Original Article
A Prospective Study of Cholesterol, Apolipoproteins, and the Risk of Myocardial Infarction
N Engl J Med 1991; 325:373-381August 8, 1991
- Abstract
- Abstract
Background.
The independent contributions of subfractions of high-density lipoprotein (HDL) cholesterol (HDL2 and HDL3) and apolipoproteins in predicting the risk of myocardial infarction are unclear. Prospective data are sparse, but HDL2 is widely believed to be a more important predictor than HDL3.
Methods.
Blood samples were collected at base line from 14,916 men (ages, 40 to 84 years) who were participants in the Physicians' Health Study. After five years of follow-up, plasma samples from 246 men with new myocardial infarction (case subjects) were analyzed together with specimens from 246 men matched to them for age and smoking status who had not had a myocardial infarction.
Results.
The levels of total cholesterol and apolipoprotein B-100 were significantly associated with an increased risk of myocardial infarction (data on levels of low-density lipoprotein cholesterol were unavailable). Both HDL cholesterol and HDL2 levels were associated with a substantially decreased risk of myocardial infarction, but the HDL3 level was the strongest predictor; the relative risk was 0.3 (95 percent confidence interval, 0.2 to 0.6) for those in the fifth of the group with the highest HDL3 levels, as compared with the fifth with the lowest levels. The benefit of a higher HDL cholesterol level was most pronounced among those with lower total cholesterol levels. Levels of apolipoprotein A-I and apolipoprotein A-II were also associated with decreased risk. However, the levels of HDL subfractions and apolipoproteins did not add significantly to the value of a multivariate model that included the ratio of total to HDL cholesterol in predicting myocardial infarction, whereas that ratio remained a significant independent predictor of risk. After adjustment for other risk factors, a change of one unit in the ratio of total to HDL cholesterol was associated with a 53 percent change in risk (95 percent confidence interval, 26 percent to 85 percent).
Conclusions.
This study underscores the importance of HDL cholesterol in predicting the risk of myocardial infarction and demonstrates protective effects of both the HDL3 and HDL2 subfractions of HDL cholesterol. We found little or no predictive value for the levels of apolipoproteins A-I A-II, and B or HDL subfractions after conventional risk factors and the ratio of total to HDL cholesterol were considered. (N Engl J Med 1991; 325: 373–81.)
Media in This Article
Figure 1
Relative Risks of Myocardial Infarction for Subjects with Values above and below the Median for Total and HDL Cholesterol Levels.Figure 2
Relative Risk of Myocardial Infarction for Subjects in the Sample Divided According to Quintile Values for the Ratio of Total Cholesterol to HDL Cholesterol and According to Aspirin Use.Article Activity
- Article
MANY studies have demonstrated that low levels of high-density lipoprotein (HDL) cholesterol are associated with an increased risk of coronary disease and myocardial infarction.1 2 3 4 5 Nonetheless, several important questions remain to be answered, including the role of HDL cholesterol subfractions. A widely held view is that any benefit of HDL cholesterol is mainly or solely associated with the HDL2 subfraction.6 7 8 As reviewed by Miller,5 however, the evidence supporting this view is sparse; the one, small prospective study9 found that the levels of both principal subfractions (HDL2 and HDL3) were inversely related to the risk of myocardial infarction. Whether apolipoprotein levels can add to the value of total and HDL cholesterol levels in predicting the risk of myocardial infarction has also been unclear. Interest has focused as well on HDL particles with and without apolipoprotein A-II.10 We addressed these issues by analyzing blood samples collected prospectively from participants in the Physicians' Health Study.
Methods
Study Population and Collection of Specimens
The Physicians' Health Study is an ongoing randomized, double-blind, placebo-controlled trial of aspirin and beta carotene with a two-by-two factorial design.11 , 12 A total of 22,071 male physicians in the United States, who were 40 to 84 years of age in 1982, were randomly assigned to treatment groups. Men were excluded if they had a history of myocardial infarction, stroke, or transient ischemic attack, cancer (except nonmelanoma skin cancer), current renal or liver disease, peptic ulcer or gout, contraindications to aspirin use, or current use of aspirin, other platelet-active agents, or vitamin A supplements. The aspirin component of the trial was terminated on January 25, 1988, principally because a marked reduction in the frequency of myocardial infarction was observed in the aspirin group. The present analysis includes cases of myocardial infarction diagnosed before that date.
Before randomization, between August 1982 and December 1984, we sent kits for blood sampling to the participants, who were instructed to have their blood drawn into Vacutainer tubes containing EDTA, to centrifuge the blood, and to return the plasma in the polypropylene cryopreservation vials by prepaid overnight courier. The kit included a cold pack to keep the specimens cool (but not frozen) until their receipt at the Channing Laboratory the following morning, when they were divided into aliquots and stored at —80°C. During storage, no specimen thawed or warmed substantially. We received specimens from 14,916 (68 percent) of the physicians randomly assigned to treatment groups; more than 70 percent of these were received between September and November 1982.
Ascertainment and Confirmation of End Points
Cases of nonfatal myocardial infarction were reported on questionnaires returned by mail every six months by the participants. Deaths were usually reported by the families or by postal authorities. Physicians who did not respond to the questionnaires were contacted by telephone. Follow-up for nonfatal events was 99.7 percent complete, and that for fatal events was 100 percent complete. Medical records were reviewed by the End Points Committee without knowledge of the subjects' treatment assignment. All cases included in this analysis met the World Health Organization criteria for myocardial infarction,13 which require symptoms plus either elevations in cardiac-enzyme levels or diagnostic changes on the electrocardiogram. For fatal myocardial infarctions, we also accepted diagnoses based on autopsies and deaths confirmed by records as due to coronary heart disease (International Classification of Diseases codes 411 to 414). Silent infarcts discovered on routine examination were not included since they could not be assigned an accurate date of occurrence. Sudden deaths (n = 21) in men with no history of coronary disease were not included because coronary disease could not be confirmed as the cause of death.
Selection of Controls
Each subject with a confirmed myocardial infarction (case subject) was matched with a subject who was free of myocardial infarction at the time of the diagnosis (control). Controls were randomly selected from among the participants who met the matching criteria of age (±1 year), smoking status (current smoker, past smoker, or never smoked), and length of time since randomization (in 6-month intervals). Aliquots of the plasma samples from the case and control subjects were paired, with the positions varied at random within the pairs. The pairs of samples were handled together and identically throughout processing and analysis.
