Higher Activation of the Rostromedial Prefrontal Cortex During Mental Stress Predicts Major Cardiovascular Disease Events in Individuals With Coronary Artery Disease.
Higher Activation of the Rostromedial Prefrontal Cortex During Mental Stress Predicts Major Cardiovascular Disease Events in Individuals With Coronary Artery Disease.
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DOI：
10.1161/circulationaha.119.044442
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发表时间：
2020-08-04
期刊：
影响因子：
37.8
通讯作者：
Shah AJ
中科院分区：
文献类型：
--
作者：
Moazzami K;Wittbrodt MT;Lima BB;Nye JA;Mehta PK;Pearce BD;Almuwaqqat Z;Hammadah M;Levantsevych O;Sun YV;Raggi P;Garcia EV;Goetz M;Quyyumi AA;Bremner JD;Vaccarino V;Shah AJ
心理压力是冠状动脉疾病（CAD）患者发生重大心血管不良事件（MACE）的危险因素。某些控制情绪状态和心脏生理的大脑区域可能与这种关系有关。吻内侧前额叶皮层（rmPFC）是处理应激、调节免疫和自主神经功能的重要脑区。rmPFC活性随情绪应激（反应性）的变化可能是未来MACE风险的信息。稳定CAD的参与者进行了急性精神压力测试，使用一系列标准化的语音/算术压力源，同时进行高分辨率正电子发射断层扫描脑成像的脑成像。我们将高rmPFC激活定义为应力和对照扫描之间的差异大于整个队列的中值。还评估了应激后90分钟的白细胞介素-6（IL-6）水平和应激期间的高频心率变异性（HF-HRV）。我们将MACE定义为心血管死亡、心肌梗死、不稳定型心绞痛伴血运重建和心力衰竭住院的复合事件。我们研究了148名受试者（69%为男性），平均± SD年龄为62 ± 8岁。校正基线人口统计学、危险因素和IL-6和HF-HRV基线水平后，rmPFC应激反应性升高与应激时IL-6升高和HF-HRV降低独立相关。在中位随访3年期间，34例受试者（21.3%）发生MACE。在精神压力下rmPFC激活每增加1 SD，MACE风险增加21%（HR 1.21，95% CI 1.08-1.37）。应激诱导的IL-6和HF-HRV分别解释了rmPFC反应性与MACE之间的15.5%和32.5%的关系。将rmPFC反应性添加到传统风险因素中改善了MACE预测的风险重新分类，C统计量从0.71改善至0.76（p=0.03）。更大的rmPFC应激反应与MACE事件相关。免疫和自主神经对精神压力的反应可能起着促进作用。
Psychological stress is a risk factor for major adverse cardiovascular events (MACE) in individuals with coronary artery disease (CAD). Certain brain regions that control both emotional states and cardiac physiology may be involved in this relationship. The rostromedial prefrontal cortex (rmPFC) is an important brain region that processes stress and regulates immune and autonomic functions. Changes in rmPFC activity with emotional stress (reactivity) may be informative of future risk for MACE. Participants with stable CAD underwent acute mental stress testing using a series of standardized speech/arithmetic stressors and simultaneous brain imaging with high resolution-positron emission tomography brain imaging. We defined high rmPFC activation as a difference between stress and control scans greater than the median value for the entire cohort. Interleukin-6 (IL-6) levels 90 minutes post-stress, and high-frequency heart rate variability (HF-HRV) during stress were also assessed. We defined MACE as a composite of cardiovascular death, myocardial infarction, unstable angina with revascularization and heart failure hospitalization. We studied 148 subjects (69% male) with mean ± SD age of 62 ± 8 years. After adjustment for baseline demographics, risk factors, and baseline levels of IL-6 and HF-HRV, higher rmPFC stress reactivity was independently associated with higher IL-6 and lower HF-HRV with stress. During a median follow-up of 3 years, 34 subjects (21.3%) experienced a MACE. Each 1SD increase in rmPFC activation with mental stress was associated with a 21% increase risk of MACE (HR 1.21, 95% CI 1.08–1.37). Stress-induced IL-6 and HF-HRV explained 15.5% and 32.5% of the relationship between rmPFC reactivity and MACE, respectively. Addition of rmPFC reactivity to conventional risk factors improved risk reclassification for MACE prediction, and C-statistic improved from 0.71 to 0.76 (p=0.03). Greater rmPFC stress reactivity is associated with incident MACE. Immune and autonomic responses to mental stress may play a contributory role.