Kalp bağirsak ekseni

Many interactions play a role in the gut-heart axis. These include intestinal epithelial dysfunction, dysbiosis, butyrate-producing bacteria, bile acids, and intestinal microbe-derived metabolites. In patients with heart failure (HF), mucosal malabsorption, intestinal wall edema and barrier dysfunction develop as a result of microcirculation disorders in the gut due to decreased perfusion, increased congestion and sympathetically mediated vasoconstriction. Toxic, pathogenic, immunogenic and inflammatory factors, through the increase in intestinal permeability as a result of damaged tight junctions in the intestine, pass through the mucosa and reach the systemic circulation, causing local-systemic inflammation. Many factors that cause dysbiosis by changing the intestinal flora, which are frequently seen in HF, lead to bacterial overgrowth, bacterial translocation and formation of many toxic substances, including lipopolysaccharide (LPS), trimethylamine N-oxide (TMAO), p-cresylsulfate (PCS) and indoxyl sulfate (IS). Depending on the increase in intestinal permeability, these toxic substances reach the systemic circulation; it increases the risk of atherosclerosis by playing a role in thrombosis, platelet invasion, foam cell formation and inflammation processes. Decreased levels of butyrate, one of the short-chain fatty acids that have many effects on the gastrointestinal tract, including maintaining intestinal barrier integrity; It promotes foam cell formation, exacerbates dysbiosis, and plays a role in the disruption of intestinal barrier function, causing endotoxins to reach the general circulation. With this review, it is aimed to inform about the physiopathological processes in the gut-heart axis, in the light of the current literature.