From the Divisions of Preventive Medicine (P.M.R., R.J.G., C.H.H.) and
Cardiovascular Diseases (P.M.R.), Department of Medicine, Brigham and
Women's Hospital, and the Department of Ambulatory Care and Prevention
(C.H.H.), Harvard Medical School, Boston, Mass.
Correspondence to Dr Paul Ridker, Brigham and Women's Hospital, 900 Commonwealth Ave East, Boston, MA 02215. E-mail pmridker{at}bics.bwh.harvard.edu
Methods and Results—Among 14 916 apparently healthy men
participating in the Physicians' Health Study, baseline levels of CRP,
TC, and HDL-C were measured among 245 study subjects who subsequently
developed a first MI (cases) and among 372 subjects who remained free
of cardiovascular disease during an average follow-up
period of 9 years (controls). In univariate
analyses, high baseline levels of CRP, TC, and TC:HDL-C ratio
were each associated with significantly increased risks of future MI
(all P values <0.001). In multivariate
analyses, models incorporating CRP and lipid
parameters provided a significantly better method to
predict risk than did models using lipids alone (all likelihood ratio
test P values <0.003). For example, relative risks of
future MI among those with high levels of both CRP and TC (RR=5.0,
P=0.0001) were greater than the product of the
individual risks associated with isolated elevations of either CRP
(RR=1.5) or TC (RR=2.3). In stratified analyses, baseline CRP
level was predictive of risk for those with low as well as high levels
of TC and the TC:HDL-C ratio. These findings were virtually identical
in analyses limited to nonsmokers and after control for other
cardiovascular risk factors.
Conclusions—In prospective data from a large cohort of apparently
healthy men, baseline CRP level added to the predictive value of lipid
parameters in determining risk of first MI.
From a clinical perspective, the question has been raised as to
whether CRP adds to the ability to predict atherothrombotic risk with
more confidence than currently achievable with standard lipid
screening. We therefore reexamined data from the Physicians' Health
Study to determine whether measuring CRP added to the predictive value
of TC and HDL-C in determining subsequent risk of first MI. In
addition, we sought to determine whether the risks of future MI
associated with CRP were present among those with low-risk as well
as high-risk profiles as assessed by baseline lipid status.
In our original description of CRP in the Physicians' Health Study, we
reported data from 246 initially healthy study participants who
subsequently developed a first MI (cases) and from a group of 543 age-
and smoking-matched study participants who remained free of
cardiovascular disease during study follow-up
(controls).1 For each of these case and control
subjects, blood collected at enrollment was thawed and assayed for CRP
by methods described elsewhere.1 In addition,
baseline blood samples of 245 cases (99%) and 372 controls (69%) were
successfully analyzed for TC and HDL-C.8
These 617 initially healthy participants in the Physicians' Health
Study form the basis for this report.
Means or proportions for baseline clinical characteristics and measured
risk factors were computed for the case and control groups and compared
by Student's t test or the
On an a priori basis, we evaluated the combined role of
hypercholesterolemia and elevations of CRP in
predicting risk of MI in three stages, which allowed us to explore from
a clinical perspective the sensitivity and robustness of any findings
to the choice of alternative cut points. Thus, we first used the
likelihood ratio test to determine whether logistic regression models
that included lipid parameters and CRP provided a
significantly better fit than did logistic regression models limited to
lipid parameters alone. In these analyses, lipid
parameters and log-normalized CRP levels were both treated
as continuous variables.
Second, logistic regression analyses were performed in which
the referent group was those individuals with both TC and CRP levels
below the 75th percentile cut point for each of these
parameters (TC-, CRP-). In this analysis,
relative risks of developing a first MI were computed for individuals
with hypercholesterolemia alone (TC+, CRP-),
for individuals with elevations of CRP alone (TC-, CRP+), and for
individuals with both hypercholesterolemia and
elevations of CRP (TC+, CRP+).