Laboratory Analyses
Plasma samples were analyzed in the Lipid Research Laboratory of Brigham and Women's Hospital. This laboratory participates in the standardization program for total and HDL cholesterol of the Centers for Disease Control and the National Heart, Lung and Blood Institute. Levels of apolipoprotein A-I and apolipoprotein B were calibrated to those of reference serum samples supplied by the Centers for Disease Control. All laboratory personnel were blinded as to the subjects' status (case vs. control). Total cholesterol, HDL cholesterol, and HDL3 cholesterol were measured with use of enzymatic reagents (Boehringer—Mannhcim, Indianapolis). HDL cholesterol was separated by precipitating low-density lipoprotein (LDL) and very-low-density lipoprotein cholesterol with dextran sulfate and magnesium chloride.14 HDL3 was isolated by precipitating HDL2 from total HDL cholesterol by increasing the concentrations of these reagents.14 The amount of HDL2 cholesterol was determined by subtracting HDL3 cholesterol from HDL cholesterol. We did not measure LDL cholesterol because of insufficient plasma for ultracentrifugation. However, apolipoprotein B-100 is the principal apoprotein associated with LDL particles, and its concentration reflects that of LDL cholesterol. Because most of the blood samples were drawn at random (only 15 percent were drawn after a 12-hour fast), we did not measure triglyceride levels. Apolipoproteins A-I and A-II were measured in total HDL cholesterol and in HDL3 by radial immunodiffusion (Tago, Burlingame, Calif., for apolipoprotein A-I; Daiichi Pure Chemicals, Tokyo, for apolipoprotein A-II). Apolipoprotein B-100 was measured in plasma by radial immunodiffusion at end point (Tago). HDL particles containing both apolipoprotein A-I and apolipoprotein A-II are thought to have a fixed molar ratio of 3:2 for these apoproteins.10 Hence, we could calculate the concentrations of apolipoprotein A-I in the two kinds of HDL particles, those with and those without apolipoprotein A-II.
At least one pair of specimens from a pooled plasma sample was included in each batch of 40 specimens for blinded analysis. The pooled plasma specimens were stored under the same conditions as those from the participating physicians. The coefficients of variation calculated on the basis of the analyses of these blinded samples were as follows: total cholesterol, 1.2 percent; HDL cholesterol, 2.7 percent; HDL2 cholesterol, 11.0 percent; HDL3 cholesterol, 6.9 percent; apolipoprotein A-I, 4.1 percent; apolipoprotein A-II, 5.3 percent; and apolipoprotein B-100, 12.2 percent. To examine the variation in lipid levels over time, we measured them in serum from 23 participants in the Boston area who were selected at random to provide serum samples for a compliance study.15 We assayed these samples along with aliquots of plasma from the same men collected at base line an average of 51 months earlier; the resulting correlation coefficients were 0.89 for total cholesterol, 0.72 for HDL cholesterol, 0.85 for HDL2 cholesterol, 0.50 for HDL3 cholesterol, 0.51 for apolipoprotein A-I, 0.72 for apolipoprotein A-II, and 0.90 for apolipoprotein B-100. Analysis of variance of the results of assays of serum and plasma specimens collected at the same time showed that most of the reductions in the correlations for HDL3 cholesterol, apolipoprotein A-I, and apolipoprotein A-II were due to the difference between serum and plasma rather than to the time between base line and the collection of the second sample.
Statistical Analysis
Data on coronary risk factors were collected by means of questionnaires before randomization. These included height and weight, which were used to calculate the Quetelet index (the body mass expressed as weight in kilograms divided by the square of the height in meters), systolic and diastolic blood pressure (reported by the participants), smoking habits, and history of coronary disease, diabetes, and alcohol consumption.
Univariate analyses, including paired and unpaired t-tests, were performed and Pearson's and Spearman's correlation coefficients were calculated with SAS software.16 , 17 To account for the matching variables and potential confounding factors simultaneously, we performed conditional logistic-regression analyses, using the EGRET software package18 to estimate relative risks by calculating the odds ratio. Lipid and lipoprotein levels were treated as continuous variables; we also analyzed these levels after dividing the sample into five groups according to quintiles for the distribution of values among the controls. The analysis according to quintiles required fewer assumptions about the shape of the curve relating lipid levels to the risk of myocardial infarction. All P values are two-tailed.
Results
Age and smoking were matching variables and hence distributed identically between the case subjects and the controls. As expected, the case subjects had a higher mean Quetelet index and blood pressure and a higher prevalence of angina and diabetes (Table 1Table 1
Risk Factors for Cardiovascular Disease in 246 Men with Myocardial Infarction (Case Subjects) and 246 Matched Controls in the Physicians' Health Study.*). They also had significantly higher levels of total cholesterol, higher ratios of total to HDL cholesterol, and significantly lower levels of HDL, HDL2, and HDL3 cholesterol, apolipoprotein A-I, and HDL particles without apolipoprotein A-II. Case subjects also had lower mean levels of apolipoprotein A-II and apolipoprotein A-II—containing HDL particles and higher levels of apolipoprotein B-100, but these differences were not statistically significant (Table 2Table 2
Lipid and Lipoprotein Levels in 246 Men with Myocardial Infarction (Case Subjects) and 246 Matched Controls in the Physicians' Health Study.*). Among the case subjects, 33.3 percent had plasma cholesterol levels below 5.2 mmol per liter (200 mg per deciliter, the level recommended as desirable by the National Cholesterol Education Program19), and 37.8 percent had levels between 5.2 and 6.2 mmol per liter (240 mg per deciliter, the borderline range). Among the controls, the corresponding percentages were 35.7 and 44.1.Table 3Table 3
Relative Risk of Myocardial Infarction for Fifths of the Sample in Terms of Plasma Lipid and Lipoprotein Levels, from a Matched Analysis of 246 Case–Control Pairs, after Adjustment for Age and Cigarette Smoking.* shows the relative risks of myocardial infarction and their 95 percent confidence intervals for the various levels of the lipids and lipoproteins; for each lipid or lipoprotein, the risk in each fifth of the sample is compared with that of the fifth with the lowest levels, and the P value for the test for trend across the quintiles is shown. Increasing levels of total cholesterol and apolipoprotein B-100 were associated with significant increases in the risk of myocardial infarction. Higher levels of HDL cholesterol and its subfractions and of HDL particles without apolipoprotein A-II were associated with a markedly lower risk, as were higher levels of apolipoprotein A-I and, to a lesser extent, apolipoprotein A-II and the apolipoprotein A-II—containing HDL particles (P not significant). The ratio of total to HDL cholesterol was a more powerful predictor of risk than the level of either type of cholesterol alone. Men in the highest fifth for this ratio (median, 6.35) had a relative risk of 3.73 (95 percent confidence interval, 1.95 to 7.12) as compared with men in the lowest fifth (median, 2.99). Only 9.3 percent of the subjects with myocardial infarctions had ratios of 3.5 or less, as compared with 19.1 percent of the controls, whereas 18.7 percent of the case subjects had ratios of 6.5 or more, as compared with 7.7 percent of the controls. We found that the interaction between the total cholesterol level and the HDL cholesterol level was statistically significant (P = 0.01); higher HDL cholesterol levels were more strongly associated with protection among those with lower levels of total cholesterol (Fig. 1Figure 1Relative Risks of Myocardial Infarction for Subjects with Values above and below the Median for Total and HDL Cholesterol Levels.). A similar interaction, though less strong, was also observed between the levels of apolipoprotein B-100 and HDL cholesterol.As expected, the levels of several of the lipids and apolipoproteins were highly intercorrelated. The total cholesterol level was correlated with the apolipoprotein B-100 level (r = 0.64), the HDL cholesterol level with that of apolipoprotein A-I (r = 0.79), and that of apolipoprotein A-I with that of apolipoprotein A-II (r = 0.57). Also as expected, the HDL cholesterol level was inversely related to the Quetelet index (r = 0.23), and the HDL cholesterol and HDL3 cholesterol levels were correlated with alcohol intake (r = 0.20 and 0.22). The full correlation matrix is available elsewhere.*
The percent changes in risk associated with given molar increases in the lipid or lipoprotein level (corresponding to an increase of 1 mg per deciliter) are shown in Table 4Table 4
