title: Remarkably high prevalence of small dense low-density lipoprotein in Japanese men with coronary artery disease, irrespective of the presence of diabetes.
abstract: To examine how prevalence of the small dense LDL phenotype (LDL particle diameter < or =25.5 nm) is associated with coronary artery disease (CAD) in type 2 diabetic and non-diabetic Japanese men, an ethnic group with a low incidence of CAD, 85 non-diabetic men and 45 type 2 diabetic men with angiographically documented CAD, and 142 control men and 76 type 2 diabetic men without CAD were studied. Mean LDL particle diameter was determined using 2-16% polyacrylamide gel electrophoresis. LDL particle diameters in CAD patients were much smaller than those in controls (25.2+/-0.7 vs. 26.0+/-0.4 nm, mean+/-S.D., P<0.0001). LDL size was smaller in diabetic subjects (25.6+/-0.6 nm) and became even smaller in diabetics with CAD (25.0+/-1.0 nm). Prevalence of small dense LDL was markedly higher in both non-diabetic and diabetic CAD patients than that in non-diabetic and diabetic patients without CAD (71, 76, 23 and 42%, respectively). CAD patients had lower HDL-cholesterol and apo A1 levels, and higher triglyceride levels than those in diabetic and non-diabetic CAD-free patients, while total- and LDL-cholesterol levels were even lower in CAD group, and remnant-like particle-cholesterol, lipoprotein (a) and insulin levels were comparable among four groups. LDL size was significantly associated with triglyceride, HDL-cholesterol and glycemic control. Logistic regression analysis revealed that the small dense LDL phenotype was significantly associated with the incidence of CAD independent of low levels of HDL-cholesterol or high levels of triglyceride in both non-diabetic and diabetic cases. These results suggest that high prevalence of small dense LDL is a leading cause of CAD in both diabetic and non-diabetic Japanese men. Type 2 diabetes shows a greater capacity to reduce LDL size, which may contribute to the high incidence of CAD in the diabetic population.
authors.affiliation: Third Department of Internal Medicine, Showa University School of Medicine, Tokyo, Japan.
authors.forename: Shinji
authors.initials: S
authors.lastname: Koba
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Hirano
authors.forename: Gen
authors.initials: G
authors.lastname: Yoshino
authors.forename: Keiko
authors.initials: K
authors.lastname: Sakai
authors.forename: Taro
authors.initials: T
authors.lastname: Sakaue
authors.forename: Mitsuru
authors.initials: M
authors.lastname: Adachi
authors.forename: Takashi
authors.initials: T
authors.lastname: Katagiri
mesh_terms: D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D003324:Coronary Artery Disease / Q000097:blood* / Q000188:drug therapy / Q000453:epidemiology*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy / Q000453:epidemiology*; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D007564:Japan / Q000453:epidemiology; D017270:Lipoprotein(a) / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood; D008077:Lipoproteins, LDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use; D015995:Prevalence; D019821:Simvastatin / Q000627:therapeutic use; D014280:Triglycerides / Q000097:blood
chemical_list: D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D000960:Hypolipidemic Agents; D017270:Lipoprotein(a); D008075:Lipoproteins, HDL; D008077:Lipoproteins, LDL; D017035:Pravastatin; D019821:Simvastatin; D014280:Triglycerides