Strike Philip C, Magid Kesson, Whitehead Daisy L, Brydon Lena, Bhattacharyya Mimi R, Steptoe Andrew
Psychobiology Group, Department of Epidemiology and Public Health, University College London, London WC1E 6BT, United Kingdom.
Proc Natl Acad Sci U S A. 2006 Mar 14;103(11):4322-7. doi: 10.1073/pnas.0507097103. Epub 2006 Mar 2.
Acute negative emotional states may act as triggers of acute coronary syndrome (ACS), but the biological mechanisms involved are not known. Heightened platelet activation and hemodynamic shear stress provoked by acute stress may contribute. Here we investigated whether patients whose ACS had been preceded by acute anger, stress, or depression would show heightened hemodynamic and platelet activation in response to psychophysiological stress testing. We studied 34 male patients an average of 15 months after they had survived a documented ACS. According to an interview conducted within 5 days of hospital admission, 14 men had experienced acute negative emotion in the 2 h before symptom onset, and 20 men had not experienced any negative emotion. Hemodynamic variables and platelet activation were monitored during performance of challenging color-word interference and public speaking tasks and over a 2-h poststress recovery period. The emotion trigger group showed significantly greater increases in monocyte-platelet, leukocyte-platelet, and neutrophil-platelet aggregate responses to stress than the nontrigger group, after adjusting for age, body mass, smoking status, and medication. Monocyte-platelet aggregates remained elevated for 30 min after stress in the emotion trigger group. The emotion trigger group also showed poststress delayed recovery of systolic pressure and cardiac output compared with the nontrigger group. These results suggest that some patients with coronary artery disease may be particularly susceptible to emotional triggering of ACS because of heightened platelet activation in response to psychological stress, coupled with impaired hemodynamic poststress recovery.
急性负面情绪状态可能是急性冠状动脉综合征（ACS）的触发因素，但其涉及的生物学机制尚不清楚。急性应激引发的血小板活化增强和血流动力学切应力可能起了作用。在此，我们研究了在ACS发作前经历过急性愤怒、应激或抑郁的患者在接受心理生理应激测试时是否会表现出血流动力学和血小板活化增强。我们研究了34名男性患者，他们在确诊ACS后平均存活了15个月。根据入院后5天内进行的访谈，14名男性在症状发作前2小时经历了急性负面情绪，20名男性未经历任何负面情绪。在执行具有挑战性的颜色-单词干扰任务和公开演讲任务期间以及应激后2小时的恢复期内，监测血流动力学变量和血小板活化情况。在调整年龄、体重、吸烟状况和用药情况后，情绪触发组对应激的单核细胞-血小板、白细胞-血小板和中性粒细胞-血小板聚集反应的增加明显大于非触发组。情绪触发组在应激后30分钟内单核细胞-血小板聚集仍保持升高。与非触发组相比时，情绪触发组在应激后还表现出收缩压和心输出量恢复延迟。这些结果表明，一些冠心病患者可能由于对心理应激的血小板活化增强以及应激后血流动力学恢复受损，而特别容易受到情绪触发ACS的影响。