Third, we divided case and control subjects into nine groups according
to tertile of TC and CRP level. In this analysis, logistic
regression was used to simultaneously evaluate the risks of
first MI in each of these groups, with those with the lowest tertile of
both TC and CRP used as the referent group. Similar analyses
were performed after case and control subjects were divided into nine
groups according to tertile of the TC:HDL-C ratio.
Finally, to evaluate whether increasing levels of CRP were a predictor
of risk for first MI among those with low as well as high lipid
parameters, we performed stratified analyses in
which tests for trends across increasing quartiles of CRP were computed
separately for those with levels of TC and the TC:HDL-C ratio above or
below the approximate median value for the study group.
All analyses were repeated for the subgroup of nonsmokers, and
additional multivariate analyses were used to
control for the presence or absence of other
cardiovascular risk factors. P values are
two-tailed, and 95% CIs were computed.
Correlations between log-normalized CRP and TC (r=0.15) and
between log-normalized CRP and HDL-C (r=-0.15) were small
in magnitude. Thus, <3% of the variance in CRP levels in these data
was explained by the lipid parameters.
In univariate analyses, baseline levels of CRP, TC,
and the TC:HDL-C ratio were each associated with increased risk of
future MI (all P values <0.001). As shown in Table 2
To evaluate whether CRP added to the predictive value of lipids on risk
of first MI, likelihood ratio tests were used to compare the fit of
prediction models using CRP and lipids to the fit of models using
lipids alone. In these analyses, the assessment of both
parameters provided a significantly improved ability to
predict risk. For example, models including both CRP and TC provided a
significant improvement in prediction (P=0.003) compared
with models including onlyTC, whereas models involving CRP
significantly improved prediction compared with models based solely on
the TC:HDL-C ratio (P=0.002) or on TC and HDL-C entered as
separate variables (P=0.002). These relationships were
not significantly altered in models limited to nonsmokers or that
further controlled for the effects of other
cardiovascular risk factors.
Table 3
Fig 2
Table 4
The present data describing at least additive relationships between
CRP and lipids in terms of risk prediction extend prior findings
relating CRP to cardiovascular
disease.1 2 3 4 5 6 Specifically, elevated levels of CRP
are associated with increased risks of MI or sudden death among those
with stable and unstable angina pectoris,2 3 4 as
well as coronary heart disease in the
elderly5 and coronary mortality among
high-risk patients.6 However, because CRP levels
increase in response to acute ischemia and are chronically
elevated among smokers,9 it had been uncertain
whether the inflammation detected by CRP in these studies is causal or
due to the effects of other factors, such as ischemia or
cigarette consumption. Moreover, these prior studies did not evaluate
whether the effects of CRP were present among those with high- as
well as low-risk lipid profiles or whether the risks associated with
CRP were additive to those determined by standard lipid
analysis.
All the apparently healthy men in the Physicians' Health Study were
free of any history of cardiovascular disease when
blood samples were obtained. Thus, the potential for confounding by the
presence of symptomatic ischemia in these data is
unlikely. Moreover, the risks of future MI associated with CRP in the
Physicians' Health Study were present for nonsmokers, providing
evidence against the possibility that observed effects are simply the
result of cigarette consumption.9
The fact that lipid parameters and CRP levels were measured
only once at baseline in our study is a potential limitation, because
random fluctuation in these parameters over time would tend
to increase the variance in our data. However, if random, such
variation would most likely bias our findings toward a null result and
lead to an underestimation of true predictive values. Conversely,
because assays for CRP as well as all lipid parameters were
performed on the same baseline plasma sample, these data are compatible
with the potential utility of simultaneous assessment of
inflammatory markers and lipid parameters as a method of
risk detection.
It is currently estimated that up to half of all MIs in the United
States occur among individuals with moderate to low risk as determined
by assessment of TC and HDL-C levels.10 The
present data raise the possibility that assessment of CRP may
provide a method of determining risk of future MI among apparently
low-risk individuals, including nonsmokers. Because relatively simple
interventions such as exercise, weight loss, and diet restriction can
lead to substantial reductions in risk of first
MI,10 assessment of CRP might have clinical
utility if improved risk stratification leads to improved compliance
with lifestyle modification. Confirmation of these data in other
prospective cohorts is thus of critical importance, as are studies in
women, for whom data are lacking on the predictive value of
inflammatory markers.
