Are Inflammatory Cytokines Associated with Pain during Acute Myocardial Infarction?

Abstract

Objective: Pain and inflammation during acute myocardial infarction (AMI) have been associated with the development of posttraumatic stress disorder and may also impact negatively on somatic outcome. We investigated the relationship between pain during AMI and levels of circulating proinflammatory (tumor necrosis factor [TNF]-α, interleukin [IL]-6) and anti-inflammatory (IL-33 and tissue growth factor [TGF]-β₁) cytokines. Methods: Data were collected as part of the Myocardial Infarction - Stress Prevention Intervention (MI-SPRINT) study. We included 140 patients (mean age 59.6 years, 82.1% male) with high acute psychological distress within 48 h after MI. Fasting blood samples were drawn thereafter to measure cytokine levels. Sociodemographic factors, psychological and medical data, as well as cardiometabolic markers were assessed with questionnaires and patient interviews. Results: Linear regression models showed a significant positive correlation of pain with TGF-β₁ (b = 770.91, p = 0.031) and a significant inverse correlation of pain with IL-33 (b = -0.11, p = 0.015) after controlling for age, gender, body mass index, lifetime depression, acute stress disorder symptoms, and the prognostic Global Registry of Acute Coronary Events (GRACE) score. Pain was not associated with IL-6 but with the GRACE score (b = 0.01, p = 0.003). Pain showed no significant association with TNF-α. Conclusion: Pain during MI was associated with anti- but not proinflammatory cytokines. As IL-33 has been shown to be cardioprotective, lower IL-33 levels with more intense pain may suggest a pathway through which increased pain during MI may have an impact on the medical prognosis.

Protein Cytokines, Cytokine Gene Polymorphisms, and Potential Acute Coronary Syndrome Symptoms

“…They found that a significantly higher proportion of patients with chronic low-back pain had increased TNF-α levels during a 6-month course compared to a healthy control group. Unlike in previous studies, Imholz et al (2017) found no significant association between chest pain and either TNF-α or IL-6 levels in patients with myocardial infarction. They suggested that during the period between symptom onset and blood collection, pro-inflammatory cytokines may have been downregulated by anti-inflammatory mediators, making any initial association between levels of these cytokines and pain intensity difficult to detect.…”