<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Girard A</submitter><funding>Joseph C. Edwards</funding><funding>Canada Research Chair on Women’s Cardiac Valvular Health</funding><funding>Medical Research Council</funding><funding>Canadian Institutes of Health</funding><funding>Quebec Heart and Lung Institute</funding><pagination>oead032</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC10108885</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>3(2)</volume><pubmed_abstract>&lt;h4>Aims&lt;/h4>Elevated lipoprotein(a) [Lp(a)] levels are associated with the risk of coronary artery disease (CAD) and calcific aortic valve stenosis (CAVS). Observational studies revealed that Lp(a) and C-reactive protein (CRP) levels, a biomarker of systemic inflammation, may jointly predict CAD risk. Whether Lp(a) and CRP levels also jointly predict CAVS incidence and progression is unknown.&lt;h4>Methods and results&lt;/h4>We investigated the association of Lp(a) with CAVS according to CRP levels in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study (&lt;i>n&lt;/i> = 18 226, 406 incident cases) and the UK Biobank (&lt;i>n&lt;/i> = 438 260, 4582 incident cases), as well as in the ASTRONOMER study (&lt;i>n&lt;/i> = 220), which assessed the haemodynamic progression rate of pre-e</pubmed_abstract><journal>European heart journal open</journal><pubmed_title>Impact of C-reactive protein levels on lipoprotein(a)-associated aortic stenosis incidence and progression.</pubmed_title><pmcid>PMC10108885</pmcid><funding_grant_id>MC_UU_00006/1</funding_grant_id><pubmed_authors>Boekholdt SM</pubmed_authors><pubmed_authors>Puri R</pubmed_authors><pubmed_authors>Mathieu P</pubmed_authors><pubmed_authors>Gaillard E</pubmed_authors><pubmed_authors>Theriault S</pubmed_authors><pubmed_authors>Paulin A</pubmed_authors><pubmed_authors>Dumesnil J</pubmed_authors><pubmed_authors>Capoulade R</pubmed_authors><pubmed_authors>Stroes ESG</pubmed_authors><pubmed_authors>Chan KL</pubmed_authors><pubmed_authors>Tam JW</pubmed_authors><pubmed_authors>Clavel MA</pubmed_authors><pubmed_authors>Pibarot P</pubmed_authors><pubmed_authors>Girard A</pubmed_authors><pubmed_authors>Tsimikas S</pubmed_authors><pubmed_authors>Wareham NJ</pubmed_authors><pubmed_authors>Teo KK</pubmed_authors><pubmed_authors>Couture C</pubmed_authors><pubmed_authors>Arsenault BJ</pubmed_authors><pubmed_authors>Manikpurage HD</pubmed_authors></additional><is_claimable>false</is_claimable><name>Impact of C-reactive protein levels on lipoprotein(a)-associated aortic stenosis incidence and progression.</name><description>&lt;h4>Aims&lt;/h4>Elevated lipoprotein(a) [Lp(a)] levels are associated with the risk of coronary artery disease (CAD) and calcific aortic valve stenosis (CAVS). Observational studies revealed that Lp(a) and C-reactive protein (CRP) levels, a biomarker of systemic inflammation, may jointly predict CAD risk. Whether Lp(a) and CRP levels also jointly predict CAVS incidence and progression is unknown.&lt;h4>Methods and results&lt;/h4>We investigated the association of Lp(a) with CAVS according to CRP levels in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Norfolk study (&lt;i>n&lt;/i> = 18 226, 406 incident cases) and the UK Biobank (&lt;i>n&lt;/i> = 438 260, 4582 incident cases), as well as in the ASTRONOMER study (&lt;i>n&lt;/i> = 220), which assessed the haemodynamic progression rate of pre-e</description><dates><release>2023-01-01T00:00:00Z</release><publication>2023 Mar</publication><modification>2026-05-28T08:06:27.354Z</modification><creation>2024-11-20T15:16:49.27Z</creation></dates><accession>S-EPMC10108885</accession><cross_references><pubmed>37077580</pubmed><doi>10.1093/ehjopen/oead032</doi></cross_references></HashMap>