Received September 12, 1997;
revision received January 13, 1998;
accepted January 23, 1998.
2.
Liuzzo G, Biasucci LM, Gallimore JR, Grillo RL,
Rebuzzi AG, Pepys MB, Maseri A. The prognostic value of C-reactive
protein and serum amyloid A protein in severe unstable angina.
N Engl J Med. 1994;331:417–424.
3.
Thompson SG, Kienast J, Pyke SDM, Haverkate F, van de
Loo JCW, for the European Concerted Action on Thrombosis, and
Disabilities Angina Pectoris Study Group. Hemostatic factors and the
risk of myocardial infarction or sudden death in patients with angina
pectoris. N Engl J Med. 1995;332:635–641.
4.
Haverkate F, Thompson SG, Pyke SDM, Gallimore JR,
Pepys MB, for the European Concerted Action on Thrombosis, and
Disabilities Angina Pectoris Study Group. Production of
C-reactive protein and risk of coronary events in stable and
unstable angina. Lancet. 1997;349:462–466.[Medline]
[Order article via Infotrieve]
5.
Tracy RP, Lemaitre RN, Psaty BM, Ives DG, Evans RW,
Cushman M, Meilahn EN, Kuller LH. Relationship of C-reactive protein to
risk of cardiovascular disease in the elderly: results
from the Cardiovascular Health Study and the Rural
Health Promotion Project. Arterioscler Thromb Vasc Biol. 1997;17:1121–1127.
6.
Kuller LH, Tracy RP, Shaten J, Meilahn EN, for the
MRFIT Research Group. Relationship of C-reactive protein and
coronary heart disease in the MRFIT nested case-control study.
Am J Epidemiol. 1996;144:537–547.
7.
Steering Committee of the Physicians' Health Study
Research Group. Final report of the aspirin component of the ongoing
Physicians' Health Study. N Engl J Med. 1989;321:129–135.[Abstract]
8.
Stampfer MJ, Sacks FM, Salvini S, Willett WC,
Hennekens CH. A prospective study of cholesterol,
apolipoproteins, and the risk of myocardial infarction. N
Engl J Med. 1991;325:373–381.[Abstract]
9.
Das I. Raised C-reactive protein levels in serum from
smokers. Clin Chim Acta. 1985;153:9–13.[Medline]
[Order article via Infotrieve]
10.
Manson JE, Tosteson H, Ridker PM, Satterfield S, Hebert
P, O'Connor GJ, Buring JE, Hennekens CH. Current concepts: primary
prevention of myocardial infarction. N Engl J Med. 1992;326:1406–1416.[Medline]
[Order article via Infotrieve]
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
C-Reactive Protein Adds to the Predictive Value of Total and HDL Cholesterol in Determining Risk of First Myocardial Infarction
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—C-reactive protein (CRP)
is a sensitive marker of inflammation, and elevated levels have been
associated with future risk of myocardial infarction (MI). However,
whether measurement of CRP adds to the predictive value of total
cholesterol (TC) and HDL cholesterol (HDL-C) in
determining risk is uncertain.
