THE ROLE OF TRIMETHYLAMINE N-OXIDE (TMAO) IN DIFFERENT CARDIOVASCULAR PHENOTYPES

Abstract

Cardiovascular diseases (CVDs) are the leading cause of death worldwide. Increased trimethylamine N-oxide (TMAO) levels have been shown to associate with cardiovascular disease and predict outcomes in the presence of multiple CVD phenotypes. The present review focuses on TMAO’s involvement in the main pathogenetic pathways causing or aggravating the development and progression of different CVD phenotypes, as well as the correlation between higher TMAO values in a certain cardiovascular disorder and its prognostic value of future outcomes. Different studies demonstrate the importance of the TMAO in atherosclerotic and thrombotic processes which result in more severe peripheral artery disease and its worse outcomes. In addition to atherosclerosis, TMAO induced platelet hyper-reactivity and foam cell formation lead to myocardial ischemia manifesting as a stable coronary artery disease (CAD) or acute coronary syndrome (ACS). TMAO is also involved in the progression of heart failure (HF) as it directly promotes cardiac damage and indirectly exacerbates the procession of HF by causing renal impairment. The findings suggest assessing TMAO concentration for CVD prophylaxis purposes and using measured TMAO levels as a prognostic value and a valid mortality risk assessment independently as well as combined with other current clinical risk predictors.