Kop Willem J, Weissman Neil J, Zhu Jianhui, Bonsall Robert W, Doyle Margaret, Stretch Micah R, Glaes Sami B, Krantz David S, Gottdiener John S, Tracy Russell P
University of Maryland Medical Center, Baltimore, Maryland, USA.
Am J Cardiol. 2008 Mar 15;101(6):767-73. doi: 10.1016/j.amjcard.2007.11.006. Epub 2008 Feb 21.
Physical and mental stressors result in increased inflammation markers in populations free of coronary artery disease (CAD). However, inflammatory responses to mental and exercise challenges have not been established in patients with CAD. This study investigated the responses of inflammatory markers, including C-reactive protein (CRP), interleukin-6 (IL-6), and soluble intercellular adhesion molecule-1, in patients with CAD after successful elective percutaneous coronary intervention (n = 36, 59 +/- 8 years of age, 33% women) and healthy controls without a history of CAD (n = 28, 54 +/- 10 years of age, 36% women). Increases in inflammatory markers were examined in response to mental challenge tasks (anger recall and mental arithmetic) and treadmill exercise. Stress echocardiography was used to rule out stress-induced ischemia as a possible confounding factor. Results showed that CRP increased significantly to mental challenge and exercise (p values <0.01), and CRP responses were higher in patients with CAD than in controls (change in mental arithmetic 0.19 +/- 0.11 vs 0.01 +/- 0.03 mg/L, p = 0.003; change in exercise 0.57 +/- 0.11 vs 0.08 +/- 0.0.03 mg/L, p = 0.001). Increased norepinephrine responses were related to larger CRP and IL-6 increases to mental challenge tasks (p values <0.05). Exercise elicited increased CRP, IL-6, and soluble intercellular adhesion molecule-1 levels (p values <0.01), and these responses were larger than with mental challenge tasks (p values <0.05). In conclusion, mental stress and exercise induce increased levels of inflammatory markers in patients with CAD. These stress-induced increases are larger than in healthy subjects, occur in the absence of myocardial ischemia, and are related to the neurohormonal stress response.
身心应激源会导致无冠状动脉疾病（CAD）人群的炎症标志物增加。然而，CAD患者对精神和运动应激的炎症反应尚未明确。本研究调查了成功接受择期经皮冠状动脉介入治疗的CAD患者（n = 36，年龄59±8岁，女性占33%）和无CAD病史的健康对照者（n = 28，年龄54±10岁，女性占36%）中炎症标志物的反应，包括C反应蛋白（CRP）、白细胞介素-6（IL-6）和可溶性细胞间黏附分子-1。研究了对精神应激任务（愤怒回忆和心算）和跑步机运动的炎症标志物增加情况。采用负荷超声心动图排除应激诱导的心肌缺血这一可能的混杂因素。结果显示，CRP对精神应激和运动均显著增加（p值<0.01），且CAD患者的CRP反应高于对照组（心算时变化为0.19±0.11 vs 0.01±0.03 mg/L，p = 0.003；运动时变化为0.57±0.11 vs 0.08±0.03 mg/L，p = 0.001）。去甲肾上腺素反应增加与精神应激任务时更大的CRP和IL-6增加相关（p值<0.05）。运动引起CRP、IL-6和可溶性细胞间黏附分子-1水平升高（p值<0.01），且这些反应大于精神应激任务时的反应（p值<0.05）。总之，精神应激和运动可诱导CAD患者炎症标志物水平升高。这些应激诱导的升高在健康受试者中更大，在无心肌缺血的情况下发生，且与神经激素应激反应相关。
