<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Perak AM</submitter><funding>American Heart Association</funding><funding>NCATS NIH HHS</funding><funding>NHLBI NIH HHS</funding><funding>National Heart, Lung, and Blood Institute</funding><funding>National Institutes of Health</funding><pagination>388-400</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8026546</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>34(4)</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Little is known about the timing of preclinical heart failure (HF) development, particularly among blacks. The primary aims of this study were to delineate age-related left ventricular (LV) structure and function evolution in a biracial cohort and to test the hypothesis that young-adult LV parameters within normative ranges would be associated with incident stage B-defining LV abnormalities over 25 years, independent of cumulative risk factor burden.&lt;h4>Methods&lt;/h4>Data from the Coronary Artery Risk Development in Young Adults study were analyzed. Participants (n = 2,833) had a mean baseline age of 30.1 years; 45% were black, and 56% were women. Generalized estimating equation logistic regression was used to estimate age-related probabilities of stage B LV abnormalities (remodeling, hypertrophy, or dysfunction) and logistic regression to examine risk factor-adjusted associations between baseline LV parameters and incident abnormalities. Cox regression was used to assess whether baseline LV parameters associated with incident stage B LV abnormalities were also associated with incident clinical (stage C/D) HF events over >25 years' follow-up.&lt;h4>Results&lt;/h4>Probabilities of stage B LV abnormalities at ages 25 and 60 years were 10.5% (95% CI, 9.4%-11.8%) and 45.0% (95% CI, 42.0%-48.1%), with significant race-sex disparities (e.g., at age 60, black men 52.7% [95% CI, 44.9%-60.3%], black women 59.4% [95% CI, 53.6%-65.0%], white men 39.1% [95% CI, 33.4%-45.0%], and white women 39.1% [95% CI, 33.9%-44.6%]). Over 25 years, baseline LV end-systolic dimension indexed to height was associated with incident systolic dysfunction (adjusted odds ratio per 1 SD higher, 2.56; 95% CI, 1.87-3.52), eccentric hypertrophy (1.34; 95% CI, 1.02-1.75), concentric hypertrophy (0.69; 95% CI, 0.51-0.91), and concentric remodeling (0.68; 95% CI, 0.58-0.79); baseline LV mass indexed to height&lt;sup>2.7&lt;/sup> was associated with incident eccentric hypertrophy (1.70; 95% CI, 1.25-2.32]), concentric hypertrophy (1.63; 95% CI, 1.19-2.24), and diastolic dysfunction (1.24; 95% CI, 1.01-1.52). Among the entire cohort with baseline echocardiographic data available (n = 4,097; 72 HF events), LV end-systolic dimension indexed to height and LV mass indexed to height&lt;sup>2.7&lt;/sup> were significantly associated with incident clinical HF (adjusted hazard ratios per 1 SD higher, 1.56 [95% CI, 1.26-1.93] and 1.42 [95% CI, 1.14-1.75], respectively).&lt;h4>Conclusions&lt;/h4>Stage B LV abnormalities and related racial disparities were present in young adulthood, increased with age, and were associated with baseline variation in indexed LV end-systolic dimension and mass. Baseline indexed LV end-systolic dimension and mass were also associated with incident clinical HF. Efforts to prevent the LV abnormalities underlying clinical HF should start from a young age.</pubmed_abstract><journal>Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography</journal><pubmed_title>Age-Related Development of Cardiac Remodeling and Dysfunction in Young Black and White Adults: The Coronary Artery Risk Development in Young Adults Study.