ABSTRACT
Background: High density lipoproteins are an heterogeneous population of particles. Two main subpopulations have been identified, one contains Apo A-I and Apo A-II and is denominated LpA-I:A-II and another one contains only Apo A-I and is denominated LpA-I. Aim: To measure the concentrations of these particles in patients with stable coronary artery disease. Patients and Methods: Serum lipids, A-I and B apolipoproteins, LpA-I, LpA-I:A-II and LpB particles were measured in 73 men aged 33 to 82 years with angiographically documented coronary artery disease (CAD) and 33 control subjects aged 39 to 76 years. LpA-I, LpA-I:A-II and LpB were measured by a noncompetitive enzyme linked immunoassay using previously characterized monoclonal antibodies against ApoA-I, ApoA-II and apoB. Results: Patients with CAD had significantly higher mean levels of LDL cholesterol than the control group (p= 0.038). The mean concentration of LpA-I particles in patients with CAD was significantly lower (p= 0.031) than in control subjects, while the concentration of LpA-I:A-II particles was significantly higher (p=0.016). The percentage of coronary stenosis correlated negatively with LpA-I and positively with LpA-I:A-II. The best relative risk (RR) indicator in these patients was LDL-cholesterol. The relative risk increases 2.5 fold when LpA-I falls below the cut-off level. Likewise, the relative risk increases 3-fold when LpA-I:A-II raises over the cut-off level. Conclusions: Our findings indicate that the quantification of LpA-I and LpA-I:A-II particles might allow a more accurate evaluation of the CAD risk than HDL cholesterol. LpA-I might represent the antiatherogenic fraction of HDL
Subject(s)
Humans , Male , Adult , Middle Aged , Coronary Disease/blood , Lipoproteins/blood , Enzyme-Linked Immunosorbent Assay , Case-Control Studies , Cholesterol/blood , Cholesterol, HDL/blood , Apolipoproteins/bloodABSTRACT
LDLs obtainded from blood of healthy subjects, were glycated or altered with malondialbehyde and used as antigens. Serum autoantibodies against these LDLs were measured by ELISA in 22 patients with non insulin dependent diabetes mellitus aged 46 to 67 years old and 13 healthy controls aged 41 to 64 years old. Basal and LDL stimulated tumor necrosis factor production in vitro, by peripheral leukocytes of diabetics and controls was also measured. Results: The ratio of glycated LDL/native LDL antibodies was higher in diabetics than in controls (9.37 ñ 2.72 and 0.41 ñ 0.11 respectively p < 0.05) and the ratio of MDA modified LDL/native LDL antibodies was not significantly different (8.64 ñ 3.83 and 2.14 ñ 1.26 respectively, NS). Tumor necrosis or production by leukocytes was higher in diabetics than in controls in basal conditions (53.3 ñ 15.3 and 26.9 ñ 14.7 arbitrary units (a.u.) respectively), when stimulated withnative LDL (46.5 ñ 5 and 24.3 ñ 9.4 a.u. respectively), when stimulated with malondialdehyde modified LDL (50 ñ 16.2 and 24.4 ñ 7.7 a.u. respectively) or when stimulated with glycated LDL (38.3 ñ 8.8 and 14.4 ñ 7.5 a.u. respectively). Conclusions: Diabetic patients have an enhanced immune response against low density lipoproteins, factor that could contribute to the accelared atherogenesis of this disease