Did you know?
Heart Failure affects approximately 64.3 million people worldwide, yet nearly half of them are unaware they have it because the symptoms can be subtle or mistaken for other conditions.

Heart Failure

Researched by:

Karen Pendergrass ID

Karen Pendergrass

Karen 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.

August 9, 2024

Recent research reveals that the gut microbiome significantly influences heart failure progression, contributing to inflammation and other complications.

Research feed

Karen Pendergrass

Karen 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.

Researched by:

Karen Pendergrass ID

Karen Pendergrass

Karen 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.

Last Updated: August 8, 2024

Overview

Heart failure (HF) is a complex syndrome affecting millions worldwide, characterized by the heart’s inability to fill or eject blood properly. Emerging research highlights the role of gut microbiota in HF, suggesting that changes in gut metabolites are closely related to HF progression. The gut hypothesis of HF posits that reduced cardiac output and systemic congestion lead to intestinal ischemia and barrier dysfunction, resulting in bacterial translocation and inflammation. We explore the microbiome signature and gut microbiota’s involvement in HF, mechanisms mediated by gut metabolites, as well as potential interventions, including dietary changes, probiotics, fecal microbiota transplantation (FMT), and antibiotics.

Gut Hypothesis of Heart Failure

The gut hypothesis of HF, first introduced in the late 1990s, proposed that circulatory congestion and low cardiac output reduce intestinal perfusion, causing ischemia and intestinal barrier damage, leading to bacterial translocation, endotoxemia, and systemic inflammation. ^[1][2] Several studies have further supported the idea that metabolites like trimethylamine-n-oxide (TMAO) and SCFAs, produced by the gut microbiota, significantly impact HF progression. ^[3]

Primer

Research indicates that heart failure (HF) patients exhibit distinct gut microbiota profiles compared to healthy individuals. Key findings reveal an increased prevalence of pro-inflammatory bacteria such as Bacteroides/Prevotella, Campylobacter, Shigella,Salmonella, Enterococcus, and Clostridium difficile in HF patients. Conversely, there is a reduction in families like Coriobacteriaceae, Erysipelotrichaceae, and Ruminococcaceae, as well as anti-inflammatory genera such as Blautia and Collinsella. ^[4] Additionally, HF patients show reduced gut microbiota diversity, and an increased Firmicutes/ Bacteroidetes (F/B) ratio, which contributes to systemic conditions like persistent T-cell activation, and heightened susceptibility to hospitalization with a Clostridium difficile infection. ^[5][6]

Associated Conditions

Hospitalized HF patients are more frequently affected by Clostridium difficile infection, which is associated with in-hospital mortality. ^[7]

Metabolomic Signature of Heart Failure

Elevated metabolites contributing to heart failure (HF) have been identified, highlighting the influence of gut-derived compounds. Key metabolites include trimethylamine N-oxide (TMAO), which is produced from dietary nutrients by gut microbiota and is associated with cardiac fibrosis, hypertrophy, inflammation, and endothelial dysfunction. ^[8] Short-chain fatty acids (SCFAs), such as acetate, propionate, and butyrate, are derived from dietary fibers and provide energy to failing hearts, reduce inflammation, and prevent cardiac fibrosis and hypertrophy. ^[9]

Interventions

The gut hypothesis of HF underscores the potential of targeting gut microbiota for HF treatment. Changes in gut microbiota composition and metabolites like TMAO and SCFAs are significant in HF pathophysiology. Interventions such as dietary changes, probiotics, and possibly fecal microbiota transplantation FMT are often suggested as promising avenues for HF management.

Intervention	Findings
Pharmacological
Rifaximin	Rifaximin is commonly used to treat microbiota toxicity and translocation by exerting anti-inflammatory effects and promoting the growth of beneficial bacteria like bifidobacteria and lactobacillus. Despite these potential benefits, the effects of antibiotics on gut microbiota in heart failure (HF) have not been extensively studied. It is crucial to balance the potential benefits and risks of antibiotic use.
Captopril	Captopril effectively modulates neurohormonal pathways, improves renal function, reduces cardiac workload, and corrects electrolyte imbalances, contributing to improved clinical outcomes. ^[10] While captopril’s mechanism of action traditionally involves inhibiting the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, studies suggest that captopril modulates the gut microbiota, leading to a reduction in systemic inflammation and improvement in gut barrier function, both of which are implicated in the pathogenesis of HF. ^[11]

