Differential implications of gut-related metabolites on outcomes between heart failure and myocardial infarction.

Gut metabolites, through their role in atherosclerotic plaque formation,1 myocardial fibrosis,2 and myocardial function suppression,3 have been implicated in the pathophysiology of various cardiovascular (CV) diseases.4,5 Clinical studies have shown the association of gut metabolites with adverse outcomes, severity, and risk stratification in several CV diseases [e.g. heart failure (HF)6 and myocardial infarction (MI)7].

Despite most of the past studies having focused mainly on a single metabolite (i.e. trimethylamine N-oxide—TMAO), it has been suggested that additional metabolites of this pathway, involving choline and carnitine (e.g. acetyl-L-carnitine, L-carnitine, betaine, and γ-butyrobetaine), may have an additional role to play.8,9 However, to date, the proper contribution of the different metabolites in the spectrum of the CV diseases still remains unclear; therefore, the aim of the present study is to investigate whether there is a differential contribution of metabolite biomarkers of the choline/carnitine–metabolic pathway in association with the adverse outcomes of MI and HF.