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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1995;15:228-231.)
© 1995 American Heart Association, Inc.

Articles

The Role of Lipoprotein A-I and Lipoprotein A-I/A-II in Predicting Coronary Artery Disease

T. O'Brien; T. T. Nguyen; B. J. Hallaway; D. Hodge; K. Bailey; D. Holmes; B. A. Kottke

From the Atherosclerosis Research Unit (T.O., T.T.N., B.J.H., B.A.K.); Division of Endocrinology/Metabolism and Internal Medicine (T.O., T.T.N.); Division of Biostatistics, Department of Health Related Sciences (D.H., K.B.); and the Division of Cardiovascular Disease (B.A.K.), Mayo Clinic and Foundation, Rochester, Minn.

Correspondence to B.A. Kottke, Watson Clinic, PO Box 95000, 1600 Lakeland Hills Blvd, Lakeland, FL 33804-5000.

	Abstract

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Abstract The aim of this study was to examine the role of HDL subparticles with apolipoprotein (apo) A-I alone (LpA-I) and with apoA-I and apoA-II (LpA-I/A-II) in predicting coronary artery disease. Concentrations of these HDL subparticles were compared in 184 subjects with angiographically confirmed significant coronary artery disease (>50% stenosis of at least one vessel) and 191 age- and sex-matched control subjects without clinical coronary artery disease. LpA-I and LpA-I/A-II were measured with magnetic beads coated with anti–apoA-II antibodies to separate particles containing apoA-II from plasma. Total plasma cholesterol and triglyceride levels were similar in both groups. Although subjects with coronary artery disease had lower HDL cholesterol, plasma apoA-I, LpA-I, and LpA-I/A-II than age- and sex-matched control subjects without coronary artery disease, plasma apoA-I was the best predictor of coronary artery disease. In conclusion, LpA-I and LpA-I/A-II are lower in subjects with coronary artery disease but do not add to plasma apoA-I in predicting the presence of coronary artery disease.

Key Words: lipids • lipoproteins • HDL • coronary artery disease

	Introduction

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An inverse relation between HDL cholesterol levels and coronary artery disease (CAD) risk has been described.¹ HDL particles, however, are heterogeneous in nature, and not all HDL subparticles may be equally protective. This may in part explain why some studies have not found this association.^{2 3} A number of methods have been used to separate HDL subparticles. HDL can be separated into HDL₂ and HDL₃ with ultracentrifugation. Although it was thought that HDL₂ was a more important predictor of CAD,⁴ recent work has shown that HDL₂ and HDL₃ are equally cardioprotective.⁵ Furthermore, lipoprotein separation by ultracentrifugation results in artifactual changes in the apolipoprotein composition of these particles.⁶

Classification systems based on the apolipoprotein content of HDL particles have also been used. One such example is the use of heparin affinity chromatography to separate apolipoprotein E (apoE)–poor and apoE-rich HDL subparticles.^{7 8} This classification has both functional and clinical significance. ApoE-rich HDL subparticles have been shown to be lower in CAD⁹ and may have a distinct role in reverse cholesterol transport.¹⁰

HDL can also be separated into particles that contain apoA-I without apoA-II (LpA-I) and particles that contain both apoA-I and apoA-II (LpA-I/A-II).^{11 12} In vivo metabolic studies have shown that apoA-I on LpA-I is catabolized more rapidly than apoA-I on LpA-I/A-II,¹³ suggesting that LpA-I and LpA-I/A-II have divergent metabolic pathways. In a comparison of subjects with and without CAD, LpA-I has been shown to be the protective subfraction.¹⁴ It has also been shown that cholesterol efflux from cultured adipose cells is mediated by LpA-I but not by LpA-I/A-II particles.¹⁵ However, results of in vitro studies have been inconsistent, with one study¹⁶ showing LpA-I/A-II to be more efficient in promoting cholesterol efflux and another showing both to be equally effective.¹⁷ Furthermore, in Tangier disease, HDL subparticles with apoA-I and subparticles with apoA-II are equally effective at promoting cellular cholesterol efflux.¹⁸

The aim of the current study was to examine the relative cardioprotective roles of LpA-I and LpA-I/A-II by comparing levels of these HDL subparticles in subjects with angiographically confirmed significant CAD and age- and sex-matched control subjects.

