<?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>2026-06-30T03:04:03Z</responseDate><request verb="GetRecord" identifier="oai:repisalud.isciii.es:20.500.12105/11189" metadataPrefix="marc">https://repisalud.isciii.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:repisalud.isciii.es:20.500.12105/11189</identifier><datestamp>2024-11-28T15:51:47Z</datestamp><setSpec>com_20.500.12105_19604</setSpec><setSpec>com_20.500.12105_2051</setSpec><setSpec>com_20.500.12105_15322</setSpec><setSpec>col_20.500.12105_19605</setSpec><setSpec>col_20.500.12105_16938</setSpec><setSpec>col_20.500.12105_16967</setSpec><setSpec>col_20.500.12105_16969</setSpec><setSpec>col_20.500.12105_16977</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">Rossello, Xavier</subfield>
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      <subfield code="a">Fuster, Valentin</subfield>
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      <subfield code="a">Oliva, Belen</subfield>
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      <subfield code="a">Sanz, Javier</subfield>
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      <subfield code="a">Fernandez-Friera, Leticia</subfield>
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      <subfield code="a">Lopez-Melgar, Beatriz</subfield>
      <subfield code="e">author</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Mendiguren, Jose M</subfield>
      <subfield code="e">author</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Lara-Pezzi, Enrique</subfield>
      <subfield code="e">author</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Bueno, Hector</subfield>
      <subfield code="e">author</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Fernandez-Ortiz, Antonio</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Ibáñez, Borja</subfield>
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   <datafield ind2=" " ind1=" " tag="720">
      <subfield code="a">Ordovas, Jose M</subfield>
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      <subfield code="c">2020-12-01</subfield>
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      <subfield code="a">Context: The underlying relationship between body mass index (BMI), cardiometabolic disorders, and subclinical atherosclerosis is poorly understood. Objective: To evaluate the association between body size phenotypes and subclinical atherosclerosis. Design: Cross-sectional. Setting: Cardiovascular disease-free cohort. Participants: Middle-aged asymptomatic subjects (n = 3909). A total of 6 cardiometabolic body size phenotypes were defined based on the presence of at least 1 cardiometabolic abnormality (blood pressure, fasting blood glucose, triglycerides, low high-density lipoprotein cholesterol, homeostasis model assessment-insulin resistance index, high-sensitivity C-reactive protein) and based on BMI: normal-weight (NW; BMI &lt;25), overweight (OW; BMI = 25.0-29.9) or obese (08; BMI >30.0). Main Outcome Measures: Subclinical atherosclerosis was evaluated by 2D vascular ultrasonography and noncontrast cardiac computed tomography. Results: For metabolically healthy subjects, the presence of subclinical atherosclerosis increased across BMI categories (49.6%, 58.0%, and 67.7% for NW, OW, and OB, respectively), whereas fewer differences were observed for metabolically unhealthy subjects (61.1%, 69.7%, and 70.5%, respectively). When BMI and cardiometabolic abnormalities were assessed separately, the association of body size phenotypes with the extent of subclinical atherosclerosis was mostly driven by the coexistence of cardiometabolic risk factors: adjusted OR = 1.04 (95% confidence interval [CI), 0.90-1.19) for OW and OR = 1.07 (95% CI, 0.88-1.30) for OB in comparison with NW, whereas there was an increasing association between the extent of subclinical atherosclerosis and the number of cardiometabolic abnormalities: adjusted OR = 1.21 (95% CI, 1.05-1.40),1.60 (95% Cl, 1.33-1.93), 1.92 (95% CI, 1.48-2.50), and 2.27 (95% Cl, 1.67-3.09) for 1, 2, 3, and >3, respectively, in comparison with noncardiometabolic abnormalities. Conclusions: The prevalence of subclinical atherosclerosis varies across body size phenotypes. Pharmacologic and lifestyle interventions might modify their cardiovascular risk by facilitating the transition from one phenotype to another.</subfield>
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      <subfield code="a">J Clin Endocrinol Metab. 2020; 105(12):dgaa620</subfield>
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      <subfield code="a">10.1210/clinem/dgaa620</subfield>
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      <subfield code="a">1945-7197</subfield>
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   <datafield ind1="8" ind2=" " tag="024">
      <subfield code="a">The Journal of clinical endocrinology and metabolism</subfield>
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   <datafield ind1="8" ind2=" " tag="024">
      <subfield code="a">http://hdl.handle.net/20.500.13003/15219</subfield>
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      <subfield code="a">32879953</subfield>
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      <subfield code="a">L2010072475</subfield>
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      <subfield code="a">2-s2.0-85092120313</subfield>
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      <subfield code="a">http://hdl.handle.net/20.500.12105/11189</subfield>
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      <subfield code="a">584547800050</subfield>
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      <subfield code="a">Body size phenotypes</subfield>
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      <subfield code="a">Obesity</subfield>
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      <subfield code="a">Subclinical atherosclerosis</subfield>
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      <subfield code="a">Association Between Body Size Phenotypes and Subclinical Atherosclerosis</subfield>
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