Key Words: myocardial infarction • epidemiology • C-reactive protein • risk factors • cholesterol
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
C-reactive protein is
a sensitive marker of systemic inflammation, and prospective data from
a population of apparently healthy men indicate that baseline levels
predict risk of first MI.1 Specifically, among
men free of prior cardiovascular disease participating
in the Physicians' Health Study, we recently reported that those with
baseline levels of CRP in the highest quartile had a threefold increase
in risk of developing future MI compared with those with levels in the
lowest quartile (relative risk, 2.9;
P<0.001).1 In this population, risk
estimates were stable over long periods of time, were significant among
the subgroup of nonsmokers, and were independent of a number of other
risk factors for cardiovascular disease. As such, these
data demonstrate that CRP is a marker of cardiovascular
risk not only among those with stable and unstable
angina,2 3 4 the elderly,5
and selected high-risk patients6 but also among
individuals with no current evidence of cardiovascular
disease.1
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
In the US Physicians' Health Study,7
14 916 men initially free of reported cardiovascular
disease, cancer, or other chronic illness provided a baseline plasma
sample before randomization and were prospectively followed up for the
first occurrence of MI. Details of the Physicians' Health Study, a
randomized, double-blind, placebo-controlled trial of aspirin and
ß-carotene in the primary prevention of
cardiovascular disease and cancer, have been described
elsewhere, as have the methods used to collect, store, and process
baseline blood specimens.1 7 Morbidity follow-up
was >99% complete and mortality follow-up was 100% over the 
9
years of follow-up in the present analysis. Reported MI
that occurred during the study follow-up period was confirmed if
medical record review demonstrated symptoms consistent with
MI and the presence of either diagnostic ECG changes or
cardiac enzymes. Silent MIs were not included because they could not be
accurately dated. Deaths due to MI were confirmed when autopsy reports,
symptoms, circumstances of death, and a history of coronary
disease were consistent with this diagnosis. 
2
statistic. Univariate logistic regression analyses
were used to determine whether baseline levels of CRP, TC, and the
TC:HDL-C ratio were predictive of future risk of MI. In these
analyses, baseline levels were divided into quartiles based on
the distribution of the control values.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Table 1
presents the baseline
clinical characteristics of the subjects evaluated. Because study
participants in our original report were matched on smoking and age,
these variables were similar among those who subsequently developed
a first MI (cases) and among those who remained free of reported
cardiovascular disease over the follow-up period
(controls). As expected, case subjects had less favorable lipid
profiles than did control subjects.
View this table:
[in a new window]
Table 1. Baseline Characteristics of Study Participants Who
Subsequently Developed First MI (Cases) and Those Who Remained Free of
Reported Vascular Disease During the Average 8-Year Follow-up Period
(Controls) , the relative risk of future MI
increased 38% with each increasing quartile of CRP (95% CI, 19% to
61%; P<0.001), 62% for each increasing quartile of TC
(95% CI, 39% to 90%; P<0.001), and 59% for each
increasing quartile of the TC:HDL-C ratio (95% CI, 37% to 86%;
P<0.001). The 95% CIs for these risk estimates overlap and
are consistent with prior reports from the entire
cohort.1 4
View this table:
[in a new window]
Table 2. Relative Risks of First MI Associated With Each
Quartile Increase of CRP, TC, and TC:HDL-C Ratio presents the relative risks
of first MI in analyses in which study subjects were
categorized as being above or below the 75th percentile cut point for
TC and CRP. As shown, compared with those with levels of TC and CRP
less than the 75th percentile cut point for each parameter
(TC-, CRP-), those with elevations of TC alone (TC+, CRP-) had a
2.3-fold increase in risk, whereas those with elevations of CRP alone
(TC-, CRP+) had a 1.5-fold increase in risk. In contrast, the risk of
first MI associated with elevations of both TC and CRP (TC+, CRP+) was
increased 5-fold (RR=5.0; 95% CI, 2.5 to 9.8; P=0.0001). As
shown in Table 3 and in Fig 1, these
effects were not significantly altered in analyses controlling
for other risk factors.
