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Background: Chronic heart failure (HF) patients have reduced microbiota diversity. Leakage of microbes and their metabolites into the bloodstream may activate neutrophils. Neutrophil extracellular traps (NETs) consist of chromatin and proteases, and may contribute to HF pathogenesis. We assessed associations between circulating NETs and 1) cardiac function, 2) the degree of gut microbiota diversity and 3) gut leakage and microbial metabolites in HF patients., Methods: A cross-sectional study including 124 patients with chronic HF and left ventricular ejection fraction ≤40 %. Severe HF was defined as N-terminal pro-B-type natriuretic peptide concentrations above median. We measured citrullinated histone H 3 (CitH 3 ), myeloperoxidase- and double-stranded-DNA in the blood. Gut leakage markers included bacterial lipopolysaccharides and soluble cluster of differentiation 14. The microbial metabolites included circulating trimethylamine N-oxide and butyrate producing capacity. We used the Shannon diversity-index and a dysbiosis-index based on bacteria with altered relative abundance to characterize the gut microbiota profile., Results: Quartile 4 of CitH 3 was associated with more severe HF compared to quartiles 1-3, after adjustments for age, gender and hypertension (adjusted odds ratio [95 %CI] 3.21[1.18-8.69], p = 0.022). CitH 3 was moderately associated with hypertension (p = 0.04), higher CRP levels (p = 0.016) and lower Shannon diversity index , (p = 0.039). No other NET marker associated with severe HF., Conclusions: In chronic HF patients with reduced LVEF, high levels of CitH 3 were associated with disease severity, inflammation and reduced gut microbiota diversity. Our results suggest that enhanced release of NETs could be involved in progressive HF, although the contribution of the gut microbiota seems limited in this context., Competing Interests: Declaration of competing interest The authors declare no competing interests., (Copyright © 2024 The Author(s). Published by Elsevier B.V. All rights reserved.)

Background: Circulating microparticles (cMPs) have been proposed as novel biomarkers of cardiovascular disease (CVD). We aimed to investigate the prognostic relevance of cMPs for future major adverse cardiovascular events (MACE) in STEMI patients., Methods: We included 200 STEMI patients treated with percutaneous coronary intervention (PCI). One hundred patients with a primary composite end point (recurrent nonfatal acute MI, rehospitalization for heart failure, unscheduled PCI or death because of CV causes) were case-matched for sex, age, and CVD risk factors to 100 patients without a primary endpoint at the end of study follow-up (4.4 (1.4) years). cMPs from vascular cells were measured by flow cytometer at a mean of 28h after onset of symptoms., Results: No differences were observed in MP shedding between patients with or without a MACE at the end of the study follow-up. However, compared to patients who survived during follow-up, patients who died because of CV causes (n=24) presented with increased total cMPs (Annexin V-AV- + ), cMPs carrying tissue factor, and increased MP shedding from platelets, lymphocytes, monocytes, and activated leukocytes, and ~10% lower left ventricular ejection fraction (LVEF). ROC-curve analyses showed that monocyte-derived cMPs (CD14 + /AV + , CD11b + /CD14 + /AV + and CD142 + /CD14 + /AV + ) considered together with LVEF best predicted cardiovascular mortality., Conclusions: Monocyte-derived cMPs assessed in the acute phase relate to the prognosis of CV death at the long term. These findings may be of clinical interest in the risk assessment of STEMI patients., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)