que se leu este artigo
array:24 [ "pii" => "S0870255120304200" "issn" => "08702551" "doi" => "10.1016/j.repc.2020.10.002" "estado" => "S300" "fechaPublicacion" => "2020-11-01" "aid" => "1622" "copyrightAnyo" => "2020" "documento" => "simple-article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "dis" "cita" => "Rev Port Cardiol. 2020;39:623-4" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "itemSiguiente" => array:19 [ "pii" => "S0870255120304157" "issn" => "08702551" "doi" => "10.1016/j.repc.2020.03.017" "estado" => "S300" "fechaPublicacion" => "2020-11-01" "aid" => "1617" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Port Cardiol. 2020;39:625-33" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Original Article</span>" "titulo" => "Influence of EPICardial adipose tissue in HEART diseases (EPICHEART) study: Protocol for a translational study in coronary atherosclerosis" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "pt" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "625" "paginaFinal" => "633" ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Influência do Tecido Adiposo Epicárdico nas Doenças Cardíacas (EPICHEART): protocolo para um estudo de translação em aterosclerose coronário" ] ] "contieneResumen" => array:2 [ "en" => true "pt" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0010" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr2.jpeg" "Alto" => 1290 "Ancho" => 2766 "Tamanyo" => 239026 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0050" class="elsevierStyleSimplePara elsevierViewall">EPICHEART study aims. The EPICHEART study is a prospective translational study enrolling severe aortic stenosis (AS) patients referred for aortic valve replacement, in which we will provide clinical associations between epicardial adipose tissue (EAT) volume assessed by computed tomography and different outcomes of heart disease, namely coronary artery disease, left atrial remodeling and incidence of postoperative atrial fibrillation, and frailty syndrome in severe AS patients referred to aortic valve replacement (Arm 1). In addition, the proteomic profile of EAT and mediastinal and subcutaneous thoracic fat samples collected from matched case-control pairs will be investigated and compared (Arm 2). In this paper, we focused on the methodology employed to address Aim 1. AVR: aortic valve replacement; CAD: coronary artery disease; CT: computed tomography; EAT: epicardial adipose tissue; echo: echocardiography; ICA: invasive coronary angiography; LA: left atrial; MAT: mediastinal adipose tissue; MRI: magnetic resonance imaging; SWATH-MS: sequential windowed acquisition of all theoretical fragment ion mass spectra mass spectrometry.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Jennifer Mancio, António S. Barros, Glória Conceicão, Cátia Santa, Guilherme Pessoa-Amorim, Carla Bartosch, Mariana Fragao-Marques, Wilson Ferreira, Mónica Carvalho, Nuno Ferreira, Luís Vouga, Isabel M. Miranda, Rui Vitorino, Ricardo Fontes-Carvalho, Bruno Manadas, Inês Falcão-Pires, Vasco Gama Ribeiro, Adelino Leite-Moreira, Nuno Bettencourt" "autores" => array:19 [ 0 => array:2 [ "nombre" => "Jennifer" "apellidos" => "Mancio" ] 1 => array:2 [ "nombre" => "António S." "apellidos" => "Barros" ] 2 => array:2 [ "nombre" => "Glória" "apellidos" => "Conceicão" ] 3 => array:2 [ "nombre" => "Cátia" "apellidos" => "Santa" ] 4 => array:2 [ "nombre" => "Guilherme" "apellidos" => "Pessoa-Amorim" ] 5 => array:2 [ "nombre" => "Carla" "apellidos" => "Bartosch" ] 6 => array:2 [ "nombre" => "Mariana" "apellidos" => "Fragao-Marques" ] 7 => array:2 [ "nombre" => "Wilson" "apellidos" => "Ferreira" ] 8 => array:2 [ "nombre" => "Mónica" "apellidos" => "Carvalho" ] 9 => array:2 [ "nombre" => "Nuno" "apellidos" => "Ferreira" ] 10 => array:2 [ "nombre" => "Luís" "apellidos" => "Vouga" ] 11 => array:2 [ "nombre" => "Isabel M." "apellidos" => "Miranda" ] 12 => array:2 [ "nombre" => "Rui" "apellidos" => "Vitorino" ] 13 => array:2 [ "nombre" => "Ricardo" "apellidos" => "Fontes-Carvalho" ] 14 => array:2 [ "nombre" => "Bruno" "apellidos" => "Manadas" ] 15 => array:2 [ "nombre" => "Inês" "apellidos" => "Falcão-Pires" ] 16 => array:2 [ "nombre" => "Vasco Gama" "apellidos" => "Ribeiro" ] 17 => array:2 [ "nombre" => "Adelino" "apellidos" => "Leite-Moreira" ] 18 => array:2 [ "nombre" => "Nuno" "apellidos" => "Bettencourt" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2174204920303858" "doi" => "10.1016/j.repce.2020.12.009" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2174204920303858?idApp=UINPBA00004E" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S0870255120304157?idApp=UINPBA00004E" "url" => "/08702551/0000003900000011/v2_202012020712/S0870255120304157/v2_202012020712/en/main.assets" ] "itemAnterior" => array:20 [ "pii" => "S087025512030411X" "issn" => "08702551" "doi" => "10.1016/j.repc.2019.12.009" "estado" => "S300" "fechaPublicacion" => "2020-11-01" "aid" => "1613" "copyright" => "Sociedade Portuguesa de Cardiologia" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Port Cardiol. 