Apolipoprotein A-I-Containing Particles in Patients With Hypoalphalipoproteinemia

This study was performed to determine relations among concentrations of high-density lipoprotein (HDL) apolipoprotein (apo) A-I and apoA-II and lipoproteins with apoA-I only (LpA-I) and with both apoA-I and apoA-II (LpA-I:A-II) in patients with low plasma levels of HDL cholesterol. Seventyseven middle-aged men with low HDL cholesterol levels (<40 mg/dL) were compared with 37 middle-aged men with normal HDL cholesterol levels (>40 mg/dL). Low-HDL patients were divided into those with nonnotrigh/ceridemia (trigh/cerides <250 mg/dL; n=49) and hypertriglyceridemia (trigh/cerides £250 mg/dL; n=28). Total apoA-I and apoA-II concentrations and apoA-I levels in LpA-I were significantly lower in the two There is growing evidence ' and recognition' of an inverse relation between levels of highdensity lipoprotein (HDL) and risk of coronary heart disease (CHD). This link has been most commonly identified by the increased CHD risk associated with a low HDL cholesterol (HDL-C) concentration,and low HDL-C has been designated as a major risk factor for CHD. Moreover, a high HDL-C level appears to be "protective" against CHD. Even so, HDL consists of several subtractions that may vary in their antiatherogenic potential, and the identification and differentiation of these subfractions could prove useful in CHD risk assessment in individual patients. For example, larger HDL particles (ie, HDL2) appear to be more closely linked in an inverse way to CHD risk than do smaller HDL3 particles.Differences in antiatherogenic potential may also be related to the apolipoprotein concentrations and composition of HDL. Several reports suggest that reduced concentrations of HDL apolipoproteins are associated with increased CHD risk. Furthermore, two types of HDL particles have been identified, ie, those having apolipoprotein (apo) A-I only (LpA-I) and those having both apoA-I and apoA-II (LpA-I:A-II). The HDL2 subfraction is enriched in LpA-I, and LpA-I levels have a stronger inverse correlation with CHD risk than do LpA-I:A-II levels. Received October 4, 1993; revision accepted January 5, 1994. From The Center for Human Nutrition (A.M., G.LV., S.M.G.) and the Departments of Internal Medicine (S.M.G.), Biochemistry (S.M.G.), and Clinical Nutrition (G.L.V., S.M.G.) of the University of Texas Southwestern Medical Center, Dallas, and the Veterans Affairs Medical Center at Dallas, Tex. Correspondence to Scott M. Grundy, MD, PhD, The Center for Human Nutrition and the Departments of Internal Medicine, Biochemistry, and Clinical Nutrition, University of Texas Southwestern Medical Center, Dallas, TX 75235-9052. low-HDL groups compared with control subjects. Although low-HDL patients' apoA-I levels were numerically lower in LpA-I:A-II compared with control subjects' levels, the differences were not statistically significant. Thus, there is a preferential reduction in apoA-I levels of LpA-I compared with LpA-I:A-II in patients with low HDL cholesterol. This preferential reduction in LpA-I levels was observed in both normotrigh/ceridemic and hypertrigh/ceridemic patients. However, among low-HDL patients levels of apoA-I in LpA-I did not distinguish between those with and without coronary heart disease. (ArterioscUr Thromb. 1994;14:511-517.)