Dysbiosis of Gut Microbiota in Patients With Acute Myocardial Infarction

Ying Han; Zhaowei Gong; Guizhi Sun; Jing Xu; Changlu Qi; Weiju Sun; Huijie Jiang; Peigang Cao; Hong Ju

doi:10.3389/fmicb.2021.680101

Dysbiosis of Gut Microbiota in Patients With Acute Myocardial Infarction

Front Microbiol. 2021 Jul 5:12:680101. doi: 10.3389/fmicb.2021.680101. eCollection 2021.

Authors

Ying Han¹, Zhaowei Gong¹, Guizhi Sun¹, Jing Xu¹, Changlu Qi², Weiju Sun³, Huijie Jiang⁴, Peigang Cao⁵, Hong Ju⁶

Affiliations

¹ Department of Cardiovascular, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, China.
² College of Bioinformatics Science and Technology, Harbin Medical University, Harbin, China.
³ Department of Cardiovascular, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
⁴ Department of Radiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
⁵ Department of Cardiology, Heilongjiang Province Land Reclamation Headquarters General Hospital, Harbin, China.
⁶ Department of Information Engineering, Heilongjiang Biological Science and Technology Career Academy, Harbin, China.

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.

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