Brief Report

Abstract

Recent evidence has shown a complex relationship between the gut microbiota, dietary nutrients, and cardiovascular disease (CVD). Trimethylamine-N-oxide (TMAO) production, initiated by the microbiota, has been associated with CVD events. We sought to test if this association exists in HIV-infected persons. After adjusting for aspirin use and CVD risk factors, HIV-infected men were more likely to have coronary stenosis in the second and third TMAO quartiles compared to the first quartile, but did not differ significantly in the fourth quartile. We found an inverted U-shaped association between TMAO levels and the presence of coronary artery stenosis among HIV-infected men.

Gut microbial diversity in HIV infection post combined antiretroviral therapy

“…The lack of direct association with platelet hyperactivation in this study may in part be explained by the multitude of HIV-associated factors that may interfere with platelet activation. This may also explain earlier reports showing an inverted U-shaped association between TMAO levels and the presence of coronary artery stenosis among HIV-infected men [ 58 ▪ ]. In this last study, it was only the middle subpopulation within the second and third TMAO quartiles, compared with the first and fourth quartile, that showed an association with coronary stenosis, which suggests the involvement of other pathways.…”

Gut microbiota in coronary artery disease: a friend or foe?

“…In recent years, there is an increase in the interest in gut resident microbiota due to the unfolding of their greater participation in human diseases [10][11][12]. In relation to CAD, studies have shown the beneficial as well as deleterious effects of gut microbiota [15][16][17][18][19][20]. The studies have shown that gut microorganisms may produce beneficial effects in the myocardial ischemic state either directly in the form of exogenous administration like Lactobacillus [14,15] or indirectly by acting on plant-dominated fiber-rich food to produce important components including enterolactone [33].…”

“…Trimethylamine-N-oxide (TMAO) is formed in the liver from trimethylamine, which is almost exclusively generated from dietary phosphatidylcholine by gut microbiota. Studies have shown the close association between TMAO and the development of CAD [20]. In Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation (COURAGE) trial-like patient cohort, a relationship between fasting plasma TMAO levels and mortality rate over 5 years in CAD patients (n = 2235) was investigated.…”

“…Gut microbe-mediated modulation of the cardiovascular diseases, including atherosclerosis and coronary artery disease, may be due to structural components of bacteria, including lipopolysaccharide or generation of diverse metabolites, including trimethylamine-N-oxide (TMAO), short-chain fatty acids, secondary bile acids, and uremic toxins like p-cresol sulfate and indoxyl sulfate. The data from the literature show that gut microbiota may be beneficial to the heart patients [15,17,18], or it may produce deleterious effects in CAD patients [19][20][21].…”

HIV, Cancer, and the Microbiota: Common Pathways Influencing Different Diseases

“…Trimethylamine-N-oxide (TMAO) is a gut microbiota-dependent choline and carnitine metabolite that is responsible for an increased risk of atherogenesis and cardiovascular disease risk (47), particularly in individuals who consume large quantities of meat and possess a specific microbiome signature with enriched proportions of the genus Prevotella (48). This metabolite has also been associated with atherosclerotic plaque burden in HIV in some (49, 50) but not all (51) studies. A recent cohort study comparing the fecal microbiota of HIV-infected individuals with and without ischemic heart disease showed that high TMAO plasma levels was a marker of cardiovascular heart disease and correlated with the fecal abundance of Phascolarctobacterium, Desulfovibrio, Sutterella , and Faecalibacterium (52).…”