(Circulation. 2000;102:1082.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Lipoprotein(a) and Coronary Heart Disease
Meta-Analysis of Prospective Studies
From the Clinical Trial Service Unit and Epidemiological Studies Unit, Nuffield Department of Clinical Medicine, University of Oxford, Radcliffe Infirmary, Oxford, UK.
Correspondence to Dr John Danesh, CTSU, Radcliffe Infirmary, Oxford OX2 6HE, UK.
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Abstract |
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Background—Studies of the association between the plasma concentration of lipoprotein(a) [Lp(a)] and coronary heart disease (CHD) have reported apparently conflicting findings. We report a meta-analysis of the prospective studies with at least 1 year of follow-up published before 2000.
Methods and Results—The following information was abstracted for each study: geographical location of study, size, type of cohort (population-based or selected because of previous disease), mean age, follow-up duration, blood storage temperature and duration, assay methods, degree of adjustment for potential confounders, and relationship of baseline Lp(a) measurement with subsequent CHD risk. There were 5436 deaths from CHD or nonfatal myocardial infarctions during a weighted mean follow-up of 10 years in the 27 eligible studies. Comparison of individuals in the top third of baseline plasma Lp(a) measurements with those in the bottom third in each study yielded a combined risk ratio of 1.6 (95% CI 1.4 to 1.8, 2P<0.00001), with similar findings when the analyses were restricted to the 18 studies of general populations (combined risk ratio 1.7, 95% CI 1.4 to 1.9; 2P<0.00001). Despite differences among studies in blood storage techniques and assay methods, there was no significant heterogeneity among the results from the 18 population-based studies or among those from the 9 studies of patients with previous disease. Lp(a) was only weakly correlated with classical vascular risk factors, and adjustment for those that had been recorded made little difference to the reported risk ratios.
Conclusions—These prospective studies demonstrate a clear association between Lp(a) and CHD, but further studies are needed to determine the extent to which this is causal.
Key Words: lipoproteins • coronary disease • meta-analysis
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Epidemiological studies of coronary heart disease (CHD) and blood concentrations of lipoprotein(a) [Lp(a)], a large protein attached to an LDL particle (Table
), have yielded apparently
conflicting results, ranging from a strongly positive association to no
association at all.1 2 3 A previous
meta-analysis4 involved 
1600 CHD cases in 12
prospective studies, but since the publication of that review, the
evidence has increased to >5400 cases of CHD death or nonfatal
myocardial infarction in 27 prospective studies. This article provides
an updated meta-analysis of the published studies in which CHD
events were recorded for some years after "baseline" blood
collection. Such prospective studies should be less prone to bias than
retrospective studies because they limit any influence of preexisting
disease itself on blood concentrations of Lp(a).
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Methods |
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Search Methods and Data Abstraction
Prospective studies with at least 1 year of follow-up that reported before 2000 on correlations between blood concentrations of Lp(a) and CHD death or nonfatal myocardial infarction were sought by Medline (http://igm.nlm.nih.gov) searches; by scanning relevant reference lists; by hand searching cardiology, epidemiology, and other relevant journals; and by discussion and correspondence with authors of relevant reports.5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 Computer searches used combinations of key words relating to disease (CHD, myocardial infarction, atherosclerosis, and vascular disease) and Lp(a). Articles in languages other than English were to be translated. The following information was abstracted according to a fixed protocol (with discussion and checks to resolve any discrepancies): geographical location of study, size, type of cohort (population-based or selected because of previous disease), mean age, follow-up duration, blood storage temperature and duration, assay methods, and degree of adjustment for potential confounders.
Studies Identified
Twenty-seven published prospective studies involving a
total of 5436 CHD cases were identified, of which 9 involved patients
with preexisting CHD,23 26 27 28 30 31
diabetes,29 or renal disease.24 25 The
studies were conducted in Nordic
countries,9 12 15 17 18 20 22 23 28 31
Germany,14 19 the United Kingdom,8 21 27 30
the United States,5 6 7 10 11 13 24 26 29
Canada,16 and Japan25 ; most involved only
white participants, and 4 were "nested" within randomized
trials.6 7 12 23 The weighted mean age at the time of the
CHD event was 61 years, which represented a weighted mean
age at baseline of 51 years and a weighted mean follow-up of 10 years.
