Comparison of thrombus, gut, and oral microbiomes in Korean patients with ST-elevation myocardial infarction: a

Ju-Seung Kwun1,2, Si-Hyuck Kang3,4, Hyo-Jung Lee5

  • 1Cardiovascular Center, Seoul National University Bundang Hospital, Seongnam-si, Korea.

Insights

The gut and oral microbiomes of ST-segment elevation myocardial infarction (STEMI) patients show distinct microbial compositions, correlating with thrombus microbiome findings. This suggests a link between systemic microbial dysbiosis and coronary artery disease pathogenesis.

Area of Science:

  • Microbiology
  • Cardiology
  • Genomics

Background:

  • ST-segment elevation myocardial infarction (STEMI) involves coronary artery occlusion due to atherosclerotic plaque rupture.
  • The gut microbiome is increasingly recognized for its role in cardiovascular disease pathogenesis.

Purpose of the Study:

  • To investigate the microbial diversity and composition of coronary thrombi in STEMI patients.
  • To compare thrombus microbiome composition with oral and gut microbiomes in STEMI patients versus healthy controls.

Main Methods:

  • A case-control study involving 22 STEMI patients and 20 healthy controls.
  • Collection of coronary thrombi, oral swabs, and stool samples.
  • 16S rRNA sequencing and metagenomic microbiome analysis.

Main Results:

  • Microbial DNA was detected in 4 of 22 coronary thrombi, with Proteobacteria and Bacteroidetes as dominant phyla.
  • Significant differences in oral and gut microbiomes were observed between STEMI patients and controls, indicating dysbiosis.
  • STEMI patients exhibited higher gut Proteobacteria and Enterobacteriaceae, and lower oral Firmicutes and Haemophilus.
  • Specific genera like Escherichia and Bacteroides were abundant in coronary thrombi of STEMI patients.

Conclusions:

  • The study identified specific microbial signatures in coronary thrombi of STEMI patients.
  • Correlations were found between the relative abundance of gut/oral microbiomes and the thrombus microbiome.
  • These findings suggest a potential role for microbial dysbiosis in STEMI pathogenesis.