Gut microbiota alterations in acute myocardial infarction: (diabetic) context is everything.
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ABSTRACT:
SUBMITTER: Lymperopoulos A
PROVIDER: S-EPMC10777215 | biostudies-literature | 2023 Dec
REPOSITORIES: biostudies-literature
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Gut microbiota alterations in acute myocardial infarction: (diabetic) context is everything.
Annals of translational medicine 20230905 12
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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.
| S-EPMC10316093 | biostudies-literature
Project description: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.
| S-EPMC8290895 | biostudies-literature
Project description:Recent studies suggested that gut microbiota was involved in the development of coronary artery disease. However, the changes of gut microbiota following acute myocardial infarction (AMI) remain unknown. In this study, a total of 66 male Wistar rats were randomly divided into control, AMI and SHAM groups. The controls (n = 6) were sacrificed after anesthesia. The AMI model was built by ligation of left anterior descending coronary artery. The rats of AMI and SHAM groups were sacrificed at 12 h, 1 d, 3 d, 7 d and 14 d post-operation respectively. Gut microbiota was analyzed by 16S rDNA high throughput sequencing. The gut barrier injuries were evaluated through histopathology, transmission electron microscope and immunohistochemical staining. The richness of gut microbiota was significantly higher in AMI group than SHAM group at 7 d after AMI (P<0.05). Principal coordinate analysis with unweighted UniFrac distances revealed microbial differences between AMI and SHAM groups at 7 d. The gut barrier impairment was also the most significant at 7 d post-AMI. We further identified the differences of microorganisms between AMI and SHAM group at 7 d. The abundance of Synergistetes phylum, Spirochaetes phylum, Lachnospiraceae family, Syntrophomonadaceae family and Tissierella Soehngenia genus was higher in AMI group compared with SHAM group at 7 d post-operation (q<0.05). Our study showed the changes of gut microbiota at day 7 post AMI which was paralleled with intestinal barrier impairment. We also identified the microbial organisms that contribute most.
| S-EPMC5501596 | biostudies-literature
Project description:BackgroundAn increasing number of studies have shown that gut microbiota are associated with human cardiovascular disease, but the characteristics of intestinal flora in patients with acute myocardial infarction (AMI) are still unclear. In this study, we aimed to investigate the difference of intestinal microflora between patients with AMI and healthy people, and to find the effect of percutaneous coronary intervention (PCI) on intestinal microflora.MethodsA total of 60 stool samples and 60 peripheral blood samples were collected from 20 previously diagnosed AMI patients and 20 healthy people serving as controls. Gut microbiota communities were analyzed via 16 ribosomal RNA-sequencing (16S rRNA). Gut microbiota-derived metabolites, trimethylamine N-oxide (TMAO) and short-chain fatty acids (SCFA), in the blood were detected using stable isotope dilution high-performance liquid chromatography with on line electrospray ionization tandem mass spectrometry (LC/MS/MS).ResultsThe results showed that a distinct pattern of gut microbiota was observed in AMI patients compared to healthy controls. AMI patients had lower microbiological richness but no significant change in diversity. Bacteroidetes and Verrucomicobia showed an upward trend, whereas Proteobacteria showed a downward trend in AMI patients. During a longitudinal study to compare the changes in bacteria before and after treatment, we found routine cardiac admission therapy 1 week after PCI surgery had no effect on the microbial community structure in patients. There were significantly higher levels of plasma TMAO in AMI patients' microbiota than that in the control group. Contrarily, there was no obvious change in SCFA.ConclusionsThe gut microbiota of patients with AMI differs from that of normal people, and the metabolic products of microflora are more abundant in the plasma of AMI than control cases. Microflora may act on the cardiovascular system through metabolites, and regulation of the microfloral structure may be used in the future treatment of cardiovascular diseases.
| S-EPMC9843380 | biostudies-literature
Project description:Gut microbiome alterations might be considered a metabolic disorder. However, the relationship between the microbiome and acute myocardial infarction (AMI) has not been properly validated. The feces of 44 subjects (AMI: 19; control: 25) were collected for fecal genomic DNA extraction. The variable region V3-V4 of the 16S rRNA gene was sequenced using the Illumina MiSeq platform. The metabolite amounts were analyzed using the Kyoto Encyclopedia of Genes and Genomes (KEGG) metabolic pathways. The bacteria were more enriched in the AMI group both in the observed operational taxonomic units (OTUs) and faith phylogenetic diversity (PD) (p-value = 0.01 and <0.001 with 95% CI, individually). The Selenomonadales were less enriched in the AMI group at the family, genus, and species levels (all linear discriminant analysis (LDA) scores > 2). Seleno-compounds were more abundant in the AMI group at the family, genus, and species levels (all LDA scores > 2). This is the first study to demonstrate the association of Selenomonadales and seleno-compounds with the occurrence of AMI. Our findings provide an opportunity to identify a novel approach to prevent and treat AMI.