A few studies made measurements in fresh
samples,5 10 13 19 22 31 but most stored the blood for
some years at low temperatures (range -20°C to -90°C)
before thawing and analyzing samples from those who had
subsequently suffered a CHD event and from age- and sex-matched
controls for nested case-control comparisons. Different studies used
different methods to measure Lp(a) concentrations, including
electrophoresis,5 10 13 22
ELISA,6 7 8 11 12 14 16 17 20 25 26 27 28 29 30
radioimmunoassay,9 21 23 24
electroimmunodiffusion,19
electroimmunoassay,31 and immunoradiometric
assay.15 18 Most studies made adjustments for smoking,
blood lipid concentrations, and other classical vascular risk factors,
such as blood pressure (see Figure legend).
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Statistical Methods
The present meta-analysis is based only on
within-study comparisons, thereby avoiding any biases being caused by
methodological differences between studies. Plasma concentrations of
Lp(a) had been measured by various assay methods, with different
studies reporting risk ratios on the basis of different cutoff levels
(including comparisons of mean values, thirds, quarters, fifths, etc)
or as increases in risk for a given increase in Lp(a). The risk ratios
derived for the present review compare individuals in the top third
of single baseline measurements versus those in the bottom third; see
previous publication for statistical details.32 Studies
based on the interpretation of electrophoretic
bands5 10 13 22 involved only a few Lp(a) categories. For
the present meta-analysis, the highest was taken to
correspond with the top third of baseline values; the lowest, with the
bottom third. The standard error of the log risk ratio in each study
was estimated from the number of standard errors by which the reported
relationship differed from zero.32 Summary estimates of
the risk ratios from all studies were obtained by combining the
separate estimates of inverse-variance–weighted log risk ratios from
each study. This is valid even though different studies used different
assay methods, because cases were compared directly only with controls
within the same studies. CIs were obtained by normal approximations to
the log relative risk, with 99% CIs used for the individual study
results to take account of the increased scope for the play of chance
in multiple comparisons and 95% CIs used for the overall results.
Heterogeneity was assessed by standard
2 tests.
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Results |
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The Figure
displays the results for
each separate study, with separate subtotals for studies in general
populations and in patients with preexisting disease. Overall, in the
18 population-based cohorts, the combined risk ratio for the comparison
of CHD rates in the top third of baseline Lp(a) measurement versus
those in the bottom third was 1.7 (95% CI 1.4 to 1.9,
2P<0.00001). There was no significant
heterogeneity between the risk ratios in these 18
studies (217=19.6,
P>0.1). One of those 18 studies5 accounts
for almost half the cases, but the risk ratio of 1.66 (95% CI 1.41 to
1.95) in that study is almost identical to the risk ratio of 1.69 (95%
CI 1.45 to 1.96) in the aggregated results of the others, and in none
of the 17 smaller studies was the risk ratio significantly different
from the overall result. The risk ratios were also similar when
population-based studies were grouped by various characteristics,
including studies that made measurements in fresh samples versus those
that froze and thawed samples before measurement (1.72 versus 1.59,
21=0.4; P>0.1),
those that stored samples for <5 years versus that stored samples for
5 years (1.58 versus 1.59,
21=0.3; P>0.1),
or those that used ELISAs versus those that used other assay methods
(1.65 versus 1.67, 21=0.0;
P>0.1).
Overall, in the 9 studies of patients who already had some disease at
baseline, the combined risk ratio was 1.3 (95% CI 1.1 to 1.6,
2P<0.001), which is significantly smaller than that for the
population-based studies
(21=3.8, P=0.05).
This result for studies in patients with preexisting disease is
dominated by just one large study of patients with a history of
myocardial infarction,23 which accounted for three
fourths of the evidence. The other 8 studies were all small; hence,
although their results are all statistically compatible with a relative
risk of 1.3 (and there was no significant heterogeneity
among the 9 studies; 28=9.7,
P>0.1), they add little information to the one large study
in patients with preexisting disease.