Drug Repurposing
Metformin	Originally indicated to treat type 2 diabetes mellitus, metformin has been explored for its cardioprotective effects, primarily due to its ability to improve endothelial function, reduce oxidative stress, and exert anti-inflammatory effects. It may also improve myocardial energetics and reduce the risk of HF in diabetic and non-diabetic patients. Clinical trials are assessing metformin’s efficacy in improving outcomes in patients with HF, particularly HF with preserved ejection fraction (HFpEF). ^[12]
SGLT2 inhibitors	SGLT2 inhibitors such as empagliflozin and dapagliflozin have shown significant benefits in reducing HF-related hospitalizations and cardiovascular mortality in both HF with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). ^[13] SGLT2 inhibitors are reported to influence gut microbiota composition, potentially by reducing glucose availability in the gut, which may inhibit pathogenic bacteria and support beneficial microbial populations. Preliminary studies in both animal models and humans suggest that these drugs can increase beneficial microbes and reduce pro-inflammatory bacteria, which might contribute to the observed reduction in inflammation and improved cardiovascular outcomes in heart failure patients treated with SGLT2 inhibitors. ^[14]
Spironolactone	Ongoing trials are investigating the effects of spironolactone in HFpEF and its potential to reduce fibrosis and improve diastolic function. As a mineralocorticoid receptor antagonist, spironolactone reduces aldosterone-induced sodium retention and cardiac remodeling. It is especially effective in reducing morbidity and mortality in HFrEF. ^[15] Spironolactone can modulate the gut microbiota by reducing inflammation and improving the gut barrier function, potentially reducing the translocation of gut-derived endotoxins that contribute to systemic inflammation in HF. ^[16]
Colchicine	There is emerging evidence that colchicine may influence the gut microbiota by decreasing pro-inflammatory bacteria and promoting the growth of bacteria that produce SCFAs, which have anti-inflammatory effects. These changes could help mitigate the inflammatory response in HF. Further, colchicine significantly increases Firmicutes while reducing Bacteroidetes. Overall, colchicine intervention notably decreases the abundance of Bacteroidetes, Candida, and Clostridium, which are elevated in the microbiome signature of HF. ^[17]

Diet
DASH Diet	A cohort study of 35,004 participants over 22 years indicated that the DASH diet reduces heart failure (HF) risk. In HF patients, the DASH diet improves walking test performance, arterial compliance, exercise capacity, and quality of life over a 3-month intervention.^[18]

Non-Pharmacological
Fecal microbiota transplantation (FMT)	Fecal microbiota transplantation (FMT) has primarily been used to treat recurrent Clostridium difficile infection, but holds promise for several other conditions hallmarked by the microbe. While the potential effects of FMT on HF are not well studied, FMT may hold promise as a supplementary treatment for HF given the consistent findings of Clostridium difficile in HF patients. ^[19]
*Lactobacillus rhamnosus GR-1*	Lactobacillus rhamnosus GR-1 can reduce hypertrophy and improve both systolic and diastolic functions of the left ventricle, indicating potential benefits for heart failure (HF) patients. ^[20]
*Saccharomyces boulardii*	A randomized, double-blind, placebo-controlled pilot trial targeting HF patients using Saccharomyces boulardii for 3 months showed that it could improve LVEF, shorten left atrial diameter, and lower total cholesterol and uric acid levels. ^[21] *Saccharomyces boulardii* can reduce filamentation, adhesion and biofilm formation of candida species, which are found elevated in HF patients. ^[22]
Probiotic yogurt	A triple-blind, controlled trial suggested that probiotic yogurt might help relieve inflammatory status in CHF patients by elevating sTWEAK levels, a cytokine involved in inflammation, tissue regeneration, and apoptosis. ^[23]

Supplements
Berberine	Oral intake of berberine for 4 months has been shown to decrease TMAO production in animal intestines and reduce TMA and TMAO levels in both the feces and plasma of patients, exerting effects similar to those of vitamins. ^[24]
Vitamin D+ B Vitamins	A study has suggested that combining B vitamins with vitamin D can alter choline metabolism, leading to a greater reduction in TMAO levels compared to the use of vitamin D alone. ^[25]
3,3-dimethyl-1-butanol (DMB)	DMB has been reported to improve cardiac function and reduce cardiac remodeling in heart failure (HF) mice induced by pressure overload. It achieves this by lowering plasma TMAO levels, which inhibits the TGF-β1/Smad3 and p65 NF-κB signaling pathways, thereby attenuating cardiac hypertrophy, fibrosis, and inflammation. ^[26]
High-Fiber Diet + Acetate Supplementation	High-Fiber Diet and acetate supplementation has been found to reduce the F/B ratio, while significantly increasing the abundance of the bacteria Bacteroides acidifaciens. This species has recently been shown to prevent obesity and the evolution of hypertension and heart failure in hypertensive mice.^[27]

