The researchers found that unlike gut bacteria, certain bacteria in coronary plaques were pro-inflammatory. In addition, patients with acute coronary syndrome (heart attack) had different bacteria in their guts compared to patients with stable angina.
Diet, smoking, pollution, age, and medications have a major impact on cell physiology, the immune system, and metabolism. Several previous researches indicate that these effects are moderated by microorganisms in the intestinal tract. This study investigated the contribution of the microbiota to the instability of coronary plaques.
In order to understand better, the researchers enrolled 30 patients with acute coronary syndrome and ten patients with stable angina. They isolated gut bacteria from faeces samples. Coronary plaque bacteria were extracted from angioplasty balloons.
Comparison of microbiota in faeces and coronary plaques revealed a different composition in the two sites. While faecal bacteria had a heterogeneous composition, and a pronounced presence of Bacteroidetes and Firmicutes, coronary plaques primarily contained microbes with pro-inflammatory phenotypes belonging to Proteobacteria and Actinobacteria.
Eugenia Pisano, lead author of the study from Catholic University, Rome, Italy said “This suggests selective retention of pro-inflammatory bacteria in atherosclerotic plaques, which could provoke an inflammatory response and plaque rupture.”
The analyses also revealed differences in gut microbiota between the two groups of patients. Those with the acute coronary syndrome had more Firmicutes, Fusobacteria and Actinobacteria, while Bacteroidetes and Proteobacteria were more abundant in those with stable angina.
Pisano said “We found a different make-up of the gut microbiome in acute and stable patients. The varying chemicals emitted by these bacteria might affect plaque destabilisation and consequent heart attack. Studies are needed to examine whether these metabolites do influence plaque instability.”
“Microbiota in the gut and coronary plaque could have a pathogenetic function in the process of plaque destabilisation and might become a potential therapeutic target,” she concluded.