Kuebler Ulrike, Trachsel Manuel, von Känel Roland, Abbruzzese Elvira, Ehlert Ulrike, Wirtz Petra H
Clinical Psychology and Psychotherapy, University of Zurich, Zurich, Switzerland.
Institute of Biomedical Ethics, University of Zurich, Zurich, Switzerland.
J Psychosom Res. 2014 Jul;77(1):51-6. doi: 10.1016/j.jpsychores.2014.04.004. Epub 2014 Apr 24.
Hypertension and an atherogenic lipid profile are known risk factors for coronary heart disease (CHD). Hypertensives show greater changes in atherogenic plasma lipids to acute stress than normotensives. In this study, we investigated whether attribution of failure is associated with lipid stress reactivity in hypertensive compared with normotensive men.
18 normotensive and 17 hypertensive men (mean±SEM; 45±2.2 years) underwent an acute standardized psychosocial stress task that can be viewed as a situation of experimentally induced failure. We assessed external-stable (ES), external-variable (EV), internal-stable (IS), and internal-variable (IV) attribution of failure and psychological control variables (i.e. extent of depression and neuroticism). Moreover, total cholesterol (TC), low-density-lipoprotein cholesterol (LDL-C), and norepinephrine were measured immediately before and several times after stress.
ES moderated TC- and LDL-C-stress reactivity in hypertensives as compared to normotensives (interaction mean arterial pressure [MAP]-by-ES for TC: F=3.71, p=.015; for LDL-C: F=3.61, p=.016). TC and LDL-C levels were highest in hypertensives with low ES immediately after stress (p≤.039). In contrast, hypertensives with high ES did not differ from normotensives in TC and LDL-C immediately after stress (p's>.28). Controlling for norepinephrine, depression, and neuroticism in addition to age and BMI did not significantly change results. There were no significant associations between lipid baseline levels or aggregated lipid secretion and IS, IV, or EV (p's>.23).
Our data suggest that ES may independently protect from elevated lipid stress reactivity in hypertensive individuals. ES thus might be a protective factor against CHD in hypertension.
高血压和致动脉粥样硬化血脂谱是已知的冠心病(CHD)危险因素。与血压正常者相比,高血压患者在急性应激时致动脉粥样硬化血浆脂质变化更大。在本研究中,我们调查了与血压正常男性相比,高血压男性的失败归因是否与脂质应激反应性相关。
18名血压正常男性和17名高血压男性(均值±标准误;45±2.2岁)接受了一项急性标准化心理社会应激任务,该任务可被视为实验诱导失败的情境。我们评估了失败的外部稳定(ES)、外部可变(EV)、内部稳定(IS)和内部可变(IV)归因以及心理控制变量(即抑郁程度和神经质)。此外,在应激前即刻和应激后多次测量总胆固醇(TC)、低密度脂蛋白胆固醇(LDL-C)和去甲肾上腺素。
与血压正常者相比,ES调节了高血压患者的TC和LDL-C应激反应性(TC的平均动脉压[MAP]×ES交互作用:F = 3.71,p = 0.015;LDL-C:F = 3.61,p = 0.016)。应激后即刻,ES低的高血压患者的TC和LDL-C水平最高(p≤0.039)。相反,ES高的高血压患者在应激后即刻的TC和LDL-C水平与血压正常者无差异(p>0.28)。除年龄和BMI外,控制去甲肾上腺素、抑郁和神经质后,结果无显著变化。脂质基线水平或总脂质分泌与IS、IV或EV之间无显著关联(p>0.23)。
我们的数据表明,ES可能独立保护高血压个体免受脂质应激反应性升高的影响。因此,ES可能是高血压患者预防冠心病的保护因素。