Dysbiosis of oral bacteriome and mycobiome associated with the severity of heart failure.

BACKGROUND

Heart failure (HF) is accompanied by chronic inflammation and metabolic stress, but the relationship between HF severity and the oral microbial ecosystem remains incompletely understood. This study aimed to investigate bacterial, fungal, and predicted functional alterations in supragingival plaque from patients with HF.

METHODS

This case-control study enrolled 63 patients with HF and 31 healthy controls (HC). Supragingival plaque samples were profiled by 16S rRNA and ITS sequencing. Community structure, differential amplicon sequence variants (ASVs), bacterial-fungal co-abundance networks, HF severity-associated ASVs and predicted MetaCyc pathways were analyzed using QIIME2, SparCC, weighted LASSO regression, and PICRUSt2. Pathway-ASV correlations were further assessed to explore links between taxonomic and predicted functional shifts.

RESULTS

HF status and NYHA class were among the strongest explanatory factors for oral bacterial and fungal community variation. Differential abundance analysis identified 102 bacterial and 68 fungal ASVs between HF and control groups. Weighted LASSO analysis retained six ASVs associated with the NYHA III-IV phenotype: ASV586 (Geotrichum candidum), ASV238 (Nectriaceae), and ASV182 (Neisseria bacilliformis) showed positive coefficients, whereas Haemophilus (ASV1), Streptococcus (ASV0), and Pseudopropionibacterium (ASV148) showed negative coefficients. A combined 6-ASV score discriminated HF from controls with an AUC of 0.804 and NYHA III-IV from the remaining cohort with an AUC of 0.842. PICRUSt2 identified 165 pathways differing between HF and controls. TCA cycle I was enriched in HF and positively correlated with NYHA class, whereas pyruvate fermentation to butanoate, a butyrate-related fermentative pathway, was enriched in controls and negatively correlated with NYHA class. Robust pathway-ASV correlations linked HC-enriched oral biofilm taxa with HC-enriched functional modules, suggesting functional uncoupling of the supragingival plaque ecosystem in more severe HF.

CONCLUSIONS

HF severity is associated with oral bacterial-fungal dysbiosis, characterized by enrichment of opportunistic pathogens, depletion of commensal biofilm organisms and predicted functional shifts involving microbial TCA cycle and fermentative capacity. These findings support an "oral-heart axis" in HF and warrant validation by longitudinal multi-omics studies.