<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-14T03:53:31Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/12148" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/12148</identifier><datestamp>2025-05-08T08:53:44Z</datestamp><setSpec>com_20.500.12105_2052</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>col_20.500.12105_19627</setSpec></header><metadata><record xmlns="http://www.loc.gov/MARC21/slim" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.loc.gov/MARC21/slim http://www.loc.gov/standards/marcxml/schema/MARC21slim.xsd">
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      <subfield code="a">Bermejo, Javier</subfield>
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      <subfield code="a">González-Mansilla, Ana</subfield>
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      <subfield code="a">Mombiela, Teresa</subfield>
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      <subfield code="a">Fernández, Ana I</subfield>
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      <subfield code="a">Martínez-Legazpi, Pablo</subfield>
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      <subfield code="a">Yotti-Alvarez, Raquel</subfield>
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      <subfield code="a">García-Orta, Rocío</subfield>
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      <subfield code="a">Sánchez-Fernández, Pedro L</subfield>
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      <subfield code="a">Castaño, Mario</subfield>
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      <subfield code="a">Segovia-Cubero, Javier</subfield>
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      <subfield code="a">Escribano-Subias, Pilar</subfield>
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      <subfield code="a">Alberto San Román, J</subfield>
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      <subfield code="a">Borrás, Xavier</subfield>
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      <subfield code="a">Alonso-Gómez, Angel</subfield>
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      <subfield code="a">Botas, Javier</subfield>
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      <subfield code="a">Crespo-Leiro, María G</subfield>
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      <subfield code="a">Velasco, Sonia</subfield>
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      <subfield code="a">Bayes-Genis, Antoni</subfield>
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      <subfield code="a">López, Amador</subfield>
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      <subfield code="a">Muñoz-Aguilera, Roberto</subfield>
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      <subfield code="a">Jiménez-Navarro, Manuel</subfield>
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      <subfield code="a">Gonzalez-Juanatey, Jose R</subfield>
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      <subfield code="a">Evangelista, Arturo</subfield>
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      <subfield code="a">Elizaga, Jaime</subfield>
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      <subfield code="a">Martín-Moreiras, Javier</subfield>
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      <subfield code="a">González-Santos, José M</subfield>
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      <subfield code="a">Moreno-Escobar, Eduardo</subfield>
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      <subfield code="a">Fernández-Avilés, Francisco</subfield>
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   <datafield ind2=" " ind1=" " tag="260">
      <subfield code="c">2021-01-19</subfield>
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      <subfield code="a">Background The determinants and consequences of pulmonary hypertension after successfully corrected valvular heart disease remain poorly understood. We aim to clarify the hemodynamic bases and risk factors for mortality in patients with this condition. Methods and Results We analyzed long-term follow-up data of 222 patients with pulmonary hypertension and valvular heart disease successfully corrected at least 1 year before enrollment who had undergone comprehensive hemodynamic and imaging characterization as per the SIOVAC (Sildenafil for Improving Outcomes After Valvular Correction) clinical trial. Median (interquartile range) mean pulmonary pressure was 37 mm Hg (32-44 mm Hg) and pulmonary artery wedge pressure was 23 mm Hg (18-26 mm Hg). Most patients were classified either as having combined precapillary and postcapillary or isolated postcapillary pulmonary hypertension. After a median follow-up of 4.5 years, 91 deaths accounted for 4.21 higher-than-expected mortality in the age-matched population. Risk factors for mortality were male sex, older age, diabetes mellitus, World Health Organization functional class III and higher pulmonary vascular resistance-either measured by catheterization or approximated from ultrasound data. Higher pulmonary vascular resistance was related to diabetes mellitus and smaller residual aortic and mitral valve areas. In turn, the latter correlated with prosthetic nominal size. Six-month changes in the composite clinical score and in the 6-minute walk test distance were related to survival. Conclusions Persistent valvular heart disease-pulmonary hypertension is an ominous disease that is almost universally associated with elevated pulmonary artery wedge pressure. Pulmonary vascular resistance is a major determinant of mortality in this condition and is related to diabetes mellitus and the residual effective area of the corrected valve. These findings have important implications for individualizing valve correction procedures. Registration URL: https://www.clinicaltrials.gov; Unique identifier: NCT00862043.</subfield>
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      <subfield code="a">J Am Heart Assoc  . 2021 Jan 19;10(2):e019949.</subfield>
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      <subfield code="a">10.1161/JAHA.120.019949</subfield>
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      <subfield code="a">2047-9980</subfield>
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      <subfield code="a">Journal of the American Heart Association</subfield>
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      <subfield code="a">33399006</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/12148</subfield>
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      <subfield code="a">Heart failure</subfield>
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      <subfield code="a">Pulmonary hypertension</subfield>
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   <datafield tag="653" ind2=" " ind1=" ">
      <subfield code="a">Valvular heart diseas</subfield>
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   <datafield ind2="0" ind1="0" tag="245">
      <subfield code="a">Persistent Pulmonary Hypertension in Corrected Valvular Heart Disease: Hemodynamic Insights and Long-Term Survival</subfield>
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