Background: Japanese patients with coronary heart disease (CHD) usually have slightly elevated triglyceride levels but virtually normal low-density lipoprotein (LDL)-cholesterol levels.
Design: Case–control study.
Methods: To explore the atherogenecity of mild hypertriglyceridemia, we measured very-low-density lipoprotein (VLDL) composition and apolipoprotein (apo) B in VLDL, intermediate-density lipoprotein (IDL), light LDL and dense LDL fractions separated by ultracentrifugation in 61 men with angiographically proven CHD and in 69 men without CHD. Apo B, E, C1 and C3 in VLDL were measured by enzyme-linked immunosorbent assay.
Results: Although total- and LDL-cholesterol levels were similar in CHD and control participants, triglyceride levels were significantly higher and high-density lipoprotein (HDL)-cholesterol levels were lower in CHD patients. Triglyceride, cholesterol and apo C1 and E levels in VLDL were two-fold higher and VLDL-apo B level was three-fold higher in CHD than control patients. IDL-triglyceride levels were significantly elevated in CHD, but IDL-cholesterol level was not. Apo B levels of the dense LDL fraction were significantly elevated in CHD groups, but those of the light LDL fraction were not. These differences were constant when triglyceride levels matched between both groups. Multiple logistic regression analysis revealed that the VLDL-apo B and VLDL-apo C1 levels were significantly associated with the incidence of CHD independent of the plasma triglyceride, HDL-cholesterol or apo B levels in dense LDL.
Conclusion: These results suggest that an increased number of VLDL particles is strongly associated with CHD, independently of traditional risk factors or newly recognized atherogenic lipoproteins, such as IDL or small, dense LDL, in Japanese men.
bFirst Departments of Internal Medicine, Showa University School of Medicine, Tokyo, Japan
Sponsorship: This study was supported in part by a grant-in-aid (11671136) from the Japanese Ministry of Education, Science and Culture, and Showa University Medical Foundation (Kyoudo-Kennkyu, H12-Year).
Correspondence and requests for reprints to Tsutomu Hirano MD, First Department of Internal Medicine, Showa University School of Medicine, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo 142-8666, Japan.
Tel: +81 3 3784 8722; fax: +81 3 3784 8742; e-mail: firstname.lastname@example.org
This study was presented at the 73rd Annual Scientific Meeting of the American Heart Association in New Orleans, Louisiana, USA, 13 November 2000.
Received 12 February 2002 Revised 08 July 2002 Accepted 12 July 2002