Wong Ma-Li, Dong Chuanhui, Esposito Karin, Thakur Sarika, Liu Weiqing, Elashoff Robert M, Licinio Julio
Department of Psychiatry and Behavioral Sciences, Leonard M. Miller School of Medicine, University of Miami, Miami, Florida, USA.
PLoS One. 2008;3(7):e2350. doi: 10.1371/journal.pone.0002350. Epub 2008 Jul 16.
Major depressive disorder (MDD) is an independent risk factor for cardiovascular disease (CVD); the presence of MDD symptoms in patients with CVD is associated with a higher incidence of cardiac complications following acute myocardial infarction (MI). Stress-hemoconcentration, a result of psychological stress that might be a risk factor for the pathogenesis of CVD, has been studied in stress-challenge paradigms but has not been systematically studied in MDD.
Secondary analysis of stress hemoconcentration was performed on data from controls and subjects with mild to moderate MDD participating in an ongoing pharmacogenetic study of antidepressant treatment response to desipramine or fluoxetine. Hematologic and hemorheologic measures of stress-hemoconcentration included blood cell counts, hematocrit, hemoglobin, total serum protein, and albumin, and whole blood viscosity.
Subjects with mild to moderate MDD had significantly increased hemorheologic measures of stress-hemoconcentration and blood viscosity when compared to controls; these measures were correlated with depression severity. Measures of stress-hemoconcentration improved significantly after 8 weeks of antidepressant treatment. Improvements in white blood cell count, red blood cell measures and plasma volume were correlated with decreased severity of depression.
Our secondary data analyses support that stress-hemoconcentration, possibly caused by decrements in plasma volume during psychological stress, is present in Mexican-American subjects with mild to moderate MDD at non-challenged baseline conditions. We also found that after antidepressant treatment hemorheologic measures of stress-hemoconcentration are improved and are correlated with improvement of depressive symptoms. These findings suggest that antidepressant treatment may have a positive impact in CVD by ameliorating increased blood viscosity. Physicians should be aware of the potential impact of measures of hemoconcentration and consider the implications for cardiovascular risk in depressed patients.
重度抑郁症（MDD）是心血管疾病（CVD）的独立危险因素；CVD患者中MDD症状的存在与急性心肌梗死（MI）后心脏并发症的较高发生率相关。应激性血液浓缩是心理应激的结果，可能是CVD发病机制的一个危险因素，已在应激挑战范式中进行了研究，但尚未在MDD中进行系统研究。
对参与正在进行的关于地昔帕明或氟西汀抗抑郁治疗反应的药物遗传学研究的对照组和轻度至中度MDD受试者的数据进行应激性血液浓缩的二次分析。应激性血液浓缩的血液学和血液流变学指标包括血细胞计数、血细胞比容、血红蛋白、总血清蛋白、白蛋白和全血粘度。
与对照组相比，轻度至中度MDD受试者的应激性血液浓缩和血液粘度的血液流变学指标显著升高；这些指标与抑郁严重程度相关。抗抑郁治疗8周后，应激性血液浓缩指标显著改善。白细胞计数、红细胞指标和血浆容量的改善与抑郁严重程度的降低相关。
我们的二次数据分析支持，在未受挑战的基线条件下，轻度至中度MDD的墨西哥裔美国受试者中存在可能由心理应激期间血浆容量减少引起的应激性血液浓缩。我们还发现，抗抑郁治疗后，应激性血液浓缩的血液流变学指标得到改善，且与抑郁症状的改善相关。这些发现表明，抗抑郁治疗可能通过改善血液粘度增加对CVD产生积极影响。医生应意识到血液浓缩指标的潜在影响，并考虑对抑郁症患者心血管风险的影响。