The published reports of these 27 studies contained insufficient information to produce combined analyses within subgroups defined by other potentially relevant characteristics (eg, age, sex, and fatal versus nonfatal CHD).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This meta-analysis of 27 prospective studies with information on 5436 CHD cases observed during mean follow-up of 10 years provides the most reliable assessment so far of the association between plasma Lp(a) and CHD. It indicates that people in the general population with Lp(a) levels in the top third of baseline measurement are at
70% increased risk of CHD compared with those in the bottom
third. The risk ratio appeared to be less extreme in the 9 studies of
patients with preexisting disease, but those studies may be less
directly relevant than the population-based studies in the assessment
of cause-and-effect relationships. Concentrations of plasma Lp(a) and
classical vascular risk factors have not been found to be strongly
correlated (Table), and these prospective studies of CHD
generally reported little or no change in risk ratios after adjustment
for other risk factors. This suggests that any effects of Lp(a) are
unlikely to be accounted for by effects on, or confounding with,
classical vascular risk factors.
In the present meta-analysis, cases were compared directly
only with controls within the same studies, thereby avoiding any bias
due to the use of different assay methods, reagents, and blood storage
conditions among the different studies. There was no evidence of
significant heterogeneity of the CHD risk ratios among
the 18 population-based cohorts (or among the 9 cohorts defined on the
basis of previous disease). However, several potential limitations of
the present meta-analysis warrant attention. First, assays
for Lp(a) are now widely available, so other prospective studies of
Lp(a) and CHD that have not yet been reported may well exist. But, any
exaggeration of the CHD risk ratio due to the preferential publication
of reports with more extreme associations is unlikely to be
substantial, particularly because the combined risk ratio for the 17
smaller population-based studies was so similar to that for the single
largest study.5 Second, certain chronic conditions (such
as inflammatory diseases) might both alter Lp(a) concentrations and be
associated with CHD, but this would be expected to have only a small
effect on the association of Lp(a) with CHD. Moreover, attempts in
certain studies to control for the possible effects of preexisting
disease on Lp(a) by the exclusion of those known to have certain
conditions or by omission of any CHD events during the first few years
of follow-up did not appear to change the reported associations
substantially. Conversely, it is possible that the published studies
have somewhat underestimated the role of Lp(a) in CHD. Only slight
underestimation is likely to be due to the lack of correction in most
studies for regression dilution,33 because
within-individual fluctuations of measured Lp(a) concentrations over
time are relatively small (self-correlation 0.9, Table).
However, more substantial underestimation is possible if Lp(a) variants
in people with higher blood concentrations were selectively degraded in
studies with suboptimal blood storage conditions.34
Moreover, there are great differences between individuals in the nature
of Lp(a), with different isoforms of the protein differing widely in
molecular weight (Table) and, hence, perhaps also in biological
activity. Some studies have suggested stronger associations between CHD
and certain apolipoprotein(a) isoforms than with
others,35 36 37 but this question has not yet been studied
with appropriately large numbers.
More detailed combined analysis of the prospective studies of Lp(a), perhaps with the use of individual participant data from each study, could help to characterize the shapes of any dose-response relationship, reduce any bias related to the selection of particular cutoff levels, allow more complete adjustment for other risk factors, and assess associations in particular subgroups. If practicable treatments become available that substantially lower Lp(a),38 then randomized trials might eventually become relevant to assessing the causal nature of this association (and, hence, the potential for reducing CHD risk). Studies of CHD and genetic polymorphisms that are associated with Lp(a) concentrations may also help to elucidate causality. Thus, much further study is still needed to determine the relevance of Lp(a) in the causation of CHD, but at least the existence of a moderately strong association of Lp(a) with CHD, independent of the standard vascular risk factors, is now clearly established.