Microbiome Targeted Interventions (MBTIs)
Carvacrol	Carvacrol (CR) shows potential as a candidate for microbiome-targeted interventions for heart failure due to its ability to positively modulate gut microbiota and reduce pathogen-induced dysbiosis. The study found that CR supplementation improved clinical outcomes in C. difficile infections, a pathogen also associated with the microbiome signature of HF. CR achieved this by increasing the abundance of beneficial bacteria like Firmicutes and reducing harmful bacteria like Proteobacteria, without significantly disrupting overall microbiome diversity. Given that gut dysbiosis and the presence of pathogens like C. difficile are linked to heart failure, CR’s ability to restore healthy gut flora suggests it could be beneficial in managing gut microbiota imbalances associated with heart failure. ^[28] Hypertension-induced left ventricular hypertrophy is the most important risk factor for heart failure. This study finds that carvacrol was able to ameliorate cardiac hypertrophy in in-vivo and in-vitro models. ^[29]

FAQs

What are the main treatments for heart failure (HF) and what medications are commonly used?

Treatments for HF include pharmacological interventions, device and interventional therapies, mechanical circulatory support (MCS), and heart transplantation. Common medications include renin-angiotensin system inhibitors (ACE inhibitors, ARBs, ARNi), beta-blockers, mineralocorticoid receptor antagonists, SGLT2 inhibitors, hydralazine, isosorbide dinitrate, and others.

What are the device and interventional therapies for HF and their associated risks?

Device therapies include implantable cardioverter defibrillators (ICDs) and cardiac resynchronization therapy (CRT), which aim to prevent sudden cardiac death. These therapies can be invasive, costly, and may carry risks such as infection, lead displacement, and device malfunction.

What is mechanical circulatory support (MCS) and what complications are associated with it?

The most widely used MCS is the left ventricular assist device (LVAD), which serves as both a bridge to transplantation and destination therapy. Complications include thromboembolism, bleeding, infection, device failure, and the need for lifelong anticoagulation therapy.

What challenges are associated with heart transplantation and how do they impact patients?

Heart transplantation faces challenges such as limited donor organ availability, potential for organ rejection, and the need for lifelong immunosuppressive therapy, which increases the risk of infections and other complications. Additionally, heart transplantation is expensive and not universally accessible.

What are the biggest concerns with current HF treatment options and why is there a need for more personalized approaches?

Significant concerns include medication adherence and side effects, limitations of device and interventional therapies, complications of MCS, and challenges with heart transplantation. HF is a heterogeneous condition, and current treatments may not be equally effective for all patients. There is a need for more personalized approaches to optimize outcomes, improve quality of life, and provide more effective and sustainable long-term solutions.

What are the potential benefits of microbiome-targeted interventions or therapies for HF?

Microbiome-targeted interventions, such as the use of probiotics, prebiotics, and dietary modifications, can positively influence gut health and potentially reduce inflammation, improve metabolic function, and lower harmful metabolite levels like TMAO. These interventions may help alleviate HF symptoms, enhance overall cardiovascular health, and offer a complementary approach to traditional HF treatments.

Research Feed

July 10, 2023

•

What was reviewed?

The Gut Microbiota in Heart Failure and Related Interventions Review article examines the relationship between heart failure (HF) and the gut microbiota, exploring the gut hypothesis of HF, the role of gut microbiota metabolites, and potential microbiome-targeted interventions (MBTIs). The review provides a comprehensive overview of the current understanding of how changes in gut microbiota composition and its metabolites contribute to HF progression and discusses various interventions, including dietary changes, probiotic therapy, fecal microbiota transplantation (FMT), antibiotics, and other novel approaches.

Who was reviewed?