View this table:
[in a new window]
Table 3. Relative Risks of First MI According to the Presence
(TC+) or Absence (TC-) of TC Levels in Excess of the 75th Percentile
of the Control Distribution (234 mg/dL) and/or the Presence (CRP+) or
Absence (CRP-) of CRP Levels in Excess of the 75th Percentile of
the Control Distribution (2.11 mg/L)
View larger version (10K):
[in a new window]
Figure 1. Adjusted relative risks of first MI according to
baseline levels of TC above (TC+) or below (TC-) 75th percentile of
control group (234 mg/dL) and baseline CRP levels above (CRP+) or below
(CRP-) 75th percentile of control group (2.11 mg/L). illustrates the relative risks of
first MI in analyses in which study participants were
stratified into nine groups according to tertile of TC as well as
tertile of CRP. As shown, risks of future MI increased with each of
these parameters such that those in the highest tertile of
both TC and CRP had a relative risk of first MI 5.3 times that of
individuals in the lowest tertile of both parameters (95%
CI, 2.4 to 11.7; P=0.0001). Similarly, Fig 3 illustrates the relative risks of first
MI in analyses in which study participants were stratified into
nine groups according to tertile of the TC:HDL-C ratio as well as
tertile of CRP.
View larger version (20K):
[in a new window]
Figure 2. Relative risks of first MI among apparently
healthy men associated with high (>223 mg/dL), middle (191 to 223
mg/dL), and low (<191 mg/dL) tertiles of TC and high (>1.69 mg/L),
middle (0.72 to 1.69 mg/L), and low (<0.72 mg/L) tertiles of
CRP.
View larger version (19K):
[in a new window]
Figure 3. Relative risks of first MI among apparently
healthy men associated with high (>5.01), middle (3.78 to 5.01), and
low (<3.78) tertiles of the TC:HDL-C ratio and high (>1.69 mg/L),
middle (0.72 to 1.69 mg/L), and low (<0.72 mg/L) tertiles of
CRP. presents the relative risks
of first MI according to baseline levels of CRP in analyses in
which the study population was stratified according to baseline lipid
profile. As shown, statistically significant associations were found
between baseline level of CRP and risk of first MI for study
participants with low as well as high levels of TC and the TC:HDL-C
ratio. Similar relationships were found in analyses limited to
nonsmokers.
View this table:
[in a new window]
Table 4. Relative Risks of First MI According to Baseline
Levels of CRP, Stratified by Baseline Lipid and Lipoprotein Levels
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
In these prospective data deriving from a large cohort of
apparently healthy men, baseline CRP level added to the predictive
value of TC and HDL-C in determining risk of first MI. Indeed,
interactive models evaluating elevations of CRP and lipids raise the
possibility that the joint effects of both risk factors may be slightly
greater than the product of the individual effects of each risk
factor considered separately. Moreover, baseline level of CRP is a
predictor of risk of first MI for men at low as well as high risk as
determined by their lipid profiles. These relationships were minimally
altered in analyses either limited to nonsmokers or adjusted
for other risk factors, including hypertension, body mass, diabetes,
and family history of coronary disease. Finally, these results
were robust to the choice of several cut points for both CRP and lipid
parameters.
Selected Abbreviations and Acronyms
CRP
=
C-reactive protein
HDL-C
=
HDL cholesterol
MI
=
myocardial infarction
TC
=
total cholesterol
Acknowledgments
This study was supported by funding from the National Institutes
of Health, Bethesda, Md. Dr Ridker is supported by an Established
Investigator Award from the American Heart Association. The authors
wish to acknowledge the prior work of Drs Mary Cushman and Russell
Tracy in determining CRP levels in the Physicians' Health Study
cohort, as well as the prior work of Drs Frank Sacks and Meir Stampfer
in determining lipid parameters.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
1.
Ridker PM, Cushman M, Stampfer MJ, Tracy RP,
Hennekens CH. Inflammation, aspirin, and risks of
cardiovascular disease in apparently healthy men.
N Engl J Med. 1997;336:973–979.
