<?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>1688-0420</journal-id>
<journal-title><![CDATA[Revista Uruguaya de Cardiología]]></journal-title>
<abbrev-journal-title><![CDATA[Rev.Urug.Cardiol.]]></abbrev-journal-title>
<issn>1688-0420</issn>
<publisher>
<publisher-name><![CDATA[Sociedad Uruguaya de Cardiología]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1688-04202017000100023</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Alteraciones electrocardiográficas en una cohorte de pacientes con miocardiopatía hipertrófica septal asimétrica]]></article-title>
<article-title xml:lang="en"><![CDATA[Electrocardiographic changes in patients with septal asymmetric hypertrophic cardiomyopathy]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ferrando-Castagnetto]]></surname>
<given-names><![CDATA[Federico]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Pedemonte]]></surname>
<given-names><![CDATA[Óscar]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Torterolo]]></surname>
<given-names><![CDATA[Alicia]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ricca-Mallada]]></surname>
<given-names><![CDATA[Roberto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Hospital de Clínicas Centro Cardiovascular Universitario Departamento de Cardiología]]></institution>
<addr-line><![CDATA[Montevideo ]]></addr-line>
<country>Uruguay</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>04</month>
<year>2017</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>04</month>
<year>2017</year>
</pub-date>
<volume>32</volume>
<numero>1</numero>
<fpage>23</fpage>
<lpage>34</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.edu.uy/scielo.php?script=sci_arttext&amp;pid=S1688-04202017000100023&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.edu.uy/scielo.php?script=sci_abstract&amp;pid=S1688-04202017000100023&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.edu.uy/scielo.php?script=sci_pdf&amp;pid=S1688-04202017000100023&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción:  ciertos hallazgos del electrocardiograma (ECG) de superficie sugieren el diagnóstico de miocardiopatía hipertrófica (MCH) y se correlacionan directamente con su expresión fenotípica. Sin embargo, las modificaciones ECG han sido escasamente descritas en series locales y regionales. El objetivo de este estudio fue caracterizar los cambios ECG en la MCH, correlacionándolos con variables clínicas y estructurales.  Método:  se interpretaron los ECG en una cohorte de 26 pacientes con MCH septal asimétrica referidos a la policlínica especializada del Centro Cardiovascular Universitario del Uruguay. Todos los pacientes fueron estudiados con ecocardiograma Doppler y 13 de ellos, además, con resonancia nuclear magnética cardíaca (RNMC) para evaluar la presencia, extensión y distribución del realce tardío de gadolinio (RTG) como marcador de fibrosis intramiocárdica. La correlación de los hallazgos ECG con los síntomas, severidad de la hipertrofia y presencia y extensión de la fibrosis intramiocárdica se analizó mediante la prueba exacta de Fisher o el test no paramétrico de Mann-Whitney.  Resultados:  el hallazgo de un ECG normal fue muy infrecuente en nuestra serie (8,0%). Las alteraciones ECG más comunes se observaron en la repolarización ventricular (76,9%) bajo forma de sobrecarga sistólica (42,3%) e inversión de la onda T (30,7%). Los signos de sobrecarga auricular izquierda (53,8%), hipertrofia ventricular izquierda (61,5%), fragmentación del QRS (46,2%) y ondas Q anormales (30,7%) fueron menos frecuentes. Los criterios de hipertrofia no se correlacionaron con los síntomas, el espesor parietal, la obstrucción al tracto de salida del ventrículo izquierdo ni la presencia de RTG en la RNMC. No encontramos asociación significativa entre la fragmentación del QRS o la presencia de ondas Q y el hallazgo de RTG en la RNMC. Aunque los pacientes con hipertrofia septal más severa presentaban extensas áreas de fibrosis, esta relación no alcanzó significación estadística.  Conclusión:  el trazado ECG es anormal en la gran mayoría (92,0%) de los pacientes con MCH septal asimétrica, y se caracteriza por alteraciones diversas, lo que confirma su utilidad como herramienta de tamizaje. Sin embargo, en nuestra serie los hallazgos ECG no se correlacionan con los síntomas, el espesor parietal ni la presencia de fibrosis intramiocárdica. La contribución diagnóstica de signos ECG combinados y su potencial valor pronóstico en diferentes variantes fenotípicas de MCH merecen ser evaluados en series locales más amplias.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Summary  Introduction:  in many cases, surface ECG suggests the diagnosis of hypertrophic cardiomyopathy (HCM) and is directly related to phenotypic expression. However, ECG changes have been not fully described in regional and local case series. Our study was aimed to characterize the ECG abnormalities in patients with HCM, correlating these findings with clinical and structural variables.  Method:  ECG recordings were interpreted in a cohort of 26 subjects with asymmetric septal HCM. All patients were studied by echocardiogram, adding MRI in 13 cases to evaluate the presence, extension and distribution of late gadolinium enhancement (LGE) as a marker of myocardial fibrosis. The correlation of ECG findings with symptoms, severity of hypertrophy and presence and extension of myocardial fibrosis was analyzed using Fisher&#8217;s exact test or non-parametric Mann-Whitney test.  Results:  the presence of a normal ECG was very infrequent in our sample (8,0%). The most common ECG abnormalities were observed in ventricular repolarization (76,9%) as systolic overload (42,3%) and T wave inversion (30,7%). ECG signs suggesting left atrium dilation (53,8%), left ventricle hypertrophy (LVH) criteria (61,5%), QRS fragmentation (46,2%) and abnormal Q waves (30,7%) were less frequently found. LVH was not correlated with symptoms, wall thickness, left ventricular outflow tract obstruction or presence of LGE. We found no significant relationship between LGE and fragmented QRS or abnormal Q waves. While patients with more severe septal hypertrophy exhibited large areas of LGE, this relationship did not reach statistical significance.  Conclusion:  in our cohort, the ECG is abnormal in 92,0% of patients with asymmetric septal HCM and is characterized by various alterations, confirming its usefulness as a screening tool. However, the findings in the ECG did not correlate closely with symptoms, amount of hypertrophy or presence of myocardial fibrosis. Larger local series must evaluate diagnostic contribution of combined ECG findings and its potential prognostic value in different phenotypic variants of HCM.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[CARDIOMIOPATÍA HIPERTRÓFICA]]></kwd>
<kwd lng="es"><![CDATA[ELECTROCARDIOGRAFÍA]]></kwd>
<kwd lng="es"><![CDATA[FIBROSIS.]]></kwd>
<kwd lng="en"><![CDATA[HYPERTROPHIC CARDIOMYOPATHY]]></kwd>
<kwd lng="en"><![CDATA[ELECTROCARDIOGRAPHY]]></kwd>
<kwd lng="en"><![CDATA[FIBROSIS.]]></kwd>
</kwd-group>
</article-meta>
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