The review synthesizes findings from various studies involving HF patients and animal models to understand the connection between gut microbiota and HF. It also evaluates research on different interventions and their effects on gut microbiota and HF. Specific studies cited include investigations of bacterial species present in HF patients compared to healthy controls, the impact of gut microbiota metabolites like trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFAs) on HF, and the efficacy of interventions like the DASH diet, Mediterranean diet, probiotics, FMT, and antibiotics.

What were the most important findings of this review?

The review highlights the gut hypothesis of heart failure (HF), where reduced cardiac output and systemic congestion lead to diminished intestinal perfusion, ischemia, and barrier dysfunction. This allows bacterial translocation and endotoxin release, worsening inflammation and HF. HF patients show increased pathogenic bacteria (e.g., Bacteroides, Eubacterium rectale) and decreased beneficial bacteria (e.g., Lachnospiraceae, Ruminococcaceae). Key gut microbiota metabolites, such as TMAO, SCFAs, TMAVA, and PAGln, significantly impact HF. TMAO promotes cardiac fibrosis, hypertrophy, and inflammation, while SCFAs have protective effects, preventing cardiac hypertrophy and fibrosis, reducing inflammation, and providing energy to the failing heart.

What are the greatest implications of this review?

The greatest implications of the Gut Microbiota in Heart Failure and Related Interventions review are manifold. It highlights the therapeutic potential of targeting gut microbiota as a promising avenue for heart failure (HF) treatment, suggesting that a deeper understanding of the interactions between gut microbiota and HF could lead to novel strategies that complement existing therapies. Personalized medicine approaches, including dietary changes, probiotics, and potentially fecal microbiota transplantation (FMT), could be tailored to individual patients to address specific microbial imbalances contributing to HF. The review also underscores the importance of preventive strategies, such as adopting diets that support a healthy gut microbiota, in reducing the risk and progression of HF, which could have significant public health implications. Additionally, the review calls for further research to elucidate the mechanisms linking gut microbiota and HF, assess the long-term efficacy and safety of various interventions, and explore the roles of other metabolites and bacterial species in HF. Such research could pave the way for new diagnostic and therapeutic tools in HF management. Overall, the review emphasizes the critical role of gut microbiota in HF and suggests that targeting it could revolutionize HF treatment and prevention.

January 31, 2022

•

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.

August 21, 2020

•

What Was Reviewed?

This review focused on the involvement of gut microbiota in the pathogenesis and progression of cardiovascular diseases, particularly heart failure (HF). It emphasized the role of gut microbiota-derived metabolite trimethylamine N-oxide (TMAO) in heart failure and explored the potential of the gut–TMAO–HF axis as a therapeutic target for HF treatment.

Who Was Reviewed?

The review considered patients with various forms of heart failure, including acute heart failure (AHF), chronic heart failure (CHF), heart failure with preserved ejection fraction (HFpEF), and heart failure with reduced ejection fraction (HFrEF). It also encompassed studies involving animal models and in vitro experiments that investigated the pathophysiological mechanisms of TMAO in HF.

What Were the Most Important Findings of This Review?

This review highlights the critical role of gut microbiota in heart failure (HF). Gut dysbiosis contributes to HF pathogenesis through mechanisms like splanchnic hypoperfusion and intestinal barrier dysfunction. Trimethylamine N-oxide (TMAO), a gut-derived metabolite, significantly impacts cardiovascular pathology by promoting myocardial hypertrophy and fibrosis, inducing inflammatory responses, and causing endothelial dysfunction. Elevated TMAO levels correlate with poorer prognosis and higher mortality in HF patients, serving as an independent predictor for HF outcomes. Potential therapeutic targets include dietary interventions, probiotics, prebiotics, and inhibitors of TMA synthesis, such as 3,3-dimethyl-1-butanol (DMB). Fecal microbial transplantation (FMT) and certain antibiotics also show promise in modulating gut microbiota and reducing TMAO production. These findings support a multifaceted approach to HF management by targeting gut microbiota and its metabolites.

What Are the Greatest Implications of This Review?

The "TMAO: how gut microbiota contributes to heart failure" review highlights the importance of novel therapeutic strategies, the prognostic value of TMAO, and future research directions.

Novel Therapeutic Strategies: The review suggests that targeting the gut–TMAO–HF axis could be a revolutionary approach in treating HF. By modulating gut microbiota composition and reducing TMAO levels, it may be possible to improve HF prognosis and patient outcomes. Personalized dietary interventions and the use of probiotics, prebiotics, and phytochemicals hold significant potential for HF management.

