Letter to the Editor
Hypertrophic cardiomyopathy: New pathogenic variant in MYH7
Miocardiopatía hipertrófica: nueva variante patogénica en MYH7
a Servicio de Neumología, Complexo Hospitalario Universitario de Vigo, Vigo, Pontevedra, Spain
b Grupo de Investigación NEUMOVIGO I+I, Instituto de Investigación Sanitaria Galicia, Sur (IIS Galicia Sur), SERGAS-UVIGO, Vigo, Pontevedra, Spain
c Servicio de Cardiología, Complexo Hospitalario Universitario de Vigo, Vigo, Pontevedra, Spain
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The most commonly involved proteins are beta myosin heavy chain (MYH7) and the cardiac form of myosin-binding protein C (MYBPC3).<a class="elsevierStyleCrossRef" href="#bib0005"><span class="elsevierStyleSup">1</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">A case of a family with HCM associated with a missense single nucleotide polymorphism in MYH7 (g.23899810C>T, c.958G>A, p.Val320Met) is presented. The family tree is detailed in <a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>. The index case is a 72-year-old woman whose first available echocardiographic report (at the age of 58) already included a diagnosis of HCM in her personal history. She had no left ventricular outflow tract (LVOT) obstruction and, to date, no progression was observed on follow-up imaging tests. The patient was admitted at 72 years of age for cardiogenic syncope, which required PM/ICD implantation as she had an estimated 5-year risk of sudden cardiac death (HCM Risk-SCD) of 11.65%.</p><elsevierMultimedia ident="fig0005"></elsevierMultimedia><p id="par0015" class="elsevierStylePara elsevierViewall">In this case, an HCM panel was performed using next-generation sequencing of 18 genes related to familial HCM, detecting a heterozygous missense mutation in the gene <span class="elsevierStyleItalic">MYH7</span> (g.23899810C>T, c.958G>A, p.Val320Met). At the time of this publication, according to the National Center for Biotechnology Information, this mutation is considered pathogenic/likely pathogenic with a level of evidence of 2/4 according to their own classification scale.<a class="elsevierStyleCrossRef" href="#bib0010"><span class="elsevierStyleSup">2</span></a></p><p id="par0020" class="elsevierStylePara elsevierViewall">A review of the family medical history revealed the documented presence of two cases of first-degree relatives with the same heterozygous mutation of <span class="elsevierStyleItalic">MYH7</span> and diagnosed with HCM. In addition, there are 2 confirmed cases of HCM in the family pending genetic testing and there is a high suspicion that 3 more relatives could be carriers of this mutation due to the family history collected, including a sudden death at 65 years of age in one of the cases, of which there is no autopsy record. Therefore, there are 5 confirmed cases of HCM (3 confirmed with the previously described mutation, with autosomal dominant inheritance pattern) and 3 suspected cases in total (<a class="elsevierStyleCrossRef" href="#fig0005">Fig. 1</a>). One of the 3 cases of HCM carrying the mutation that is the subject of this publication also carries a mutation in gene <span class="elsevierStyleItalic">HCN4</span> (g.73660595G>T, c.17C>A, p.Pro6Gln), something previously unpublished in the literature, with no differences in clinical course/phenotype at follow-up. To date, the only 2 confirmed carrier offspring have not shown clinical expression, probably due to the later age of onset of disease with this mutation, as the first of their affected relatives was diagnosed at the age of 53.</p><p id="par0025" class="elsevierStylePara elsevierViewall">A mean age at diagnosis of 34.6 years is described in cases published in the literature on this mutation. Left ventricular hypertrophy was observed in 55.6% of cases, of which 55.6% and 60% had LVOT obstruction and ventricular arrhythmias, respectively.