Percent Change in the Risk of Myocardial Infarction Associated with an Increase of 1 mg per Deciliter for Each Lipid Level, after Adjustment for Age, Smoking, Other Risk Factors, and Other Lipid Levels.*. Those estimates are derived from conditional logistic regression, with use of continuous variables. For the ratio of total to HDL cholesterol, the estimated percent change in risk is that associated with a change of one unit in the ratio. The associations between the levels of specific lipids and apolipoproteins and the risk of myocardial infarction were not materially altered after additional adjustment for a history of angina, diabetes, or hypertension, assignment to the aspirin group, and Quetelet index. After such adjustment, we found that an increase of one unit in the ratio of total to HDL cholesterol was associated with an average increase in risk of 53 percent (95 percent confidence interval, 26 to 85 percent).To assess the independent predictive values of the various lipoprotein and apolipoprotein levels, we included them simultaneously in conditional logistic models (Table 4). Because total HDL cholesterol is the sum of HDL2 cholesterol and HDL3 cholesterol, we ran separate models, one that included the HDL subfractions but not total HDL cholesterol, and one with total HDL cholesterol but not the subfractions. In these models, only HDL cholesterol and total cholesterol remained significant predictors of risk. In the model with both HDL2 cholesterol and HDL3 cholesterol, only total cholesterol and HDL3 cholesterol remained significant. Although minor changes in the data set could produce substantial differences in the coefficients for different lipid levels that are highly intercorrelated (as is the case for apolipoprotein A-I with HDL and HDL3 cholesterol), there was no evidence to suggest any appreciable increase in the value of the model in predicting the risk of myocardial infarction with the addition of the levels of apolipoprotein or the HDL subfractions to a multivariate model that included the ratio of total to HDL cholesterol and nonlipid risk factors (P>0.5 by likelihood-ratio test). The same findings emerged when we considered levels of apolipoprotein A-I and apolipoprotein A-II in the specific HDL subfractions as well as the ratio of apolipoprotein A-I to apolipoprotein A-II and the ratio of apolipoprotein A-I plus apolipoprotein A-II to HDL cholesterol. Analyses omitting the 13 case subjects with a history of angina yielded virtually identical results.
To determine whether the protective effect of aspirin varied according to the lipid profile, we divided the population on the basis of the ratio of total to HDL cholesterol (Fig. 2Figure 2
Relative Risk of Myocardial Infarction for Subjects in the Sample Divided According to Quintile Values for the Ratio of Total Cholesterol to HDL Cholesterol and According to Aspirin Use.). Among men with ratios below the median value, the relative risk of myocardial infarction associated with assignment to the aspirin group was 0.46 (95 percent confidence interval, 0.27 to 0.80). In contrast, among those with ratios above the median, aspirin was apparently less beneficial; the relative risk for this group was 0.87 (95 percent confidence interval, 0.51 to 1.47). These estimates remained virtually unchanged after further adjustment for other coronary risk factors and lipid levels. The interaction between assignment to the aspirin group and the ratio of total to HDL cholesterol (as a continuous variable) was marginally significant (P = 0.05). When we divided the group separately at the median value for total cholesterol level and HDL cholesterol level, we observed similar results: those with higher cholesterol levels and lower HDL cholesterol levels appeared to benefit less from taking aspirin. The association of the ratio of total to HDL cholesterol with risk was statistically significant in both the aspirin and placebo groups.To assess the change in the predictive value of a single lipid-profile determination over time, we divided the case–control pairs into two groups according to the date of diagnosis of the cases of myocardial infarction, which ranged from 1 to 66 months after blood sampling. The pattern of differences between case subjects and controls was generally similar in the two groups. We noted a trend toward a weaker association with total cholesterol level but a stronger association with HDL cholesterol level among those with a longer period between the blood sampling and the diagnosis of infarction. After adjusting for nonlipid risk factors, we observed relative risks of 1.7 (95 percent confidence interval, 1.2 to 2.3) for a change of one unit in the ratio of total to HDL cholesterol among the men with myocardial infarction diagnosed in the first half of the interval and 1.5 (95 percent confidence interval, 1.1 to 1.9) among those with myocardial infarction diagnosed in the second half.
Discussion
In this selected population, for whom base-line blood samples were available, the HDL cholesterol level was a powerful predictor of the risk of myocardial infarction. Contrary to prevailing thought, this inverse association was not limited to the level of HDL2 cholesterol. Indeed, the level of HDL3 cholesterol was even more strongly associated with a decreased risk of myocardial infarction, but the HDL subfractions did not add significantly to the value of our model for predicting the risk of myocardial infarction after we considered the ratio of total to HDL cholesterol. This ratio was a particularly strong discriminator of risk; a change of one unit in this ratio corresponded to a 37 percent change in risk (53 percent after adjustment for risk factors for coronary disease). Although apolipoproteins A-I, A-II, and B-100 and the concentration of apolipoprotein A-I in HDL particles without apolipoprotein A-II were significant predictors of risk individually, they did not contribute materially to the prediction of the risk of myocardial infarction after the ratio of total to HDL cholesterol was taken into consideration, or when total and HDL cholesterol were considered as separate variables in the multiple regression analysis. LDL cholesterol levels were not available. Had they been available, it is possible that the ratio of LDL to HDL cholesterol might have been a better predictor of risk than the ratio of total to HDL cholesterol. However, the level of apolipoprotein B-100, the main apoprotein in LDL, used as a surrogate for LDL in calculating such a ratio, was not as good a predictor as the ratio of total to HDL cholesterol.
The prospective collection of blood rules out any effect of the diagnosis on lipid levels, either directly or through behavioral changes that may affect lipids. The laboratory was standardized by the Centers for Disease Control, thus reducing potential misclassifications due to laboratory error, although these analyses were based on a single venipuncture. Our data and those of others20 show that a single measurement provides a reasonable but imperfect assessment of the true long-term level. Because this error, due to both variability in laboratory procedures and biologic variability, is random with respect to the outcome of disease, it will cause the true relation between the lipid level and the risk of myocardial infarction to be underestimated.
In general, participants in the Physicians' Health Study are unusually healthy, with cardiovascular mortality only 15 percent that of the general population of white men of comparable age in the United States, and they have lower levels of total cholesterol than have been found in other studies. For example, in the Framingham Study,4 the mean value for the population (5.73 mmol per liter) was higher than that of the controls (5.52) and about the same as that for case subjects in our study (5.72). Despite these differences, the findings are consistent with those of other studies,21 which showed that HDL cholesterol was the single best predictor of the risk of myocardial infarction. In our data, the 0.7 percent increase in risk associated with an increase of 0.026 mmol per liter (1 mg per deciliter) in the total cholesterol level (after adjustment for other risk factors) was similar to the 0.5 percent increase in risk observed in the Framingham Study.22 We observed a 3.5 percent decrease in risk associated with an increase of 0.026 mmol per liter (1 mg per deciliter) in the HDL cholesterol level, also similar to the Framingham finding of a 3.1 percent decrease in risk.22
Several studies have examined the relation between subfractions of HDL cholesterol and the risk of coronary disease5 , 23 among survivors of myocardial infarctions or among patients with angiographically documented atherosclerosis24 25 26 27 28 and healthy controls. These studies have generally found significantly lower levels of HDL2 among the survivors of myocardial infarction than among the controls,29 30 31 32 33 34 and several have also observed significantly lower levels of HDL3 among the patients with myocardial infarction.30 , 32 , 34 Generally, the differences were more pronounced for HDL2. Two studies35 , 36 found, however, that HDL3 but not HDL2 was significantly associated with the extent of atherosclerosis.