	Methods

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The study received Institutional Review Board approval.

Subjects
Subjects Without Clinical CAD
This control group consisted of healthy individuals (participants in a community-based study of CAD) from the general population of Rochester, Minn, without clinical evidence of CAD based on clinical examination, electrocardiogram, and review of the medical history. The age of the group was 66±10 years (mean±SD) and contained 141 men and 43 women. They were matched to the cases exactly for age and sex. When multiple matches existed, one was chosen randomly (for a small number of cases, two control subjects were chosen).

Subjects With Angiographically Confirmed CAD
This group consisted of nondiabetic individuals who underwent coronary arteriography. After informed consent was obtained, blood was drawn at the time of coronary arteriography. Individuals in whom at least a 50% stenosis of one coronary artery was seen at coronary arteriography were classified as having significant CAD. Subjects on lipid-lowering medications were excluded.

Laboratory Analysis
Fasting blood samples were drawn into tubes containing EDTA. Plasma was separated by centrifugation in a tabletop centrifuge machine (model TJ-6, Beckman Instruments, Inc) at 4°C and 1500g for 20 minutes, and aliquots were frozen at -70°C for later LpA-I and LpA-I/A-II analysis. We have previously shown that freezing at -70°C does not influence LpA-I and LpA-I/A-II levels.¹⁹ Samples were thawed only once before analysis. Cholesterol and triglyceride levels were measured by standard enzymatic methods with the use of quality-control plasma pools.^{20 21} HDL cholesterol was measured with polyethylene glycol 6000 precipitation as previously described.^{21 22}

LpA-I levels were measured by a previously described assay that used immunomagnetic beads coated with anti–apoA-II antibodies to separate particles containing apoA-II from those not containing apoA-II.¹⁹ In brief, Dynabeads coated with anti-human apoA-II antibodies were mixed with the plasma samples on a titer plate shaker and incubated for 16 hours at room temperature. The Dynabeads were separated with a 96-magnet apparatus, and apoA-I levels in the supernatant were measured by radioimmunoassay. This represented LpA-I. LpA-I/A-II was the difference between plasma apoA-I and supernatant apoA-I. The supernatant was repeatedly negative for apoA-II by radioimmunoassay, suggesting that the separation of particles containing apoA-II was complete.

Statistical Methods
Levels of total cholesterol, triglycerides, HDL cholesterol, apoA-I, and HDL subparticles were compared between groups using the Wilcoxon rank sum test. The probability value and rank sum Z-score along with the means and standard deviations are reported. A value of P <.05 was considered significant.

The question of which factors were the most important in the prediction of CAD was approached in two ways. The first was a paired comparison between each pair of parameters. Each parameter was standardized to have mean zero and unit variance when considered in both groups combined. The difference between the standardized variables was calculated and compared between groups by a two-sample t test. Significance of this test would imply a significantly larger standardized group difference for one parameter than the other. For example, if the standardized version of apoA-I is significantly lower than the standardized version of HDL cholesterol among subjects with CAD relative to their respective values in healthy subjects, this would imply that apoA-I has a stronger association with CAD than does HDL cholesterol.

The second approach used a multiple linear regression analysis of the four parameters HDL cholesterol, apoA-I, LpA-I, and LpA-I/A-II in predicting CAD. Since the latter three parameters are linearly related, two models, one with apoA-I included and one with it excluded, were estimated. These analyses address the slightly different question of whether, for example, LpA-I/A-II adds significant predictive information to LpA-I or apoA-I.