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Acknowledgments |
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Dr Danesh was supported by a Merton College fellowship and a Frohlich award, and Dr Collins holds a British Heart Foundation personal chair. M.J. Meyer assisted with data abstraction. P. Appleby plotted the figure. The following investigators kindly provided additional information for their studies: Gosta Dahlen,17 Peter Cremer,14 Ronald Klein,29 Santica Marcovina,11 Dorothea Nagel,14 Tu Nguyen,5 and Nicholas Wald.8
Received November 22, 1999; revision received March 21, 2000; accepted March 29, 2000.
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P. R. Kamstrup, M. Benn, A. Tybjaerg-Hansen, and B. G. Nordestgaard Extreme Lipoprotein(a) Levels and Risk of Myocardial Infarction in the General Population: The Copenhagen City Heart Study Circulation, January 15, 2008; 117(2): 176 - 184. [Abstract] [Full Text] [PDF]
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S. Tsimikas, L. D. Tsironis, and A. D. Tselepis New Insights Into the Role of Lipoprotein(a)-Associated Lipoprotein-Associated Phospholipase A2 in Atherosclerosis and Cardiovascular Disease Arterioscler. Thromb. Vasc. Biol., October 1, 2007; 27(10): 2094 - 2099. [Abstract] [Full Text] [PDF]
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M. M. Luke, J. P. Kane, D. M. Liu, C. M. Rowland, D. Shiffman, J. Cassano, J. J. Catanese, C. R. Pullinger, D. U. Leong, A. R. Arellano, et al. A Polymorphism in the Protease-Like Domain of Apolipoprotein(a) Is Associated With Severe Coronary Artery Disease Arterioscler. Thromb. Vasc. Biol., September 1, 2007; 27(9): 2030 - 2036. [Abstract] [Full Text] [PDF]
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S. Kiechl, J. Willeit, M. Mayr, B. Viehweider, M. Oberhollenzer, F. Kronenberg, C. J. Wiedermann, S. Oberthaler, Q. Xu, J. L. Witztum, et al. Oxidized Phospholipids, Lipoprotein(a), Lipoprotein-Associated Phospholipase A2 Activity, and 10-Year Cardiovascular Outcomes: Prospective Results From the Bruneck Study Arterioscler. Thromb. Vasc. Biol., August 1, 2007; 27(8): 1788 - 1795. [Abstract] [Full Text] [PDF]
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B. Dieplinger, A. Lingenhel, N. Baumgartner, W. Poelz, H. Dieplinger, M. Haltmayer, F. Kronenberg, and T. Mueller Increased Serum Lipoprotein(a) Concentrations and Low Molecular Weight Phenotypes of Apolipoprotein(a) Are Associated with Symptomatic Peripheral Arterial Disease Clin. Chem., July 1, 2007; 53(7): 1298 - 1305. [Abstract] [Full Text] [PDF]
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I. Tzoulaki, G. D. Murray, A. J. Lee, A. Rumley, G. D.O. Lowe, and F. G. R. Fowkes Relative Value of Inflammatory, Hemostatic, and Rheological Factors for Incident Myocardial Infarction and Stroke: The Edinburgh Artery Study Circulation, April 24, 2007; 115(16): 2119 - 2127. [Abstract] [Full Text] [PDF]
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G. T. Jones, A. M. van Rij, J. Cole, M. J.A. Williams, E. H. Bateman, S. M. Marcovina, M. Deng, and S. P.A. McCormick Plasma Lipoprotein(a) Indicates Risk for 4 Distinct Forms of Vascular Disease Clin. Chem., April 1, 2007; 53(4): 679 - 685. [Abstract] [Full Text] [PDF]
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P. M Ridker, J. E. Buring, N. Rifai, and N. R. Cook Development and Validation of Improved Algorithms for the Assessment of Global Cardiovascular Risk in Women: The Reynolds Risk Score JAMA, February 14, 2007; 297(6): 611 - 619. [Abstract] [Full Text] [PDF]
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J. Suk Danik, N. Rifai, J. E. Buring, and P. M Ridker Lipoprotein(a), measured with an assay independent of apolipoprotein(a) isoform size, and risk of future cardiovascular events among initially healthy women. JAMA, September 20, 2006; 296(11): 1363 - 1370. [Abstract] [Full Text] [PDF]
