Tulner Dorien M, Smith Otto R F, de Jonge Peter, van Melle Joost P, Slomp Jennichjen, Storm Huib, Quere Michel, den Boer Johan A, Honig Adriaan, Korf Jakob
Department of Hospital Psychiatry, Medical Centre, Leeuwarden, The Netherlands.
Neuropsychobiology. 2009;59(2):87-95. doi: 10.1159/000209860. Epub 2009 Mar 27.
Prevalence of depressive symptoms in the post-myocardial infarction (MI) period varies from 8 to 30%. Cerebral damage after MI, caused by transient ischemia, an inflammatory response or both, may contribute to development of post-MI depression. S100B is an established protein marker of cerebral damage. In a pilot study, the authors assessed whether S100B serum levels are: (1) increased during the week after MI, and (2) related to depressive symptoms during index hospital admission and the year following MI.
This pilot study is a substudy of the Myocardial Infarction and Depression Intervention Trial (MIND-IT). In 48 patients, serum levels of S100B were available at 1, 2, 3, 4 and 8 days following MI. Subsequently, in 27 patients, depressive symptoms were measured at 0, 3, 6, 9 and 12 months following MI with the Beck Depression Inventory (BDI). In 21 of the initial 48 patients, BDI data were lacking due to refusals to fill out BDI forms or missing data.
Significant and transient increases in serum S100B were observed in 81.3% of the 48 patients: 37.5% reached S100B serum levels comparable to serum levels found in acute brain injury (>0.20 microg/l) and 43.8% reached mildly elevated S100B serum levels comparable to serum levels found in depressive disorder (0.10-0.20 microg/l). In 18.7%, no S100B was detected in serum. Using non-parametric Spearman rank correlation tests, a trend towards an association was found between serum S100B and depressive symptoms during the post-MI year (rho values between 0.16 and 0.53) in 27 patients who completed both the S100B serum study and the BDI study.
Transiently elevated levels of S100B are suggestive of minor acute cerebral damage in the first days following MI and associated with depressive symptoms in the year following MI. Cerebral damage could be an important mechanism in the pathogenesis in a subtype of post-MI depression.
心肌梗死(MI)后抑郁症状的发生率在8%至30%之间。MI后由短暂性缺血、炎症反应或两者共同引起的脑损伤,可能促使MI后抑郁症的发生。S100B是一种已确定的脑损伤蛋白标志物。在一项初步研究中,作者评估了S100B血清水平是否:(1)在MI后的一周内升高,以及(2)与住院期间及MI后一年的抑郁症状相关。
这项初步研究是心肌梗死与抑郁干预试验(MIND-IT)的一项子研究。48例患者在MI后第1、2、3、4和8天可获得S100B血清水平。随后,在27例患者中,在MI后0、3、6、9和12个月用贝克抑郁量表(BDI)测量抑郁症状。在最初的48例患者中,有21例因拒绝填写BDI表格或数据缺失而缺乏BDI数据。
48例患者中有81.3%观察到血清S100B显著且短暂升高:37.5%的患者S100B血清水平达到与急性脑损伤时发现的血清水平相当(>0.20μg/l),43.8%的患者S100B血清水平轻度升高,与抑郁症时发现的血清水平相当(0.10 - 0.20μg/l)。18.7%的患者血清中未检测到S100B。在完成S100B血清研究和BDI研究的27例患者中,使用非参数Spearman等级相关检验发现,MI后一年血清S100B与抑郁症状之间存在关联趋势(rho值在0.16至0.53之间)。
S100B水平短暂升高提示MI后最初几天存在轻度急性脑损伤,并与MI后一年的抑郁症状相关。脑损伤可能是MI后抑郁症一种亚型发病机制中的重要机制。