Wirtz Petra H, von Känel Roland
Biological Work and Health Psychology, Department of Psychology, University of Konstanz, Universitaetsstrasse 10, 78457, Constance, Baden-Wuerttemberg, Germany.
Department of Neurology, Inselspital, Bern University Hospital, and University of Bern, Bern, Switzerland.
Curr Cardiol Rep. 2017 Sep 20;19(11):111. doi: 10.1007/s11886-017-0919-x.
In this review, we summarize evidence on the risk factor psychological stress in the context of coronary heart disease (CHD) in humans and explore the role of inflammation as a potential underlying mechanism.
While chronic stress increases the risk of incident CHD and poor cardiovascular prognosis, acute emotional stress can trigger acute CHD events in vulnerable patients. Evidence supporting a potential role for inflammation as a promising biological mechanism comes from population-based studies showing associations between chronic stress and increased inflammation. Similarly, experimental studies demonstrate acute stress-induced increases in inflammatory markers and suggest modulatory potential for pharmacological and biobehavioral interventions. So far, studies investigating patients with cardiovascular disease are few and the full sequence of events from stress to inflammation to CHD remains to be established. Psychological stress is an independent CHD risk factor associated with increased inflammation. Although promising, causality needs to be further explored.
在本综述中,我们总结了关于人类冠心病(CHD)背景下心理应激这一危险因素的证据,并探讨炎症作为潜在潜在机制的作用。
虽然慢性应激会增加冠心病发病风险和不良心血管预后,但急性情绪应激可在易患患者中引发急性冠心病事件。支持炎症作为一种有前景的生物学机制的潜在作用的证据来自基于人群的研究,这些研究表明慢性应激与炎症增加之间存在关联。同样,实验研究表明急性应激会导致炎症标志物增加,并提示药物和生物行为干预具有调节潜力。到目前为止,针对心血管疾病患者的研究较少,从应激到炎症再到冠心病的完整事件序列仍有待确定。心理应激是与炎症增加相关的独立冠心病危险因素。尽管前景广阔,但因果关系仍需进一步探索。