<?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>2026-04-14T03:40:31Z</responseDate><request verb="GetRecord" identifier="oai:www.recercat.cat:2445/224922" metadataPrefix="oai_dc">https://recercat.cat/oai/request</request><GetRecord><record><header><identifier>oai:recercat.cat:2445/224922</identifier><datestamp>2026-04-08T13:58:14Z</datestamp><setSpec>com_2072_1057</setSpec><setSpec>col_2072_478916</setSpec><setSpec>col_2072_478917</setSpec></header><metadata><oai_dc:dc xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
   <dc:title>One-year longitudinal changes of peripheral CD4+ T-lymphocyte counts, gut microbiome, and plaque vulnerability after an acute coronary syndrome</dc:title>
   <dc:creator>Fernández Ávila, Ana I.</dc:creator>
   <dc:creator>Gutiérrez Ibañes, Enrique</dc:creator>
   <dc:creator>Martín de Miguel, Irene</dc:creator>
   <dc:creator>Sanz Ruiz, Ricardo</dc:creator>
   <dc:creator>Gabaldón, Álvaro</dc:creator>
   <dc:creator>Fernández Avilés, Francisco</dc:creator>
   <dc:creator>Gómez Lara, Josep</dc:creator>
   <dc:creator>Fernández Castillo, Marta</dc:creator>
   <dc:creator>Vázquez Cuesta, Silvia</dc:creator>
   <dc:creator>Martínez Legazpi, Pablo</dc:creator>
   <dc:creator>Lozano Garcia, Nuria</dc:creator>
   <dc:creator>Blázquez López, Elena</dc:creator>
   <dc:creator>Yotti, Raquel</dc:creator>
   <dc:creator>López Cade, Igor</dc:creator>
   <dc:creator>Reigadas, Elena</dc:creator>
   <dc:creator>Muñoz, Patricia</dc:creator>
   <dc:creator>Elízaga, Jaime</dc:creator>
   <dc:creator>Correa, Rafael</dc:creator>
   <dc:creator>Bermejo, Javier</dc:creator>
   <dc:subject>Microbiota intestinal</dc:subject>
   <dc:subject>Sistema immunitari</dc:subject>
   <dc:subject>Malalties coronàries</dc:subject>
   <dc:subject>Gastrointestinal microbiome</dc:subject>
   <dc:subject>Immune system</dc:subject>
   <dc:subject>Coronary diseases</dc:subject>
   <dc:description>Background: Longitudinal changes in gut microbiome and inflammation may be involved in the evolution of atherosclerosis after an acute coronary syndrome (ACS). We aimed to characterize repeated profiles of gut microbiota and peripheral CD4 + T lymphocytes during the first year after an ACS, and to address their relationship with atherosclerotic plaque changes. Methods: Over one year we measured the microbiome, peripheral counts of CD4 + T populations and cytokines in 67 patients shortly after a first ACS. We compared baseline measurements to those of a matched population of 40 chronic patients. A subgroup of 20 ACS patients underwent repeated assessment of fibrous cap thickness (FCT) of a non-culprit lesion. Results: At admission, ACS patients showed gut dysbiosis compared with the chronic group, which was rapidly reduced and remained low at 1-year. Also, their Th1 and Th2 CD4 + T counts were increased but decreased over time. The CD4 + T counts were related to ongoing changes in gut microbiome. Unsupervised clustering of repeated CD4 + Th0, Th1, Th2, Th17 and Treg counts in ACS patients identified two different cell trajectory patterns, related to cytokines. The group of patients following a high-CD4 + T cell trajectory showed a one-year reduction in their FCT [net effect = -24.2 mu m; p = 0.016]. Conclusions: Patients suffering an ACS show altered profiles of microbiome and systemic inflammation that tend to mimic values of chronic patients after 1-year. However, in one-third of patients, this inflammatory state remains particularly dysregulated. This persistent inflammation is likely related to plaque vulnerability as evident by fibrous cap thinning (Clinical Trial NCT03434483).</dc:description>
   <dc:date>2025-12-15T12:53:06Z</dc:date>
   <dc:date>2025-12-15T12:53:06Z</dc:date>
   <dc:date>2024-06-04</dc:date>
   <dc:date>2025-12-11T15:05:13Z</dc:date>
   <dc:type>info:eu-repo/semantics/article</dc:type>
   <dc:type>info:eu-repo/semantics/publishedVersion</dc:type>
   <dc:identifier>2352-9067</dc:identifier>
   <dc:identifier>https://hdl.handle.net/2445/224922</dc:identifier>
   <dc:identifier>38912228</dc:identifier>
   <dc:language>eng</dc:language>
   <dc:relation>Reproducció del document publicat a: https://doi.org/10.1016/j.ijcha.2024.101438</dc:relation>
   <dc:relation>IJC Heart &amp; Vasculature, 2024, vol. 53, 101438</dc:relation>
   <dc:relation>https://doi.org/10.1016/j.ijcha.2024.101438</dc:relation>
   <dc:rights>cc-by (c) Fernández Ávila, Ana I. et al., 2024</dc:rights>
   <dc:rights>https://creativecommons.org/licenses/by/4.0/</dc:rights>
   <dc:rights>info:eu-repo/semantics/openAccess</dc:rights>
   <dc:format>9 p.</dc:format>
   <dc:format>application/pdf</dc:format>
   <dc:publisher>Elsevier BV</dc:publisher>
   <dc:source>Articles publicats en revistes (Institut d'lnvestigació Biomèdica de Bellvitge (IDIBELL))</dc:source>
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