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M. A. Mittleman A 39-year-old woman with hypercholesterolemia. JAMA, July 19, 2006; 296(3): 319 - 326. [Abstract] [Full Text] [PDF]
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L. B. Goldstein, R. Adams, M. J. Alberts, L. J. Appel, L. M. Brass, C. D. Bushnell, A. Culebras, T. J. DeGraba, P. B. Gorelick, J. R. Guyton, et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Circulation, June 20, 2006; 113(24): e873 - e923. [Abstract] [Full Text] [PDF]
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S. Tsimikas, S. Kiechl, J. Willeit, M. Mayr, E. R. Miller, F. Kronenberg, Q. Xu, C. Bergmark, S. Weger, F. Oberhollenzer, et al. Oxidized Phospholipids Predict the Presence and Progression of Carotid and Femoral Atherosclerosis and Symptomatic Cardiovascular Disease: Five-Year Prospective Results From the Bruneck Study J. Am. Coll. Cardiol., June 6, 2006; 47(11): 2219 - 2228. [Abstract] [Full Text] [PDF]
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J. D. Spence Lipoprotein(a): Involved in Events, but Not Burden of Atherosclerotic Disease? Stroke, June 1, 2006; 37(6): 1350 - 1351. [Full Text] [PDF]
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L. B. Goldstein, R. Adams, M. J. Alberts, L. J. Appel, L. M. Brass, C. D. Bushnell, A. Culebras, T. J. DeGraba, P. B. Gorelick, J. R. Guyton, et al. Primary Prevention of Ischemic Stroke: A Guideline From the American Heart Association/American Stroke Association Stroke Council: Cosponsored by the Atherosclerotic Peripheral Vascular Disease Interdisciplinary Working Group; Cardiovascular Nursing Council; Clinical Cardiology Council; Nutrition, Physical Activity, and Metabolism Council; and the Quality of Care and Outcomes Research Interdisciplinary Working Group: The American Academy of Neurology affirms the value of this guideline. Stroke, June 1, 2006; 37(6): 1583 - 1633. [Abstract] [Full Text] [PDF]
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J. Rubin, H. J. Kim, T. A. Pearson, S. Holleran, R. Ramakrishnan, and L. Berglund Apo[a] size and PNR explain African American-Caucasian differences in allele-specific apo[a] levels for small but not large apo[a] J. Lipid Res., May 1, 2006; 47(5): 982 - 989. [Abstract] [Full Text] [PDF]
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S. Tsimikas, J. T. Willerson, and P. M. Ridker C-reactive protein and other emerging blood biomarkers to optimize risk stratification of vulnerable patients. J. Am. Coll. Cardiol., April 18, 2006; 47(8 Suppl): C19 - C31. [Abstract] [Full Text] [PDF]
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T. Pischon, C. J. Girman, F. M. Sacks, N. Rifai, M. J. Stampfer, and E. B. Rimm Non-High-Density Lipoprotein Cholesterol and Apolipoprotein B in the Prediction of Coronary Heart Disease in Men Circulation, November 29, 2005; 112(22): 3375 - 3383. [Abstract] [Full Text] [PDF]
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D. T. Holmes, B. A. Schick, K. H. Humphries, and J. Frohlich Lipoprotein(a) Is an Independent Risk Factor for Cardiovascular Disease in Heterozygous Familial Hypercholesterolemia Clin. Chem., November 1, 2005; 51(11): 2067 - 2073. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden Inflammation, Atherosclerosis, and Aspects of Insulin Action Diabetes Care, September 1, 2005; 28(9): 2312 - 2319. [Full Text] [PDF]
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I. Shai, E. B. Rimm, S. E. Hankinson, C. Cannuscio, G. Curhan, J. E. Manson, N. Rifai, M. J. Stampfer, and J. Ma Lipoprotein (a) and coronary heart disease among women: beyond a cholesterol carrier? Eur. Heart J., August 2, 2005; 26(16): 1633 - 1639. [Abstract] [Full Text] [PDF]
