Dysbiotic microbiota contributes to the extent of acute myocardial infarction in rats

Marc-André Gagné1,2, Claude Barbeau1, Geneviève Frégeau1

  • 1Research Center, CIUSSS du Nord-de-l'Île-de-Montréal, Hôpital Sacré-Cœur, Montreal, Canada.

Scientific Reports
|October 3, 2022
PubMed

Insights

Altered gut microbiota from a dysbiotic diet increases heart attack size. Probiotics can help reduce this effect by improving gut barrier function and reducing inflammation.

Area of Science:

  • Microbiology
  • Cardiology
  • Gastroenterology

Background:

  • Intestinal microbiota composition is increasingly linked to pathologies like hypertension, obesity, and diabetes.
  • Diet-induced gut dysbiosis may influence cardiovascular outcomes.

Purpose of the Study:

  • To investigate if intestinal microbiota dysbiosis exacerbates myocardial infarction size.
  • To determine if probiotics can attenuate the effects of dysbiosis on myocardial infarction.

Main Methods:

  • Rats received microbiota transplants from donors on dysbiotic or non-dysbiotic diets, with or without probiotics, after antibiotic treatment.
  • Myocardial infarction was induced via coronary artery occlusion, and infarct size was measured.
  • Intestinal barrier resistance, plasma lipopolysaccharides (LPS), NF-κB, Akt signaling, and microbiota composition were analyzed.

Main Results:

  • Dysbiotic microbiota without probiotics significantly increased infarct size compared to other groups.
  • Increased infarct size correlated with a higher Firmicutes/Bacteroidetes ratio, elevated NF-κB phosphorylation, and higher plasma LPS.
  • Probiotic intervention with dysbiotic microbiota attenuated infarct size, improved intestinal barrier resistance, and modulated signaling pathways.

Conclusions:

  • Diet-induced intestinal dysbiosis promotes larger myocardial infarction size.
  • Probiotics can mitigate the detrimental effects of gut dysbiosis on cardiac injury.
  • Gut microbiota modulation represents a potential therapeutic target for cardiovascular diseases.