Abstract 12979: Increase in Exogenous Lipoproteins Characterized by Apolipoprotein B48 and Cholesterol Absorption/Synthesis Markers Represents Residual Risks for Coronary Artery Disease during Intensive LDL-Lowering Therapy
Objective: Recent clinical trials suggest that there remain residual risks for coronary artery disease (CAD) during low-density lipoprotein cholesterol (LDL-C) lowering therapy with statins. Exogenously derived lipids such as remnant lipoproteins are considered as a candidate representing residual risks. We investigated whether apolipoprotein (apo) B48 and cholesterol absorption/synthesis markers could be useful for CAD progression and residual risk stratification.
Methods: Patients with CAD who underwent percutaneous coronary intervention (PCI) were enrolled. These patients underwent follow-up coronary angiography 8 months after the initial PCI, and were divided into three groups; 1) patients without major coronary stenosis (no-stenosis: NS, n=258), 2) patients with de novo coronary stenosis (de novo-stenosis: DNS, n=74), and 3) patients with major in-stent coronary restenosis (instent-restenosis: ISR, n=90). Biochemical analyses were done on fasting serum samples at the time of PCI and follow-up admission.
Results: Serum levels of LDL-C and total apoB in patients with CAD (n=552) were significantly lower than those without CAD (n=275) (p<0.05), presumably due to receiving the statin treatment. There were no differences in LDL-C and total apoB levels among the NS-, DNS-, and ISR-group. Thus, LDL-C or total apoB did not predict residual risks in the secondary prevention. In contrast, apoB48 was significantly higher in CAD than in without CAD (5.0±3.4, vs. 4.1±2.7 µg/ml, p<0.05). Among the CAD patients, apoB48 was higher in DNS than in NS (5.7±3.8, vs. 4.6±2.8 µg/ml, p<0.05). Moreover, in DNS, apoB48 was 93% increased for 8 months from the initial PCI, while it was unchanged in ISR during the observation period. Furthermore, in DNS, cholesterol absorption markers were higher than those in ISR (3.91±1.67 vs. 3.08±0.81, p<0.05).
Conclusion: During the intensive lipid-lowering therapy by statins, cholesterol absorption predominates over cholesterol synthesis and serum apoB48 level is concomitantly increased, which leads to the progression of de novo lesions. Fasting apoB48 and cholesterol absorption/synthesis markers could be a predictor of lesion progression and a possible therapeutic target for secondary prevention of CAD.
- © 2012 by American Heart Association, Inc.