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M. Y. Desai, A. Rodriguez, B. A. Wasserman, G. Gerstenblith, S. Agarwal, M. Kennedy, D. A Bluemke, and J. A.C. Lima Association of Cholesterol Subfractions and Carotid Lipid Core Measured by MRI Arterioscler. Thromb. Vasc. Biol., June 1, 2005; 25(6): e110 - e111. [Full Text] [PDF]
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C. Hernandez, G. Francisco, P. Chacon, and R. Simo Lipoprotein(a) as a Risk Factor for Cardiovascular Mortality in Type 2 Diabetic Patients: A 10-year follow-up study Diabetes Care, April 1, 2005; 28(4): 931 - 933. [Full Text] [PDF]
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R. Guerra, Z. Yu, S. Marcovina, R. Peshock, J. C. Cohen, and H. H. Hobbs Lipoprotein(a) and Apolipoprotein(a) Isoforms: No Association With Coronary Artery Calcification in The Dallas Heart Study Circulation, March 29, 2005; 111(12): 1471 - 1479. [Abstract] [Full Text] [PDF]
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E. M. Stuveling, S. J. L. Bakker, H. L. Hillege, P. E. de Jong, R. O. B. Gans, and D. de Zeeuw Biochemical risk markers: a novel area for better prediction of renal risk? Nephrol. Dial. Transplant., March 1, 2005; 20(3): 497 - 508. [Full Text] [PDF]
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L. Berglund and R. Ramakrishnan Lipoprotein(a): An Elusive Cardiovascular Risk Factor Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2219 - 2226. [Abstract] [Full Text] [PDF]
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I. J. Kullo, K. R. Bailey, L. F. Bielak, P. F. Sheedy II, G. G. Klee, S. L. Kardia, P. A. Peyser, E. Boerwinkle, and S. T. Turner Lack of Association Between Lipoprotein(a) and Coronary Artery Calcification in the Genetic Epidemiology Network of Arteriopathy (GENOA) Study Mayo Clin. Proc., October 1, 2004; 79(10): 1258 - 1263. [Abstract] [PDF]
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K. Hoffmann, B.-C. Zyriax, H. Boeing, and E. Windler A dietary pattern derived to explain biomarker variation is strongly associated with the risk of coronary artery disease Am. J. Clinical Nutrition, September 1, 2004; 80(3): 633 - 640. [Abstract] [Full Text] [PDF]
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N. Rifai, J. Ma, F. M. Sacks, P. M. Ridker, W. J. L. Hernandez, M. J. Stampfer, and S. M. Marcovina Apolipoprotein(a) Size and Lipoprotein(a) Concentration and Future Risk of Angina Pectoris with Evidence of Severe Coronary Atherosclerosis in Men: The Physicians' Health Study Clin. Chem., August 1, 2004; 50(8): 1364 - 1371. [Abstract] [Full Text] [PDF]
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P. M Ridker, N. J. Brown, D. E. Vaughan, D. G. Harrison, and J. L. Mehta Established and Emerging Plasma Biomarkers in the Prediction of First Atherothrombotic Events Circulation, June 29, 2004; 109(25_suppl_1): IV-6 - IV-19. [Full Text] [PDF]
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S. C. Smith Jr, R. V. Milani, D. K. Arnett, J. R. Crouse III, M. M. McDermott, P. M Ridker, R. S. Rosenson, K. A. Taubert, and P. W.F. Wilson Atherosclerotic Vascular Disease Conference: Writing Group II: Risk Factors Circulation, June 1, 2004; 109(21): 2613 - 2616. [Full Text] [PDF]
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H. D. Wu, L. Berglund, C. Dimayuga, J. Jones, R. R. Sciacca, M. R. Di Tullio, and S. Homma High lipoprotein(a) levels and small apolipoprotein(a) sizes are associated with endothelial dysfunction in a multiethnic cohort J. Am. Coll. Cardiol., May 19, 2004; 43(10): 1828 - 1833. [Abstract] [Full Text] [PDF]
