<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>1405-9940</journal-id>
<journal-title><![CDATA[Archivos de cardiología de México]]></journal-title>
<abbrev-journal-title><![CDATA[Arch. Cardiol. Méx.]]></abbrev-journal-title>
<issn>1405-9940</issn>
<publisher>
<publisher-name><![CDATA[Instituto Nacional de Cardiología Ignacio Chávez]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1405-99402020000100059</article-id>
<article-id pub-id-type="doi">10.24875/acme.m20000085</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Genes frequently associated with sudden death in primary hypertrophic cardiomyopathy]]></article-title>
<article-title xml:lang="es"><![CDATA[Genes frecuentemente asociados con muerte súbita en miocardiopatía hipertrófica primaria]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Herrera-Rodríguez]]></surname>
<given-names><![CDATA[Diana L.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Totomoch-Serra]]></surname>
<given-names><![CDATA[Armando]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rosas-Madrigal]]></surname>
<given-names><![CDATA[Sandra]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Luna-Limón]]></surname>
<given-names><![CDATA[Claudia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Marroquín-Ramírez]]></surname>
<given-names><![CDATA[Daniel]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Carnevale]]></surname>
<given-names><![CDATA[Alessandra]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rosendo-Gutiérrez]]></surname>
<given-names><![CDATA[Rigoberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Villarreal-Molina]]></surname>
<given-names><![CDATA[María T.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Márquez-Murillo]]></surname>
<given-names><![CDATA[Manlio F.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto Politécnico Nacional  ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Instituto Politécnico Nacional Center of Research and Advanced Studies Department of Genetics and Molecular Biology]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad de la Frontera PhD Program in Medical Sciences ]]></institution>
<addr-line><![CDATA[Temuco ]]></addr-line>
<country>Chile</country>
</aff>
<aff id="Af4">
<institution><![CDATA[,Instituto Nacional de Medicina Genómica Laboratory of Cardiovascular Diseases ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af5">
<institution><![CDATA[,Instituto Nacional de Cardiología Department of Electrocardiology ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<aff id="Af6">
<institution><![CDATA[,Instituto Nacional de Medicina Genómica Laboratory of Mendelian Diseases ]]></institution>
<addr-line><![CDATA[Mexico City ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2020</year>
</pub-date>
<volume>90</volume>
<numero>1</numero>
<fpage>59</fpage>
<lpage>68</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1405-99402020000100059&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1405-99402020000100059&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1405-99402020000100059&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Hypertrophic cardiomyopathy (HCM) is characterized by left ventricular hypertrophy without apparent cardiac justification. Sudden cardiac death may be the first manifestation of the disease. It occurs mainly in adulthood and can be seen in childhood and adolescence where genetic origin predominates. Primary HCM (“familial”) is inherited in an autosomal dominant pattern in the 25 subtypes informed in Online Mendelian Inheritance in Man. The proteins encoded by the mutated genes are part of the sarcomere in the cardiac cells, being the thick filament the most frequently affected, with the worst prognosis. In the present article, we describe the Mendelian inheritance of the disease and the two most associated genes with sudden death: MYBPC3 and MYH7.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen La miocardiopatía hipertrófica (MCH) es el aumento de grosor de la pared ventricular izquierda no relacionada con otras alteraciones cardíacas. Es una enfermedad que puede presentar como primera manifestación clínica la muerte súbita y de ahí su relevancia clínica. Aunque se presenta sobre todo en la edad adulta, puede aparecer durante la infancia y adolescencia, en las que predominan los casos de origen hereditario. La MCH primaria, de causa genética, muestra en particular un patrón de herencia autosómico dominante en los 25 subtipos reconocidos en OMIM (Online Mendelian Inheritance in Man). Las proteínas codificadas por los genes mutantes forman parte del sarcómero en células musculares cardíacas, y las variantes patogénicas de filamentos gruesos son las de mayor frecuencia y peor pronóstico. En este artículo se describen la herencia mendeliana de la enfermedad y la relación con muerte súbita de los genes más frecuentemente encontrados en ella: MYBPC3 y MYH7.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Hypertrophic cardiomyopathy]]></kwd>
<kwd lng="en"><![CDATA[Genes]]></kwd>
<kwd lng="en"><![CDATA[Gene variants]]></kwd>
<kwd lng="en"><![CDATA[MYBPC3]]></kwd>
<kwd lng="en"><![CDATA[MYH7]]></kwd>
<kwd lng="en"><![CDATA[Sudden cardiac death]]></kwd>
<kwd lng="es"><![CDATA[Miocardiopatía hipertrófica]]></kwd>
<kwd lng="es"><![CDATA[Genes]]></kwd>
<kwd lng="es"><![CDATA[MYBPC3]]></kwd>
<kwd lng="es"><![CDATA[MYH7]]></kwd>
<kwd lng="es"><![CDATA[Variantes genéticas]]></kwd>
<kwd lng="es"><![CDATA[Muerte súbita]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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