4.6 Article

Dysbiosis of Gut Microbiota in Patients With Acute Myocardial Infarction

Journal

FRONTIERS IN MICROBIOLOGY
Volume 12, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fmicb.2021.680101

Keywords

acute myocardial infarction; gut microflora; 16S rRNA gene; patients; dysbiosis

Categories

Funding

  1. National Key Research andDevelopment Program of China [2019YFC0118100]
  2. NationalNatural Science Foundation of China [81671760, 81873910]
  3. Excellent youth project of the Fourth Affiliated Hospital ofHarbin Medical University [HYDSYYXQN202007]

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This study revealed significant differences in gut microbiota composition between AMI patients and healthy controls, with AMI patients showing lower abundance of Firmicutes and higher abundance of Bacteroidetes. The study also found correlations between specific gut microbiota and clinical characteristics of AMI patients, suggesting potential pathways through which gut flora may influence AMI pathogenesis. Additionally, differences in fecal microflora were observed among subgroups of AMI patients, providing insight into potential functional pathways based on the fecal microfloral composition in AMI patients.
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.

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