Prognostic Value of TMAO: TMAO can serve as a valuable prognostic marker for HF, aiding clinicians in identifying high-risk patients and tailoring more effective treatment strategies. Further research is needed to validate TMAO's role across diverse populations and to explore its utility in clinical practice.

Future Research Directions: Prospective studies are needed to establish a causal relationship between gut microbiota changes and HF. Investigating the detailed mechanisms of how TMAO influences HF progression will be crucial for developing targeted therapies.

References

Elevated Soluble CD14 Receptors and Altered Cytokines in Chronic Heart Failure.. Anker, Stefan D., Karl R. Egerer, Hans-Dieter Volk, Wolfgang J. Kox, Philip A. Poole-Wilson, and Andrew J. S. Coats.. (The American Journal of Cardiology 79: 1426–30. (1997))
Endotoxin and Immune Activation in Chronic Heart Failure: a Prospective Cohort Study.. Niebauer, Josef, Hans-Dieter Volk, Michael Kemp, Martin Dominguez, Ralf R. Schumann, Mathias Rauchhaus, Philip A. Poole-Wilson, Andrew J. S. Coats, and Stefan D. Anker.. (The Lancet 353: 1838–42. (1999))
Gut Microbiota in Heart Failure and Related Interventions.. Chen, An-Tian, Jian Zhang, and Yuhui Zhang.. (iMeta 2, e125. (2023))
Alterations of the Gut Microbiota in Patients With Severe Chronic Heart Failure.. Sun, Weiju, Debing Du, Tongze Fu, Ying Han, Peng Li, and Hong Ju.. (Frontiers in Microbiology 12: 813289.(2022))
Gut Microbiota in Heart Failure Patients With Preserved Ejection Fraction (GUMPTION Study).. Huang, Ziyin, Xiaofei Mei, Yufeng Jiang, Tan Chen, and Yafeng Zhou.. (Frontiers in Cardiovascular Medicine 8: 803744. (2022))
Hospitalized Patients with Heart Failure and Common Bacterial Infections: A Nationwide Analysis of Concomitant Clostridium Difficile Infection Rates and In-Hospital Mortality.. Mamic, Petra, Paul A. Heidenreich, Haley Hedlin, Lakshika Tennakoon, and Kristan L. Staudenmayer.. (Journal of Cardiac Failure 22: 891–900. (2016))
TMAO: how gut microbiota contributes to heart failure.. Zhang Y, Wang Y, Ke B, Du J.. (Transl Res. (2021))
Short-Chain Fatty Acids Outpace Ketone Oxidation in the Failing Heart.. Carley, Andrew N., Santosh K. Maurya, Matthew Fasano, Yang Wang, Craig H. Selzman, Stavros G. Drakos, and E. Douglas Lewandowski.. (Circulation. (2021))
Captopril in heart failure. A double blind controlled trial.. Cleland JG, Dargie HJ, Hodsman GP, et al.. (Br Heart J. (1984))
Hypotensive effect of captopril on deoxycorticosterone acetate-salt-induced hypertensive rat is associated with gut microbiota alteration.. Wu H, Lam TYC, Shum TF, Tsai TY, Chiou J.. (Hypertens Res. (2022))
Effects of Metformin in Heart Failure: From Pathophysiological Rationale to Clinical Evidence.. Salvatore T, Galiero R, Caturano A, et al.. (Biomolecules. (2021))
SGLT-2 Inhibitors in Heart Failure: A Review of Current Evidence.. Talha KM, Anker SD, Butler J.. (Int J Heart Fail. (2023))
Effects of Oral Glucose-Lowering Agents on Gut Microbiota and Microbial Metabolites.. Wang D, Liu J, Zhou L, Zhang Q, Li M, Xiao X.. (Front Endocrinol (Lausanne). (2022))
The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone Evaluation Study Investigators.. Pitt B, Zannad F, Remme WJ, et al.. (N Engl J Med. (1999))
Mineralocorticoid receptor blockade improved gut microbiota dysbiosis by reducing gut sympathetic tone in spontaneously hypertensive rats.. González-Correa, Moleón,Miñano et al.. (Biomedicine & Pharmacotherapy (2023))
Potential roles of gut microbiota and microbial metabolites in chronic inflammatory pain and the mechanisms of therapy drugs.. Li JS, Su SL, Xu Z, et al.. (Ther Adv Chronic Dis. (2022))
The DASH diet is associated with a lower risk of heart failure: a cohort study.. Ibsen DB, Levitan EB, Åkesson A, Gigante B, Wolk A.. (Eur J Prev Cardiol. (2022))