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 M. B. Clearfield C-Reactive Protein: A New Risk Assessment Tool for Cardiovascular Disease J Am Osteopath Assoc, September 1, 2005; 105(9): 409 - 416. [Abstract] [Full Text] [PDF]
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M. Cushman, A. M. Arnold, B. M. Psaty, T. A. Manolio, L. H. Kuller, G. L. Burke, J. F. Polak, and R. P. Tracy C-Reactive Protein and the 10-Year Incidence of Coronary Heart Disease in Older Men and Women: The Cardiovascular Health Study Circulation, July 5, 2005; 112(1): 25 - 31. [Abstract] [Full Text] [PDF]
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 J. J.P. Kastelein The realities of dyslipidaemia: what do the studies tell us? Eur. Heart J. Suppl., July 1, 2005; 7(suppl_F): F27 - F33. [Abstract] [Full Text] [PDF]
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S. C. Smith Jr, J. L. Anderson, R. O. Cannon III, Y. Y. Fadl, W. Koenig, P. Libby, S. E. Lipshultz, G. A. Mensah, P. M Ridker, and R. Rosenson CDC/AHA Workshop on Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: Report From the Clinical Practice Discussion Group Circulation, December 21, 2004; 110(25): e550 - e553. [Full Text] [PDF]
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K. B. Vallbracht, P. L. Schwimmbeck, U. Kuhl, B. Seeberg, and H.-P. Schultheiss Endothelium-Dependent Flow-Mediated Vasodilation of Systemic Arteries Is Impaired in Patients With Myocardial Virus Persistence Circulation, November 2, 2004; 110(18): 2938 - 2945. [Abstract] [Full Text] [PDF]
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 G. Zhao, T. D. Etherton, K. R. Martin, S. G. West, P. J. Gillies, and P. M. Kris-Etherton Dietary {alpha}-Linolenic Acid Reduces Inflammatory and Lipid Cardiovascular Risk Factors in Hypercholesterolemic Men and Women J. Nutr., November 1, 2004; 134(11): 2991 - 2997. [Abstract] [Full Text] [PDF]
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L. Branen, L. Hovgaard, M. Nitulescu, E. Bengtsson, J. Nilsson, and S. Jovinge Inhibition of Tumor Necrosis Factor-{alpha} Reduces Atherosclerosis in Apolipoprotein E Knockout Mice Arterioscler. Thromb. Vasc. Biol., November 1, 2004; 24(11): 2137 - 2142. [Abstract] [Full Text] [PDF]
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 H.-B. Leu, C.-P. Lin, W.-T. Lin, T.-C. Wu, and J.-W. Chen Risk Stratification and Prognostic Implication of Plasma Biomarkers in Nondiabetic Patients With Stable Coronary Artery Disease: The Role of High-Sensitivity C-Reactive Protein Chest, October 1, 2004; 126(4): 1032 - 1039. [Abstract] [Full Text] [PDF]
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S. S. Levinson, J. J. Miller, and R. J. Elin Poor Predictive Value of High-Sensitivity C-Reactive Protein Indicates Need for Reassessment Clin. Chem., October 1, 2004; 50(10): 1733 - 1735. [Full Text] [PDF]
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 P Jepsen, S P Johnsen, M W Gillman, and H T Sorensen Interpretation of observational studies Heart, August 1, 2004; 90(8): 956 - 960. [Full Text] [PDF]
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 R. J. Glynn, N. R. Cook, P. Libby, J. T. Willerson, E. Braunwald, J. M. Foody, A. M. Gotto, N. Wenger, P. M. Ridker, W. Koenig, et al. C-Reactive Protein and Coronary Heart Disease N. Engl. J. Med., July 15, 2004; 351(3): 295 - 298. [Full Text] [PDF]
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C. Chrysohoou, D. B. Panagiotakos, C. Pitsavos, U. N. Das, and C. Stefanadis Adherence to the Mediterranean diet attenuates inflammation and coagulation process in healthy adults: The Attica study J. Am. Coll. Cardiol., July 7, 2004; 44(1): 152 - 158. [Abstract] [Full Text] [PDF]
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C. Kluft Identifying patients at risk of coronary vascular disease: the potential role of inflammatory markers Eur. Heart J. Suppl., July 1, 2004; 6(suppl_C): C21 - C27. [Abstract] [Full Text] [PDF]
