Remnant cholesterol has attracted interest as a marker of cardiovascular event risk. The power of remnant cholesterol to predict major cardiovascular events (MACE) in patients with differing fasting glucose state is unclear and is addressed in the present study. We prospectively recorded MACE including cardiovascular death, non-fatal myocardial infarction and non-fatal stroke in a high-risk cohort of 1787 patients with cardiovascular disease,1472 had angiographically proven coronary artery disease and 315 had sonographically proven peripheral artery disease, over a mean follow-up period of 10.7±5.0 years. At baseline, remnant cholesterol significantly increased from patients with NFG (n=690) over those with IFG (n=505) to those with T2DM (n=592; 19±21 mg/dl, 24±23 mg/dl and 26±24 mg/dl, respectively; ptrend<0.001). During follow-up, 719 of our patients suffered MACE; the incidence of MACE in subjects with NFG, IFG and T2DM was 37.8%, 34.4% and 49.1%, respectively, ptrend<0.001.Remnant cholesterol in the total study population predicted MACE (standardized adjusted HR 1.17 [1.09-1.27], p<0.001) in Cox regression models adjusting for age, sex, hypertension, smoking, body mass index and LDL cholesterol and also after additional adjustment for the baseline glycemic state (HR=1.15 [1.07-1.23], p<0.001). In subgroup analyses, standardized adjusted HR were 1.19 [1.05-1.35], p=0.005), 1.12 [0.96-1.30], p=0.146) and 1.15 [1.02-1.29], p=0.025) in patients with NFG, IFG and T2DM, respectively. An interaction term remnant cholesterol by glycemic state was not significant (p=0.363), indicating that the glycemic state did not significantly impact the power of remnant cholesterol to predict MACE. From our data we conclude that remnant cholesterol is a predictor of MACE in CVD patients irrespective of the baseline glycemic state.

Disclosure

H. Drexel: None. T. Plattner: None. B. Larcher: None. A. Mader: None. A. Vonbank: None. P. Elsner: None. A. Leiherer: None. A. Muendlein: None. C.H. Saely: None.

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