Abstract
There is a bidirectional relationship between the heart and the gut. The gut microbiota, the community of gut micro-organisms themselves, is an excellent gut-homeostasis keeper since it controls the growth of potentially harmful bacteria and protects the microbiota environment. There is evidence suggesting that a diet rich in fatty acids can be metabolized and converted by gut microbiota and hepatic enzymes to trimethyl-amine N-oxide (TMAO), a product that is associated with atherogenesis, platelet dysfunction, thrombotic events, coronary artery disease, stroke, heart failure (HF), and, ultimately, death. HF, by inducing gut ischemia, congestion, and, consequently, gut barrier dysfunction, promotes the intestinal leaking of micro-organisms and their products, facilitating their entrance into circulation and thus stimulating a low-grade inflammation associated with an immune response. Drugs used for HF may alter the gut microbiota, and, conversely, gut microbiota may modify the pharmacokinetic properties of the drugs. The modification of lifestyle based mainly on exercise and a Mediterranean diet, along with the use of pre- or probiotics, may be beneficial for the gut microbiota environment. The potential role of gut microbiota in HF development and progression is the subject of this review.
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