	Results

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Total plasma cholesterol and triglyceride levels were similar in both groups. Mean total cholesterol was 201±38 mg/dL in the CAD group versus 205±35 mg/dL in control subjects (P=NS by rank sum test). Mean triglycerides were 142±88 mg/dL (median, 114) in the CAD group versus 133±62 mg/dL (median, 115) in control subjects (P=.17 by rank sum test). The CAD group had lower levels of HDL cholesterol (39±12 mg/dL) than control subjects (42±12 mg/dL, P=.031). Plasma apoA-I, LpA-I, and LpA-I/A-II levels were all significantly lower in the CAD group (Table 1). Total cholesterol, triglycerides, HDL cholesterol, apoA-I, LpA-I, and LpA-I/A-II levels were not significantly related within the CAD group to the use of ß-blockers or diuretics (Table 2). Therefore, these subjects were not excluded from the analysis.

View this table: [in this window] [in a new window]   Table 1. Plasma Lipid, ApoA-I, LpA-I, and LpA-I/A-II Levels in Subjects With Angiographically Confirmed Significant CAD and Age- and Gender-Matched Control Subjects

View this table: [in this window] [in a new window]   Table 2. Comparison of Lipids and HDL Subparticles in Subjects With CAD on ß-Blockers and/or Diuretics and Those Not on Medications

The results of the paired comparison between each pair of parameters is shown in Table 3. This analysis showed that apoA-I, LpA-I, and LpA-I/A-II were better than HDL cholesterol at predicting CAD. Moreover, apoA-I was significantly better than LpA-I and marginally better than LpA-I/A-II at predicting CAD. Finally, there was modest evidence that LpA-I/A-II was slightly better than LpA-I at predicting CAD.

View this table: [in this window] [in a new window]   Table 3. Paired Comparison Between Variables to Determine Which Variable Is Better at Predicting CAD

The results of the multivariate logistic analyses are shown in Table 4. The first model suggests that both LpA-I and LpA-I/A-II, as well as HDL cholesterol, independently relate to the probability of CAD. Lower levels of LpA-I, at given levels of LpA-I/A-II and HDL cholesterol, are associated with a higher probability of CAD. Similarly, lower levels of LpA-I/A-II, at given levels of LpA-I and HDL cholesterol, are associated with a higher probability of CAD. However, the incremental level of HDL cholesterol is reversed; ie, if the levels of LpA-I and LpA-I/A-II are fixed, then an increased level of HDL cholesterol is associated with a higher probability of CAD, the opposite of the simple association of HDL cholesterol with CAD. The coefficient for LpA-I of -.107 suggests an 11% decrease in the odds of CAD per unit increase in LpA-I, whereas the coefficient for LpA-I/A-II of -.071 suggests a corresponding 7% decrease.

View this table: [in this window] [in a new window]   Table 4. Multiple Linear Regression Analysis of Four Parameters in Predicting CAD

The second model, in which apoA-I is substituted for LpA-I, though formally a different model, is algebraically equivalent to the first model but indicates that this difference in the effects of the two subparticles is statistically significant (P=.02). That is, if the total amount of apoA-I is constant, then an increase in the amount of LpA-I/A-II (necessitating a corresponding decrease in LpA-I) acts to increase the probability of CAD. Thus, given a choice, it is better to have the apoA-I in the form of LpA-I.

	Discussion

Top Abstract Introduction Methods Results Discussion References

 
HDL particles are heterogeneous in nature, and a number of classification systems have been proposed to further define this heterogeneity. The separation of lipoprotein particles based on apolipoprotein content was initially described by Alaupovic.²³ This system of classification is useful, as the apolipoprotein content of lipoprotein particles plays an important role in their metabolic fate.²⁴

In the current study, HDL particles were separated into those that contained apoA-I (LpA-I) and those that contained both apoA-I and apoA-II (LpA-I/A-II). Magnetic beads coated with anti–apoA-II antibodies were used to separate particles containing apoA-II. It should be noted that apoA-II was absent from the supernatant, suggesting that the separation of apoA-II–containing particles was complete. With the use of this method, approximately 33% of plasma apoA-I is present on particles containing apoA-I alone (LpA-I), and the remaining 67% is on LpA-I/A-II particles. This is consistent with values previously reported using other methods of measurement.¹⁴

