未经评估:不良儿童经历(ACE)是不良行为的主要危险因素,精神和健康的结果在以后的生活。然而,ACE传达这些风险的确切途径,特别是关于心血管疾病等健康结果,仍然未知。这里,我们将精神病学和心脏方法结合起来,研究儿童逆境可能导致成人不良心血管健康的途径,重点关注心外膜脂肪组织(EAT)作为风险标志物。
未经评估:210名成人先天性心脏病门诊患者(平均年龄35.5岁,43%的女性)完成了彻底的心脏和精神病学评估。精神病学测量包括专家访谈,儿童创伤问卷(CTQ),贝克的抑郁症清单II(BDI-II),生活质量和全球功能规模,在其他人中。所有患者均完成了完整的心脏检查,包括使用超声心动图进行的EAT评估。然后,我们使用ACE作为预测器来计算引导中介模型,抑郁和体力活动作为中介,饮食作为过程中的因变量。
UNASSIGNED:CTQ评分通过BDI和体力活动的连续介导对EAT有显著的间接影响[a*b2*d=0.0260,95%BCaCI[0.0047,0.0619]]。
未经评估:使用中介分析,我们发现不良儿童事件与抑郁症状增加有关,这与身体活动减少有关,这反过来又与较高量的心外膜脂肪组织有关。虽然其他途径肯定存在并且需要复制,这表明ACEs导致不良心血管健康的有意义的途径,随着时间的推移,有几个潜在的健康干预目标。
UNASSIGNED: Adverse childhood experiences (ACEs) are a major risk factor for unfavorable behavioral, mental and health outcomes later in life. However, the precise pathway via which ACEs convey these risks, in particular regarding health outcomes such as cardiovascular disease, remains unknown. Here, we combined psychiatric and cardiac methods to investigate the pathway via which childhood adversities may lead to adult adverse cardiovascular health, with a focus on epicardial adipose tissue (EAT) as a risk marker.
UNASSIGNED: 210 adult congenital heart disease outpatients (mean age 35.5 y, 43% female) completed a thorough cardiac and psychiatric evaluation. Psychiatric measurements included an expert interview, the childhood trauma questionnaire (CTQ), Beck\'s depression inventory II (BDI-II), quality of life and the global scale of functioning, amongst others. All patients completed a full cardiac workup including EAT assessment using echocardiography. We then computed bootstrapping mediation models using ACEs as a predictor, depression and physical activity as mediators and EAT as dependent variable in PROCESS.
UNASSIGNED: CTQ scores had a significant indirect effect on EAT via a serial mediation of BDI and physical activity [a*b2*d = 0.0260, 95% BCa CI [0.0047, 0.0619]].
UNASSIGNED: Using mediation analyses, we show that adverse childhood events are linked to increased depressive symptoms, which are linked to decreased physical activity, which in turn are linked to a higher amount of epicardial adipose tissue. While other pathways most certainly exist and replication is needed, this suggests a meaningful pathway via which ACEs lead to adverse cardiovascular health, with several potential targets for health interventions across time.