Vaccarino Viola, Johnson B Delia, Sheps David S, Reis Steven E, Kelsey Sheryl F, Bittner Vera, Rutledge Thomas, Shaw Leslee J, Sopko George, Bairey Merz C Noel
Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia 30306, USA.
J Am Coll Cardiol. 2007 Nov 20;50(21):2044-50. doi: 10.1016/j.jacc.2007.07.069. Epub 2007 Nov 5.
The purpose of this study was to examine prospectively whether inflammation explains the relationship between depression and cardiovascular disease (CVD).
It is unclear whether inflammation is a mechanism linking depression to CVD.
We measured C-reactive protein (CRP) and interleukin (IL)-6 in 559 women with suspected coronary ischemia who completed the Beck Depression Inventory (BDI) at baseline and were followed over 5.9 years. We considered indicators of past and current depression to classify women into 3 groups: 1) depression, having both elevated depressive symptoms (BDI > or =10) and a previous diagnosis of depression requiring treatment; 2) possible depression, having either indicator but not both; and 3) no depression, having neither indicator of depression. The main outcome was incidence of CVD events (hospital stays for nonfatal myocardial infarction, stroke, congestive heart failure, and CVD-related mortality).
Compared with women without depression, women with depression had a 70% higher CRP (p = 0.0008) and a 25% higher IL-6 (p = 0.04), whereas women with possible depression had 30% higher CRP (p = 0.02) and 28% higher IL-6 (p = 0.01). Depression was a significant predictor of CVD (hazard ratio 2.58, p = 0.0009), but possible depression was not (hazard ratio 1.12, p = 0.68). Adjustment for other patient factors did not substantially affect the results. Addition of CRP decreased the estimate for depression by 13% and addition of IL-6 decreased it by 4%. Both depression and inflammatory biomarkers remained independent predictors of outcome.
Despite their robust association with depression, inflammatory biomarkers explain only a small portion of the association between depression and CVD incidence.
本研究的目的是前瞻性地检验炎症是否能解释抑郁症与心血管疾病(CVD)之间的关系。
炎症是否是将抑郁症与心血管疾病联系起来的一种机制尚不清楚。
我们对559名疑似冠状动脉缺血的女性进行了C反应蛋白(CRP)和白细胞介素(IL)-6的测量,这些女性在基线时完成了贝克抑郁量表(BDI),并随访了5.9年。我们根据过去和当前抑郁症的指标将女性分为3组:1)抑郁症组,抑郁症状升高(BDI≥10)且既往有需要治疗的抑郁症诊断;2)可能患有抑郁症组,有其中一项指标但并非两项指标都有;3)无抑郁症组,两项抑郁症指标均无。主要结局是心血管疾病事件的发生率(非致命性心肌梗死、中风、充血性心力衰竭的住院治疗以及与心血管疾病相关的死亡率)。
与无抑郁症的女性相比,患有抑郁症的女性CRP高70%(p = 0.0008),IL-6高25%(p = 0.04),而可能患有抑郁症的女性CRP高30%(p = 0.02),IL-6高28%(p = 0.01)。抑郁症是心血管疾病的显著预测因素(风险比2.58,p = 0.0009),但可能患有抑郁症不是(风险比1.12,p = 0.68)。对其他患者因素进行调整并未实质性影响结果。加入CRP使抑郁症的估计值降低了13%,加入IL-6使其降低了4%。抑郁症和炎症生物标志物仍然是结局的独立预测因素。
尽管炎症生物标志物与抑郁症有密切关联,但它们仅解释了抑郁症与心血管疾病发生率之间关联的一小部分。