2020;39:615-21" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Original Article</span>" "titulo" => "Late gadolinium enhancement location assessed by magnetic resonance and arrhythmogenic risk in hypertrophic cardiomyopathy" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "pt" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "615" "paginaFinal" => "621" ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Localização do realce tardio avaliado por ressonância magnética e risco arritmogénico na miocardiopatia hipertrófica" ] ] "contieneResumen" => array:2 [ "en" => true "pt" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1605 "Ancho" => 2500 "Tamanyo" => 603267 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Cardiac magnetic resonance imaging of two patients with hypertrophic cardiomyopathy included in the study showing late gadolinium enhancement (LGE) and the respective bull's eyes marking location and extent of LGE. (A) Patient with a pathogenic mutation in <span class="elsevierStyleItalic">TNNI3</span>; LGE was documented in four segments – basal inferior, basal inferolateral, mid anterior and distal septal; (B) patient with no pathogenic mutation found on genetic testing; LGE was documented in five segments – basal and mid inferoseptal, basal and mid inferolateral, and basal anteroseptal.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Ana Raquel Barbosa, João Almeida, Cláudio Guerreiro, Pedro Teixeira, Ricardo Ladeiras Lopes, Nuno Dias Ferreira, Olga Sousa, Pedro Braga" "autores" => array:8 [ 0 => array:2 [ "nombre" => "Ana Raquel" "apellidos" => "Barbosa" ] 1 => array:2 [ "nombre" => "João" "apellidos" => "Almeida" ] 2 => array:2 [ "nombre" => "Cláudio" "apellidos" => "Guerreiro" ] 3 => array:2 [ "nombre" => "Pedro" "apellidos" => "Teixeira" ] 4 => array:2 [ "nombre" => "Ricardo" "apellidos" => "Ladeiras Lopes" ] 5 => array:2 [ "nombre" => "Nuno" "apellidos" => "Dias Ferreira" ] 6 => array:2 [ "nombre" => "Olga" "apellidos" => "Sousa" ] 7 => array:2 [ "nombre" => "Pedro" "apellidos" => "Braga" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2174204920303834" "doi" => "10.1016/j.repce.2020.12.008" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2174204920303834?idApp=UINPBA00004E" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S087025512030411X?idApp=UINPBA00004E" "url" => "/08702551/0000003900000011/v2_202012020712/S087025512030411X/v2_202012020712/en/main.assets" ] "asociados" => array:1 [ 0 => array:20 [ "pii" => "S087025512030411X" "issn" => "08702551" "doi" => "10.1016/j.repc.2019.12.009" "estado" => "S300" "fechaPublicacion" => "2020-11-01" "aid" => "1613" "copyright" => "Sociedade Portuguesa de Cardiologia" "documento" => "article" "crossmark" => 1 "licencia" => "http://creativecommons.org/licenses/by-nc-nd/4.0/" "subdocumento" => "fla" "cita" => "Rev Port Cardiol. 2020;39:615-21" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "en" => array:13 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Original Article</span>" "titulo" => "Late gadolinium enhancement location assessed by magnetic resonance and arrhythmogenic risk in hypertrophic cardiomyopathy" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => array:2 [ 0 => "en" 1 => "pt" ] "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "615" "paginaFinal" => "621" ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Localização do realce tardio avaliado por ressonância magnética e risco arritmogénico na miocardiopatia hipertrófica" ] ] "contieneResumen" => array:2 [ "en" => true "pt" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:7 [ "identificador" => "fig0005" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 1605 "Ancho" => 2500 "Tamanyo" => 603267 ] ] "descripcion" => array:1 [ "en" => "<p id="spar0045" class="elsevierStyleSimplePara elsevierViewall">Cardiac magnetic resonance imaging of two patients with hypertrophic cardiomyopathy included in the study showing late gadolinium enhancement (LGE) and the respective bull's eyes marking location and extent of LGE. (A) Patient with a pathogenic mutation in <span class="elsevierStyleItalic">TNNI3</span>; LGE was documented in four segments – basal inferior, basal inferolateral, mid anterior and distal septal; (B) patient with no pathogenic mutation found on genetic testing; LGE was documented in five segments – basal and mid inferoseptal, basal and mid inferolateral, and basal anteroseptal.