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Updated: Feb 12, 2026
Postconditioning with Lactate-enriched Blood for Cardioprotection in ST-segment Elevation Myocardial Infarction
Published on: May 28, 2019
Gut-dependent microbial translocation induces inflammation and cardiovascular events after ST-elevation myocardial
Xin Zhou1, Jing Li2,3, Junli Guo4
1Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Pingjin Hospital Heart Center, 220, Cheng-Lin Street, Tianjin, 300162, China.
Background:
Post-infarction cardiovascular remodeling and heart failure are the leading cause of myocardial infarction (MI)-driven death during the past decades. Experimental observations have involved intestinal microbiota in the susceptibility to MI in mice; however, in humans, identifying whether translocation of gut bacteria to systemic circulation contributes to cardiovascular events post-MI remains a major challenge.
Results:
Here, we carried out a metagenomic analysis to characterize the systemic bacteria in a cohort of 49 healthy control individuals, 50 stable coronary heart disease (CHD) subjects, and 100 ST-segment elevation myocardial infarction (STEMI) patients. We report for the first time higher microbial richness and diversity in the systemic microbiome of STEMI patients. More than 12% of post-STEMI blood bacteria were dominated by intestinal microbiota (Lactobacillus, Bacteroides, and Streptococcus). The significantly increased product of gut bacterial translocation (LPS and D-lactate) was correlated with systemic inflammation and predicted adverse cardiovascular events. Following experimental MI, compromised left ventricle (LV) function and intestinal hypoperfusion drove gut permeability elevation through tight junction protein suppression and intestinal mucosal injury. Upon abrogation of gut bacterial translocation by antibiotic treatment, both systemic inflammation and cardiomyocyte injury in MI mice were alleviated.
Conclusions:
Our results provide the first evidence that cardiovascular outcomes post-MI are driven by intestinal microbiota translocation into systemic circulation. New therapeutic strategies targeting to protect the gut barrier and eliminate gut bacteria translocation may reduce or even prevent cardiovascular events post-MI.
Insights
Gut bacteria translocating into the bloodstream after myocardial infarction (MI) worsen cardiovascular outcomes. Targeting gut barrier integrity and bacterial translocation may prevent heart events.
Area of Science:
- Microbiology
- Cardiovascular Medicine
- Gastroenterology
Background:
- Post-infarction cardiovascular remodeling and heart failure are primary causes of myocardial infarction (MI)-related mortality.
- While mouse studies suggest a role for intestinal microbiota in MI susceptibility, human evidence linking gut bacteria translocation to cardiovascular events post-MI is lacking.
Purpose of the Study:
- To investigate the role of systemic bacterial translocation from the gut in patients following ST-segment elevation myocardial infarction (STEMI).
- To characterize the systemic microbiome in healthy individuals, coronary heart disease (CHD) patients, and STEMI patients.
Main Methods:
- Metagenomic analysis of systemic bacteria in a cohort of 49 healthy controls, 50 stable CHD subjects, and 100 STEMI patients.
- Measurement of gut bacterial translocation products (LPS and D-lactate).
- Experimental MI induction in mice to assess gut permeability changes and the effect of antibiotic treatment.
Main Results:
- STEMI patients exhibited higher microbial richness and diversity in their systemic microbiome compared to controls.
- Intestinal microbiota (Lactobacillus, Bacteroides, Streptococcus) constituted over 12% of bacteria in post-STEMI blood.
- Elevated LPS and D-lactate levels correlated with systemic inflammation and predicted adverse cardiovascular events.
- Experimental MI led to increased gut permeability via tight junction protein suppression and mucosal injury.
- Antibiotic treatment abrogating gut bacterial translocation reduced systemic inflammation and cardiomyocyte injury in MI mice.
Conclusions:
- This study provides the first human evidence that intestinal microbiota translocation into systemic circulation drives cardiovascular outcomes post-MI.
- Therapeutic strategies aimed at protecting the gut barrier and preventing bacterial translocation could mitigate or prevent cardiovascular events after MI.
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