Fecal microbiota transplant, its usefulness beyond Clostridioides difficile in gastrointestinal diseases.. Núñez F P, Quera R, Bay C, Thomson P.. (Gastroenterol Hepatol. (2022).)
Probiotic Therapy With Saccharomyces Boulardii for Heart Failure Patients: A Randomized, Double-Blind, Placebo-Controlled Pilot Trial.. Costanza, Annelise C., Samuel D. Moscavitch, Hugo C. C. Faria Neto, and Evandro T. Mesquita.. (International Journal of Cardiology 179: 348–50. (2015))
The antagonistic effect of Saccharomyces boulardii on Candida albicans filamentation, adhesion and biofilm formation.. Krasowska A, Murzyn A, Dyjankiewicz A, Łukaszewicz M, Dziadkowiec D.. (FEMS Yeast Res. (2009))
The Impact of Probiotic Yogurt Versus Ordinary Yogurt on Serum sTWEAK, sCD163, ADMA, LCAT and BUN in Patients with Chronic Heart Failure: A Randomized, Triple-Blind, Controlled Trial.. Pourrajab, Behnaz, Nasim Naderi et al.. (Journal of the Science of Food and Agriculture 102: 6024–35. 2022.)
Berberine Treats Atherosclerosis Via A Vitamine-Like Effect Down-Regulating Choline-TMA-TMAO Production Pathway in Gut Microbiota.. Ma, Shu-Rong, Qian Tong, Yuan Lin, Li-Bin Pan, Jie Fu, Ran Peng, Xian-Feng Zhang, et al.. (Signal Transduction and Targeted Therapy 7: 207. (2022))
Plasma Trimethylamine-N-Oxide Following Supplementation with Vitamin D or D Plus B Vitamins.. Obeid, Rima, Hussain M. Awwad, Susanne H. Kirsch, Christiane Waldura, Wolfgang Herrmann, Stefan Graeber, and Juergen Geisel.. (Molecular Nutrition & Food Research 61: 1600358. (2017))
3,3-Dimethyl-1-butanol Attenuates Cardiac Remodeling in Pressure-Overload-Induced Heart Failure Mice. Wang, Guangji, Bin Kong, Wei Shuai, Hui Fu, Xiaobo Jiang, and He Huang.. (The Journal of Nutritional Biochemistry 78: 108341 (2020))
A High-Fiber Diet or Dietary Supplementation of Acetate Attenuate Hyperoxia-Induced Acute Lung Injury.. Chu SJ, Tang SE, Pao HP, Wu SY, Liao WI.. (Nutrients. (2022))
Protective Effect of Carvacrol against Gut Dysbiosis and Clostridium difficile Associated Disease in a Mouse Model.. Mooyottu S, Flock G, Upadhyay A, Upadhyaya I, Maas K, Venkitanarayanan K.. (Front Microbiol. (2017))
Carvacrol Ameliorates Pathological Cardiac Hypertrophy in Both In-vivo and In-vitro Models.. Jamhiri M, Safi Dahaj F, Astani A, et al.. (Iran J Pharm Res. (2019))

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Overview

Gut Hypothesis of Heart Failure

Primer

Associated Conditions

Metabolomic Signature of Heart Failure

Interventions

FAQs

Research Feed

What was reviewed?

Who was reviewed?

What were the most important findings of this review?

What are the greatest implications of this review?

What Was Studied?

Who Was Studied?

What Were the Most Important Findings?

What Are the Greatest Implications of This Study?

What Was Reviewed?

Who Was Reviewed?

What Were the Most Important Findings of This Review?

What Are the Greatest Implications of This Review?

References

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Heart Failure

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Overview

Gut Hypothesis of Heart Failure

Primer

Associated Conditions

Metabolomic Signature of Heart Failure

Interventions

FAQs

Research Feed

What was reviewed?

Who was reviewed?

What were the most important findings of this review?

What are the greatest implications of this review?

What Was Studied?

Who Was Studied?

What Were the Most Important Findings?

What Are the Greatest Implications of This Study?

What Was Reviewed?

Who Was Reviewed?

What Were the Most Important Findings of This Review?

What Are the Greatest Implications of This Review?

References

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