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Dysbiosis of Gut Microbiota in Patients With Acute Myocardial Infarction.

ABSTRACT: Acute myocardial infarction (AMI) continues as the main cause of morbidity and mortality worldwide. Interestingly, emerging evidence highlights the role of gut microbiota in regulating the pathogenesis of coronary heart disease, but few studies have systematically assessed the alterations and influence of gut microbiota in AMI patients. As one approach to address this deficiency, in this study the composition of fecal microflora was determined from Chinese AMI patients and links between gut microflora and clinical features and functional pathways of AMI were assessed. Fecal samples from 30 AMI patients and 30 healthy controls were collected to identify the gut microbiota composition and the alterations using bacterial 16S rRNA gene sequencing. We found that gut microflora in AMI patients contained a lower abundance of the phylum Firmicutes and a slightly higher abundance of the phylum Bacteroidetes compared to the healthy controls. Chao1 (P = 0.0472) and PD-whole-tree (P = 0.0426) indices were significantly lower in the AMI versus control group. The AMI group was characterized by higher levels of the genera Megasphaera, Butyricimonas, Acidaminococcus, and Desulfovibrio, and lower levels of Tyzzerella 3, Dialister, [Eubacterium] ventriosum group, Pseudobutyrivibrio, and Lachnospiraceae ND3007 group as compared to that in the healthy controls (P < 0.05). The common metabolites of these genera are mostly short-chain fatty acids, which reveals that the gut flora is most likely to affect the occurrence and development of AMI through the short-chain fatty acid pathway. In addition, our results provide the first evidence revealing remarkable differences in fecal microflora among subgroups of AMI patients, including the STEMI vs. NSTEMI, IRA-LAD vs. IRA-Non-LAD and Multiple (≥2 coronary stenosis) vs. Single coronary stenosis groups. Several gut microflora were also correlated with clinically significant characteristics of AMI patients, including LVEDD, LVEF, serum TnI and NT-proBNP, Syntax score, counts of leukocytes, neutrophils and monocytes, and fasting serum glucose levels. Taken together, the data generated enables the prediction of several functional pathways as based on the fecal microfloral composition of AMI patients. Such information may enhance our comprehension of AMI pathogenesis.

SUBMITTER: Han Y

PROVIDER: S-EPMC8290895 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundType 2 diabetes mellitus (T2DM) is a risk factor for acute myocardial infarction (AMI) and a common comorbidity in patients with AMI. T2DM doubles the fatality rate of patients with AMI in the acute phase of AMI and the follow-up period. However, the mechanisms by which T2DM increases the fatality rate remain unknown. This study sought to investigate changes in the gut microbiota of patients with AMI and T2DM (AMIDM) to extend understandings of the relative mechanisms from the aspects of gut microbiota.MethodsPatients were recruited and divided into 2 groups comprising 15 patients with AMIDM and 15 patients with AMI but without T2DM (AMINDM). Their stool samples and clinical information were collected. 16S ribosomal DNA sequencing was used to analyze the structure and composition of the gut microbiota based on the operational taxonomic units.ResultsA significant difference was observed in the gut microbiota β diversity between the 2 groups. At the phylum level, the AMIDM patients showed an increase in the abundance of Firmicutes and a decrease in the abundance of Bacteroidetes compared to the AMINDM patients. At the genus level, the AMIDM patients showed an increase in the abundance of Companilactobacillus, Defluvitaleaceae UCG-011 and UCG-009, and a decrease in the abundance of Phascolarctobacterium and CAG 56 compared to the AMINDM patients. At the species level, the AMIDM patients showed an increase in the abundance of species unclassified NK4A214 group, Bacteroides clarus, Coprococcus comes, unclassified Defluviltaleaceae UCG-011, uncultured rumen bacterium, unclassified CAG 56, Barnesiella intestinihominis, Lachnospiraceae bacterium, Bacteroides nordii, unclassified UCG-009, and the Family XIII AD3011 group compared to the AMINDM patients. The gut microbiota function predictions indicated that the nucleotide metabolism-related pathway was significantly more increase in the patients with AMIDM than those with AMINDM. Additionally, the patients with AMIDM showed an increase in gram-positive bacteria and a decrease in the proportion of gram-negative bacteria. Our correlation analysis results on the gut microbiota and clinical parameters might extend understandings of the progression of AMI.ConclusionsChanges in the gut microbiota composition of patients with AMIDM affect the severity of the metabolic disturbance and may be responsible for poorer clinical outcomes and worse disease progression in patients with AMIDM compared to those with AMINDM.

Project description:Background: The bidirectional interaction between the gut and brain after stroke through the immune-mediated pathway has been studied. However, the long-term effects of gut microbiota and systemic immune homeostasis after cerebral ischemia remain unclear. We examined long-term changes in the gut microbiota and systemic inflammatory cytokines after cerebral infarction in cynomolgus monkeys. Methods: Twelve monkeys underwent successful distal M1 segment of the left middle cerebral artery occlusion (MCAO) and were randomly and equally assigned to the MCAO-1.5 m, MCAO-6 m, and MCAO-12 m groups, which were sacrificed 1.5, 6, and 12 months after cerebral infarction induction, respectively. Four monkeys that underwent a sham operation were sacrificed 12 months later. The gut microbiota and short-chain fatty acids (SCFAs) were analyzed by 16S rDNA sequencing and gas chromatography mass spectrometry, respectively. Histological examinations of the transverse colon were performed. Plasma D-lactate, zonulin, lipopolysaccharide (LPS), tumor necrosis factor (TNF-α), interferon (IFN)-γ, and interleukin (IL)-6 were detected by immunoassay kits. Results: The levels of the Bacteroidetes phylum and Prevotella genus were significantly increased, while the Firmicutes phylum as well as the Faecalibacterium, Oscillospira, and Lactobacillus genera were decreased after cerebral infarction. Gut-originating SCFAs were significantly decreased 6 and 12 months after cerebral infarction (P < 0.05). We observed intestinal mucosal damage, evaluated by Chiu's score. Plasma D-lactate, zonulin, LPS, TNF-α, IFN-γ, and IL-6 were significantly increased after cerebral infarction (P < 0.05). Additionally, the increases in plasma LPS, TNF-α, IFN-γ, and IL-6 after cerebral infarction coincided with overgrowth of the Bacteroidetes phylum (P < 0.001). Conclusion: Cerebral infarction induces persistent host gut microbiota dysbiosis, intestinal mucosal damage, and chronic systemic inflammation in cynomolgus monkeys.

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Dysbiosis of Gut Microbiota in Patients With Acute Myocardial Infarction.

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