Carney Robert M, Freedland Kenneth E, Steinmeyer Brian, Rubin Eugene H, Mann Douglas L, Rich Michael W
From the Departments of Psychiatry (Carney, Freedland, Steinmeyer, Rubin) and Medicine (Mann, Rich), Washington University School of Medicine, St Louis, Missouri.
Psychosom Med. 2016 Jan;78(1):49-59. doi: 10.1097/PSY.0000000000000245.
Depression is associated with an increased risk of mortality in patients with coronary heart disease. There is evidence that this risk may be reduced in patients who respond to depression treatment. The purpose of this study was to determine whether cardiac risk markers predict poor response to depression treatment and, second, whether they improve with successful treatment.
One hundred fifty-seven patients with stable coronary heart disease who met the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria for a moderate to severe major depressive episode were treated with cognitive behavior therapy, either alone or combined with an antidepressant, for up to 16 weeks. Depression, physical activity, sleep quality, thyroid hormones (total thyroxine [T4] and free T4), and inflammatory blood markers (C-reactive protein, interleukin-6, tumor necrosis factor) were assessed at baseline and after 16 weeks of treatment.
The mean (SD) Beck Depression Inventory scores were 30.2 (8.5) at baseline and 8.5 (7.8) at 16 weeks. More than 50% of the participants met the criteria for depression remission (17-item Hamilton Rating Scale for Depression ≤ 7) at 16 weeks. Only free T4 thyroid hormone at baseline predicted poor response to depression treatment after adjustment for potential confounders (p = .004). Improvement in sleep quality (p = .012) and physical activity level (p = .041) correlated with improvement in depression. None of the inflammatory markers predicted posttreatment depression or changed with depression.
Thyroid hormone (T4) level predicted depression treatment outcome, and improvement in depression correlated with improvement in sleep and physical activity. More detailed studies of thyroid function and objective assessments of sleep and physical activity in relation to depression improvement and cardiac outcomes are needed.
抑郁症与冠心病患者的死亡风险增加有关。有证据表明,对抑郁症治疗有反应的患者,这种风险可能会降低。本研究的目的,一是确定心脏风险标志物是否能预测抑郁症治疗反应不佳,二是确定它们是否会随着治疗成功而改善。
157例符合《精神障碍诊断与统计手册》第四版中重度重度抑郁发作标准的稳定型冠心病患者,接受认知行为疗法单独治疗或联合抗抑郁药治疗,为期16周。在基线和治疗16周后,评估抑郁、身体活动、睡眠质量、甲状腺激素(总甲状腺素 [T4] 和游离T4)以及炎症血液标志物(C反应蛋白、白细胞介素-6、肿瘤坏死因子)。
基线时贝克抑郁量表平均(标准差)评分为30.2(8.5),16周时为8.5(7.8)。超过50%的参与者在16周时达到抑郁缓解标准(17项汉密尔顿抑郁量表≤7)。在调整潜在混杂因素后,仅基线时的游离T4甲状腺激素可预测抑郁症治疗反应不佳(p = 0.004)。睡眠质量改善(p = 0.012)和身体活动水平改善(p = 0.041)与抑郁改善相关。没有一种炎症标志物能预测治疗后的抑郁情况,也没有随抑郁情况而变化。
甲状腺激素(T4)水平可预测抑郁症治疗结果,抑郁改善与睡眠和身体活动改善相关。需要对甲状腺功能进行更详细的研究,并对与抑郁改善和心脏结局相关的睡眠和身体活动进行客观评估。