纽约（路透社健康）11月21日：根据11月出版的《动脉粥样硬化、血栓与血管生物学》上发表的研究结果，心理应激后血压恢复正常缓慢与颈动脉内膜中层厚度有关。研究结果显示心理社会因素与心血管疾病相关。
英国伦敦大学的Andrew Steptoe 博士及他的同事指出，“心理应激后血压（BP）恢复延迟与社会经济状况低下以及未来临床血压增加相关。”
为了了解应激后血压是否与颈动脉粥样硬化有关，在白厅II研究中，研究团队对受试者的一个健康亚群进行了心理生理学应激检测（颜色-词语干扰试验和镜画实验）。试验后监测40至45分钟应激后收缩压的恢复。
应激测试三年后，136名受试者（平均年龄55.3岁）进行了颈动脉超声扫描：37例收缩压在恢复期返回到基线水平（充分恢复），99例血压保持升高（延迟恢复）。
消除相关变异后，与充分恢复相比，在社会经济状况低下的受试者中，颈动脉内膜中层厚度与延迟恢复相关（平均0.78比0.65毫米），但是在社会经济状况较好的受试者中二者没有相关关系（平均0.75比0.74毫米）。
Dr. Steptoe的研究团队总结道：“我们的研究显示，应激相关因素影响CHD发展的途径是通过干扰稳态调节导致应激后心血管功能延迟恢复或者无法恢复而实现的。”
最后更新：2006-11-20 11:22:18 -0400 （路透社 健康）
Delayed blood pressure recovery after stress is linked to atherosclerosis
11/21/2006
By: Reuters Health
http://www.auntminnie.com/index.asp?Sec=sup&Sub=ult&Pag=dis&ItemId=73603
NEW YORK (Reuters Health), Nov 21 - Slow blood pressure normalization after psychological stress is associated with carotid intima-media thickness, according to study results published in the November issue of Arteriosclerosis, Thrombosis, and Vascular Biology. The findings suggest a link between psychosocial factors and cardiovascular disease.
"Delayed blood pressure (BP) recovery after psychological stress is associated with low socioeconomic status (SES) and prospectively with increases in clinic BP," Dr. Andrew Steptoe and colleagues from University College London, U.K., write.
To see if poststress BP is associated with carotid atherosclerosis, the team performed psychophysiological stress testing (color-word interference testing and mirror tracing) in a healthy subgroup of subjects in the Whitehall II study. Poststress recovery systolic BP was monitored for 40 to 45 minutes after the tasks.
Three years after stress testing, carotid ultrasound scanning was conducted in 136 subjects (mean age 55.3 years) -- 37 whose systolic BP returned to baseline in the recovery period (adequate recovery) and 99 whose BP remained elevated (delayed recovery).
After adjustment for a number of covariates, carotid intima-media thickness was associated with delayed recovery compared with adequate recovery (mean 0.78 versus 0.65 mm) in lower SES subjects but not in higher SES participants (mean 0.75 versus 0.74 mm).
"Our results suggest that one of the pathways through which stress-related factors influence the development of CHD is through disturbances of homeostatic regulation leading to delayed or ineffective poststress recovery of cardiovascular function," Dr. Steptoe's team concludes.
Last Updated: 2006-11-20 11:22:18 -0400 (Reuters Health)
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