Psychosomatic syndromes are associated with IL-6 pro-inflammatory cytokine in heart failure patients

Abstract

Psychosomatic syndromes have emerged as an important source of comorbidity in cardiac patients and have been associated with increased risk for adverse outcomes in patients with heart failure (HF). Understanding of the mechanisms underlying this connection is limited, however immune activity represents a possible pathway. While there have been numerous studies connecting immune activity to psychosomatic psychopathology, there is a lack of research on patients with HF. We examined forty-one consecutive outpatients affected by HF. We assessed psychosomatic psychopathology using the Diagnostic Criteria for Psychosomatic Research (DCPR) and the Patient Health Questionnaire-15 (PHQ-15). The Psychosocial Index (PSI) was used for assessing stress and psychosocial dimensions. Depression was evaluated with Beck Depression Inventory-II (BDI-II). Circulating levels of proinflammatory cytokines IL-6 and TNF-alpha were ascertained. Univariate and multivariable regression models were used to test for associations between inflammatory cytokines and psychosomatic psychopathology (i.e., DCPR syndromes, PHQ-15) and psychological dimensions (i.e., BDI-II, PSI). A significant positive correlation was found between IL-6 levels and psychosomatic psychopathology even when controlling for any confounding variables (i.e., Body-mass index (BMI), New York Heart Association (NYHA) class, smoking habits, alcohol consumption, statin use, aspirin use, beta blockers use, age, and gender). In contrast, the associations between TNF-alpha levels were non-significant. These findings can contribute to research in support of a psychoneuroimmune connection between psychosomatic psychopathology and HF. Findings also suggest the possibility that elevated IL-6 levels are more relevant for the pathogenesis of psychosomatic syndromes than for depression in patients with HF.

A daily diary study on stressors, hurt feelings, aggression, and somatic symptoms: The role of rejection sensitivity and negative emotion differentiation

“…Consistent with the literature (Irwin, 2011; Kiecolt‐Glaser et al, 2005; Takahashi et al, 2018), the current study revealed that more stressors and hurt feelings predicted more SOMA and worse general health. Neuroimmunological studies reveal that stressors increase the level of proinflammatory cytokines, which are associated with nonspecific sickness symptoms (Altamura et al, 2022; Schwarz, 2003). As a result, these detrimental effects may embody more SOMA and worse physical health.…”

“…Neuroimmunology research shows that dysregulated immune systems underly the association between social stress and aggression (Takahashi et al, 2018). Stressors are associated with inflammatory cytokines, which may lead to sickness behaviors (e.g., fever, anorexia, hyperalgesia, weakness) (Altamura et al, 2022; Irwin, 2011; Schwarz, 2003). Stressful events trigger the state of anger and increase the level of cytokines (Kiecolt‐Glaser et al, 2005; Pesce et al, 2013).…”

Potential Cardioprotective Effect of Genipin via Cyclooxidase 2 Suppression and P53 Signal Pathway Attenuation in Induced Myocardial Infarction in Rats

“…This study also showed that genipin could regulate the COX2-PGD2 pathway to inhibit the structure-function remodeling in response to MI. Interleukin 6 and TNF-α were serum inflammatory markers, associated with HF and used for clinical evaluation of HF (32,33). The inflammatory markers activated the AA metabolism pathways to accelerate HF development (34).…”

Psychosocial risk factors for cardiovascular disease: vital exhaustion and its associations with biochemical markers of inflammation among persons 25-44 years old

“…Как известно, вирусные инфекции, воспаление и эндотелиальная дисфункция участвуют в атерогенезе. Присутствие пожизненных латентных вирусов герпеса в атеросклеротических бляшках может оказывать патогенетическое действие, проникая через артериальную стенку, модифицируя липидный обмен и стимулируя выработку провоспалительных цитокинов и факторов роста [6]. Кумулятивная подверженность множественным инфекционным патогенам, известная как патогенная нагрузка, связана с повышением риска ИБС, воспаления и эндотелиальной дисфункции.…”