<?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>S1405-99402016000100064</article-id>
<article-id pub-id-type="doi">10.1016/j.acmx.2015.09.009</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Estudio comparativo de los cambios funcionales y estructurales producidos en un modelo porcino de infarto de miocardio agudo y crónico]]></article-title>
<article-title xml:lang="en"><![CDATA[Comparative study of functional and structural changes produced in a porcine model of acute and chronic heart attack]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hernándiz]]></surname>
<given-names><![CDATA[Amparo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Cerrada]]></surname>
<given-names><![CDATA[Inmaculada]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Díez]]></surname>
<given-names><![CDATA[José Luis]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Ferrando]]></surname>
<given-names><![CDATA[Mónica]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sepúlveda]]></surname>
<given-names><![CDATA[Pilar]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Instituto de Investigación Sanitaria La Fe Unidad de Cardiología Experimental ]]></institution>
<addr-line><![CDATA[Valencia ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Hospital General Universitario Servicio de Cardiología ]]></institution>
<addr-line><![CDATA[Valencia ]]></addr-line>
<country>Spain</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Hospital Universitario Dr. Peset Unidad de Hemodinámica ]]></institution>
<addr-line><![CDATA[Valencia ]]></addr-line>
<country>Spain</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>03</month>
<year>2016</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>03</month>
<year>2016</year>
</pub-date>
<volume>86</volume>
<numero>1</numero>
<fpage>64</fpage>
<lpage>74</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1405-99402016000100064&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1405-99402016000100064&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1405-99402016000100064&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen:  Introducción y objetivos:  Los modelos animales son una herramienta muy útil para la evaluación de los mecanismos de la enfermedad y las tecnologías de diagnóstico y tratamiento. En este estudio hemos realizado un análisis descriptivo de los cambios funcionales y estructurales cardíacos acontecidos como consecuencia de un infarto agudo por oclusión coronaria en cerdos y su evolución a 5 semanas.  Métodos:  Se utilizaron 19 cerdos, Large White, de 20 kg de peso, distribuidos aleatorizadamente en 3 series experimentales. Tras estereotomía, se ocluyó la arteria coronaria descendente anterior. Duración de la oclusión: serie 1 (n = 6) 60 min; serie 2 (n = 8) 90 min; serie 3 (n = 5) 60 min, con seguimiento de 5 semanas. Se evaluaron parámetros de función cardíaca global (ECG, presiones de ventrículo y aurícula izquierdos, flujo aórtico y ecocardiografía cardíaca), regional (sonometría), niveles de troponina T y CK-MB, análisis macroscópico e histológico.  Resultados:  La oclusión coronaria alteró la función cardíaca global transitoriamente y produjo daño celular con incremento de marcadores, alteración de la contractilidad regional y cambios histológicos. El incremento de tiempo de isquemia (60 vs. 90 min) aumentó el tamaño del infarto (13.4 ± 5.4% S1 vs. 22.9 ± 7.8% S2; p = 0.04). A las 5 semanas eran patentes los cambios morfológicos por remodelado. En el 79% de los casos la isquemia desencadenó fibrilación ventricular.  Conclusión:  El modelo porcino de infarto agudo y reperfusión posterior a tórax abierto es válido para el estudio de la fisiopatología de la isquemia coronaria, permite el análisis directo de la función miocárdica regional y es fácilmente recuperable en caso de arritmias graves.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract:  Introduction and objectives:  Animal models are a useful tool for the evaluation of disease mechanisms and also for technologies for diagnosis and treatment. In this study we performed a descriptive analysis of the functional and structural cardiac changes occurred as a result of acute coronary occlusion in pigs and its evolution during 5 weeks.  Methods:  19-Large White pigs, weighing 20 kg, randomized into 3-experimental series were used. After sternotomy, anterior descending coronary artery was occluded. Duration of occlusion: Series 1 (n = 6) 60 min; series 2 (n = 8) 90 min; series 3 (n = 5) 60 min followed for 5 weeks. The following parameters where then analyzed: global cardiac function (ECG, left ventricular and atrium pressures, aortic flow and cardiac echocardiography), regional contractility, troponin T and CK-MB levels, macroscopic and histological analyzes.  Results:  Coronary occlusion transiently altered the global cardiac function and produced increased cell damage markers, impaired regional contractility and produced histological changes. The increment of ischemic time (60 vs. 90 min) increased infarct size (13.4 ± 5.4% vs. 22.9 ± 7.8 S1 S2%; P=.04). After 5 weeks, morphological remodelling changes were evident. In 79% of cases ischemia triggered ventricular fibrillation.  Conclusion:  The porcine open chest model of acute myocardial infarction and reperfusion is valid for studying the pathophysiology of coronary ischemia, allows direct analysis of regional myocardial function and is easily retrievable in the event of serious arrhythmias.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[Isquemia cardíaca]]></kwd>
<kwd lng="es"><![CDATA[Remodelado cardíaco]]></kwd>
<kwd lng="es"><![CDATA[Modelo experimental]]></kwd>
<kwd lng="es"><![CDATA[España]]></kwd>
<kwd lng="en"><![CDATA[Cardiac ischaemia]]></kwd>
<kwd lng="en"><![CDATA[Cardiac remodeling]]></kwd>
<kwd lng="en"><![CDATA[Experimental model]]></kwd>
<kwd lng="en"><![CDATA[Spain]]></kwd>
</kwd-group>
</article-meta>
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