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Increased Plasma Lipid-Poor Apolipoprotein A-I in Patients with Coronary Artery Disease

Departments of ¹ Informative Clinical Medicine and ² Cardiology, Regeneration and Advanced Medical Science, Gifu University Graduate School of Medicine, Gifu, Japan.
³ Daiichi Pure Chemicals Company, Tokyo, Japan.

^aAddress correspondence to this author at: Department of Informative Clinical Medicine, Gifu University Graduate School of Medicine, Yanagido, Gifu 501-1194, Japan. Fax 81-58-230-6431; seishima{at}cc.gifu-u.ac.jp.

Background: Pre-ß1-HDL participates in a cyclic process involved in the retrieval of cholesterol from peripheral tissues. Although pre-ß1-HDL can be measured by two-dimensional electrophoresis or crossed immunoelectrophoresis, these methods are time-consuming and require technical expertise. In this study, we separated plasma lipid-poor apolipoprotein A-I (apo A-I) by high-performance size-exclusion chromatography.

Methods: We measured plasma lipid-poor apo A-I in 20 male patients with coronary artery disease [CAD; mean (SD) age, 64.0 (18) years] and 15 male controls [54.7 (17) years] and in 7 female CAD patients [70.3 (7.7) years] and 9 female controls [65.1 (4.7) years].

Results: Lipid-poor apo A-I was most stable when stored at –80 °C in the presence of aprotinin (final concentration, 50 kIU/L). The lipid-poor apo A-I concentration decreased during incubation at 37 °C, and this was not prevented by the addition of 2 mmol/L of the lecithin:cholesterol acyltransferase (LCAT) inhibitor 5,5'-dithiobis(2-nitrobenzoic acid). Lipid-poor apo A-I was significantly higher in CAD patients than in controls [38.3 (7.9) mg/L for male CAD patients vs 29.3 (7.3) mg/L for male controls; 43.3 (11) mg/L for female CAD patients vs 27.1 (7.4) mg/L for female controls (P <0.01 for both)]. There were no significant differences in LCAT activity or cholesteryl ester transfer protein (CETP) concentration between patients and controls. Moreover, the plasma lipid-poor apo A-I concentration was not significantly correlated with LCAT or CETP activities.

Conclusions: Although the production of lipid-poor apo A-I in plasma is not fully understood, our results indicate that lipid-poor apo A-I could be used as a marker for arteriosclerosis and demonstrate that it is not identical to the pre-ß1-HDL measured by other methods.

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