The effect of heart failure on gut microbial richness and diversity; [O efeito da insuficiência cardíaca estável na riqueza e diversidade microbiana intestinal]

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Özet

Introduction 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.

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https://rdlopen.rawdatalibrary.net/r/bayburt/11797Resmi atıflarda kullanılan kalıcı adres
DOI
https://doi.org/10.1016/j.repc.2022.06.016Yayıncı resmi DOI adresi
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AlanDeğerDil
dc.contributor.authorKilic, Oguz
dc.contributor.authorKaya, Halil Ibrahim
dc.contributor.authorSecme, Mucahit
dc.contributor.authorKilinc, Mehmet
dc.contributor.authorSevgican, Cihan Ilyas
dc.contributor.authorBuber, Ipek
dc.contributor.authorDodurga, Yavuz
dc.contributor.authorSimsek, Omer
dc.contributor.authorErgin, Cagrı
dc.contributor.authorKilic, Ismail Dogu
dc.date.accessioned2026-10-29T19:08:48.813022932Z
dc.date.available2026-10-29T19:08:48.813022932Z
dc.date.issued2023
dc.description.abstractIntroduction 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.
dc.description.sponsorshipPamukkale Üniversitesi, PAÜ, (2018TIPF005)
dc.description.sponsorshipPamukkale Üniversitesi, PAÜ
dc.identifier.doi10.1016/j.repc.2022.06.016
dc.identifier.endpage551
dc.identifier.issn0870-2551
dc.identifier.issue6
dc.identifier.pmid36893840
dc.identifier.scopus2-s2.0-85162925468
dc.identifier.startpage543
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/bayburt/11797
dc.identifier.volume42
dc.language.isoen
dc.publisherSociedade Portuguesa de Cardiologia
dc.relation.ispartofRevista Portuguesa de Cardiologia
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectCoronary artery disease
dc.subjectDiversity
dc.subjectHeart failure
dc.subjectIntestinal
dc.subjectMicrobiota
dc.subject.otheracetylsalicylic acid
dc.subject.otheramino terminal pro brain natriuretic peptide
dc.subject.otherangiotensin receptor antagonist
dc.subject.otherbeta adrenergic receptor blocking agent
dc.subject.otherC reactive protein
dc.subject.otherdipeptidyl carboxypeptidase inhibitor
dc.subject.otherDNA 16S
dc.subject.otherendotoxin
dc.subject.otherfurosemide
dc.subject.othergalectin 3
dc.subject.otherhydroxymethylglutaryl coenzyme A reductase inhibitor
dc.subject.otherinterleukin 1beta
dc.subject.otherinterleukin 6
dc.subject.otherlipopolysaccharide binding protein
dc.subject.otherproton pump inhibitor
dc.subject.otherpurinergic P2Y receptor antagonist
dc.subject.otherRNA 16S
dc.subject.otherspironolactone
dc.subject.othertumor necrosis factor
dc.subject.otheradult
dc.subject.otherAnoxybacillus
dc.subject.otherAnoxybacillus ayderensis
dc.subject.otherArticle
dc.subject.otherBacteroidetes
dc.subject.otherBifidobacterium
dc.subject.otherBifidobacterium angulatum
dc.subject.otherBifidobacterium gallicum
dc.subject.otherclinical article
dc.subject.othercontrolled study
dc.subject.othercoronary artery disease
dc.subject.otherdiuretic therapy
dc.subject.otherDNA sequencing
dc.subject.otherEnterococcus
dc.subject.otherenzyme linked immunosorbent assay
dc.subject.otherfeces analysis
dc.subject.otherfemale
dc.subject.otherFirmicutes
dc.subject.otherheart failure with reduced ejection fraction
dc.subject.otherheart left ventricle ejection fraction
dc.subject.otherhuman
dc.subject.otherillumina sequencing
dc.subject.otherintestine flora
dc.subject.otherLactobacillus
dc.subject.otherLactobacillus letivazi
dc.subject.othermale
dc.subject.othermicrobial diversity
dc.subject.othermiddle aged
dc.subject.otheroperational taxonomic unit
dc.subject.otherPeptoniphilus
dc.subject.otherPeptoniphilus gorbachii
dc.subject.otherphylum
dc.subject.otherpolymerase chain reaction
dc.subject.otherProteobacteria
dc.subject.otherProvidencia
dc.subject.otherProvidencia burhodogranariea
dc.subject.otherRNA sequencing
dc.subject.otherShannon index
dc.subject.otherspecies richness
dc.titleThe effect of heart failure on gut microbial richness and diversity; [O efeito da insuficiência cardíaca estável na riqueza e diversidade microbiana intestinal]
dc.typeArticle
rdl.citation.openalex7
rdl.citation.scopus8
rdl.departmentDepartment of Cardiology, Karaman Training and Research Hospital, Karaman, Turkey
rdl.departmentDepartment of Cardiology, Pamukkale University Hospitals, Denizli, Turkey
rdl.departmentDepartment of Food Engineering, University of Bayburt University, Bayburt, Turkey
rdl.departmentDepartment of Medical Biology, Faculty of Medicine, Pamukkale University, Denizli, Turkey
rdl.departmentDepartment of Cardiology, Konya City Hospital, Konya, Turkey
rdl.departmentDepartment of Food Engineering, University of Pamukkale University, Denizli, Turkey
rdl.departmentDepartment of Medical Microbiology, Faculty of Medicine, Pamukkale University, Denizli, Turkey
rdl.oa.statusgold
rdl.oa.urlhttps://doi.org/10.1016/j.repc.2022.06.016
rdl.scopus.quartileQ3
rdl.sdgSDG03
rdl.source.indexSCOPUS
rdl.source.indexPUBMED