Department of Dermatology, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha City, Hunan Province 410008, China.
Hunan Key Laboratory of Aging Biology, Xiangya Hospital, Central South University, No. 87, Xiangya Road, Changsha City, Hunan Province 410008, China.
Eur Heart J Cardiovasc Imaging. 2024 Aug 26;25(9):1315-1323. doi: 10.1093/ehjci/jeae126.
Advanced age is associated with an increased risk of adverse cardiovascular events. The relationship between biological age acceleration (BAA), cardiac size, cardiac function, and heart failure (HF) is not well-defined.
Utilizing the UK Biobank cohort, we assessed biological age using the Klemera-Doubal and PhenoAge methods. BAA was quantified by residual analysis compared with chronological age. Cardiovascular magnetic resonance (CMR) imaging provided detailed insights into cardiac structure and function. We employed multivariate regression to examine links between BAA and CMR-derived cardiac phenotypes. Cox proportional hazard regression models analysis was applied to explore the causative relationship between BAA and HF. Additionally, Mendelian randomization was used to investigate the genetic underpinnings of these associations. A significant correlation was found between increased BAA and deleterious changes in cardiac structure, such as diminished left ventricular mass, lower overall ventricular volume, and reduced stroke volumes across ventricles and atria. Throughout a median follow-up of 13.8 years, participants with greater biological aging showed a heightened risk of HF [26% per standard deviation (SD) increase in KDM-BA acceleration, 95% confidence intervals (CI): 23-28%; 33% per SD increase in PhenoAge acceleration, 95% CI: 32-35%]. Mendelian randomization analysis suggests a likely causal link between BAA, vital cardiac metrics, and HF risk.
In this cohort, accelerated biological aging may serve as a risk indicator for altered cardiac dimensions, functionality, and the onset of heart failure among middle-aged and elderly adults. It holds promise as a focal point for evaluating risk and developing targeted interventions.
高龄与心血管不良事件风险增加相关。生物学年龄加速（BAA）、心脏大小、心脏功能和心力衰竭（HF）之间的关系尚未明确。
利用英国生物库队列，我们使用 Klemera-Doubal 和 PhenoAge 方法评估了生物学年龄。通过与实际年龄的残差分析来量化 BAA。心血管磁共振（CMR）成像提供了对心脏结构和功能的详细了解。我们采用多元回归分析来研究 BAA 与 CMR 衍生的心脏表型之间的关系。Cox 比例风险回归模型分析用于探索 BAA 和 HF 之间的因果关系。此外，还使用孟德尔随机化来研究这些关联的遗传基础。BAA 增加与心脏结构的有害变化之间存在显著相关性，例如左心室质量降低、整体心室容积降低以及心室和心房的每搏量降低。在中位随访 13.8 年期间，生物学老化程度较高的参与者 HF 风险增加[KDM-BA 加速每标准差（SD）增加 26%，95%置信区间（CI）：23-28%；PhenoAge 加速每 SD 增加 33%，95%CI：32-35%]。孟德尔随机化分析表明 BAA、重要心脏指标与 HF 风险之间存在可能的因果关系。
在该队列中，加速的生物学老化可能是中年和老年人心脏结构、功能和心力衰竭发生改变的风险指标。它有望成为评估风险和制定针对性干预措施的焦点。
