Associations between psychosocial burden and prognostic biomarkers in patients with chronic coronary syndrome: a STABILITY substudy

Abstract

Abstract Aims To investigate associations between psychosocial (PS) burden and biomarkers reflecting pathophysiological pathways in patients with chronic coronary syndrome. Methods and results Psychosocial factors were collected from self-assessed questionnaires and biomarkers representing inflammation [high-sensitivity (hs)-C-reactive protein (CRP), interleukin-6 (IL-6), lipoprotein-associated phospholipase A2 (Lp-PLA2)] and cardiac injury/stress [hs-troponin T (hs-TnT), N-terminal pro-B-type natriuretic peptide (NT-proBNP)] were measured in 12 492 patients with chronic coronary syndrome in the STABILITY trial. Associations between level of each PS factor [never–rarely (reference), sometimes, often–always] and biomarkers were evaluated using linear models with adjusted geometric mean ratios (GMR). A score comprising four factors (‘feeling down’, ‘loss of interest’, financial stress’, and ‘living alone’) that previously demonstrated association with cardiovascular (CV) outcome was created, and categorized into three levels: low, moderate, and high PS burden. Associations between PS score and biomarkers were evaluated similarly. Greater PS burden was significantly associated with a gradual increase in inflammatory biomarkers [GMR (95% confidence interval) for moderate vs. low PS burden; and high vs. low PS burden]: hs-CRP [1.09 (1.04–1.14); 1.12 (1.06–1.17)], IL-6 [1.05 (1.02–1.07); 1.08 (1.05–1.11)], LpPLA2 [1.01 (1.00–1.02); 1.02 (1.01–1.04)], and cardiac biomarkers hs-TnT [1.03 (1.01–1.06); 1.06 (1.03–1.09)] and NT-proBNP [1.09 (1.04–1.13); 1.21 (1.15–1.27)]. Conclusion In patients with chronic coronary syndrome, greater PS burden was associated with increased levels of inflammatory and cardiac biomarkers. While this observational study does not establish causal nature of these associations, the findings suggest inflammation and cardiac injury/stress as plausible pathways linking PS burden to an elevated CV risk that needs to be further explored.