We are aware of only one other published prospective study of the relation between subfractions of HDL cholesterol and the risk of myocardial infarction, a follow-up study of 1961 men.9 The 38 participants in whom clinical coronary disease subsequently developed had significantly lower levels of both HDL2 and HDL3 cholesterol, but the statistical significance of the association was greater for HDL2; no multivariate analysis was reported.
As in most studies relating apolipoprotein A-I levels to coronary disease, we found that the case subjects had significantly lower levels of apolipoprotein A-I than the controls.5 Most of these studies compared the levels among survivors of myocardial infarction37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 or patients with angiographic evidence of atherosclerosis24 , 26 , 52 53 54 55 56 57 58 59 60 61 62 with those of controls. The results of these cross-sectional studies differed about whether HDL cholesterol was a better predictor of risk than apolipoprotein A-I. In three previous small, prospective studies of apolipoprotein A-I, comprising a total of 144 case subjects,63 64 65 the subjects in whom coronary disease was subsequently diagnosed had significantly lower levels of apolipoprotein A-I than those who did not. In the two previous studies in which HDL cholesterol was also measured,63 , 64 it was a better discriminator of the risk of myocardial infarction than apolipoprotein A-I. This finding is consistent with our results in studying 246 matched case–control pairs. Previous studies have been far less consistent in showing an inverse association between the level of apolipoprotein A-I and the risk of myocardial infarction.5 Although one study of survivors of infarction and controls44 found apolipoprotein A-II to be a better independent predictor of risk than HDL cholesterol or apolipoprotein A-I, several others have found either weaker associations or none at all between apolipoprotein A-II levels and the risk of myocardial infarction.24 , 45 , 47 , 49 , 53 , 55 , 59 , 61
Recently, attention has focused on HDL particles that contain apolipoprotein A-I but not apolipoprotein A-II.10 Although the levels of these particles were not significant independent predictors of risk after we accounted for the ratio of total to HDL cholesterol, our results do not rule out the possibility that these particles may be biologically relevant in the mechanisms leading to myocardial infarction. The calculation of their concentration requires measuring apolipoprotein A-I and apolipoprotein A-II, both of which can be assayed less accurately than total and HDL cholesterol. At present, the measurement of HDL particles without apolipoprotein A-II does not appear to be useful in the clinical assessment of risk, but a more accurate assay might have predictive value.
In the Physicians' Health Study, a benefit of aspirin was observed at all levels, but it was greater among the men who reported lower cholesterol levels (test for difference in the effect, P = 0.04).12 The present findings, based on measured levels of lipids, demonstrate this interaction more clearly. It is still likely that aspirin has benefit among those with a less favorable lipid profile, but its effect is not as pronounced as among those with a low ratio of total to HDL cholesterol.
We draw three main conclusions from these results. First, in this population the total HDL cholesterol level was a powerful predictor of the risk of myocardial infarction, and the inverse association appeared stronger for men with lower levels of total cholesterol. Second, we found that the levels of both the HDL2 and the HDL3 subfractions of HDL cholesterol were inversely associated with the risk of myocardial infarction; indeed, HDL3 appeared to be a better predictor of risk than HDL2. Third, the levels of the HDL subfractions, the levels of apolipoproteins A-I and B-100, and the concentration of HDL particles without apolipoprotein A-II were significantly related to the risk of myocardial infarction, but none were independently predictive of infarction after standard risk factors and the ratio of total to HDL cholesterol had been considered. Although further studies of the lipoprotein subclasses and apolipoproteins are vital, it is premature to recommend the use of their concentrations as indicators of risk in clinical practice. Our findings suggest that increased attention should be given to HDL cholesterol levels, however, not only when the serum cholesterol level is high (as recommended by the National Cholesterol Education Program19), but also when the total cholesterol level is not elevated.
Supported by research grants (CA 42182, HL 26490, HL 34595, CA 34944, and CA 40360) from the National Institutes of Health, and by an Established Investigator Award to Dr. Sacks from the American Heart Association.
We are indebted to the members of the Steering Committee of the Physicians' Health Study — Charlene Belanger, M.A., Julie E. Buring, Sc.D., Nancy Cook, Sc.D., Kimberly Eberlein, M.P.H., Samuel Z. Goldhaber, M.D., David Gordon, M.A., Sherry L. Mayrent, Ph.D., Richard Peto, F.R.S., Bernard Rosner, Ph.D., Fran Stubblefield, B.S., Thomas Blazkowski, Ph.D. (ex officio), and Andrew Vargosko, Ph.D. (ex officio); to the members of the End Points Committee — Harris Funkenstein, M.D. (deceased), Samuel Z. Goldhaber, M.D., and James O. Taylor, M.D. (chair); and to Stefanie Bechtel, Mary Ann O'Hanesian, Laura Newcomer, Mary Lou Lyons, and Georgina Friedenberg for their skilled assistance.
Source Information
From the Channing Laboratory, Departments of Medicine (M.J.S., F.M.S., S.S., W.C.W., C.H.H.) and Preventive Medicine (C.H.H.), Brigham and Women's Hospital and Harvard Medical School, and the Departments of Epidemiology (M.J.S., W.C.W.) and Nutrition (W.C.W.), Harvard School of Public Health, all in Boston. Address reprint requests to Dr. Stampfer at the Channing Laboratory, 180 Longwood Ave., Boston, MA 02115.
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CrossRef | Web of Science | Medline65
Salonen
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- Citing Articles (278)
Citing Articles
1
Roger Mallol, Miguel A. Rodríguez, Mercedes Heras, Maria Vinaixa, Núria Plana, Lluís Masana, Gareth A. Morris, Xavier Correig. (2012) Particle size measurement of lipoprotein fractions using diffusion-ordered NMR spectroscopy. Analytical and Bioanalytical Chemistry
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Deren Wang, Wendan Tao, Zilong Hao, Ming Liu, Ming Liu. 2012. Fibrates for secondary prevention of cardiovascular disease and stroke. .
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Kurt R. Schumacher, Robert J. Gajarski, Simon Urschel. (2012) Pediatric Coronary Allograft Vasculopathy-A Review of Pathogenesis and Risk Factors. Congenital Heart Diseaseno-no
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2011. Epidemiology. , 113-160.
