Age-Related Development of Cardiac Remodeling and Dysfunction in Young Black and White Adults: The Coronary Artery Risk Development in Young Adults Study.

Age-Related Development of Cardiac Remodeling and Dysfunction in Young Black and White Adults: The Coronary Artery Risk Development in Young Adults Study.
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DOI:
10.1016/j.echo.2020.11.002
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发表时间:
2021-04
期刊:
Journal of the American Society of Echocardiography : official publication of the American Society of Echocardiography
影响因子:
--
通讯作者:
Lloyd-Jones DM
Lloyd-Jones DM
中科院分区:
其他
文献类型:
--
作者:
Perak AM;Khan SS;Colangelo LA;Gidding SS;Armstrong AC;Lewis CE;Reis JP;Schreiner PJ;Sidney S;Lima JAC;Lloyd-Jones DM

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关于临床前心力衰竭(HF)发展的时间知之甚少,特别是在黑人中。本研究的主要目的是在一个双裔队列中描述与年龄相关的左室(LV)结构和功能演变,并检验在规范范围内的年轻成人左室参数与25年以上的事件b期(定义的LV异常)相关的假设,独立于累积风险因素负担。我们分析了来自年轻人冠状动脉风险发展研究的数据。参与者(N=2,833) 45%为黑人,56%为女性,平均基线年龄为30.1岁。我们使用广义估计方程逻辑回归来估计B期左室异常(重塑、肥大或功能障碍)与年龄相关的概率,并使用逻辑回归来检查基线左室参数与事件异常之间的危险因素调整的关联。我们使用Cox回归来评估基线左室参数与事件B级左室异常是否也与事件临床(C/D期)HF事件相关。25岁和60岁时B期LV异常的概率分别为10.5% (95% CI, 9.4-11.8%)和45.0%(42.0-48.1%),存在显著的种族性别差异;例如,在60岁时:黑人男性52.7%(44.9-60.3%),黑人女性59.4%(53.6-65.0%),白人男性39.1%(33.4-45.0%),白人女性39.1%(33.9-44.6%)。25年来,基线左室收缩期末期尺寸/高度与发生的收缩功能障碍(每1-SD校正比值比:2.56[1.87-3.52])、偏心肥大(1.34[1.02-1.75])、同心肥大(0.69[0.51-0.91])和同心重构(0.68[0.58-0.79])相关;基线左室质量/高度2.7与发生偏心肥大(1.70[1.25-2.32])、同心肥大(1.63[1.19-2.24])和舒张功能障碍(1.24[1.01-1.52])相关。在具有基线超声心动图数据的整个队列中(N=4097; 72例HF事件),左室收缩末期尺寸/高度和质量/高度2.7与临床HF事件显著相关(每1-SD校正风险比分别为1.56 [95% CI, 1.26-1.93]和1.42[1.14-1.75])。B期左室异常和相关的种族差异存在于青年成年期,随着年龄的增长而增加,并与索引左室收缩末期尺寸和质量的基线变化相关。基线指标左室收缩末期尺寸和质量也与临床心衰事件相关。预防临床HF的左室异常应从年轻时开始。
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. We analyzed data from the Coronary Artery Risk Development in Young Adults Study. Participants (N=2,833) were 45% black, 56% female, with mean baseline age 30.1 years. We used generalized estimating equation logistic regression 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. We used Cox regression 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. Probabilities of stage B LV abnormalities at ages 25 and 60 years were 10.5% (95% CI, 9.4–11.8%) and 45.0% (42.0–48.1%), with significant race-sex disparities; e.g., at age 60: black men 52.7% (44.9–60.3%), black women 59.4% (53.6–65.0%), white men 39.1% (33.4–45.0%), and white women 39.1% (33.9–44.6%). Over 25 years, baseline LV end-systolic dimension/height was associated with incident systolic dysfunction (adjusted odds ratio per 1-SD higher: 2.56 [1.87–3.52]), eccentric hypertrophy (1.34 [1.02–1.75]), concentric hypertrophy (0.69 [0.51–0.91]), and concentric remodeling (0.68 [0.58–0.79]); baseline LV mass/height2.7 was associated with incident eccentric hypertrophy (1.70 [1.25–2.32]), concentric hypertrophy (1.63 [1.19–2.24]), and diastolic dysfunction (1.24 [1.01–1.52]). Among the entire cohort with baseline echocardiographic data available (N=4097; 72 HF events), LV end-systolic dimension/height and mass/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 [1.14–1.75], respectively). 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.
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