Abstract 4365030: Excess Apolipoprotein B Improves Risk Assessment of All-Cause Mortality in Patients with Aortic Stenosis: Insights from the ARISTOTLE Study
Abstract
Aims: Discordance analyses showed that apolipoprotein B (apoB) is better for assessing cardiovascular disease risk than low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C). However, its additional value beyond LDL-C or non-HDL-C in aortic stenosis (AS) remains underexplored. Methods: Moderate to severe AS patients (n=467) from ARISTOTLE study were included. Excess apoB was defined as the difference between the observed apoB and the expected apoB based on their given LDL-C or non-HDL-C level. Association of excess apoB with the risk of all-cause mortality was assessed by Cox proportional hazards regressions with 95% confidence intervals (CIs). Additionally, the incremental value incorporating excess apoB into standard models for predicting outcome was evaluated. Results: ApoB and LDL-C were highly correlated (r=0.92), with LDL-C account for 84% of the variability in apoB levels. A dose-dependent association was observed between excess apoB based on LDL-C and the risk of all-cause mortality in AS patients. For each one standard deviation (SD) increase in excess apoB, the multivariate-adjusted hazard ratio (HR) for all-cause mortality was 1.021 (95%CI, 1.004-1.038). The multivariable adjusted HR for excess apoB >12.71 mg/dL was 1.998 (95% CI: 1.233-3.237). When excess apoB was added to the standard risk model, the prediction accuracy significantly improved, as indicated by notable changes in the C-statistic, continuous NRI, and IDI (all P-values < 0.05). Similar improvements in prediction were observed when excess apoB was calculated based on non-HDL-C. Conclusions: Excess apoB was dose-dependently associated with an increased risk of all-cause mortality in moderate to severe AS. Key words: excess ApoB, aortic stenosis, all-cause mortality, LDL-C, non-HDL-C
Article Details
Authors (4)
Mengjie Xie
Stanford Cardiovascular Institute, Stanford University, CA (L.R., N.B., H.Z., R.H., W.Z., X.W., M.X., J.G., H.Y.K., T.L., J.S., J.C.W.).
Zhenyu Xiong
Department of Cardiology, Kaifeng Children’s Hospital, Kaifeng, China
Liao Xinxue
Sun Yat-Sen University, Guangzhou, China
Xiaodong Zhuang
The Soft2D Lab, State Key Laboratory of Synergistic Chem-Bio Synthesis, School of Chemistry and Chemical Engineering, Shanghai Jiao Tong University, 130 Dongchuan Road, Shanghai 200240, China