<p>Gut dysbiosis (GD) influences myocardial infarction (MI), by promoting inflammation. Investigating compositional shifts in proinflammatory versus beneficial bacterial taxa may reveal novel biomarkers and therapeutic interventions. This study analysed stool samples from 30 patients who experienced myocardial infarction following COVID-19 infection or vaccination, and 20 healthy controls, using 16S rRNA sequencing to investigate gut microbial imbalances. OTUs were identified, and microbial differences were examined via PCA and PLS-DA to explore biomarkers and interventions. MI patients exhibited reduced <i>Prevotella</i> (17.19% vs. 30% in controls) and elevated <i>Escherichia</i> (16.11% vs.0. 28%), <i>Salmonella</i> (2.58% vs. 0.08%), and <i>Bacteroides</i> (15.91% vs. 8.18%), indicating proinflammatory Microbiota. At phylum level, <i>Firmicutes</i> increased (45.80% vs. 40.87%), <i>Proteobacteria</i> rose (13.27% vs. 9.91%), and beneficial <i>Actinobacteria</i> declined (2.78% vs. 3.67%). PCA showed distinct clustering, confirmed by Partial Least Squares Discriminant Analysis, highlighting heightened inflammation-driving taxa. Although <i>Faecalibacterium</i> appeared variably, it was overall diminished in MI patients, likely fueling immune activation. However, <i>Bifidobacterium</i> (2.06% vs. 2.57%) and <i>Lactobacillus</i> (0.63% v. 0.99%) decreased, compromising intestinal barrier integrity. Females had higher <i>Fusobacterium</i> (1.85% vs. ~ 0%) and <i>Streptococcus</i> (2.28% vs. 0.16%), whereas males exhibited increased <i>Desulfovibrio</i> (1.60% vs. 0.08%) and <i>Akkermansia</i> (1.02% vs. 0.04%). Finally, <i>Enterobacteriaceae</i> surged from 0.41% to 10.04%, exacerbating inflammatory cascades and underscoring dysbiosis in MI pathophysiology. Findings highlights pivotal role of dysbiosis in MI, with elevated proinflammatory bacteria (<i>Escherichia, Salmonella, Proteobacteria</i>) and reduced beneficial SCFA-producing taxa (<i>Bifidobacterium, Lactobacillus</i>) worsening inflammation. Sex-specific microbial alterations, characterized by an enrichment of <i>Fusobacterium</i> and <i>Streptococcus</i> in females and elevated levels of <i>Desulfovibrio</i> and <i>Akkermansia</i> in males, underscore their potential utility as clinical biomarkers for risk stratification. Targeted microbiota therapies can enhance cardiac care outcomes.</p> Graphical Abstract <p>Multilevel taxonomic analysis of proinflammatory gut microbiota in first-time myocardial infarction patients post-COVID-19 vaccination. Using 16S rRNA sequencing, this study identifies microbial signatures at various taxonomic levels, highlighting gut dysbiosis and its potential role in cardiovascular inflammation and myocardial infarction pathophysiology.</p> <p></p>

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Biochemical insight into gut microbial imbalance in Covid-19 and post vaccination heart attacks

  • Mohamed Gamil Mehanna,
  • Turky Omar Asar,
  • Habib Changal Mudasir,
  • Sherif Edris,
  • Hadiah Bassam Al Mahdi,
  • Ahmed F. Bakry,
  • Mustafa Zeyadi,
  • Mirza Rafi Baig,
  • Salma Naqvi,
  • Fahad A. Al-Abbasi,
  • Omar A. Al-Bar,
  • Vikas Kumar,
  • Firoz Anwar

摘要

Gut dysbiosis (GD) influences myocardial infarction (MI), by promoting inflammation. Investigating compositional shifts in proinflammatory versus beneficial bacterial taxa may reveal novel biomarkers and therapeutic interventions. This study analysed stool samples from 30 patients who experienced myocardial infarction following COVID-19 infection or vaccination, and 20 healthy controls, using 16S rRNA sequencing to investigate gut microbial imbalances. OTUs were identified, and microbial differences were examined via PCA and PLS-DA to explore biomarkers and interventions. MI patients exhibited reduced Prevotella (17.19% vs. 30% in controls) and elevated Escherichia (16.11% vs.0. 28%), Salmonella (2.58% vs. 0.08%), and Bacteroides (15.91% vs. 8.18%), indicating proinflammatory Microbiota. At phylum level, Firmicutes increased (45.80% vs. 40.87%), Proteobacteria rose (13.27% vs. 9.91%), and beneficial Actinobacteria declined (2.78% vs. 3.67%). PCA showed distinct clustering, confirmed by Partial Least Squares Discriminant Analysis, highlighting heightened inflammation-driving taxa. Although Faecalibacterium appeared variably, it was overall diminished in MI patients, likely fueling immune activation. However, Bifidobacterium (2.06% vs. 2.57%) and Lactobacillus (0.63% v. 0.99%) decreased, compromising intestinal barrier integrity. Females had higher Fusobacterium (1.85% vs. ~ 0%) and Streptococcus (2.28% vs. 0.16%), whereas males exhibited increased Desulfovibrio (1.60% vs. 0.08%) and Akkermansia (1.02% vs. 0.04%). Finally, Enterobacteriaceae surged from 0.41% to 10.04%, exacerbating inflammatory cascades and underscoring dysbiosis in MI pathophysiology. Findings highlights pivotal role of dysbiosis in MI, with elevated proinflammatory bacteria (Escherichia, Salmonella, Proteobacteria) and reduced beneficial SCFA-producing taxa (Bifidobacterium, Lactobacillus) worsening inflammation. Sex-specific microbial alterations, characterized by an enrichment of Fusobacterium and Streptococcus in females and elevated levels of Desulfovibrio and Akkermansia in males, underscore their potential utility as clinical biomarkers for risk stratification. Targeted microbiota therapies can enhance cardiac care outcomes.

Graphical Abstract

Multilevel taxonomic analysis of proinflammatory gut microbiota in first-time myocardial infarction patients post-COVID-19 vaccination. Using 16S rRNA sequencing, this study identifies microbial signatures at various taxonomic levels, highlighting gut dysbiosis and its potential role in cardiovascular inflammation and myocardial infarction pathophysiology.