</pubmed_title><pmcid>PMC8026546</pmcid><funding_grant_id>HHSN268201800005I</funding_grant_id><funding_grant_id>HHSN268201800004I</funding_grant_id><funding_grant_id>HHSN268200900041C</funding_grant_id><funding_grant_id>HHSN268201800007I</funding_grant_id><funding_grant_id>HHSN268201800006I</funding_grant_id><funding_grant_id>UL1 TR001422</funding_grant_id><funding_grant_id>T32 HL069771</funding_grant_id><funding_grant_id>HHSN268201800003I</funding_grant_id><funding_grant_id>KL2 TR001424</funding_grant_id><funding_grant_id>K23 HL145101</funding_grant_id><pubmed_authors>Lewis CE</pubmed_authors><pubmed_authors>Khan SS</pubmed_authors><pubmed_authors>Lima JAC</pubmed_authors><pubmed_authors>Colangelo LA</pubmed_authors><pubmed_authors>Armstrong AC</pubmed_authors><pubmed_authors>Sidney S</pubmed_authors><pubmed_authors>Perak AM</pubmed_authors><pubmed_authors>Schreiner PJ</pubmed_authors><pubmed_authors>Lloyd-Jones DM</pubmed_authors><pubmed_authors>Reis JP</pubmed_authors><pubmed_authors>Gidding SS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Age-Related Development of Cardiac Remodeling and Dysfunction in Young Black and White Adults: The Coronary Artery Risk Development in Young Adults Study.</name><description>&lt;h4>Background&lt;/h4>Little is known about the timing of preclinical heart failure (HF) development, particularly among blacks. The primary aims of this study were to delineate age-related left ventricular (LV) structure and function evolution in a biracial cohort and to test the hypothesis that young-adult LV parameters within normative ranges would be associated with incident stage B-defining LV abnormalities over 25 years, independent of cumulative risk factor burden.&lt;h4>Methods&lt;/h4>Data from the Coronary Artery Risk Development in Young Adults study were analyzed. Participants (n = 2,833) had a mean baseline age of 30.1 years; 45% were black, and 56% were women. Generalized estimating equation logistic regression was used to estimate age-related probabilities of stage B LV abnormalities (remodeling, hypertrophy, or dysfunction) and logistic regression to examine risk factor-adjusted associations between baseline LV parameters and incident abnormalities. Cox regression was used to assess whether baseline LV parameters associated with incident stage B LV abnormalities were also associated with incident clinical (stage C/D) HF events over >25 years' follow-up.&lt;h4>Results&lt;/h4>Probabilities of stage B LV abnormalities at ages 25 and 60 years were 10.5% (95% CI, 9.4%-11.8%) and 45.0% (95% CI, 42.0%-48.1%), with significant race-sex disparities (e.g., at age 60, black men 52.7% [95% CI, 44.9%-60.3%], black women 59.4% [95% CI, 53.6%-65.0%], white men 39.1% [95% CI, 33.4%-45.0%], and white women 39.1% [95% CI, 33.9%-44.6%]). Over 25 years, baseline LV end-systolic dimension indexed to height was associated with incident systolic dysfunction (adjusted odds ratio per 1 SD higher, 2.56; 95% CI, 1.87-3.52), eccentric hypertrophy (1.34; 95% CI, 1.02-1.75), concentric hypertrophy (0.69; 95% CI, 0.51-0.91), and concentric remodeling (0.68; 95% CI, 0.58-0.79); baseline LV mass indexed to height&lt;sup>2.7&lt;/sup> was associated with incident eccentric hypertrophy (1.70; 95% CI, 1.25-2.32]), concentric hypertrophy (1.63; 95% CI, 1.19-2.24), and diastolic dysfunction (1.24; 95% CI, 1.01-1.52). Among the entire cohort with baseline echocardiographic data available (n = 4,097; 72 HF events), LV end-systolic dimension indexed to height and LV mass indexed to height&lt;sup>2.7&lt;/sup> were significantly associated with incident clinical HF (adjusted hazard ratios per 1 SD higher, 1.56 [95% CI, 1.26-1.93] and 1.42 [95% CI, 1.14-1.75], respectively).&lt;h4>Conclusions&lt;/h4>Stage B LV abnormalities and related racial disparities were present in young adulthood, increased with age, and were associated with baseline variation in indexed LV end-systolic dimension and mass. Baseline indexed LV end-systolic dimension and mass were also associated with incident clinical HF. Efforts to prevent the LV abnormalities underlying clinical HF should start from a young age.</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Apr</publication><modification>2025-04-29T11:32:28.388Z</modification><creation>2025-04-06T19:54:30.84Z</creation></dates><accession>S-EPMC8026546</accession><cross_references><pubmed>33212181</pubmed><doi>10.1016/j.echo.2020.11.002</doi></cross_references></HashMap>