</p>" ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "Ana Raquel Barbosa, João Almeida, Cláudio Guerreiro, Pedro Teixeira, Ricardo Ladeiras Lopes, Nuno Dias Ferreira, Olga Sousa, Pedro Braga" "autores" => array:8 [ 0 => array:2 [ "nombre" => "Ana Raquel" "apellidos" => "Barbosa" ] 1 => array:2 [ "nombre" => "João" "apellidos" => "Almeida" ] 2 => array:2 [ "nombre" => "Cláudio" "apellidos" => "Guerreiro" ] 3 => array:2 [ "nombre" => "Pedro" "apellidos" => "Teixeira" ] 4 => array:2 [ "nombre" => "Ricardo" "apellidos" => "Ladeiras Lopes" ] 5 => array:2 [ "nombre" => "Nuno" "apellidos" => "Dias Ferreira" ] 6 => array:2 [ "nombre" => "Olga" "apellidos" => "Sousa" ] 7 => array:2 [ "nombre" => "Pedro" "apellidos" => "Braga" ] ] ] ] ] "idiomaDefecto" => "en" "Traduccion" => array:1 [ "en" => array:9 [ "pii" => "S2174204920303834" "doi" => "10.1016/j.repce.2020.12.008" "estado" => "S300" "subdocumento" => "" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:1 [ "total" => 0 ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2174204920303834?idApp=UINPBA00004E" ] ] "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S087025512030411X?idApp=UINPBA00004E" "url" => "/08702551/0000003900000011/v2_202012020712/S087025512030411X/v2_202012020712/en/main.assets" ] ] "en" => array:12 [ "idiomaDefecto" => true "cabecera" => "<span class="elsevierStyleTextfn">Editorial comment</span>" "titulo" => "Arrhythmogenic risk of late gadolinium enhancement in patients with hypertrophic cardiomyopathy: Burden and location?" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "623" "paginaFinal" => "624" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Mahdi Montazeri, Raymond H. Chan" "autores" => array:2 [ 0 => array:2 [ "nombre" => "Mahdi" "apellidos" => "Montazeri" ] 1 => array:4 [ "nombre" => "Raymond H." "apellidos" => "Chan" "email" => array:1 [ 0 => "raymond.chan@utoronto.ca" ] "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor0005" ] ] ] ] "afiliaciones" => array:1 [ 0 => array:2 [ "entidad" => "University Health Network, University of Toronto, Toronto, Canada" "identificador" => "aff0005" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor0005" "etiqueta" => "⁎" "correspondencia" => "Corresponding author." ] ] ] ] "titulosAlternativos" => array:1 [ "pt" => array:1 [ "titulo" => "Risco arritmogénico de realce tardio pelo gadolínio em doentes com miocardiopatia hipertrófica: quantidade e localização?" ] ] "textoCompleto" => "<span class="elsevierStyleSections"><p id="par0005" class="elsevierStylePara elsevierViewall">Hypertrophic cardiomyopathy (HCM) is a common genetic disease, and is one of the leading causes of sudden cardiac death (SCD), particularly in young athletes.<a class="elsevierStyleCrossRef" href="#bib0090"><span class="elsevierStyleSup">1</span></a> Myocardial fibrosis and scar formation are frequently observed in patients with HCM.<a class="elsevierStyleCrossRef" href="#bib0095"><span class="elsevierStyleSup">2</span></a> Quantitative late gadolinium enhancement (LGE) has emerged as a tool for risk stratification in HCM, as the presence and extent of LGE have been associated with increased risk of SCD. Quantitative LGE (through the use of various threshold methods) and semi-quantitative methods have been proposed to quantify the extent of LGE.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">3–5</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">In HCM, LGE is most commonly observed in the septal wall, usually but not always limited to hypertrophied segments in a variety of patterns that are not related to vascular territories. This is in contrast to ischemic cardiomyopathy, in which the subendocardial area related to the culprit artery is most frequently affected.<a class="elsevierStyleCrossRefs" href="#bib0100"><span class="elsevierStyleSup">3,6,7</span></a> Histopathological analysis results from postmortem or post-surgical samples in HCM patients have shown that LGE areas are indicative of myocardial scarring or interstitial fibrosis, and so the proposed mechanism has been hypothesized to be related to microvascular ischemia rather than stenosis of epicardial coronary arteries.<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">8,9</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">In this issue of the <span class="elsevierStyleItalic">Journal</span>, Barbosa and colleagues observe that the location of LGE, in addition to its extent, are important features associated with increased risk of ventricular arrhythmias in HCM patients. They hypothesize that areas of increased mechanical stress are more prone to LGE development, and that such areas may play an arrhythmogenic role.