冠心病合并焦虑和/或抑郁情绪患者血清髓过氧化物酶和脂氧素A4水平的变化

Change of serum myeloperoxidase and lipoxin A4 level in coronary heart disease patients with anxiety and/or depression

目的:探讨冠心病合并焦虑和/或抑郁情绪患者血清髓过氧化物酶(myeloperoxidase,MPO)和脂氧素A4(lipoxin A4,LXA4)水平的变化及临床意义。方法:选择2010年12月至2011年2月在中南大学湘雅二医院心内科住院确诊为冠心病的患者143例为研究对象,并以44例非冠心病者作为对照,使用医院焦虑抑郁情绪评定表(Thehospital anxiety and depression scale,HADS)评价患者的心理状态,将冠心病患者分为焦虑抑郁组(n=57)及非焦虑抑郁组(n=86)。测定所有研究对象的血清高敏C反应蛋白(high sensitive C-reactive protein,HsCRP),MPO,LXA4水平,计算LXA4与MPO比值(M/L)。结果:冠心病两组的血清HsCRP,LXA4,MPO水平和M/L均较对照组明显升高(均P<0.01),其中以冠心病焦虑抑郁组升高更为明显,与非焦虑抑郁组相比MPO和M/L差异有统计学意义(P<0.05)。相关分析发现MPO与HADS总表(HADS total,HADS-t)、焦虑亚量表(HADS-anxiety,HADS-a)或抑郁亚量表(HADS-depression,HADS-d)评分呈正相关,LXA4与HADS-t或HADS-d评分呈负相关。多因素logistic回归分析显示,较高的HADS-t评分、稳定型心绞痛、不稳定型心绞痛和急性心肌梗死是M/L升高的独立影响因子(P<0.05或P<0.01)。结论:焦虑和/或抑郁情绪可能加重冠心病患者体内的炎症反应,炎症与抗炎之间的失衡可能是其重要机制之一。

Objective： To investigate the change of serum myeloperoxidase （MPO） and lipoxin A4 （LXA4） in coronary heart disease （CHD） patients with anxiety and depression and its clinical significance. Methods： From December 2010 to February 2011, 143 CHD patients and 44 non-CHD patients （the control group） hospitalized in the Department of Cardiology at the Second Xiangya Hospital were enrolled. The hospital anxiety and depression scale （HADS） was used to evaluate the psychological state of all patients and the CHD patients were assigned to an anxiety and depression group （n=57） or a non-depression and anxiety group （n=86）. The serum levels of high sensitive C-reactive protein （Hs-CRP）, MPO, and LXA4 were examined, and the ratio of MPO and LXA4 （M/L） was calculated. Results： q-he levels of Hs-CRP, MPO, and LXA4 as well as M/L ratios in both CHD groups were significantly higher than those in the control group （all P〈0.01）. Compared with the non-anxiety and depression group, the levels of MPO and LXA4, and M/L ratios in the anxiety and depression group increased （all P〈0.05）. Correlation analysis showed that MPO was positively correlated with the score ofHADS-total （HADS-t）, HADS-anxiety （HADS-a）, or HADS-depression （HADS-d）, while LXA4 was negatively correlated with HADS-t or HADS-d. Multiple ordinal logistic regression analysis revealed that higher HADS-t score, stable angina, unstable angina, and acute myocardial infarction were the independent impact factors for the elevation of M/L ratio. Conclusion： Anxiety and depression may aggravate the inflammatory response in CHD patients. The imbalance between inflammation and anti-inflammation maybe part of the mechanism.