The comorbidities that collectively define metabolic syndrome are common in patients with heart failure. However, the role of metabolic syndrome in the pathophysiology of heart failure is not well understood. We therefore investigated the clinical and biomarker correlates of metabolic syndrome in patients with heart failure.

Introduction The risk factors that collectively define metabolic syndrome (MetS) are common in heart failure (HF) patients. More research is needed to elucidate the individual role of MetS in the pathophysiology of HF. Purpose The study investigates the differences in biomarker profiles of HF patients with MetS and without MetS. Methods and results The prevalence of MetS was 468 of the 1103 patients (42.4%) in the index cohort and 615 of 1433 (42.9%) patients in the validation cohort. With a microarray analysis of 363 biomarkers, the biomarker profiles of HF patients with versus without MetS were identified. The resulting biomarker profiles were used in network analysis to analyse the underlying pathophysiological mechanisms. The biomarker profile for MetS showed 43 upregulated and 5 downregulated biomarkers in the index cohort. In the validation cohort, there were 58 upregulated and 3 downregulated biomarkers. The most significantly upregulated biomarkers shared between the two cohorts were leptin, fatty acid-binding protein 4, interleukin-1 receptor antagonist, tumour necrosis factor receptor superfamily member 11a, and RET proto-oncogene. Network analysis identified 10 pathways in the index cohort and 6 in the validation cohort, all related to inflammation. Conclusion Pathophysiological pathways leading to HF in patients with MetS are most likely related to obesity and the chronic inflammatory state found in these patients. The role of obesity in the pathophysiology of HF should be validated in similar research to analyse and compare the outcomes. Several individual proteins were identified that might be interesting targets for future research and new treatment options for HF patients. Funding Acknowledgement Type of funding sources: None.