首页> 外文学位 >Chronic stress, inflammation, and progression of carotid artery atherosclerosis: A mediation model.
【24h】

Chronic stress, inflammation, and progression of carotid artery atherosclerosis: A mediation model.

机译:慢性应激,炎症和颈动脉粥样硬化的进展:一种中介模型。

获取原文
获取原文并翻译 | 示例

摘要

Psychosocial stress might account for some of the variance in cardiovascular disease (CVD) risk that is not explained by traditional risk factors. Most studies of stress and CVD have focused on (a) stress in a single life domain, and (b) clinical CVD outcomes. Few studies have examined physiologic mechanisms that might explain the association between stress and CVD. The primary aim of the present study was to examine whether: (1) chronic stress predicts changes in carotid artery intima-media thickness (IMT) and plaque; and (2) the association between chronic stress and changes in these surrogate CVD endpoints is mediated by inflammatory processes. A secondary aim was to investigate whether individual differences in cardiovascular reactivity (CVR) moderates the association between stress and changes in IMT and plaque. The sample (n&barbelow;=276; M&barbelow; age=60.5), was a subset of the Pittsburgh Healthy Heart Project, a longitudinal investigation of the effects of psychosocial and biological risk factors on surrogate CVD endpoints among healthy older adults. Chronic stress was assessed at baseline with the Chronic Stress Scale (CSS; Norris & Uhl, 1993), a self-report survey that measures stress in 7 life domains during the preceding 6 months. Chronic stress was computed in terms of (a) scores on the 7 CSS subscales and (b) average score across all 7 subscales. Ultrasound IMT measures were taken at baseline and 3 years later. Mean IMT was derived by taking the bilateral average of far wall common, internal and bulb measures. IMT change was computed as the arithmetic difference between follow-up and baseline values. Plaque change was computed as the number of visible lesions at follow-up less the number of lesions at baseline. Blood draws for inflammatory markers and CVR testing were conducted at separate baseline visits. Results failed to support the mediation model. Only the CSS physical stress subscale was an independent predictor of IMT change (b&barbelow;=.02, t&barbelow;=2.13, p&barbelow;=.03). CSS scores were unrelated to plaque, or to inflammatory marker levels. Results did not differ according to CVR. Findings question the importance of chronic stress, as measured by global self-report, as a predictor of change in IMT and plaque.
机译:社会心理压力可能是心血管疾病(CVD)风险中某些变化的原因,而传统风险因素并未对此做出解释。大多数关于压力和CVD的研究都集中在(a)单一生活领域的压力和(b)临床CVD结果。很少有研究检查可能解释压力与CVD之间关系的生理机制。本研究的主要目的是检查:(1)慢性应激是否可以预测颈动脉内膜中层厚度(IMT)和斑块的变化; (2)慢性应激与这些替代性CVD终点变化之间的关联是由炎症过程介导的。第二个目的是研究心血管反应性(CVR)的个体差异是否能缓解压力与IMT和斑块变化之间的联系。样本(n&barbelow; = 276; M&barbelow;年龄= 60.5)是匹兹堡健康心脏计划的子集,该计划是对心理社会和生物危险因素对健康老年人替代CVD终点的影响的纵向调查。慢性压力在基线时通过慢性压力量表(CSS; Norris&Uhl,1993)进行了自我评估,该压力表测量了前6个月中7个生活领域的压力。根据(a)7个CSS子量表的得分和(b)所有7个子量表的平均得分来计算慢性应激。基线和3年后采用超声IMT措施。平均IMT是通过对远端壁常见,内部和球泡测度的双边平均值得出的。 IMT变化计算为随访值和基线值之间的算术差。斑块变化的计算是随访时可见病变的数量减去基线的病变数量。在单独的基线访视时抽取血液用于炎性标志物并进行CVR测试。结果未能支持中介模型。只有CSS物理压力分量表是IMT变化的独立预测因子(b&barbelow; =。02,t&barbelow; = 2.13,p&barbelow; =。03)。 CSS分数与斑块或炎症标志物水平无关。根据CVR,结果没有差异。研究结果质疑以整体自我报告衡量的慢性应激作为IMT和斑块变化预测因子的重要性。

著录项

  • 作者

    Janicki, Denise L.;

  • 作者单位

    University of Pittsburgh.;

  • 授予单位 University of Pittsburgh.;
  • 学科 Psychology Clinical.
  • 学位 Ph.D.
  • 年度 2006
  • 页码 153 p.
  • 总页数 153
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医学心理学、病理心理学;
  • 关键词

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号