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G. A. Ewy The Search for the "Holy Grail" of Clinically Significant Coronary Atherosclerosis Arch Intern Med, June 28, 2004; 164(12): 1266 - 1268. [Full Text] [PDF]
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P. M Ridker, P. W.F. Wilson, and S. M. Grundy Should C-Reactive Protein Be Added to Metabolic Syndrome and to Assessment of Global Cardiovascular Risk? Circulation, June 15, 2004; 109(23): 2818 - 2825. [Abstract] [Full Text] [PDF]
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D. J Baer, J. T Judd, B. A Clevidence, and R. P Tracy Dietary fatty acids affect plasma markers of inflammation in healthy men fed controlled diets: a randomized crossover study Am. J. Clinical Nutrition, June 1, 2004; 79(6): 969 - 973. [Abstract] [Full Text] [PDF]
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 L. L Kerst and V. F Mauro Coronary Event Secondary Prevention with Statins Irrespective of LDL-Cholesterol Ann. Pharmacother., June 1, 2004; 38(6): 1060 - 1064. [Abstract] [Full Text] [PDF]
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 M. M. McDermott, P. Greenland, J. M Guralnik, L. Ferrucci, D. Green, K. Liu, M. H Criqui, J. R Schneider, C. Chan, P. Ridker, et al. Inflammatory markers, D-dimer, pro-thrombotic factors, and physical activity levels in patients with peripheral arterial disease Vascular Medicine, May 1, 2004; 9(2): 103 - 105. [Abstract] [PDF]
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A. S. Wierzbicki, P. J. Twomey, and T. M. Reynolds Use of Coronary Calcification Scores to Predict Coronary Heart Disease JAMA, April 21, 2004; 291(15): 1831 - 1831. [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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 J. T. Lane Microalbuminuria as a marker of cardiovascular and renal risk in type 2 diabetes mellitus: a temporal perspective Am J Physiol Renal Physiol, March 1, 2004; 286(3): F442 - F450. [Abstract] [Full Text] [PDF]
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C. M. Ballantyne, R. C. Hoogeveen, H. Bang, J. Coresh, A. R. Folsom, G. Heiss, and A. R. Sharrett Lipoprotein-Associated Phospholipase A2, High-Sensitivity C-Reactive Protein, and Risk for Incident Coronary Heart Disease in Middle-Aged Men and Women in the Atherosclerosis Risk in Communities (ARIC) Study Circulation, February 24, 2004; 109(7): 837 - 842. [Abstract] [Full Text] [PDF]
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M. Haim, V. Boyko, U. Goldbourt, A. Battler, and S. Behar Predictive Value of Elevated White Blood Cell Count in Patients With Preexisting Coronary Heart Disease: The Bezafibrate Infarction Prevention Study Arch Intern Med, February 23, 2004; 164(4): 433 - 439. [Abstract] [Full Text] [PDF]
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 F. Lesperance, N. Frasure-Smith, P. Theroux, and M. Irwin The Association Between Major Depression and Levels of Soluble Intercellular Adhesion Molecule 1, Interleukin-6, and C-Reactive Protein in Patients With Recent Acute Coronary Syndromes Am J Psychiatry, February 1, 2004; 161(2): 271 - 277. [Abstract] [Full Text] [PDF]
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H. R. Chandra, J. A. Goldstein, N. Choudhary, C. S. O'Neill, P. B. George, S. R. Gangasani, L. Cronin, P. A. Marcovitz, A. M. Hauser, and W. W. O'Neill Adverse outcome in aortic sclerosis is associated with coronary artery disease and inflammation J. Am. Coll. Cardiol., January 21, 2004; 43(2): 169 - 175. [Abstract] [Full Text] [PDF]
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J. M Backes, P. A Howard, and P. M Moriarty Role of C-Reactive Protein in Cardiovascular Disease Ann. Pharmacother., January 1, 2004; 38(1): 110 - 118. [Abstract] [Full Text] [PDF]
