA) (64 % frente al 28,6 %; p = 0,022) en comparación con los pacientes sin LSB.</p> <span class="elsevierStyleSectionTitle">Discusión</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">La presencia de LSB en pacientes hipertensos de mediana edad está relacionada con la severidad de la elevación de la PA y con la existencia de una HVI concéntrica. La presencia del genotipo DD del gen de la ECA podría ser un factor predisponente para el desarrollo de LSB en pacientes con hipertensión arterial.</p>" ] "en" => array:1 [ "resumen" => "<span class="elsevierStyleSectionTitle">Aim</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">The clinical meaning and pathogenesis of cerebral white matter lesions (WML) are not completely understood. Most studies suggest that age and hypertension are the most important factors related to presence of WML. Genetic factors have also been suggested in one’s susceptibility to developing WML. The aim of the present study was to evaluate possible clinical, biological and genetic factors related to the presence of WML in middle-aged essential hypertension patients.</p> <span class="elsevierStyleSectionTitle">Methods</span><p id="spar0030" class="elsevierStyleSimplePara elsevierViewall">Seventy-one essential hypertensive patients of both sexes were included. These were between the ages of 50 and 60 years old, never treated, and without any evidence of cardiovascular diseases. The following explorations were performed: 24 hour ambulatory blood pressure (BP) monitoring, echocardiogram, renin-angiotensin system genetic ploymorphism study by means of PCR. A cerebral magnetic resonance was performed in all patients to evaluate the presence or absence of WML.</p> <span class="elsevierStyleSectionTitle">Results</span><p id="spar0035" class="elsevierStyleSimplePara elsevierViewall">Twenty-eight (39.4 %) of hypertensive patients presented WML in the resonance. Patients with WML had systolic and diastolic BP values, as well as those of pulse pressure, significantly higher than hypertensive patients without WML. This was the case for both clinical and 24-hour BP monitoring. No association between WML and either circadian profile or BP variability was observed. The presence of concentric left ventricular hypertrophy (LVH) was significantly more prominent (p=0.002) in patients with WML (54 %) than in non-WML hypertensive patients (11 %). With regard to the genetic study, it was observed that patients with WML presented a higher frequency of DD genotype of the angiotensin converting enzyme (ACE) gene (64 % versus 28.6 %; p=0.022) in comparison with non-WML patients.</p> <span class="elsevierStyleSectionTitle">Conclusions</span><p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">The presence of WML in middle-aged hypertensive patients is related to both severity of BP elevation and existence of concentric LVH. The presence of the DD genotype of the ACE gene could be a predisposing factor for the development of WML in essential hypertensive patients.</p>" ] ] "bibliografia" => array:2 [ "titulo" => "Bibliografía" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:35 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1." "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Periventricular lesions in the white matter on magnetic resonance imaging in the elderly: a morphometric correlation with arteriolosclerosis and dilated perivascular spaces" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:6 [ 0 => "J.C. Van Swieten" 1 => "J.H. van den Hout" 2 => "B.A. van Ketel" 3 => "A. Hijdra" 4 => "J.H. 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Journal Information
Factores relacionados con la presencia de lesiones silentes de sustancia blanca cerebral en la hipertensión arterial
C. Sierra Benito1
, A. de la Sierra Iserte, E. Gómez-Angelats, A. Coca Payeras
Corresponding author
csierra@clinic.ub.es
Correspondencia: Unidad de Hipertensión. Hospital Clínic. Villarroel, 170. 08036 Barcelona. España.
Correspondencia: Unidad de Hipertensión. Hospital Clínic. Villarroel, 170. 08036 Barcelona. España.
Unidad de Hipertensión Arterial. Servicio de Medicina Interna. IDIBAPS (Institut d’Investigacions Biomèdiques August Pi i Sunyer). Hospital Clínic. Universidad de Barcelona. Barcelona. España