研究表明心理应激是动脉粥样硬化的危险因素，我们也证实了心理应激增加冠心病的患病危险，并且与动脉粥样硬化程度正相关。但心理应激导致动脉粥样硬化的机制尚不清楚。去甲肾上腺素（NE）和血管紧张素II（AngII）介导的内皮损伤和炎症反应是动脉粥样硬化的主要机制之一。儿茶酚抑素（catestatin，CST）是一种内源性神经内分泌活性多肽，可抑制儿茶酚胺的分泌，同时改善内皮功能。我们预实验结果表明，CST水平与平时心理紧张程度和超敏C反应蛋白均负相关。为此，我们提出心理应激使CST降低，促进动脉粥样硬化的发生发展； CST可抑制NE释放，同时减少AngII，改善内皮功能及减轻炎症反应，延缓动脉粥样硬化进程。本研究拟建立心理应激动脉粥样硬化动物模型，探讨在心理应激时CST抗动脉粥样硬化的作用及机制。该研究对明确心理应激促进动脉粥样硬化的机制及药物干预有重要的理论意义，为“双心”医学理论提供实验依据。

The previous studies have shown that psychological stress is one of the independent risk factors for atherosclerosis. We have also found that psychological stress increased the risk for coronary heart disease, and that psychological stress was positively associated with severity of atherosclerosis. However, the mechanisms of psychological stress leading to atherosclerosis is unclear. Norepinephrine (NE) and Angiotensin II (AngII) mediated endothelial injury and inflammation is one of the main mechanisms of atherosclerosis. Catestatin (CST) is an endogenous active neuroendocrinal peptides inhibiting the secretion of catecholamines, while improving endothelial function. Our experimental results show that serum CST level was negatively associated with stress levels and high-sensitivity C-reactive protein. Therefore, we propose that the reduce of CST during psychological stress promotes the development of atherosclerosis; and that CST can improve endothelial function and reduce inflammation, slowing down atherosclerosis progress by inhibition of norepinephrine release and reduce of AngII. This study will establish animal models of psychological stress leading to atherosclerosis, exploring the anti-atherosclerotic effects and mechanisms of CST during psychological stress. The study have important theoretical significances in clarifying the mechanisms of chronic psychological stress promoting atherosclerosis and drug intervention, providing experimental evidence for "double heart" medicine..