Abstract 18817: The Four Statin Benefit Groups Defined by the 2013 ACC/AHA Guideline are Characterized by Increased Plasma Level of Electronegative LDL
Background: Anion-exchange chromatography has identified L5 as the most electronegative entity of charge-defined LDL subfractions, L1-L5. In patients with ST-elevation myocardial infarction, L5 is markedly elevated and can enhance platelet aggregation. To further evaluate its clinical relevance, we examined plasma L5 distributions in patients classified as the 4 statin benefit groups (atherosclerotic cardiovascular disease, LDL cholesterol >190 mg/dL, diabetes mellitus, 10-year cardiovascular risk score >7.5%) by the 2013 ACC/AHA guideline.
Methods and results: By examining the medical history and clinical profiles, we divided a cohort of 62 asymptomatic patients (59.4±10.5 yr) with 2 or more components of the metabolic syndrome criteria into the statin benefit (n=44) and non-statin benefit (n=18) groups. Although the plasma LDL cholesterol levels did not differ between groups (147±35 vs. 153±49 mg/dL), the statin benefit group had significantly higher L5/LDL% (5.2±7.3% vs. 2.6±1.9%, P=0.031) and L5 concentration (7.4±10.4 vs 3.7±3.1 mg/dL, P=0.036) values. Linear regression showed a positive correlation between the plasma L5 concentration and the 10-year cardiovascular risk scored by the pooled cohort equation (Figure). In cultured human aortic endothelial cells, L5, but not L1-L4, induced release of inflammatory chemokines (CX3CL1, IL-8, IL-6) in a concentration-dependent manner, supporting L5’s role in clinical atherogenicity. Treatment with rosuvastatin (10 mg/day) reduced L5/LDL% and L5 concentration of the statin benefit group to the levels of the non-stating benefit group (2.5±2.1%, 3.4±2.8 mg/dL) in 3 months.
Conclusions: The 4 statin benefit groups defined by the 2013 ACC/AHA guideline represent a patient population of high cardiovascular risk. The increased risk in this population is closely related to the increased plasma distribution of L5. Statin treatment can decrease the inflammatory property of LDL by reducing its L5 content.
Author Disclosures: C. Chu: None. L. Ke: None. H. Chan: None. H. Chan: None. C. Chen: None. K. Cheng: None. H. Lee: None. H. Kuo: None. C. Chang: None. S. Sheu: None. W. Lai: None. C. Chen: None.
- © 2014 by American Heart Association, Inc.