Apolipoprotein B as the best predictor of coronary artery disease in Iranian normolipidemic patients Mehran Haidari a *, Mansour Moghadam b , Majid Chinicar b , Arsis Ahmadieh b , Mahmoud Doosti c a Cardiovascular Research Center, Tehran University of Medical Sciences, Tehran, Iran b Department of Cardiology, Shariaty Hospital, Tehran University of Medical Sciences, Tehran, Iran c Department of Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran Received 1 December 2000; received in revised form 22 January 2001; accepted 1 February 2001 Abstract Objectives: A relatively high proportion of Iranian patients with coronary artery disease (CAD) have normal levels of traditional lipid risk factors and show early onset of CAD. In this study we examined the roles of apolipoprotein B (apoB), apolipoprotein AI (apoAI) and lipoprotein (a) [LP(a)] in predicting coronary heart disease in normolipidemic patients and those with premature CAD (age #50). Design and methods: Serum levels of apoB, apoAI, and LP(a) were determined in a total of 567 Iranian patients who were candidates for coronary angiography. A subgroup of 142 patients (93 males, 49 females) with normal levels of classical lipid risk factors, and a subgroup of patients (130 males, 71 females) with age below 50 years were separately assessed for coronary risk factors. Results: ApoB concentrations were significantly higher in patients with CAD (CAD1) relative to patients without CAD (CAD2) in the two subgroups. Multiple logistic regression after controlling for age and others risk factors showed apoB as the best determinant of CAD in the normolipidemic subgroup (OR, 4.3, p , 0.001) and in the men aged #50 (OR, 5.7, p , 0.001). ApoB was the best predictor of CAD in a subgroup of very young patients (age #40, n 5 77, OR, 8.6, p , 0.009). There was a significant correlation between severity of atherosclerosis and serum apoB concentration in the normolipidemic subgroup (r 5 0.22, p , 0.008). Conclusions: Our data indicate that serum concentration of apoB is the best discriminating factor to predict the presence or absence of atherosclerosis in Iranian normolipidemic individuals and young patients undergoing coronary angiography. © 2001 The Canadian Society of Clinical Chemists. All rights reserved. Keywords: Coronary artery disease, Apolipoprotein B, Lipoprotein (a), Low density lipoprotein cholesterol. 1. Introduction Coronary heart disease is the leading cause of death in the majority of countries. To date, much of the literature has focused on modifiable traditional risk factors, which are known to be associated with CAD. However, almost 50% of patients with CAD do not exhibit any of the established risk factors (hypertension, hypercholesterolemia, cigarette smoking, diabetes mellitus, marked obesity, and physical inactivity) [1]. And almost 50% of men with premature CAD have plasma total cholesterol #5.18 mmol/l (#200 mg/dl)[2]. The presence of CAD in a significant number of these patients remains unexplained. Thus, measurement of nontraditional lipid risk factors has been proposed to better identify patients potentially at risk of ischemic heart disease. The association between low density lipoprotein choles- terol (LDL-C) levels with CAD is widely accepted, and it has been assumed that the measurement of LDL by deter- mining its cholesterol content provides an accurate assess- ment of the concentration of LDL particles. But does a normal value for LDL cholesterol mean the level of LDL is normal? Because the cholesterol content of LDL is variable, LDL cholesterol is not equivalent to the LDL particle. By contrast because each LDL particle has 1 molecule of apoB, measurement of LDL apoB gives an exact estimate of the LDL particle number [3]. The across cultural prospective studies demonstrated that at a cholesterol level of about 5.43 mmol/l (210 mg/dl), CAD mortality rates vary from 5% in Japan to 15% in northern Europe[4]. This large difference To whom correspondence should be addressed: * Mehran Haidari, Room 4011c, 555 University Ave, The Hospital for Sick Children, To- ronto, ON, M5G 1X8, Canada. Tel.: 1416 813 8754; fax: 1416 813 6257. E-mail address: mhaidari@sickkids.on.ca (M. Haidari). Clinical Biochemistry 34 (2001) 149 –155 0009-9120/01/$ – see front matter © 2001 The Canadian Society of Clinical Chemists. All rights reserved. PII: S0009-9120(01)00192-8