<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Remmelzwaal S</submitter><funding>ZonMw</funding><pagination>21046</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8548503</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(1)</volume><pubmed_abstract>We investigated the prospective associations of body composition with cardiac structure and function and explored effect modification by sex and whether inflammation was a mediator in these associations. Total body (BF), trunk (TF) and leg fat (LF), and total lean mass (LM) were measured at baseline by a whole body DXA scan. Inflammatory biomarkers and echocardiographic measures were determined both at baseline and follow-up in the Hoorn Study (n = 321). We performed linear regression analyses with body composition measures as determinant and left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI) or left atrial volume index (LAVI) at follow-up as outcome. Additionally, we performed mediation analysis using inflammation at follow-up as mediator. The study population was 67.7 ± 5.2 years and 50% were female. After adjustment, BF, TF and LF, and LM were associated with LVMI with regression coefficients of 2.9 (0.8; 5.1)g/m&lt;sup>2.7&lt;/sup>, 2.3 (0.6; 4.0)g/m&lt;sup>2.7&lt;/sup>, 2.0 (0.04; 4.0)g/m&lt;sup>2.7&lt;/sup> and - 2.9 (- 5.1; - 0.7)g/m&lt;sup>2.7&lt;/sup>. Body composition measures were not associated with LVEF or LAVI. These associations were not modified by sex or mediated by inflammation. Body composition could play a role in the pathophysiology of LV hypertrophy. Future research should focus on sex differences in regional adiposity in relation with diastolic dysfunction.</pubmed_abstract><journal>Scientific reports</journal><pubmed_title>Sex-specific associations of body composition measures with cardiac function and structure after 8 years of follow-up.</pubmed_title><pmcid>PMC8548503</pmcid><funding_grant_id>849500008</funding_grant_id><funding_grant_id>91718304</funding_grant_id><pubmed_authors>Heymans SRB</pubmed_authors><pubmed_authors>van Ballegooijen AJ</pubmed_authors><pubmed_authors>Appelman Y</pubmed_authors><pubmed_authors>Remmelzwaal S</pubmed_authors><pubmed_authors>Beulens JWJ</pubmed_authors><pubmed_authors>van Empel V</pubmed_authors><pubmed_authors>Handoko ML</pubmed_authors><pubmed_authors>Elders PJM</pubmed_authors><pubmed_authors>Stehouwer CDA</pubmed_authors></additional><is_claimable>false</is_claimable><name>Sex-specific associations of body composition measures with cardiac function and structure after 8 years of follow-up.</name><description>We investigated the prospective associations of body composition with cardiac structure and function and explored effect modification by sex and whether inflammation was a mediator in these associations. Total body (BF), trunk (TF) and leg fat (LF), and total lean mass (LM) were measured at baseline by a whole body DXA scan. Inflammatory biomarkers and echocardiographic measures were determined both at baseline and follow-up in the Hoorn Study (n = 321). We performed linear regression analyses with body composition measures as determinant and left ventricular ejection fraction (LVEF), left ventricular mass index (LVMI) or left atrial volume index (LAVI) at follow-up as outcome. Additionally, we performed mediation analysis using inflammation at follow-up as mediator. The study population was 67.7 ± 5.2 years and 50% were female. After adjustment, BF, TF and LF, and LM were associated with LVMI with regression coefficients of 2.9 (0.8; 5.1)g/m&lt;sup>2.7&lt;/sup>, 2.3 (0.6; 4.0)g/m&lt;sup>2.7&lt;/sup>, 2.0 (0.04; 4.0)g/m&lt;sup>2.7&lt;/sup> and - 2.9 (- 5.1; - 0.7)g/m&lt;sup>2.7&lt;/sup>. Body composition measures were not associated with LVEF or LAVI. These associations were not modified by sex or mediated by inflammation. Body composition could play a role in the pathophysiology of LV hypertrophy. Future research should focus on sex differences in regional adiposity in relation with diastolic dysfunction.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Oct</publication><modification>2025-04-04T14:09:56.936Z</modification><creation>2025-04-04T14:09:56.936Z</creation></dates><accession>S-EPMC8548503</accession><cross_references><pubmed>34702868</pubmed><doi>10.1038/s41598-021-00541-x</doi></cross_references></HashMap>