■心血管疾病(CVD)和抑郁症具有双向关联,炎症和代谢因素是两种情况的常见重要触发因素。然而,作为一种新的炎症和代谢标志物,血小板与HDL-C比值(PHR)与抑郁症和心血管疾病的关系尚未确定.
■20岁及以上的参与者被纳入2005-2018年NHANES数据库。PHR计算为血小板计数(1000个细胞/μL)与HDL-C(mmol/L)的比率。患者健康问卷(PHQ-9)用于诊断抑郁症,截止值为10。采用加权逻辑回归分析和限制性三次样条(RCS)分析来检查PHR与抑郁相关特征之间的关联。此外,采用加权COX回归和RCS分析抑郁症患者的PHR与CVD死亡率的相关性.使用受试者工作特征曲线来评估PHR在预测抑郁症方面是否优于HDL-C。最后,探讨了PHR在最新的心血管健康指标生活要点8和抑郁症中的中介作用。
■总共包括26,970名合格参与者,包括2308名抑郁症患者,加权时代表大约1.6亿美国成年人。完全调整后,我们估计与PHR的标准差(SD)增加相关的抑郁比值比(OR)为1.06(95%CI:1.01~1.12,P=0.03).受限三次样条(RCS)分析表明线性关联(非线性P=0.113)。当PHR根据四分位数分为四组,并在对抑郁症危险因素进行充分校正后纳入模型时,与最低四分位数组相比,PHR四分位数2,四分位数3和四分位数4的参与者显示出抑郁风险增加的趋势(P趋势=0.01).此外,加权COX回归和RCS显示,在抑郁症患者中,PHR每SD增加与CVD死亡风险较高相关(HR:1.38,95%CI:1.05-1.81,P=0.02,非线性P=0.400).亚组分析表明,当前饮酒增强了PHR与抑郁症之间的关联(相互作用的P=0.017)。此外,PHR的ROC曲线下面积(AUC)为0.556(95%CI,0.544-0.568;P<0.001),HDL-C为0.536(95%CI,0.524-0.549;P<0.001)(PDeLong=0.025)。最后,调解分析表明,PHR是LE8与抑郁之间的中间机制(调解比例=5.02%,P=0.02)。
■在美国成年人中,在患有抑郁症的个体中,PHR的增加线性增加了抑郁和CVD死亡率的风险.此外,与HDL-C相比,PHR对抑郁症具有更好的预测优势。此外,PHR显著介导LE8评分与抑郁之间的关联。
UNASSIGNED: Cardiovascular disease (CVD) and depression have a bidirectional association, with inflammation and metabolic factors being common important triggers for both conditions. However, as a novel inflammatory and metabolic marker, platelet-to-HDL-C ratio (PHR) has not been established in relation to depression and cardiovascular disease.
UNASSIGNED: Participants aged 20 years and older were included in the 2005-2018 NHANES database. PHR was calculated as the ratio of platelet count (1000 cells/μL) to HDL-C (mmol/L). The Patient Health Questionnaire (PHQ-9) was used to diagnose depression, with a cutoff value of 10. Weighted logistic regression analysis and restricted cubic spline (RCS) analysis were employed to examine the association between PHR and depression-related features. Additionally, weighted COX regression and RCS were used to analyze the association of PHR with CVD mortality in patients with depression. Receiver operating characteristic curves were used to assess whether PHR had an advantage over HDL-C in predicting depression. Finally, the mediating role of PHR in the latest cardiovascular health indicator Life\'s Essential 8 and depression was explored.
UNASSIGNED: A total of 26,970 eligible participants were included, including 2,308 individuals with depression, representing approximately 160 million U.S. adults when weighted. After full adjustment, we estimated that the odds ratio (OR) of depression associated with a per standard deviation (SD) increase in PHR was 1.06 (95% CI: 1.01-1.12, P=0.03). The restricted cubic spline (RCS) analysis indicated a linear association (Nonlinear P=0.113). When PHR was divided into four groups based on quartiles and included in the model after full adjustment for depression risk factors, participants in quartile 2, quartile 3, and quartile 4 of PHR showed a trend of increasing risk of depression compared to the lowest quartile group (P trend=0.01). In addition, weighted COX regression and RCS revealed that a per SD increase in PHR was associated with a higher risk of CVD mortality among patients with depression (HR: 1.38, 95% CI: 1.05-1.81, P=0.02, Nonlinear P=0.400). Subgroup analyses showed that current alcohol consumption enhanced the association between PHR and depression (P for interaction=0.017). Furthermore, the areas under the ROC curves (AUC) were 0.556 (95% CI, 0.544-0.568; P < 0.001) for PHR and 0.536 (95% CI, 0.524-0.549; P < 0.001) for HDL-C (PDeLong = 0.025). Finally, mediation analysis indicated that PHR was an intermediate mechanism between LE8 and depression (mediation proportion=5.02%, P=0.02).
UNASSIGNED: In U.S. adults, an increase in PHR linearly increases the risk of depression and CVD mortality among individuals with depression. Additionally, PHR has a better predictive advantage for depression compared to HDL-C. Furthermore, PHR significantly mediates the association between LE8 scores and depression.