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Patty W. Siri-Tarino. (2011) Effects of Diet on High-Density Lipoprotein Cholesterol. Current Atherosclerosis Reports 13:6, 453-460
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L. Camont, J. Chapman, A. Kontush. (2011) Functionality of HDL particles: Heterogeneity and relationships to cardiovascular disease. Archives of Cardiovascular Diseases Supplements 3:4, 258-266
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E L Vyth, M A H Hendriksen, A J C Roodenburg, I H M Steenhuis, J M A van Raaij, H Verhagen, J Brug, J C Seidell. (2011) Consuming a diet complying with front-of-pack label criteria may reduce cholesterol levels: a modeling study. European Journal of Clinical Nutrition
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Kerry-Anne Rye, Philip J. Barter. (2011) Predictive value of different HDL particles for the protection against or risk of coronary heart disease. Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
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V. V. Miroshnikova, T. I. Rodygina, E. P. Demina, P. S. Kurjanov, S. A. Urazgildeeva, V. S. Gurevich, A. L. Schwarzman. (2011) Association of apoprotein A-1 genetic variants with development of atherosclerosis in the population of St. Petersburg. Russian Journal of Genetics: Applied Research 1:5, 411-415
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Zinat Nadia Hatmi, Mitra Mahdavi-Mazdeh, Seyed Saeid Hashemi-Nazari, Ebrahim Hajighasemi, Behnaz Nozari, Azita Mahdavi. (2011) Trend of lipid ratios associated with well known risk factors of coronary artery disease in different age: A population based study of 31,999 healthy individuals. International Journal of Cardiology 151:3, 328-332
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Yoshiyuki Kawano, Akira Tamura, Junichi Kadota. (2011) Association between the severity of obstructive sleep apnea and the ratio of low-density lipoprotein cholesterol to high-density lipoprotein cholesterol. Metabolism
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Chang-Nam Ko, Seong-Uk Park, Gyu-Tae Chang, Woo-Sang Jung, Sang-Kwan Moon, Jung-Mi Park, Ki-Ho Cho. (2011) Antihyperlipidemic and Antioxidant Effects of the Mixture of Ginseng Radix and Crataegi Fructus: Experimental Study and Preliminary Clinical Results. Journal of Ginseng Research 35:2, 162-169
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Carlos G. Santos-Gallego, Chiara Giannarelli, Juan José Badimón. (2011) Experimental Models for the Investigation of High-Density Lipoprotein–Mediated Cholesterol Efflux. Current Atherosclerosis Reports 13:3, 266-276
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Dan Yang, Xianbao Liu, Meixiang Xiang. (2011) The Correlation between Lipids Ratio and Degree of Coronary Artery Stenosis. High Blood Pressure & Cardiovascular Prevention 18:2, 53-56
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Deniz Agirbasli, Beyazit Cirakoglu, Fatih Eren, Mutlu Sumerkan, Sukru Aksoy, Cenk Aral, Mehmet Agirbasli. (2011) Effects of lecithin: Cholesterol acyltransferase genotypes, enzyme levels, and activity on high-density lipoprotein levels. Journal of Clinical Lipidology 5:3, 152-158
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Stephanie J. Morris, Mary Chester M. Wasko, Jana L. Antohe, Jennifer A. Sartorius, H. Lester Kirchner, Sorina Dancea, Androniki Bili. (2011) Hydroxychloroquine use associated with improvement in lipid profiles in rheumatoid arthritis patients. Arthritis Care & Research 63:4, 530-534
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José R. González-Juanatey, Jesús Millán, Eduardo Alegría, Carlos Guijarro, Jose V. Lozano, Gustavo C. Vitale. (2011) Prevalencia y características de la dislipemia en pacientes en prevención primaria y secundaria tratados con estatinas en España. Estudio DYSIS-España. Revista Española de Cardiología 64:4, 286-294
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Meriam Messedi, Kamel Jamoussi, Makram Frigui, François Laporte, Mouna Turki, Khansa Chaabouni, Emna Mnif, Moez Jaloulli, Neila Kaddour, Zouhir Bahloul, Fatma Ayedi. (2011) Atherogenic Lipid Profile in Behçet’s Disease: Evidence of Alteration of HDL Subclasses. Archives of Medical Research 42:3, 211-218
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Paul Muntner, Fleur Lee, Brad C. Astor. (2011) Association of High-Density Lipoprotein Cholesterol With Coronary Heart Disease Risk Across Categories of Low-Density Lipoprotein Cholesterol: The Atherosclerosis Risk in Communities Study. The American Journal of the Medical Sciences 341:3, 173-180
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José R. González-Juanatey, Jesús Millán, Eduardo Alegría, Carlos Guijarro, Jose V. Lozano, Gustavo C. Vitale. (2011) Prevalence and Characteristics of Lipid Abnormalities in Patients Treated With Statins in Primary and Secondary Prevention in Spain. DYSIS-Spain Study. Revista Española de Cardiología (English Edition)
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Mark S. Nash, John E. Lewis, Trevor A. Dyson-Hudson, Yaga Szlachcic, Florence Yee, Armando J. Mendez, Ann M. Spungen, William A. Bauman. (2011) Safety, Tolerance, and Efficacy of Extended-Release Niacin Monotherapy for Treating Dyslipidemia Risks in Persons With Chronic Tetraplegia: A Randomized Multicenter Controlled Trial. Archives of Physical Medicine and Rehabilitation 92:3, 399-410
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Paul T. Williams, Daniel E. Feldman. (2011) Prospective study of coronary heart disease vs. HDL2, HDL3, and other lipoproteins in Gofman's Livermore Cohort. Atherosclerosis 214:1, 196-202
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Anselm K. Gitt, Claus Jünger, Wenefrieda Smolka, Kurt Bestehorn. (2010) Prevalence and overlap of different lipid abnormalities in statin-treated patients at high cardiovascular risk in clinical practice in Germany. Clinical Research in Cardiology 99:11, 723-733
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Angel Brea Hernando, José Puzo Foncillas. (2010) Enfermedad del hígado graso no alcohólico y riesgo cardiovascular. Clínica e Investigación en Arteriosclerosis 22:6, 259-271
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Kiran Musunuru. (2010) Atherogenic Dyslipidemia: Cardiovascular Risk and Dietary Intervention. Lipids 45:10, 907-914
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Naim Alkhouri, Tarek Abu-Rajab Tamimi, Lisa Yerian, Rocio Lopez, Nizar N. Zein, Ariel E. Feldstein. (2010) The Inflamed Liver and Atherosclerosis: A Link Between Histologic Severity of Nonalcoholic Fatty Liver Disease and Increased Cardiovascular Risk. Digestive Diseases and Sciences 55:9, 2644-2650
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M. J. L. Peters, A. E. Voskuyl, N. Sattar, B. A. C. Dijkmans, Y. M. Smulders, M. T. Nurmohamed. (2010) The interplay between inflammation, lipids and cardiovascular risk in rheumatoid arthritis: why ratios may be better. International Journal of Clinical Practice 64:10, 1440-1443
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Xavier Pintó, Jesús Millán, Anna Muñoz, Emili Corbella, Antonio Hernández-Mijares, Manuel Zuñiga, Alipio Mangas, Juan Pedro-Botet. (2010) A Very High Prevalence of Low HDL Cholesterol in Spanish Patients With Acute Coronary Syndromes. Clinical Cardiology 33:7, 418-423
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Coleman Pratt. (2010) Alternative Prevention and Treatment of Cardiovascular Disease Part 1. Primary Care: Clinics in Office Practice 37:2, 325-337