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">10</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">There is a paucity of evidence linking LGE location and increased arrhythmogenic risk in HCM patients. The exception is LGE that is isolated to the right ventricular insertion point. This has been shown not to be correlated with SCD, as here it in fact represents areas of expanded extracellular space rather than replacement fibrosis.<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">11</span></a> Amano et al.<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">12</span></a> have shown that in addition to the total number of LGE segments, the presence of LGE in non-septal segments may also be related to arrhythmias and could add important information beyond fibrosis extent. Nojiri et al.<a class="elsevierStyleCrossRef" href="#bib0100"><span class="elsevierStyleSup">3</span></a> showed that the basal anteroseptal, mid anteroseptal, mid inferoseptal and apical septal segments, in that order, are the segments most often involved in HCM patients with preserved left ventricular ejection fraction, and also that mid-wall area involvement is more prevalent than subepicardial or subendocardial involvement. Based on the study's findings, and dividing the heart into 18 segments and 3 layers, they defined a scoring model up to 48 points and proposed that a higher score (i.e. higher LGE) is correlated with a higher rate of cardiac events including heart failure or ventricular tachycardia.</p><p id="par0025" class="elsevierStylePara elsevierViewall">Of interest, Basso et al.<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">13</span></a> showed that in patients with mitral valve prolapse, LGE at the papillary muscles and basal inferior segment were associated with arrhythmia. They hypothesized that mechanical stretch by the prolapsing leaflet (and the subsequent development of LGE in the aforementioned segments) could act as a trigger of electrical instability. Maurer et al.<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">14</span></a> suggested that there is an association between increased myocardial wall stress and increased metabolic demand, mostly in locations corresponding to the basal inferior and lateral segments. Excitation-contraction coupling plays an important role in cardiac physiology. In addition, mechanical stress could be a trigger for electrical activity and instability, termed mechano-electrical feedback, as in commotio cordis, which is more pronounced in non-uniform cardiac muscle.<a class="elsevierStyleCrossRefs" href="#bib0160"><span class="elsevierStyleSup">15,16</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The association between the location of LGE in HCM patients and clinical risk factors and subsequent premature cardiac death demonstrated by Barbosa et al.<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">10</span></a> represents an important first step. Nevertheless, there is a wide range and overlap in the extent of LGE within patient subgroups. Due to the small number of patients (n=61) and of events (n=15) in their study, it is difficult to independently attribute the increased arrhythmogenic risk to the location of LGE, rather than to the presence (or more likely, the overall burden) of LGE. It is also important to remember that using two or more clinical risk factors has just 45% sensitivity and 23% positive predictive value to predict sudden cardiac death in HCM patients.<a class="elsevierStyleCrossRef" href="#bib0170"><span class="elsevierStyleSup">17</span></a> However, the important data presented by Barbosa et al. indicate that further research into the prognostic value of LGE location in HCM patients is warranted.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Conflicts of interest</span><p id="par0035" class="elsevierStylePara elsevierViewall">The author has no conflicts of interest to declare.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:2 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Conflicts of interest" ] 1 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0015" "bibliografiaReferencia" => array:17 [ 0 => array:3 [ "identificador" => "bib0090" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "Hypertrophic cardiomyopathy: a systematic review" "autores" => array:1 [ 0 => array:2 [ "etal" => false "autores" => array:1 [ 0 => "B.J. 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