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Volume 204, Issue 2, Pages 595-600 (June 2009)


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Plasma preβ1-HDL level is elevated in unstable angina pectoris

Jun Tashiroac, Osamu MiyazakibCorresponding Author Informationemail address, Yoshitake Nakamurac, Akira Miyazakic, Isamu Fukamachib, Hideaki Bujod, Yasushi Saitoe

Received 30 June 2008; received in revised form 8 October 2008; accepted 10 October 2008. published online 03 December 2008.

Abstract 

Preβ1-HDL, a minor HDL subfraction consisting of apolipoprotein A-I (apoA-I), phospholipids and unesterified cholesterol, plays an important role in reverse cholesterol transport. Plasma preβ1-HDL levels have been reported to be increased in patients with coronary artery disease (CAD) and dyslipidemia. To clarify the clinical significance of measuring plasma preβ1-HDL levels, we examined those levels in 112 patients with CAD, consisting of 76 patients with stable CAD (sCAD) and 36 patients with unstable angina pectoris (uAP), and in 30 patients without CAD as controls. The preβ1-HDL levels were determined by immunoassay using a specific monoclonal antibody (Mab55201) that we established earlier. The mean preβ1-HDL level in the CAD patients was significantly higher than the level in the controls (34.8±12.9mg/L vs. 26.6±6.9mg/L, p<0.001). In addition, the mean preβ1-HDL level was markedly higher in the uAP subgroup than in the sCAD subgroup (43.1±11.5mg/L vs. 30.9±11.7mg/L, p<0.0001). These tendencies remained even after excluding dyslipidemic subjects.

These results suggest that elevation of the plasma preβ1-HDL level is associated with the atherosclerotic phase of CAD and may be useful for identifying patients with uAP.

a Department of Internal Medicine, Matsudo City Hospital, 4005, Kamihongo, Matsudo, Chiba 271-8511, Japan

b Tsukuba Research Institute, Sekisui Medical Co. Ltd. (Daiichi Pure Chemicals Co. Ltd.), 3-3-1, Koyodai, Ryugasaki, Ibaraki 301-0852, Japan

c Department of Cardiology, Chiba Cardiovascular Center, 575, Tsurumai, Ichihara, Chiba 290-0512, Japan

d Department of Genome Research and Clinical Application, Chiba University Graduate School of Medicine, 1-8-1, Inohana, Chuo-ku, Chiba 260-8670, Japan

e Department of Clinical Cell Biology, Chiba University Graduate School of Medicine, Chiba University, 1-8-1, Inohana, Chuo-ku, Chiba 260-8670, Japan

Corresponding Author InformationCorresponding author. Tel.: +81 297 62 6425; fax: +81 297 62 8635.

PII: S0021-9150(08)00755-7

doi:10.1016/j.atherosclerosis.2008.10.015


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