| S-EPMC8911090 | biostudies-literature
Project description:BackgroundDiabetes is a metabolic disorder characterized by enhanced production of free radicals hence oxidative stress. The aim of this study was to evaluate the activity of cardiac and antioxidant enzymes in diabetic and non-diabetic acute myocardial infarction (AMI) patients.MethodsThis case-control study was conducted on 450 subjects (70-85 years). Subjects were divided into three groups (Normal, N; Non-diabetic AMI, N-AMI; and Diabetic AMI, D-AMI). Each individual was subjected to a detailed history, clinical examination, and cardiovascular parameters analysis (fasting blood sugar, HbA1c, systolic and diasystolic blood pressure, total cholesterol (TC), triglycerides (TG), low-density lipoprotein (LDL), high-density lipoprotein (HDL), TC/HDL and LDL/HDL ratios). Cardiac markers (Troponin-I, creatine phosphokinase (CPK), creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), C-reactive protein (CRP) and aspartate aminotransferase (AST)) and oxidative stress markers (superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), catalase (CAT)) were also assessed. All these parameters were compared between diabetic and non-diabetic AMI patients.ResultsD-AMI individuals had high level of TC, TG, LDL, and low level of HDL in comparison to N-AMI individuals. Study suggests that cardiac markers such as Troponin I, CPK, CK-MB, AST, LDH, and CRP levels were significantly increased in patients suffering from myocardial infarction with diabetes mellitus (DM) compared to patients of myocardial infarction without DM. The activity levels of antioxidant SOD and GSH were lower in D-AMI patients than in N-AMI. However, levels of MDA and CAT were higher in D-AMI than in N-AMI controls.ConclusionStudy suggests elevated cardiac markers and reduced antioxidants in D-AMI patients compared to N-AMI patients.
| S-EPMC4911449 | biostudies-literature
Project description:Acute kidney injury (AKI) predicts poor prognosis in patients with acute myocardial infarction (MI) and diabetes mellitus (DM) is an independent risk factor of AKI. Recent clinical studies have shown the beneficial effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors on cardiovascular and renal outcomes in patients with DM. We recently reported that canagliflozin normalized susceptibility of diabetic rats to AKI after acute MI via ?-hydroxybutyrate-mediated suppression of NOX expression. Here we examined whether the same renoprotective effect is shared by empagliflozin. Serum creatinine levels were not changed by MI induced by coronary artery occlusion in LETO, non-diabetic control rats, and OLETF, obese type 2 diabetic rats. However, immunohistochemistry revealed that MI increased renal expression of NGAL and KIM-1, early markers of tubular injury, by 3.2-fold and 2.6-fold, respectively, in OLETF. These increases in injury markers were not observed in LETO. Pretreatment with empagliflozin of OLETF for 2 weeks improved hyperglycemia, increased blood ?-hydroxybutyrate level, and suppressed MI-induced expression of NGAL and KIM-1. Empagliflozin suppressed upregulation of NOX2 and NOX4 in the kidney of OLETF. Taken together with the results of our previous study, it was concluded that treatment with the SGLT2 inhibitor protects the diabetic kidney from MI-induced AKI.
| S-EPMC7190820 | biostudies-literature
Project description:BackgroundIn recent years, numerous studies have suggested that the gut microbiota and its metabolites are closely related to myocardial infarction. Utilizing insights from these research findings may be advantageous in the prevention, treatment, and prognosis of myocardial infarction. We have employed bibliometric methodology to summarize the progress made in this research area over the past 20 years, identify the hotspots, and highlight the developmental tendencies, providing a reference for future research in this field.MethodsWe searched the content related to this field in the Web of Science Core Collection database, with a time range from 2001 to 2023. We used VOSviewer, CiteSpace, and Scimago Graphica software to visualize the search results.ResultsWe included 889 reports in this study. The country with the most publications was China, while the country with the greatest influence was the United States. An analysis of institutions showed that the Chinese Academy of Medical Sciences had the largest volume of publications, whereas the Cleveland Clinic had the most influential ones. An author analysis showed Stanley L Hazen to have published the most and to also have been the most influential researcher. An analysis of all the journals publishing articles related to the search terms showed that PLoS One journal had the highest number of publications (18 articles), while Atherosclerosis journal had the most influential articles. The results of our reference analysis showed a strong association between Trimethylamine N-oxide and myocardial infarction. We found that increased intestinal permeability may be related to the progression of cardiovascular diseases, a high-fiber diet may help in the prevention of diseases such as myocardial infarction, and populations with a high intake of red meat may have an increased risk of myocardial infarction. Keyword analysis suggested that 'cardiac fibrosis' and 'major bleeding' were promising research directions in the future, and supplementing food intake with short-chain fatty acids was looked upon as a promising approach to treating coronary heart disease.ConclusionThe gut microbiota are closely related to myocardial infarction, and investigating this relationship is crucial for the prevention and treatment of myocardial infarction, where interdisciplinary research and international cooperation are indispensable.
