Ellins Elizabeth, Halcox Julian, Donald Ann, Field Bryony, Brydon Lena, Deanfield John, Steptoe Andrew
Vascular Physiology Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1N 1EH, UK.
Brain Behav Immun. 2008 Aug;22(6):941-8. doi: 10.1016/j.bbi.2008.01.009. Epub 2008 Mar 7.
The processes through which psychological stress influences cardiovascular disease are poorly understood, but may involve activation of hemodynamic, neuroendocrine and inflammatory responses. We assessed the relationship between carotid arterial stiffness and inflammatory responses to acute psychophysiologic stress. Participants were 155 healthy men and women aged 55.3, SD 2.7 years. Blood samples for the assessment of plasma fibrinogen, tumor necrosis factor (TNF) alpha and interleukin (IL) 6 were drawn at baseline, immediately following standardized behavioral tasks, and 45 min later. Carotid artery stiffness was measured ultrasonically three years later, and blood pressure and heart rate responses were recorded. The tasks induced substantial increases in blood pressure and heart rate, together with increased fibrinogen, TNFalpha and IL-6 concentration. Carotid stiffness was positively associated with body mass, waist/hip ratio, blood pressure, low density lipoprotein cholesterol, and C-reactive protein, and inversely with high density lipoprotein and grade of employment. Baseline levels of inflammatory variables were not related to carotid artery stiffness. But carotid stiffness was greater in participants with larger fibrinogen (p=0.037) and TNFalpha (p=0.036) responses to psychophysiological stress. These effects were independent of age, gender, grade of employment, smoking, body mass, waist/hip ratio, systolic and diastolic pressure, high and low density lipoprotein cholesterol, and C-reactive protein. There were no associations between carotid stiffness and stress responses in IL-6, blood pressure, or heart rate. We conclude that individual differences in inflammatory responses to psychophysiological stress are independently related to structural changes in artery walls that reflect increased cardiovascular disease risk.
心理压力影响心血管疾病的具体过程尚不清楚，但可能涉及血液动力学、神经内分泌和炎症反应的激活。我们评估了颈动脉僵硬度与急性心理生理应激炎症反应之间的关系。研究对象为155名年龄55.3岁（标准差2.7岁）的健康男性和女性。分别在基线、标准化行为任务结束后即刻以及45分钟后采集血样，以评估血浆纤维蛋白原、肿瘤坏死因子（TNF）α和白细胞介素（IL）6。三年后通过超声测量颈动脉僵硬度，并记录血压和心率反应。这些任务导致血压和心率大幅升高，同时纤维蛋白原、TNFα和IL-6浓度增加。颈动脉僵硬度与体重、腰臀比、血压、低密度脂蛋白胆固醇和C反应蛋白呈正相关，与高密度脂蛋白和就业等级呈负相关。炎症变量的基线水平与颈动脉僵硬度无关。但对心理生理应激时纤维蛋白原（p=0.037）和TNFα（p=0.036）反应较大的参与者，其颈动脉僵硬度更大。这些影响独立于年龄、性别、就业等级、吸烟、体重、腰臀比、收缩压和舒张压、高密度脂蛋白和低密度脂蛋白胆固醇以及C反应蛋白。颈动脉僵硬度与IL-6、血压或心率的应激反应之间无关联。我们得出结论，心理生理应激炎症反应的个体差异与动脉壁结构变化独立相关，而这种变化反映了心血管疾病风险增加。
