The dysbiosis of intestinal microbiota associated with isolated tricuspid valve regurgitation

Isolated tricuspid regurgitation (TR) is an increasingly recognized yet frequently underappreciated valvular disorder that adversely affects both survival and quality of life, with progressively worse outcomes as severity increases. Advances in high-throughput sequencing technologies have considerably expanded our understanding of the human microbiome, uncovering its close associations with a range of cardiovascular diseases, including atherosclerosis, heart failure, and hypertension. However, the potential role of intestinal dysfunction and the gut–heart axis in TR pathophysiology remains largely unexplored. A total of 20 patients diagnosed with TR and 10 healthy age- and gender-matched patients were enrolled in this study. Fecal samples were collected before the operation and subjected to 16 S rDNA gene sequencing. The gut microbiomes of TR and healthy patients were significantly different in terms of alpha-diversity and beta-diversity analysis. Indicator analysis further showed 9 indicative bacterial genera and 2 bacterial species. Genera known to produce short-chain fatty acids (SCFAs), including Faecalibacterium, Blautia, and Ruminococcus were depleted, whereas Lactobacillus and Veillonella were enriched. Their correlations with clinical features using Pearson analysis showed that Ruminococcus, Lactobacillus, and Veillonella were potentially involved in the pathophysiology of TR. Functional predictions indicated enrichment of pathways related to carbohydrate, lipid, and nucleotide metabolism, as well as immune and cardiovascular diseases, whereas pathways linked to amino acid and vitamin metabolism were reduced. Notably, pathways involving D-arginine and D-ornithine metabolism and Staphylococcus_ aureus infection were upregulated. Patients with tricuspid regurgitation (TR) exhibit gut dysbiosis, characterized by significant alterations in taxonomic composition. These findings suggest a dysregulation of the gut-host interaction in TR.