%0 Journal Article
%T Mannose as a biomarker of coronary artery disease: Angiographic evidence and clinical significance.
%A Ferrannini E
%A Marx N
%A Andreini D
%A Campi B
%A Saba A
%A Gorini M
%A Ferrannini G
%A Milzi A
%A Magnoni M
%A Maseri A
%A Maggioni AP
%A Burgmaier M
%A  
%J Int J Cardiol
%V 346
%N 0
%D Jan 2022 1
%M 34800594
%F 4.039
%R 10.1016/j.ijcard.2021.11.038
%X <B>BACKGROUND: </B>High mannose has previously associated with insulin resistance and cardiovascular disease (CVD). Our objective is to establish whether mannose is associated with anatomical evidence of coronary artery disease (CAD).<BR><B>METHODS: </B>Plasma mannose concentrations were measured by liquid chromatography/tandem mass spectrometry in a discovery cohort (n = 513) and a validation cohort (n = 221) of carefully phenotyped individuals. In both cohorts CAD was quantitated using state-of-the-art imaging techniques (coronary computed coronary tomography angiography (CCTA), invasive coronary angiography and optical coherence tomography). Information on subsequent CVD events/death was collected. Associations of mannose with angiographic variables and biomarkers were tested using univariate and multivariate regression models. Survival analysis was performed using the Kaplan-Meier estimator.<BR><B>RESULTS: </B>Mannose was related to indices of CAD and features of plaque vulnerability. In the discovery cohort, mannose was a marker of quantity and quality of CCTA-proven CAD and subjects with a mannose level in the top quartile had a significantly higher risk of CVD events/death (p = 3.6e-5). In the validation cohort, mannose was significantly associated with fibrous cap thickness < 65 μm (odds ratio = 1.32 per each 10 μmol/L mannose change [95% confidence interval, 1.05-1.65]) and was an independent predictor of death (hazard ratio for mannose≥vs < 84.6 μmol/L: 4.0(95%CI, 1.4-11.3), p = 0.006).<BR><B>CONCLUSIONS: </B>The current data add novel evidence that high mannose is a signature of CAD with a vulnerable plaque phenotype, consistently across measures of severity of vessel involvement and independent of the traditional correlates of CVD, and that it is an independent predictor of incident adverse outcomes.