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E. R. Christ, M. H. Cummings, N. Jackson, M. Stolinski, P. J. Lumb, A. S. Wierzbicki, P. H. Sonksen, D. L. Russell-Jones, and A. M. Umpleby Effects of Growth Hormone (GH) Replacement Therapy on Low-Density Lipoprotein Apolipoprotein B100 Kinetics in Adult Patients with GH Deficiency: A Stable Isotope Study J. Clin. Endocrinol. Metab., April 1, 2004; 89(4): 1801 - 1807. [Abstract] [Full Text] [PDF]
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S. E. Humphries, P. M. Ridker, and P. J. Talmud Genetic Testing for Cardiovascular Disease Susceptibility: A Useful Clinical Management Tool or Possible Misinformation? Arterioscler. Thromb. Vasc. Biol., April 1, 2004; 24(4): 628 - 636. [Abstract] [Full Text] [PDF]
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P. Muntner, L. L. Hamm, J. W. Kusek, J. Chen, P. K. Whelton, and J. He The Prevalence of Nontraditional Risk Factors for Coronary Heart Disease in Patients with Chronic Kidney Disease Ann Intern Med, January 6, 2004; 140(1): 9 - 17. [Abstract] [Full Text] [PDF]
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M. Trovati and F. Cavalot Optimization of Hypolipidemic and Antiplatelet Treatment in the Diabetic Patient with Renal Disease J. Am. Soc. Nephrol., January 1, 2004; 15(90010): S12 - 20. [Abstract] [Full Text]
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N. Sattar, D. W. McCarey, H. Capell, and I. B. McInnes Explaining How "High-Grade" Systemic Inflammation Accelerates Vascular Risk in Rheumatoid Arthritis Circulation, December 16, 2003; 108(24): 2957 - 2963. [Abstract] [Full Text] [PDF]
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S. M. Marcovina, M. L. Koschinsky, J. J. Albers, and S. Skarlatos Report of the National Heart, Lung, and Blood Institute Workshop on Lipoprotein(a) and Cardiovascular Disease: Recent Advances and Future Directions Clin. Chem., November 1, 2003; 49(11): 1785 - 1796. [Abstract] [Full Text] [PDF]
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C. Kang, M. Dominguez, S. Loyau, T. Miyata, V. Durlach, and E. Angles-Cano Lp(a) Particles Mold Fibrin-Binding Properties of Apo(a) in Size-Dependent Manner: A Study With Different-Length Recombinant Apo(a), Native Lp(a), and Monoclonal Antibody Arterioscler. Thromb. Vasc. Biol., July 12, 2002; 22(7): 1232 - 1238. [Abstract] [Full Text] [PDF]
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 M. Peltier, M. C. Iannetta Peltier, M. E. Sarano, J.-P. M. Lesbre, J.-L. Colas, and C. M. Tribouilloy Elevated Serum Lipoprotein(a) Level Is an Independent Marker of Severity of Thoracic Aortic Atherosclerosis* Chest, May 1, 2002; 121(5): 1589 - 1594. [Abstract] [Full Text] [PDF]
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 D J Byrne, I A Jagroop, H E Montgomery, M Thomas, D P Mikhailidis, N G Milton, and A F Winder Lipoprotein (a) does not participate in the early acute phase response to training or extreme physical activity and is unlikely to enhance any associated immediate cardiovascular risk J. Clin. Pathol., April 1, 2002; 55(4): 280 - 285. [Abstract] [Full Text] [PDF]
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D. B. Sacks, D. E. Bruns, D. E. Goldstein, N. K. Maclaren, J. M. McDonald, and M. Parrott Guidelines and Recommendations for Laboratory Analysis in the Diagnosis and Management of Diabetes Mellitus Clin. Chem., March 1, 2002; 48(3): 436 - 472. [Abstract] [Full Text] [PDF]
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J. Rubin, F. Paultre, C. H. Tuck, S. Holleran, R. G. Reed, T. A. Pearson, C. M. Thomas, R. Ramakrishnan, and L. Berglund Apolipoprotein [a] genotype influences isoform dominance pattern differently in African Americans and Caucasians J. Lipid Res., February 1, 2002; 43(2): 234 - 244. [Abstract] [Full Text] [PDF]
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