Altered Gut Microbiota in Chronic Heart Failure: A Pathway to New Therapies Original paper
Researched by:
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Karen Pendergrass
ID
Karen Pendergrass
Read MoreKaren Pendergrass is a microbiome researcher specializing in microbiome-targeted interventions (MBTIs). She systematically analyzes scientific literature to identify microbial patterns, develop hypotheses, and validate interventions. As the founder of the Microbiome Signatures Database, she bridges microbiome research with clinical practice. In 2012, based on her own investigative research, she became the first documented case of FMT for Celiac Disease—four years before the first published case study.
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Cardiovascular Health
Cardiovascular Health
Recent research has revealed that specific gut microbiota-derived metabolites are strongly linked to cardiovascular disease risk—potentially influencing atherosclerosis development more than traditional risk factors like cholesterol levels. This highlights the gut microbiome as a novel therapeutic target for cardiovascular interventions.
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Heart Failure
Heart Failure
Recent research reveals that the gut microbiome significantly influences heart failure progression, contributing to inflammation and other complications.
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Karen Pendergrass
Read More
Researched by:
-
Karen Pendergrass
ID
Karen Pendergrass
Read More
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
Karen Pendergrass
What Was Studied?
This original research focused on alterations in the gut microbiota composition of patients with severe chronic heart failure (CHF) using bacterial 16S rRNA gene sequencing. The study aimed to uncover microbial dysbiosis patterns and their potential functional implications in CHF.
Who Was Studied?
The study examined 29 CHF patients classified under New York Heart Association (NYHA) Class III-IV and compared them to 30 healthy controls. These individuals were recruited from Harbin Medical University hospitals in China. Inclusion criteria ensured the absence of confounding variables like recent antibiotic use or gastrointestinal surgery.
What Were the Most Important Findings?
The study found significant differences in microbial composition and diversity between CHF patients and healthy controls:
Phylum-Level Changes: CHF patients showed a significant decrease in Firmicutes (59.5% vs. 72.4%) and a marked increase in Proteobacteria (21.3% vs. 6.9%), suggesting dysbiosis.
Genus-Level Alterations: Notable reductions in SCFA-producing genera like Ruminococcaceae (UCG-004 and UCG-002), Lachnospiraceae FCS020 group, and Dialister were observed. Conversely, pathogenic genera such as Enterococcus and Klebsiella were elevated.
Diversity Metrics: Alpha diversity (Chao1, PD-whole-tree, Shannon indices) and beta diversity (weighted UniFrac distances) were significantly lower in CHF patients, reflecting reduced microbial richness and altered community structure.
Functional Implications: Predicted microbial functions (using PICRUSt) linked to CHF involved disruptions in pathways like cell cycle control, carbohydrate metabolism, and amino acid metabolism. Dysbiosis is also correlated with reduced SCFA production, potentially exacerbating inflammation and metabolic dysregulation.
What Are the Greatest Implications of This Study?
This research highlights a potential gut-heart axis, where microbial dysbiosis in CHF may contribute to systemic inflammation and metabolic disturbances via SCFA deficiencies and increased endotoxins. The findings suggest that targeting gut microbiota through therapeutic interventions could represent a novel strategy for managing severe CHF. Moreover, the identified microbial signatures could guide biomarker development for CHF diagnosis and progression monitoring.
Heart Failure
Recent research reveals that the gut microbiome significantly influences heart failure progression, contributing to inflammation and other complications.