University College London (UCL) Medical Research Council (MRC) Unit for Lifelong Health and AgeingUniversity College London London United Kingdom.
UCL Institute of Cardiovascular Science University College London London United Kingdom.
J Am Heart Assoc. 2021 Oct 5;10(19):e021877. doi: 10.1161/JAHA.121.021877. Epub 2021 Sep 25.
Background This study explored the association between childhood bradycardia and later-life cardiac phenotype using longitudinal data from the 1946 National Survey of Health and Development (NSHD) birth cohort. Methods and Results Resting heart rate was recorded at 6 and 7 years of age to provide the bradycardia exposure defined as a childhood resting heart rate <75 bpm. Three outcomes were studied: (1) echocardiographic data at 60 to 64 years of age, consisting of ejection fraction, left ventricular mass index, myocardial contraction fraction index, and E/e'; (2) electrocardiographic evidence of atrioventricular or ventricular conduction defects by 60 to 64 years of age; and (3) all-cause and cardiovascular mortality. Generalized linear models or Cox regression models were used, and adjustment was made for relevant demographic and health-related covariates, and for multiple testing. Mixed generalized linear models and fractional polynomials were used as sensitivity analyses. One in 3 older adults with atrioventricular conduction defects had been bradycardic in childhood, with defects being serious (Mobitz type II second-degree atrioventricular block or higher) in 12%. In fully adjusted models, childhood bradycardia was associated with 2.91 higher odds of atrioventricular conduction defects (95% CI, 1.59-5.31; =0.0005). Associations persisted in random coefficients mixed generalized linear models (odds ratio, 2.50; 95% CI, 1.01-4.31). Fractional polynomials confirmed a linear association between the log odds of atrioventricular conduction defects at 60 to 64 years of age and resting heart rate at 7 years of age. There was no association between bradycardia in childhood and mortality outcomes or with echocardiographic parameters and ventricular conduction defects in older age. Conclusions Longitudinal birth cohort data indicate that childhood bradycardia trebles the odds of having atrioventricular conduction defects in older age, 88% of which are benign. In addition, it does not influence mortality or heart size and function. Future research should concentrate on identifying children at risk.
背景 本研究利用 1946 年国民健康与发展纵向调查（NSHD）出生队列的纵向数据，探讨了儿童期心动过缓与晚年心脏表型之间的关系。
方法和结果 在 6 岁和 7 岁时记录静息心率，以提供心动过缓暴露，定义为儿童静息心率<75 次/分。研究了三种结局：（1）60-64 岁时的超声心动图数据，包括射血分数、左心室质量指数、心肌收缩分数指数和 E/e'；（2）60-64 岁时的房室或室性传导缺陷的心电图证据；（3）全因和心血管死亡率。使用广义线性模型或 Cox 回归模型进行分析，并对相关人口统计学和健康相关协变量以及多次检验进行了调整。混合广义线性模型和分数多项式用于敏感性分析。在有房室传导缺陷的老年成年人中，有 1/3 的人在儿童期曾出现心动过缓，其中 12%的人存在严重的房室传导缺陷（莫氏Ⅱ型二度房室传导阻滞或更严重）。在完全调整的模型中，儿童期心动过缓与房室传导缺陷的发生风险增加 2.91 倍（95%CI，1.59-5.31；=0.0005）。在随机系数混合广义线性模型中，相关性仍然存在（比值比，2.50；95%CI，1.01-4.31）。分数多项式证实了 60-64 岁时房室传导缺陷的对数几率与 7 岁时静息心率之间存在线性关系。儿童期心动过缓与死亡率或老年时的超声心动图参数和室性传导缺陷之间没有关联。
结论 纵向出生队列数据表明，儿童期心动过缓使老年人发生房室传导缺陷的几率增加两倍，其中 88%为良性。此外，它不会影响死亡率或心脏大小和功能。未来的研究应集中在识别有风险的儿童。
