Civieri Giovanni, Abohashem Shady, Grewal Simran S, Aldosoky Wesam, Qamar Iqra, Hanlon Erin, Choi Karmel W, Shin Lisa M, Rosovsky Rachel P, Bollepalli Sandeep Chandra, Lau Hui Chong, Armoundas Antonis, Seligowski Antonia V, Turgeon Sarah M, Pitman Roger K, Tona Francesco, Wasfy Jason H, Smoller Jordan W, Iliceto Sabino, Goldstein Jill, Gebhard Catherine, Osborne Michael T, Tawakol Ahmed
Cardiovascular Imaging Research Center, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Department of Cardiac, Thoracic, Vascular Sciences and Public Health, University of Padua, Padua, Italy.
JACC Adv. 2024 Aug 14;3(9):101208. doi: 10.1016/j.jacadv.2024.101208. eCollection 2024 Sep.
Prior studies have incompletely assessed whether the development of cardiometabolic risk factors (CVDRF) (hypertension, hyperlipidemia, and diabetes mellitus) mediates the association between anxiety and depression (anxiety/depression) and cardiovascular disease (CVD).
The authors aimed to evaluate the following: 1) the association between anxiety/depression and incident CVDRFs and whether this association mediates the increased CVD risk; and 2) whether neuro-immune mechanisms and age and sex effects may be involved.
Using a retrospective cohort design, Mass General Brigham Biobank subjects were followed for 10 years. Presence and timing of anxiety/depression, CVDRFs, and CVD were determined using ICD codes. Stress-related neural activity, chronic inflammation, and autonomic function were measured by the assessment of amygdalar-to-cortical activity ratio, high-sensitivity CRP, and heart rate variability. Multivariable regression and mediation analyses were employed.
Among 71,214 subjects (median age 49.6 years; 55.3% female), 27,048 (38.0%) developed CVDRFs during follow-up. Pre-existing anxiety/depression associated with increased risk of incident CVDRF (OR: 1.71 [95% CI: 1.59-1.83], < 0.001) and with a shorter time to their development (β = -0.486 [95% CI: -0.62 to -0.35], < 0.001). The development of CVDRFs mediated the association between anxiety/depression and CVD events (log-odds: 0.044 [95% CI: 0.034-0.055], < 0.05). Neuro-immune pathways contributed to the development of CVDRFs ( < 0.05 each) and significant age and sex effects were noted: younger women experienced the greatest acceleration in the development of CVDRFs after anxiety/depression.
Anxiety/depression accelerate the development of CVDRFs. This association appears to be most notable among younger women and may be mediated by stress-related neuro-immune pathways. Evaluations of tailored preventive measures for individuals with anxiety/depression are needed to reduce CVD risk.
既往研究尚未全面评估心血管代谢危险因素(CVDRF,即高血压、高脂血症和糖尿病)的发生是否介导了焦虑抑郁(焦虑/抑郁)与心血管疾病(CVD)之间的关联。
作者旨在评估以下内容:1)焦虑/抑郁与新发CVDRF之间的关联,以及这种关联是否介导了CVD风险的增加;2)神经免疫机制以及年龄和性别效应是否可能参与其中。
采用回顾性队列设计,对麻省总医院布莱根生物样本库的受试者进行了10年的随访。使用国际疾病分类代码确定焦虑/抑郁、CVDRF和CVD的存在情况及发生时间。通过评估杏仁核与皮质的活动比率、高敏C反应蛋白和心率变异性来测量与应激相关的神经活动、慢性炎症和自主神经功能。采用多变量回归和中介分析。
在71214名受试者(中位年龄49.6岁;55.3%为女性)中,27048名(38.0%)在随访期间出现了CVDRF。既往存在的焦虑/抑郁与新发CVDRF风险增加相关(比值比:1.71 [95%置信区间:1.59 - 1.83],P < 0.001),且与CVDRF发生时间缩短相关(β = -0.486 [95%置信区间:-0.62至-0.35],P < 0.001)。CVDRF的发生介导了焦虑/抑郁与CVD事件之间的关联(对数优势比:0.044 [95%置信区间:0.034 - 0.055],P < 0.05)。神经免疫途径促成了CVDRF的发生(每项P < 0.05),且存在显著的年龄和性别效应:焦虑/抑郁后,年轻女性CVDRF的发生加速最为明显。
焦虑/抑郁会加速CVDRF的发生。这种关联在年轻女性中似乎最为显著,可能由与应激相关的神经免疫途径介导。需要对焦虑/抑郁个体的针对性预防措施进行评估,以降低CVD风险。