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首页> 外文期刊>Psychosomatic Medicine: Journal of the American Psychosomatic Society >Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease.
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Toward a causal model of cardiovascular responses to stress and the development of cardiovascular disease.

机译：建立针对压力和心血管疾病发展的心血管反应的因果模型。

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OBJECTIVE: Cardiovascular reactivity is hypothesized to mediate the relationship between stress and cardiovascular disease. We describe three considerations that are crucial for a causal model of cardiovascular responses to stress: the need for laboratory-life generalizability, the role of interactions between environmental exposures and individual response predispositions, and the importance of the duration of both stressor exposure and cardiovascular responding. METHODS: We illustrate current understanding of stress-cardiovascular disease relationships with examples from the human and animal psychophysiology, epidemiology, and genetics literature. RESULTS: In a causal model of reactivity, the usefulness of laboratory assessment rests on the assumption that laboratory-based cardiovascular reactivity predicts responses in the natural environment. We find only limited generalizability and suggest that cardiovascular responses to stress can be better understood when examined in the natural environment. The interaction of individual response predispositions and stressor exposures contributes to the development and progression of cardiovascular disease; stress-disease relationships could therefore be better understood if predispositions and exposures were assessed simultaneously in interactive models. Cardiovascular responses to stress are likely to be most deleterious when responses are prolonged. Responses may vary in their magnitude, frequency, and duration; however, reactivity captures only response magnitude. The assessment of anticipatory and recovery measures, with response magnitude, may therefore lead to a more useful model of the stress-disease relationship. CONCLUSIONS: A causal model of cardiovascular responses to stress should generalize to the real world, assess interactions between individual predispositions and environmental exposures, and focus on sustained pathogenic exposures and responses.
机译：目的：假设心血管反应可介导压力与心血管疾病之间的关系。我们描述了对心血管应激反应因果模型至关重要的三个考虑因素：对实验室生活的概括性的需求，环境暴露与个体反应倾向之间相互作用的作用以及应激源暴露和心血管反应持续时间的重要性。方法：我们以人类和动物心理生理学，流行病学和遗传学文献为例，说明当前对压力-心血管疾病关系的理解。结果：在反应性的因果模型中，实验室评估的有用性基于以下假设：基于实验室的心血管反应性可预测自然环境中的反应。我们发现只有有限的普遍性，并建议在自然环境中检查时，可以更好地了解心血管对压力的反应。个体反应倾向与应激源暴露的相互作用促进了心血管疾病的发展和发展;因此，如果在互动模型中同时评估易感性和暴露程度，则可以更好地理解压力-疾病关系。当反应时间延长时，对压力的心血管反应可能是最有害的。反应的幅度，频率和持续时间可能有所不同;但是，反应性仅捕获响应幅度。因此，对预期和恢复措施的评估以及反应幅度，可能会导致建立一个更为有用的压力-疾病关系模型。结论：心血管对压力反应的因果模型应推广到现实世界，评估个体易感性和环境暴露之间的相互作用，并关注持续的病原体暴露和反应。

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