Association of lipids, lipoproteins, apolipoproteins and paraoxonase enzyme activity with premature coronary artery disease

Background and design The association of serum apolipoprotein (apo) A-I and apo B concentrations and paraoxonase (PON) enzyme activity with angiographically determined coronary artery disease (CAD) was investigated in Iranian non-diabetic patients with premature CAD and control participants in a sex- and age-matched case-control study. Methods The study population consisted of 59 non-diabetic patients with premature CAD and 55 CAD control participants. Premature CAD was defined as the presence of angiographically proven coronary stenosis (greater than or equal to50% involvement) in men and women younger than 55 and 65 years, respectively. Apolipoprotein concentrations were measured by immunoturbidometric assay and paraoxonase/arylesterase activities by spectrophotometric assay of p-nitrophenol/phenol production following addition of paraoxon/phenylacetate to serum, Results In CAD patients, increased concentrations of total cholesterol (215 +/- 43 compared with 193 +/- 43 P < 0.001), low-density lipoprotein cholesterol (137 ± 46 compared with 116 ± 39, P < 0.05) and apo B (102 +/- 24 compared with 84 +/- 17, P < 0,001) and a decreased ratio of apo A-I/apo B (1.7 ± 0.4 compared with 2.0 ± 0.6, P < 0.001) were observed compared to the control group, Other study variables were not significantly different between the two groups, On multiple logistic regression analysis, the only marker for discrimination between the CAD+ group and the CAD- control group was apo B level, Conclusions In Iranian non-diabetic patients with premature CAD, the concentration of apo B is a better marker than traditional lipids in discriminating between CAD+ and CAD- patients. The lack of significant difference in PON activity between CAD patients and control participants supports the concept of interethnic variability in PON activity and gene polymorphism observed in other studies. Coron Artery Dis 13:9-16 (C) 2002 Lippincott Williams Wilkins.