Psychological medicine · 2026
Dose-dependent association between elevated resting IL-6 levels and severity of mental stress-induced myocardial perfusion defects.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Yin Han, Chang Jinna, Jia Mengyang, Jiang Cheng, Wang Yuanhao, Liu Fengyao, Bai Bingqing, Liu Yuting, Liu Quanjun, Wang Haochen, Huang Jingnan, Xue Dahui, Jin Nana, Cheng Lixin, Liu Jingjin, Wang Shuxia, Ma Huan, Geng Qingshan
Аннотация
BACKGROUND: Mental stress-induced myocardial ischemia (MSIMI) is common in women with angina with no obstructive coronary artery disease (ANOCA) and is associated with adverse cardiovascular outcomes. Interleukin-6 (IL-6), a central mediator of chronic inflammation, predicts future cardiovascular risk, but its relationship with MSIMI remains unclear.
METHODS: Eighty women with ANOCA underwent 13N-ammonia positron emission tomography/computed tomography to assess myocardial perfusion and myocardial blood flow (MBF) at rest, during mental stress, and during adenosine-induced stress. Resting inflammatory biomarkers were measured, and multivariable logistic and linear regression models were used to evaluate associations with mental stress-induced perfusion defects. Proteomic profiling was performed in a selected subset to explore potential underlying mechanisms.
RESULTS: Mental stress induced significantly greater myocardial perfusion defects in MSIMI+ patients. Resting IL-6 levels were significantly higher in MSIMI+ patients (3.20 versus 1.80 pg/mL, p = 0.024). Although baseline CRP, hsCRP, and complement C3 levels were also higher in MSIMI+ patients, only resting IL-6 remained independently associated with both the presence of MSIMI and the severity of mental stress-induced myocardial perfusion defects after adjustment for demographic, clinical, and psychosocial factors, and resting MBF. Proteomic analyses demonstrated enrichment of innate immune-hemostatic pathways and mitochondrial oxidative phosphorylation in MSIMI+ patients with high IL-6 levels.
CONCLUSIONS: Elevated resting IL-6 is independently associated with the presence and severity of MSIMI in women with ANOCA. These findings suggest that IL-6 may serve as a biomarker of MSIMI and support IL-6-related inflammation as a key pathophysiological pathway underlying MSIMI, with potential implications for targeted therapeutic strategies.
METHODS: Eighty women with ANOCA underwent 13N-ammonia positron emission tomography/computed tomography to assess myocardial perfusion and myocardial blood flow (MBF) at rest, during mental stress, and during adenosine-induced stress. Resting inflammatory biomarkers were measured, and multivariable logistic and linear regression models were used to evaluate associations with mental stress-induced perfusion defects. Proteomic profiling was performed in a selected subset to explore potential underlying mechanisms.
RESULTS: Mental stress induced significantly greater myocardial perfusion defects in MSIMI+ patients. Resting IL-6 levels were significantly higher in MSIMI+ patients (3.20 versus 1.80 pg/mL, p = 0.024). Although baseline CRP, hsCRP, and complement C3 levels were also higher in MSIMI+ patients, only resting IL-6 remained independently associated with both the presence of MSIMI and the severity of mental stress-induced myocardial perfusion defects after adjustment for demographic, clinical, and psychosocial factors, and resting MBF. Proteomic analyses demonstrated enrichment of innate immune-hemostatic pathways and mitochondrial oxidative phosphorylation in MSIMI+ patients with high IL-6 levels.
CONCLUSIONS: Elevated resting IL-6 is independently associated with the presence and severity of MSIMI in women with ANOCA. These findings suggest that IL-6 may serve as a biomarker of MSIMI and support IL-6-related inflammation as a key pathophysiological pathway underlying MSIMI, with potential implications for targeted therapeutic strategies.