<a class="elsevierStyleCrossRefs" href="#bib0015"><span class="elsevierStyleSup">3–5</span></a></p><p id="par0030" class="elsevierStylePara elsevierViewall">The average age at diagnosis of the 4 confirmed cases of HCM was 58. All patients were symptomatic, although none experienced sudden death or ventricular arrhythmias; however, two of them required ICD implantation for elevated HCM-risk-SCD and syncope with cardiogenic features. Echocardiography showed LVOT obstruction in 50% of cases, and the mean maximum myocardial thickness was 21.6<span class="elsevierStyleHsp" style=""></span>mm.</p><p id="par0035" class="elsevierStylePara elsevierViewall">This publication presents the largest number of cases to date correlating this heterozygous mutation with the development of autosomal dominant inheritance HCM. Sixty per cent of the carriers developed the disease. The only ones who did not develop the disease could express it over the years, as at 38 and 45 years of age, respectively, have not yet reached the age of the earliest familial diagnosis, which was 53. In turn, in the same family, there are at least 3 suspected cases of HCM and 2 more confirmed cases without genetic testing. In the light of the above, we consider that the pathogenicity of this mutation in relation to the development of HCM is proven.</p><span id="sec0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0005">Ethical considerations</span><p id="par0040" class="elsevierStylePara elsevierViewall">This work has followed the ethical code of the WHO (Declaration of Helsinki), the International Committee of Medical Journal Editors and the acquisition of informed consent is confirmed.</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Funding</span><p id="par0045" class="elsevierStylePara elsevierViewall">This research has not received specific support from public, private or non-profit organisations.</p></span></span>" "textoCompletoSecciones" => array:1 [ "secciones" => array:3 [ 0 => array:2 [ "identificador" => "sec0005" "titulo" => "Ethical considerations" ] 1 => array:2 [ "identificador" => "sec0010" "titulo" => "Funding" ] 2 => array:1 [ "titulo" => "References" ] ] ] "pdfFichero" => "main.pdf" "tienePdf" => true "multimedia" => array:1 [ 0 => array:8 [ "identificador" => "fig0005" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "figura" => array:1 [ 0 => array:4 [ "imagen" => "gr1.jpeg" "Alto" => 484 "Ancho" => 3625 "Tamanyo" => 92023 ] ] "detalles" => array:1 [ 0 => array:3 [ "identificador" => "at0010" "detalle" => "Fig. " "rol" => "short" ] ] "descripcion" => array:1 [ "en" => "<p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Family tree, classified according to the presence or absence of MYH7 or HCN4 mutation and the development of hypertrophic cardiomyopathy during the lifetime of the subjects.</p>" ] ] ] "bibliografia" => array:2 [ "titulo" => "References" "seccion" => array:1 [ 0 => array:2 [ "identificador" => "bibs0005" "bibliografiaReferencia" => array:5 [ 0 => array:3 [ "identificador" => "bib0005" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:2 [ "titulo" => "2014 ESC Guidelines on diagnosis and management of hypertrophic cardiomyopathy: the Task Force for the diagnosis and management of hypertrophic cardiomyopathy of the European Society of Cardiology (ESC)" "autores" => array:1 [ 0 => array:2 [ "etal" => true "autores" => array:6 [ 0 => "Authors/Task Force members" 1 => "P.M. 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Antunes M de" 5 => "A.Q. de Araujo" ] ] ] ] ] "host" => array:1 [ 0 => array:1 [ "Revista" => array:5 [ "tituloSerie" => "Am Heart J" "fecha" => "2013" "volumen" => "166" "paginaInicial" => "775" "paginaFinal" => "782" ] ] ] ] ] ] ] ] ] ] ] "idiomaDefecto" => "en" "url" => "/23870206/0000016200000011/v1_202406091353/S2387020624002079/v1_202406091353/en/main.assets" "Apartado" => array:4 [ "identificador" => "43309" "tipo" => "SECCION" "en" => array:2 [ "titulo" => "Letters to the Editor" "idiomaDefecto" => true ] "idiomaDefecto" => "en" ] "PDF" => "https://static.elsevier.es/multimedia/23870206/0000016200000011/v1_202406091353/S2387020624002079/v1_202406091353/en/main.pdf?idApp=UINPBA00004N&text.app=https://www.elsevier.es/" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/S2387020624002079?idApp=UINPBA00004N" ]
