Kilic, OguzKaya, Halil IbrahimSecme, MucahitKilinc, MehmetSevgican, Cihan IlyasBuber, IpekDodurga, Yavuz2024-10-042024-10-0420230870-2551https://doi.org/10.1016/j.repc.2022.06.016http://hdl.handle.net/20.500.12403/4063Introduction and objective: With recent advances in genome sequencing technology, a large body of evidence has accumulated over the last few years linking alterations in microbiota with cardiovascular disease. In this study, we aimed to compare gut microbial composition using 16S ribosomal DNA (rDNA) sequencing techniques in patients with coronary artery disease (CAD) and stable heart failure (HF) with reduced ejection fraction and patients with CAD but with normal ejection fraction. We also studied the relationship between systemic inflammatory markers and microbial richness and diversity. Methods: A total of 40 patients (19 with HF and CAD, 21 with CAD but without HF) were included in the study. HF was defined as left ventricular ejection fraction <40%. Only stable ambulatory patients were included in the study. Gut microbiota were assessed from the participants’ fecal samples. The diversity and richness of microbial populations in each sample were assessed by the Chao1-estimated OTU number and the Shannon index. Results: The Chao1-estimated OTU number and Shannon index were similar between HF and control groups. There was no statistically significant relationship between inflammatory marker levels (tumor necrosis factor-alpha, interleukin 1-beta, endotoxin, C-reactive protein, galectin-3, interleukin 6, and lipopolysaccharide-binding protein) and microbial richness and diversity when analyzed at the phylum level. Conclusion: In the current study, compared to patients with CAD but without HF, stable HF patients with CAD did not show changes in gut microbial richness and diversity. At the genus level Enterococcus sp. was more commonly identified in HF patients, in addition to certain changes in species levels, including increased Lactobacillus letivazi. © 2023eninfo:eu-repo/semantics/openAccessCoronary artery diseaseDiversityHeart failureIntestinalMicrobiotaArticle42654355110.1016/j.repc.2022.06.0162-s2.0-85162925468Q3