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Eric Bruckert, Julien Labreuche, Pierre Amarenco. (2010) Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis. Atherosclerosis 210:2, 353-361
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VALERIO NOBILI, NAIM ALKHOURI, ANDREA BARTULI, MELANIA MANCO, ROCIO LOPEZ, ANNA ALISI, ARIEL E. FELDSTEIN. (2010) Severity of Liver Injury and Atherogenic Lipid Profile in Children With Nonalcoholic Fatty Liver Disease. Pediatric Research 67:6, 665-670
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Valentina Remig, Barry Franklin, Simeon Margolis, Georgia Kostas, Theresa Nece, James C. Street. (2010) Trans Fats in America: A Review of Their Use, Consumption, Health Implications, and Regulation. Journal of the American Dietetic Association 110:4, 585-592
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J. V. Patel, A. Abraheem, J. Creamer, M. Gunning, E. A. Hughes, G. Y.H. Lip. (2010) Apolipoproteins in the discrimination of atherosclerotic burden and cardiac function in patients with stable coronary artery disease. European Journal of Heart Failure 12:3, 254-259
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Arnold von Eckardstein. (2010) Implications of torcetrapib failure for the future of HDL therapy: is HDL-cholesterol the right target?. Expert Review of Cardiovascular Therapy 8:3, 345-358
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Mariann Harangi, Ildikó Seres, János Harangi, György Paragh. (2009) Benefits and Difficulties in Measuring HDL Subfractions and Human Paraoxonase-1 Activity During Statin Treatment. Cardiovascular Drugs and Therapy 23:6, 501-510
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Danielle M. Hack, Peter L. Bordi, S. William Hessert. (2009) Nutrition, sensory evaluation, and performance analysis of hydrogenated frying oils. International Journal of Food Sciences and Nutrition 60:8, 647-661
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M.T. Cooney, A. Dudina, D. De Bacquer, L. Wilhelmsen, S. Sans, A. Menotti, G. De Backer, P. Jousilahti, U. Keil, T. Thomsen, P. Whincup, I.M. Graham. (2009) HDL cholesterol protects against cardiovascular disease in both genders, at all ages and at all levels of risk. Atherosclerosis 206:2, 611-616
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Emilie Counil, Pierre Julien, Benoit Lamarche, Marie-Ludivine Château-Degat, Annie Ferland, Eric Dewailly. (2009) Association between trans-fatty acids in erythrocytes and pro-atherogenic lipid profiles among Canadian Inuit of Nunavik: possible influences of sex and age. British Journal of Nutrition 102:05, 766
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Palle V. R. Acharyulu, P. K. Dubey, P. V. V. Prasada Reddy, Thatipally Suresh. (2009) Synthesis of Novel New 2-(2-(4-((3,4-Dihydro-4-oxo-3-aryl quinazolin-2-yl)methyl)piperazin-1-yl)acetoyloxy)-2-phenyl Acetic Acid Esters. Synthetic Communications 39:18, 3217-3231
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Hassanali Vatanparast, Philip D. Chilibeck, Stephen M. Cornish, Jonathan P. Little, Lisa S. Paus-Jenssen, Allison M. Case, H. Jay Biem. (2009) DXA-derived Abdominal Fat Mass, Waist Circumference, and Blood Lipids in Postmenopausal Women. Obesity 17:8, 1635-1640
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Diana R. Chirovsky, Veronika Fedirko, Yadong Cui, Vasilisa Sazonov, Philip Barter. (2009) Prospective studies on the relationship between high-density lipoprotein cholesterol and cardiovascular risk: a systematic review. European Journal of Cardiovascular Prevention & Rehabilitation 16:4, 404-423
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Peter W. Parodi. (2009) Has the association between saturated fatty acids, serum cholesterol and coronary heart disease been over emphasized?. International Dairy Journal 19:6-7, 345-361
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Richard I. Levin. (2009) Arginine and Old MACE. Journal of the American College of Cardiology 53:22, 2068-2069
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Yuji Hirowatari, Yuko Tsunoda, Yutaka Ogura, Yasuhiko Homma. (2009) Analyzing of high-density lipoprotein subfractions and low-density lipoprotein subfractions in human serum with anion-exchange chromatography. Atherosclerosis 204:2, e52-e57
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Cristina Benincá, Everton Fernando Zanoelo, Luiz Fernando de Lima Luz, Cinthia Bittencourt Spricigo. (2009) Trans fatty acids in margarines marketed in Brazil: Content, labeling regulations and consumer information. European Journal of Lipid Science and Technology 111:5, 451-458
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Mariann Harangi, Hossein Z. Mirdamadi, Ildikó Seres, Ferenc Sztanek, Miklós Molnár, Andrea Kassai, Zoltán Derdák, László Illyés, György Paragh. (2009) Atorvastatin effect on the distribution of high-density lipoprotein subfractions and human paraoxonase activity. Translational Research 153:4, 190-198
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Danielle M. Hack, Peter L. Bordi, S. William Hessert. (2009) Nutrition, Sensory Evaluation, and Performance Analysis of Trans fat-Free, Low Alpha-Linolenic Acid Frying Oils. Journal of Foodservice Business Research 12:1, 42-54
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P. Mason, S. C. Porter, S. E. Berry, P. Stillman, C. Steele, A. Kirby, B. A. Griffin, A. M. Minihane. (2009) Saturated fatty acid consumption: outlining the scale of the problem and assessing the solutions. Nutrition Bulletin 34:1, 74-84
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Danladi I Musa, Samuel A Adeniran, A U Dikko, Stephen P Sayers. (2009) The Effect of a High-Intensity Interval Training Program on High-Density Lipoprotein Cholesterol in Young Men. Journal of Strength and Conditioning Research 23:2, 587-592
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Tanja X. Pedersen, Susanne Bro, Mikkel H. Andersen, Michael Etzerodt, Matti Jauhiainen, Søren Moestrup, Lars B. Nielsen. (2009) Effect of treatment with human apolipoprotein A-I on atherosclerosis in uremic apolipoprotein-E deficient mice. Atherosclerosis 202:2, 372-381
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Leandro A. Diehl, Bruno A. Fabris, Décio S Barbosa, Eliana C. De Faria, Susana L. Wiechmann, Alexandre J.F. Carrilho. (2008) Metformin Increases HDL3–Cholesterol and Decreases Subcutaneous Truncal Fat in Nondiabetic Patients with HIV-Associated Lipodystrophy. AIDS Patient Care and STDs 22:10, 779-786
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W A Bauman, A M Spungen. (2008) Coronary heart disease in individuals with spinal cord injury: assessment of risk factors. Spinal Cord 46:7, 466-476
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Maria C.A. Stene, Ruth Frikke-Schmidt, Børge G. Nordestgaard, Peer Grande, Peter Schnohr, Anne Tybjærg-Hansen. (2008) Functional Promoter Variant in Zinc Finger Protein 202 Predicts Severe Atherosclerosis and Ischemic Heart Disease. Journal of the American College of Cardiology 52:5, 369-377
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R P Mensink. (2008) Effects of products made from a high-palmitic acid, trans-free semiliquid fat or a high-oleic acid, low-trans semiliquid fat on the serum lipoprotein profile and on C-reactive protein concentrations in humans. European Journal of Clinical Nutrition 62:5, 617-624
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Grace Jooyoung Shin, Sina Vakili, Marie Caudill. 2008. Customizing Dietary Recommendations By Genotype In The Era Of Genomics. , 155-171.
