Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK; Psychiatry Unit, Department of Biomedical and Clinical Sciences, Luigi Sacco Hospital, Università degli Studi di Milano, Milan, Italy.
Department of Psychological Medicine, Institute of Psychiatry, Psychology and Neuroscience, King's College London, London, UK.
Brain Behav Immun. 2019 Oct;81:659-664. doi: 10.1016/j.bbi.2019.07.023. Epub 2019 Jul 22.
Depression frequently co-occurs with coronary heart disease (CHD), worsening clinical outcomes of both, and inflammation has been proposed as a biological link between these two disorders. The aim of the present study was to investigate the role of inflammation in the development of depression in CHD patients during a 3-year follow-up. We examined the inflammatory biomarker, high-sensitivity C-reactive protein (hsCRP), measured at baseline, as a potential predictor of later onset of depression. We recruited 89 CHD patients, who were assessed at baseline and then every 6 months, for three years. The sample included, at baseline, 25 depressed and 64 non-depressed CHD patients, as confirmed by Clinical Interview Schedule Revised (CIS-R). Depressive symptoms were assessed at baseline and all follow-up points by the Patient Health Questionnaire-9 (PHQ-9). In all CHD patients (n = 89), we found a significant positive correlation between hsCRP levels and the severity of depressive symptoms at baseline (PHQ-9, r = 0.23, p = 0.032). During follow-up, n = 21 patients (of the 64 non-depressed at baseline) developed depression, defined as being PHQ-9 positive (a score ≥ 10) in at least one follow-up assessment. Of these, n = 9 subjects were defined as developing clinically-significant depression, that is, having a positive PHQ-9 in at least 3 of the 6 follow-up assessments, implying a duration of symptoms of at least one year. We found that increased hsCRP values at baseline predicted future onset of depression. Specifically, baseline hsCRP values were higher in patients who later developed clinically-significant depression (mean ± SD; 6.76 ± 6.52 mg/L) compared with never-depressed (2.77 ± 3.13 mg/L; F(1,48) = 7.29, p = 0.010), even after controlling for baseline PHQ-9 scores. In conclusion, inflammation in CHD patients is associated with future development of clinically-significant depression. HsCRP, a reliable and ready-to-use biological marker of inflammation, may help to identify depression high-risk phenotypes even among CHD patients, who already have high baseline inflammation. Our study conveys important preliminary findings that will require further replication but that have the potential to affect the mental and physical health of a vulnerable group of individuals.
抑郁症常与冠心病（CHD）并存，使两者的临床预后恶化，炎症被认为是这两种疾病之间的生物学联系。本研究旨在探讨炎症在 CHD 患者 3 年随访期间发生抑郁症中的作用。我们检测了基线时的炎症生物标志物高敏 C 反应蛋白（hsCRP），作为随后发生抑郁症的潜在预测因子。我们招募了 89 名 CHD 患者，他们在基线时进行了评估，然后每 6 个月评估一次，共 3 年。该样本包括基线时 25 名抑郁和 64 名非抑郁的 CHD 患者，这是通过临床访谈时间表修订版（CIS-R）确认的。抑郁症状在基线和所有随访点均由患者健康问卷-9（PHQ-9）评估。在所有 89 名 CHD 患者中，我们发现 hsCRP 水平与基线时抑郁症状严重程度呈显著正相关（PHQ-9，r=0.23，p=0.032）。在随访期间，n=21 名患者（其中 64 名非抑郁患者在基线时无抑郁）出现了抑郁，定义为至少一次随访评估 PHQ-9 阳性（得分≥10）。其中，n=9 名患者被定义为出现临床显著抑郁，即至少有 3 次随访评估为 PHQ-9 阳性，意味着症状持续至少一年。我们发现基线 hsCRP 值升高可预测未来发生抑郁。具体而言，后来出现临床显著抑郁的患者（平均值±标准差；6.76±6.52mg/L）的基线 hsCRP 值高于从未抑郁的患者（2.77±3.13mg/L；F(1,48)=7.29，p=0.010），即使在控制基线 PHQ-9 评分后也是如此。结论：CHD 患者的炎症与未来发生临床显著抑郁有关。hsCRP 是一种可靠且现成的炎症生物标志物，即使在基线炎症水平较高的 CHD 患者中，也可能有助于识别抑郁高危表型。我们的研究提供了重要的初步发现，这些发现需要进一步复制，但有可能影响到一群弱势群体的身心健康。
