Age-Related Development of Cardiac Remodeling and Dysfunction in Young Black and White Adults: The Coronary Artery Risk Development in Young Adults Study - 31/03/21
, Sadiya S. Khan, MD, MSCI a, Laura A. Colangelo, MS a, Samuel S. Gidding, MD c, Anderson C. Armstrong, MD, MSc, PhD d, e, Cora E. Lewis, MD, MSPH f, Jared P. Reis, PhD g, Pamela J. Schreiner, PhD h, Stephen Sidney, MD, MPH i, Joao A.C. Lima, MD, MBA d, Donald M. Lloyd-Jones, MD, ScM aAbstract |
Background |
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.
Methods |
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.
Results |
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 height2.7 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 height2.7 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).
Conclusions |
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.
Le texte complet de cet article est disponible en PDF.Highlights |
• | The authors examined cardiac changes in black and white young adults over 25 years. |
• | At age 25, LV remodeling or dysfunction was present in 10%. |
• | Remodeling and dysfunction were accelerated by 10 to 15 years in blacks (vs whites). |
• | Young-adult cardiac parameters were associated with incident HF. |
• | Efforts to prevent HF should start before young adulthood. |
Keywords : Left ventricle, Disparities, Heart failure
Abbreviations : BMI, CARDIA, CV, EF, ESD, HF, LAD, LV, RWT
Plan
| CARDIA is conducted and supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham (HHSN268201800005I and HHSN268201800007I), Northwestern University (HHSN268201800003I), the University of Minnesota (HHSN268201800006I), the Kaiser Foundation Research Institute (HHSN268201800004I), and the Johns Hopkins University School of Medicine (HHSN268200900041C). Dr. Perak was supported in part by research grants from the National Heart, Lung, and Blood Institute (T32 HL069771 and K23 HL145101) and from the Northwestern University Feinberg School of Medicine Department of Pediatrics. Dr. Khan was supported in part by research grants from the National Institutes of Health (KL2TR001424) and the American Heart Association (19TPA34890060). The funding sources had no role in study design; the collection, analysis or interpretation of data; writing of the report; or the decision to submit the article for publication. All authors have read and approved submission of the manuscript. The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services. |
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| Conflicts of interest: None. |
Vol 34 - N° 4
P. 388-400 - avril 2021 Retour au numéro
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