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Kevin A. Harvey, Tyler Arnold, Tamkeen Rasool, Caryl Antalis, Steven J. Miller, Rafat A. Siddiqui. (2008) Trans-fatty acids induce pro-inflammatory responses and endothelial cell dysfunction. British Journal of Nutrition 99:04,
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Sonja de Groot, Annet J. Dallmeijer, Marcel W. Post, Edmond L. Angenot, Rita J. van den Berg-Emons, Luc H. van der Woude. (2008) Prospective Analysis of Lipid Profiles in Persons With a Spinal Cord Injury During and 1 Year After Inpatient Rehabilitation. Archives of Physical Medicine and Rehabilitation 89:3, 531-537
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Guido Franceschini, Laura Calabresi. (2008) Raising HDL cholesterol for cardiovascular disease prevention: Is this still feasible?. Current Cardiovascular Risk Reports 2:1, 35-40
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M. GRØNBAEK. (2008) Factors influencing the relation between alcohol and mortality - with focus on wine. Journal of Internal Medicine 250:4, 291
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Peter L. Bordi, Danielle M. Hack, Michele D. Rager, S. William Hessert. (2007) Sensory comparison of doughnuts fried in trans fat-free oil to those fried in oil containing trans fats. Journal of Foodservice 18:6, 227-237
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Madhuri Vemuri, Darshan Kelley. 2007. The Effects of Dietary Fatty Acids on Lipid Metabolism. , 591-630.
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Zach Pitluk, Iya Khalil. (2007) Achieving confidence in mechanism for drug discovery and development. Drug Discovery Today 12:21-22, 924-930
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J. Evans, M. Collins, C. Jennings, L. van der Merwe, I. Soderstrom, T. Olsson, N. S. Levitt, E. V. Lambert, J. H. Goedecke. (2007) The association of interleukin-18 genotype and serum levels with metabolic risk factors for cardiovascular disease. European Journal of Endocrinology 157:5, 633-640
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Peter L. Bordi, Michele D. Rager, Danielle M. Hack, S. William Hessert. (2007) Development and sensory evaluation of a trans fat-free sugar cookie. Journal of Foodservice 18:5, 167-175
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Michael H. Davidson. (2007) Targeting High-Density Lipoprotein Cholesterol in the Management of Cardiovascular Disease. The American Heart Hospital Journal 5:4, 210-216
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D Mozaffarian, M Abdollahi, H Campos, A HoushiarRad, W C Willett. (2007) Consumption of trans fats and estimated effects on coronary heart disease in Iran. European Journal of Clinical Nutrition 61:8, 1004-1010
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Kikuo Isoda, Eduardo J. Folco, Koichi Shimizu, Peter Libby. (2007) AGE-BSA decreases ABCG1 expression and reduces macrophage cholesterol efflux to HDL. Atherosclerosis 192:2, 298-304
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William C. Cromwell. (2007) High-density lipoprotein associations with coronary heart disease: Does measurement of cholesterol content give the best result?. Journal of Clinical Lipidology 1:1, 57-64
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Jean-Charles Hogue, Benoît Lamarche, Daniel Gaudet, André J. Tremblay, Jean-Pierre Després, Jean Bergeron, Claude Gagné, Patrick Couture. (2007) Association of heterozygous familial hypercholesterolemia with smaller HDL particle size. Atherosclerosis 190:2, 429-435
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Sunčica Kojić-Damjanov, Mirjana đerić, Velibor Čabarkapa, Ljiljana Vučurević-Ristić. (2007) Significance of Determining Levels of Apolipoproteins A-I and B in the Diagnostics and Assessment of Lipid-Related Atherogenic Risk in Hyperalpha-Lipoproteinemia, Hypocholesterolemia and Hypo-Hdl-Cholesterolemia. Journal of Medical Biochemistry 26:3, 206-214
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André J. Tremblay, Allan D. Sniderman, Claude Gagné, Jean Bergeron, Patrick Couture. (2007) Differential impact of plasma triglycerides on HDL-cholesterol and HDL-apo A-I in a large cohort. Clinical Biochemistry 40:1-2, 25-29
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Alexander Chernobelsky, M. Dominique Ashen, Roger S Blumenthal, Neil L. Coplan. (2007) High-Density Lipoprotein Cholesterol: A Potential Therapeutic Target for Prevention of Coronary Artery Disease. Preventive Cardiology 10:1, 26-30
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Ursula S. Schwab, James C. Callaway, Arja T. Erkkilä, Jukka Gynther, Matti I.J. Uusitupa, Tomi Järvinen. (2006) Effects of hempseed and flaxseed oils on the profile of serum lipids, serum total and lipoprotein lipid concentrations and haemostatic factors. European Journal of Nutrition 45:8, 470-477
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Brendan M. Everett, Tobias Kurth, Julie E. Buring, Paul M. Ridker. (2006) The Relative Strength of C-Reactive Protein and Lipid Levels as Determinants of Ischemic Stroke Compared With Coronary Heart Disease in Women. Journal of the American College of Cardiology 48:11, 2235-2242
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B. Aisbitt, J. L. Buttriss. (2006) Trans fats ? should we be worried?. Nutrition Bulletin 31:4, 279-281
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P L Zock. (2006) Do favourable effects of increasing unsaturated fat intake on cardiovascular disease risk outweigh the potential adverse effect on body weight?. International Journal of Obesity 30, S10-S15
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Paul M. Yip, Man Khun Chan, Joanna Nelken, Nathalie Lepage, George Brotea, Khosrow Adeli. (2006) Pediatric reference intervals for lipids and apolipoproteins on the VITROS 5,1 FS Chemistry System. Clinical Biochemistry 39:10, 978-983
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Peter P Toth, Antonio M Gotto. 2006. High-Density Lipoprotein Cholesterol. , 295-340.
