<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>4(5)</volume><submitter>Rikken SAOF</submitter><funding>CSL Behring LLC</funding><pubmed_abstract>&lt;h4>Background&lt;/h4>The AEGIS-II (ApoA-I Event Reducing in Ischemic Syndromes-II; NCT03473223) trial evaluated CSL112, a human plasma-derived apolipoprotein A-I therapy, for reducing cardiovascular events after acute myocardial infarction (AMI). Given CSL112's potential anti-inflammatory properties, we conducted an exploratory post hoc analysis to determine if its efficacy is influenced by baseline neutrophil-lymphocyte ratio (NLR), a marker of systemic inflammation, and low-density lipoprotein cholesterol (LDL-C).&lt;h4>Objectives&lt;/h4>The purpose of this study was to investigate the association of baseline NLR and cardiovascular events and explore whether NLR and LDL-C modify CSL112's efficacy in post-AMI patients.&lt;h4>Methods&lt;/h4>A total of 18,219 participants with AMI, multivessel coronary a</pubmed_abstract><journal>JACC. Advances</journal><pagination>101727</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12059331</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Impact of Apolipoprotein A-I Infusions on Cardiovascular Events Post-MI by Neutrophil-Lymphocyte Ratio and LDL-Cholesterol Levels.</pubmed_title><pmcid>PMC12059331</pmcid><pubmed_authors>Korjian S</pubmed_authors><pubmed_authors>Steg PG</pubmed_authors><pubmed_authors>White H</pubmed_authors><pubmed_authors>van 't Hof AWJ</pubmed_authors><pubmed_authors>Mahaffey KW</pubmed_authors><pubmed_authors>AEGIS-II Committees and Investigators</pubmed_authors><pubmed_authors>Cornel JH</pubmed_authors><pubmed_authors>Chi G</pubmed_authors><pubmed_authors>Anschuetz G</pubmed_authors><pubmed_authors>Duffy D</pubmed_authors><pubmed_authors>Goodman SG</pubmed_authors><pubmed_authors>Ten Berg JM</pubmed_authors><pubmed_authors>Nicholls SJ</pubmed_authors><pubmed_authors>Lopes RD</pubmed_authors><pubmed_authors>Kingwell BA</pubmed_authors><pubmed_authors>Gibson CM</pubmed_authors><pubmed_authors>Bahit MC</pubmed_authors><pubmed_authors>Mehran R</pubmed_authors><pubmed_authors>Ridker PM</pubmed_authors><pubmed_authors>Rikken SAOF</pubmed_authors><pubmed_authors>Ophuis TO</pubmed_authors><pubmed_authors>Bainey KR</pubmed_authors><pubmed_authors>Harrington RA</pubmed_authors><pubmed_authors>Nicolau JC</pubmed_authors><pubmed_authors>Lewis BS</pubmed_authors><pubmed_authors>Vinereanu D</pubmed_authors><pubmed_authors>Libby P</pubmed_authors><pubmed_authors>Mohammadnia N</pubmed_authors><pubmed_authors>Bode C</pubmed_authors><pubmed_authors>El Messaoudi S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of Apolipoprotein A-I Infusions on Cardiovascular Events Post-MI by Neutrophil-Lymphocyte Ratio and LDL-Cholesterol Levels.</name><description>&lt;h4>Background&lt;/h4>The AEGIS-II (ApoA-I Event Reducing in Ischemic Syndromes-II; NCT03473223) trial evaluated CSL112, a human plasma-derived apolipoprotein A-I therapy, for reducing cardiovascular events after acute myocardial infarction (AMI). Given CSL112's potential anti-inflammatory properties, we conducted an exploratory post hoc analysis to determine if its efficacy is influenced by baseline neutrophil-lymphocyte ratio (NLR), a marker of systemic inflammation, and low-density lipoprotein cholesterol (LDL-C).&lt;h4>Objectives&lt;/h4>The purpose of this study was to investigate the association of baseline NLR and cardiovascular events and explore whether NLR and LDL-C modify CSL112's efficacy in post-AMI patients.&lt;h4>Methods&lt;/h4>A total of 18,219 participants with AMI, multivessel coronary a</description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 May</publication><modification>2026-06-01T05:23:25.707Z</modification><creation>2026-04-08T09:36:12.868Z</creation></dates><accession>S-EPMC12059331</accession><cross_references><pubmed>40288083</pubmed><doi>10.1016/j.jacadv.2025.101727</doi></cross_references></HashMap>