The gut-heart axis: a review of gut microbiota, dysbiosis, and cardiovascular disease development

Abstract

Background: Cardiovascular diseases (CVDs) are a major cause of morbidity and mortality worldwide and there are strong links existing between gut health and cardiovascular health. Gut microbial diversity determines gut health. Dysbiosis, described as altered gut microbiota, causes bacterial translocations and abnormal gut byproducts resulting in systemic inflammation.

Objective: To review the current literature on the relationships between gut microbiota, dysbiosis, and CVD development, and explore therapeutic methods to prevent dysbiosis and support cardiovascular health.

Summary: Dysbiosis increases levels of pro-inflammatory substances while reducing those of anti-inflammatory substances. This accumulative inflammatory effect negatively modulates the immune system and promotes vascular dysfunction and atherosclerosis. High Firmicutes to Bacteroidetes ratios, high trimethylamine-n-oxide to short-chain fatty acid ratios, high indole sulfate levels, low cardiac output, and polypharmacy are all associated with worse cardiovascular outcomes. Supplementation with prebiotics and probiotics potentially alleviates some CVD risk. Blood and stool samples may be used in clinical practice to quantify and qualify gut bacterial ratios and byproducts, assess patients' risk for adverse cardiovascular outcomes, and track their gut health progress. Further research is required to set population-based cutoffs for normal and abnormal gut microbiota and byproduct ratios.

Keywords: atherosclerosis and dysbiosis; dysbiosis; gut microbiota; gut–heart axis; polypharmacy and dysbiosis.

Figure 1.

Pathways involved in the production of TMA. Created using BioRender.

Figure 2.

TMAO production in the gut. Created using MS Word.

Figure 3.

Mechanisms of atherosclerosis development due to TMAO. Created using Bio Render.

Figure 4.

The relationship between CHD and Gut Microbiota. Created using BioRender.