| S-EPMC11408004 | biostudies-literature
Project description:IntroductionAcute myocardial infarction (AMI) accounts for the majority of deaths caused by coronary artery disease (CAD). Early warning of AMI, especially for patients with stable coronary artery disease (sCAD), is urgently needed. Our previous study showed that alterations in the gut microbiota were correlated with CAD severity.ObjectivesHerein, we tried to discover accurate and convenient biomarkers for AMI by combination of gut microbiota and fecal/blood/urinary metabolomics.MethodsWe recruited 190 volunteers including 93 sCAD patients, 49 AMI patients, and 48 subjects with normal coronary artery (NCA), and measured their blood biochemical parameters, 16S rRNA-based gut microbiota and NMR-based fecal/blood/urinary metabolites. We further selected 20 subjects from each group and analyzed their gut microbiota by whole-metagenome shotgun sequencing.ResultsMulti-omic analyses revealed that AMI patients exhibited specific changes in gut microbiota and serum/urinary/fecal metabolites as compared to subjects with sCAD or NCA. Fourteen bacterial genera and 30 metabolites (11 in feces, 10 in blood, 9 in urine) were closely related to AMI phenotypes and could accurately distinguish AMI patients from sCAD patients. Some species belonging to Alistipes, Streptococcus, Ruminococcus, Lactobacillus and Faecalibacterium were effective to distinguish AMI from sCAD and their predictive ability was confirmed in an independent cohort of CAD patients. We further selected nine indicators including 4 bacterial genera, 3 fecal and 2 urinary metabolites as a noninvasive biomarker set which can distinguish AMI from sCAD with an AUC of 0.932.ConclusionCombination of gut microbiota and fecal/urinary metabolites provided a set of potential useful and noninvasive predictive biomarker for AMI from sCAD.
| S-EPMC10105070 | biostudies-literature
Project description:BackgroundPreclinical data suggest that an acute inflammatory response following myocardial infarction (MI) accelerates systemic atherosclerosis. Using combined positron emission and computed tomography, we investigated whether this phenomenon occurs in humans.Methods and resultsOverall, 40 patients with MI and 40 with stable angina underwent thoracic 18F-fluorodeoxyglucose combined positron emission and computed tomography scan. Radiotracer uptake was measured in aortic atheroma and nonvascular tissue (paraspinal muscle). In 1003 patients enrolled in the Global Registry of Acute Coronary Events, we assessed whether infarct size predicted early (≤30 days) and late (>30 days) recurrent coronary events. Compared with patients with stable angina, patients with MI had higher aortic 18F-fluorodeoxyglucose uptake (tissue-to-background ratio 2.15±0.30 versus 1.84±0.18, P<0.0001) and plasma C-reactive protein concentrations (6.50 [2.00 to 12.75] versus 2.00 [0.50 to 4.00] mg/dL, P=0.0005) despite having similar aortic (P=0.12) and less coronary (P=0.006) atherosclerotic burden and similar paraspinal muscular 18F-fluorodeoxyglucose uptake (P=0.52). Patients with ST-segment elevation MI had larger infarcts (peak plasma troponin 32 300 [10 200 to >50 000] versus 3800 [1000 to 9200] ng/L, P<0.0001) and greater aortic 18F-fluorodeoxyglucose uptake (2.24±0.32 versus 2.02±0.21, P=0.03) than those with non-ST-segment elevation MI. Peak plasma troponin concentrations correlated with aortic 18F-fluorodeoxyglucose uptake (r=0.43, P=0.01) and, on multivariate analysis, independently predicted early (tertile 3 versus tertile 1: relative risk 4.40 [95% CI 1.90 to 10.19], P=0.001), but not late, recurrent MI.ConclusionsThe presence and extent of MI is associated with increased aortic atherosclerotic inflammation and early recurrent MI. This finding supports the hypothesis that acute MI exacerbates systemic atherosclerotic inflammation and remote plaque destabilization: MI begets MI.Clinical trial registrationURL: https://www.clinicaltrials.gov. Unique identifier: NCT01749254.
| S-EPMC4599491 | biostudies-literature