As stated previously, in most studies HDL cholesterol levels are inversely associated with the risk of CAD.¹ This is felt to be due to the role of these particles in reverse cholesterol transport.²⁵ Attempts have been made to examine the roles of HDL subparticles as acceptors of cellular cholesterol, a step that may be the initial event in this process. The results of these studies, however, have produced conflicting results.^{15 16 17 18}

The primary aim of the present study was to assess the cardioprotective roles of HDL subparticles with apoA-I alone (LpA-I) and with apoA-I and A-II (LpA-I/A-II) in CAD. In a previous study,¹⁴ it was suggested that LpA-I is cardioprotective, whereas LpA-I/A-II is not. However, in studies of this issue, this has not been a universal finding. In a study of subjects about to undergo coronary artery bypass grafting,²⁶ those with CAD had lower levels of both LpA-I and LpA-I/A-II than control subjects. In the ECTIM study,²⁷ LpA-I and LpA-I/A-II were lower in subjects with a history of myocardial infarction than in control subjects in both France and Northern Ireland. Thus, the results of both in vivo and in vitro studies on the antiatherogenic role of these particles have been inconsistent. Studies in transgenic mice have suggested that, in contrast to HDL particles containing apoA-I, particles containing apoA-II may increase the risk of atherosclerosis.²⁸

The current study included consecutive nondiabetic subjects who underwent coronary arteriography. Healthy age- and sex-matched subjects without clinical evidence of CAD served as controls. In the current study, LpA-I and LpA-I/A-II were lower in the CAD group and did not add to the measurement of plasma apoA-I levels in the assessment of CAD risk. The reason for the discrepancy between our study and that of Puchois et al¹⁴ is not immediately obvious. The studies used different methodologies, which may in part explain the difference. Differences in the populations studied may also be responsible.

In the current study, although total cholesterol and triglyceride levels were the same in both groups, all measurements of HDL particles were significantly lower in the CAD group. An inverse correlation exists between apoA-I levels and CAD.⁴ Furthermore, plasma apoA-I has been shown to be the best predictor of the presence of CAD.^{29 30} This finding was confirmed in the current study. Furthermore, although HDL cholesterol is inversely associated with CAD (because of the strong correlation of HDL cholesterol with apoA-I), for a given plasma apoA-I, HDL cholesterol is positively associated with CAD. This suggests that the composition of the particle is important in determining its cardioprotective role.

The paired head-to-head analysis suggests that, with regard to HDL subparticles LpA-I/A-II is more strongly negatively related to CAD than LpA-I (although not reaching statistical significance). A likely explanation for this finding is that most apoA-I is present on LpA-I/A-II. As both subparticles were reduced in the CAD group, an attempt was made to determine the relative cardioprotective roles of these subparticles in a multivariate analysis. By fixing total plasma apoA-I levels in our model, a change in the concentration of one subparticle must be accompanied by reciprocal changes in the other, since apoA-I is present either as LpA-I or as LpA-I/A-II. This analysis suggested that for a given total plasma apoA-I level, the cardioprotective effect is greater if apoA-I is found in the form of LpA-I rather than in the form of LpA-I/A-II. This is in keeping with recent work in transgenic mice which suggests that in contrast to particles containing apoA-II, those containing apoA-I are cardioprotective.

In summary, we found decreased HDL cholesterol, apoA-I, LpA-I, and LpA-I/A-II in subjects with significant CAD. Furthermore, the measurement of HDL subparticles did not add to plasma apoA-I in CAD risk assessment. However, for a given plasma apoA-I, LpA-I may be more cardioprotective than LpA-I/A-II. The results of this study suggest that although a decrease in both HDL subparticles is found in individuals with CAD, in an even exchange LpA-I is more cardioprotective than LpA-I/A-II.

	Acknowledgments

 
This study was supported by a grant from the American Heart Association, Minnesota Affiliate. T. O'Brien is a recipient of the W.L. Stephenson Fellowship in Nutrition. We appreciate the technical assistance of Mark Wentworth and the provision of samples by George Klee.

Received February 25, 1994; accepted November 28, 1994.

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