Coronary artery disease is a collection of problems caused by insufficient oxygen getting to the heart muscle.
Diet, sedentism, and microbiota to blame
In 2012, coronary artery disease caused 7.4 million deaths according to the WHO. It is most often a complication of atherosclerosis. It is the progressive depositing of fats on the walls of the coronary arteries--the arteries that supply blood to the heart muscle. These deposits gradually form an atheromatous plaque, which narrows the diameter of the arteries and reduces blood flow. Atherosclerosis is a result of various factors, including unbalanced diet and a lack of physical activity.
The severity of coronary artery disease depends on the extent of the area deprived of oxygen and the degree of arterial narrowing. There is, therefore, a distinction between angina, myocardial infarction, and sudden death.
Heart and microbiota: a connection?
Coronary artery disease may also be linked to the nature of the microbiota. Certain intestinal bacteria produce TMA (trimethylamine), a substance which, when oxidized in the liver, favors the formation of clots capable of clogging the smallest arteries, such as the coronary arteries that supply the heart.
Revascularizing the heart muscle
In the acute phase (myocardial infarction), the goal of treatment is to unblock the affected artery in order to supply oxygen to the heart muscle. In terms of prevention, the involvement of the intestinal microbiota in the development of coronary artery disease means several therapeutic applications can be envisaged: enrichment of the intestinal flora with non-TMA-producing bacteria via probiotics, the elimination of TMA-producing bacteria, or more radically, the transplantation of a low-TMA-producing fecal microbiota.
Maladies cardiovasculaires, OMS, janvier 2015. http://www.who.int/mediacentre/factsheets/fs317/fr/
Fédération française de cardiologie https://www.fedecardio.org/Les-maladies-cardio-vasculaires/Les-traitements-des-maladies-cardio-vasculaires/la-maladie-coronarienne
Zhu W, Gregory JC, Org E, et al. Gutmicrobial metabolite TMAO enhances platelet hyperreactivity and thrombosis risk. Cell 2016 ; 165 (1) : 111-24.