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Bela F. Asztalos, Serkalem Demissie, L. Adrienne Cupples, Dorothea Collins, Caitlin E. Cox, Katalin V. Horvath, Hanna E. Bloomfield, Sander J. Robins, Ernst J. Schaefer. (2006) LpA-I, LpA-I:A-II HDL and CHD-risk: The Framingham Offspring Study and the Veterans Affairs HDL Intervention Trial. Atherosclerosis 188:1, 59-67
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Natalie Khuseyinova, Wolfgang Koenig. (2006) Apolipoprotein A-I and risk for cardiovascular diseases. Current Atherosclerosis Reports 8:5, 365-373
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F. Hadaegh, H. Harati, A. Ghanbarian, F. Azizi. (2006) Association of total cholesterol versus other serum lipid parameters with the short-term prediction of cardiovascular outcomes: Tehran Lipid and Glucose Study. European Journal of Cardiovascular Prevention & Rehabilitation 13:4, 571-577
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Sepideh Mansoub, Man Khun Chan, Khosrow Adeli. (2006) Gap analysis of pediatric reference intervals for risk biomarkers of cardiovascular disease and the metabolic syndrome. Clinical Biochemistry 39:6, 569-587
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A. THOMPSON, J. DANESH. (2006) Associations between apolipoprotein B, apolipoprotein AI, the apolipoprotein B/AI ratio and coronary heart disease: a literature-based meta-analysis of prospective studies. Journal of Internal Medicine 259:5, 481-492
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O. FAERGEMAN. (2006) Introduction: Apolipoproteins and guidelines for prevention of cardiovascular disease. Journal of Internal Medicine 259:5, 434-436
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Amy E. Griel, Penny M. Kris-Etherton. (2006) Beyond Saturated Fat: The Importance of the Dietary Fatty Acid Profile on Cardiovascular Disease. Nutrition Reviews 64:5, 257-262
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Mozaffarian, Dariush, Katan, Martijn B., Ascherio, Alberto, Stampfer, Meir J., Willett, Walter C., . (2006) Trans Fatty Acids and Cardiovascular Disease. New England Journal of Medicine 354:15, 1601-1613
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Carolyn M. Hutter, Melissa A. Austin, Federico M. Farin, Hannah-Malia Viernes, Karen L. Edwards, Donna L. Leonetti, Marguerite J. McNeely, Wilfred Y. Fujimoto. (2006) Association of endothelial lipase gene (LIPG) haplotypes with high-density lipoprotein cholesterol subfractions and apolipoprotein AI plasma levels in Japanese Americans. Atherosclerosis 185:1, 78-86
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P K Shah. (2006) HDL/apoA-I infusion for atherosclerosis management: an emerging therapeutic paradigm. Future Lipidology 1:1, 55-64
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Morten Grønbæk. (2006) Factors influencing the relation between alcohol and cardiovascular disease. Current Opinion in Lipidology 17:1, 17-21
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Fabio L. Sodré, Vera S. Castanho, Lucia N. Castilho, Silvia de Barros-Mazon, Eliana C. de Faria. (2006) High-density lipoprotein subfractions in normolipidemic individuals without clinical atherosclerosis lipoprotein subfractions in an adult population. Journal of Clinical Laboratory Analysis 20:3, 113-117
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J. Bruce German, Cora J. Dillard. (2006) Composition, Structure and Absorption of Milk Lipids: A Source of Energy, Fat-Soluble Nutrients and Bioactive Molecules. Critical Reviews in Food Science and Nutrition 46:1, 57-92
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P. L. Zock. 2006. Health problems associated with saturated and trans fatty acid intake. , 3-24.
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Tricia Psota, Kirsten Hilpert, Sarah Gebauer, Penny Kris-Etherton, Amy Griel, Yumei Coa. 2005. New Insights on the Role of Lipids and Lipoproteins in Cardiovascular Disease. , 211-263.
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Stephen Crouse. 2005. Acute Changes in Lipids and Lipoprotein-Lipids Induced by Exercise. , 283-298.
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K.A.J. Al Khaja, R.P. Sequeira, A.H.H. Damanhori. (2005) Comparison of the quality of diabetes care in primary care diabetic clinics and general practice clinics. Diabetes Research and Clinical Practice 70:2, 174-182
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Benjamin Lee, Chi-Jen Lee, Lucia Lee, Christopher Wu. 2005. Drugs for Treatment of Disorders of Lipid Metabolism. , 355-362.
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San-Chiang Wu, Jeng-Chuan Shiang, Shoa-Lin Lin, Te-Lang Wu, Wei-Chun Huang, Kuan-Rau Chiou, Chun-Peng Liu. (2005) Efficacy and safety of statins in hypercholesterolemia with emphasis on lipoproteins. Heart and Vessels 20:5, 217-223
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R. Estruch, E. Sacanella. (2005) Alcohol: ¿tónico o tóxico cardiovascular?. Clínica e Investigación en Arteriosclerosis 17:4, 183-195
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Ingrid Anderz??n, Bengt B. Arnetz. (2005) The Impact of a Prospective Survey-Based Workplace Intervention Program on Employee Health, Biologic Stress Markers, and Organizational Productivity. Journal of Occupational and Environmental Medicine 47:7, 671-682
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Xiang Guang-da, Yang Xiang-jiu, Zhao Lin-shuang, Chen Zhi-song, He Yu-sheng. (2005) Apolipoprotein e4 allele and the risk of CAD death in type 2 diabetes mellitus with ischaemia electrocardiographic change. Diabetes Research and Clinical Practice 68:3, 223-229
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Irene Lagogianni, Aggeliki Papapanagiotou, Christina Piperi, Christos Kalofoutis, George Troupis, Ariadni Zachari, Anastasios Kalofoutis. (2005) Evidence of reduced plasma HDL subfractions in patients with cutaneous discoid lupus erythematosus. Clinical Biochemistry 38:3, 286-290
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Margreet R. Olthof, Trinette van Vliet, Petra Verhoef, Peter L. Zock, Martijn B. Katan. (2005) Effect of Homocysteine-Lowering Nutrients on Blood Lipids: Results from Four Randomised, Placebo-Controlled Studies in Healthy Humans. PLoS Medicine 2:5, e135
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Naja Rod Nielsen, Lau Caspar Thygesen, Ditte Johansen, Gorm Jensen, Morten grøNbæk. (2005) The influence of duration of follow-up on the association between alcohol and cause-specific mortality in a prospective cohort study. Annals of Epidemiology 15:1, 44-55
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J.P.H. van Wijk, R. Buirma, A. van Tol, C.J.M. Halkes, P.P.Th. De Jaegere, H.W.M. Plokker, Y.J.M. van der Helm, M. Castro Cabezas. (2005) Effects of increasing doses of simvastatin on fasting lipoprotein subfractions, and the effect of high-dose simvastatin on postprandial chylomicron remnant clearance in normotriglyceridemic patients with premature coronary sclerosis. Atherosclerosis 178:1, 147-155
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J. A. Gimeno-Orna, E. Faure-Nogueras, M. A. Sancho-Serrano. (2005) Usefulness of total cholesterol/HDL-cholesterol ratio in the management of diabetic dyslipidaemia. Diabetic Medicine 22:1, 26-31
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Ute Panzenböck, Roland Stocker. (2005) Formation of methionine sulfoxide-containing specific forms of oxidized high-density lipoproteins. Biochimica et Biophysica Acta (BBA) - Proteins & Proteomics 1703:2, 171-181
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Simin Liu, Yiqing Song, Frank B. Hu, Tianhua Niu, Jing Ma, Michael Gaziano, Meir J. Stampfer. (2004) A prospective study of the APOA1 XmnI and APOC3 SstI polymorphisms in the APOA1/C3/A4 gene cluster and risk of incident myocardial infarction in men. Atherosclerosis 177:1, 119-126
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Christopher A. Girkin, William B. Kannel, David S. Friedman, Robert N. Weinreb. (2004) Glaucoma risk factor assessment and prevention: Lessons from coronary heart disease. American Journal of Ophthalmology 138:3, 11-18
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Dominic S Ng. (2004) Treating low HDL—From bench to bedside. Clinical Biochemistry 37:8, 649-659
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J. D. Curb. (2004) High Density Lipoprotein Cholesterol and the Risk of Stroke in Elderly Men: The Honolulu Heart Program. American Journal of Epidemiology 160:2, 150-157
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Bela F Asztalos. (2004) High-density lipoprotein metabolism and progression of atherosclerosis: new insights from the HDL Atherosclerosis Treatment Study. Current Opinion in Cardiology 19:4, 385-391
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Michael N. Pollak, Eva S. Schernhammer, Susan E. Hankinson. (2004) Insulin-like growth factors and neoplasia. Nature Reviews Cancer 4:7, 505-518
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