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 K. E. Watson, A. L. Peters Harmel, and G. Matson Atherosclerosis in Type 2 Diabetes Mellitus: The Role of Insulin Resistance Journal of Cardiovascular Pharmacology and Therapeutics, December 1, 2003; 8(4): 253 - 260. [Abstract] [PDF]
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P. M Ridker and on behalf of the JUPITER Study Group Rosuvastatin in the Primary Prevention of Cardiovascular Disease Among Patients With Low Levels of Low-Density Lipoprotein Cholesterol and Elevated High-Sensitivity C-Reactive Protein: Rationale and Design of the JUPITER Trial* Circulation, November 11, 2003; 108(19): 2292 - 2297. [Full Text] [PDF]
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M. Cesari, B. W.J.H. Penninx, A. B. Newman, S. B. Kritchevsky, B. J. Nicklas, K. Sutton-Tyrrell, S. M. Rubin, J. Ding, E. M. Simonsick, T. B. Harris, et al. Inflammatory Markers and Onset of Cardiovascular Events: Results From the Health ABC Study Circulation, November 11, 2003; 108(19): 2317 - 2322. [Abstract] [Full Text] [PDF]
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A. Silvestro, F. Scopacasa, A. Ruocco, G. Oliva, V. Schiano, C. Zincarelli, and G. Brevetti Inflammatory status and endothelial function in asymptomatic and symptomatic peripheral arterial disease Vascular Medicine, November 1, 2003; 8(4): 225 - 232. [Abstract] [PDF]
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D. M Cummings, D. E King, and A. G Mainous III C-Reactive Protein, Antiinflammatory Drugs, and Quality of Life in Diabetes Ann. Pharmacother., November 1, 2003; 37(11): 1593 - 1597. [Abstract] [Full Text] [PDF]
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A. B. Newman, A. M. Arnold, B. L. Naydeck, L. P. Fried, G. L. Burke, P. Enright, J. Gottdiener, C. Hirsch, D. O'Leary, and R. Tracy "Successful Aging": Effect of Subclinical Cardiovascular Disease Arch Intern Med, October 27, 2003; 163(19): 2315 - 2322. [Abstract] [Full Text] [PDF]
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 P Jousilahti, V Salomaa, V Rasi, E Vahtera, and T Palosuo Association of markers of systemic inflammation, C reactive protein, serum amyloid A, and fibrinogen, with socioeconomic status J Epidemiol Community Health, September 1, 2003; 57(9): 730 - 733. [Abstract] [Full Text] [PDF]
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D Tousoulis, G Davies, C Stefanadis, P Toutouzas, and J A Ambrose Inflammatory and thrombotic mechanisms in coronary atherosclerosis Heart, September 1, 2003; 89(9): 993 - 997. [Abstract] [Full Text] [PDF]
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T. B. Ledue and N. Rifai Preanalytic and Analytic Sources of Variations in C-reactive Protein Measurement: Implications for Cardiovascular Disease Risk Assessment Clin. Chem., August 1, 2003; 49(8): 1258 - 1271. [Abstract] [Full Text] [PDF]
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 M. T. Schram, N. Chaturvedi, C. Schalkwijk, F. Giorgino, P. Ebeling, J. H. Fuller, and C. D. Stehouwer Vascular Risk Factors and Markers of Endothelial Function as Determinants of Inflammatory Markers in Type 1 Diabetes: The EURODIAB Prospective Complications Study Diabetes Care, July 1, 2003; 26(7): 2165 - 2173. [Abstract] [Full Text] [PDF]
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 A. Y.-M. Wang, J. Woo, C. W.-K. Lam, M. Wang, M. M.-M. Sea, S.-F. Lui, P. K.-T. Li, and J. Sanderson Is a Single Time Point C-Reactive Protein Predictive of Outcome in Peritoneal Dialysis Patients? J. Am. Soc. Nephrol., July 1, 2003; 14(7): 1871 - 1879. [Abstract] [Full Text] [PDF]
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L. L. Carr Summary of the Role of Statins in the Treatment of Dyslipidemia J Am Osteopath Assoc, July 1, 2003; 103(7_suppl_3): S1 - S3. [Full Text] [PDF]
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I. M. van der Meer, M. P. M. de Maat, A. J. Kiliaan, D. A. M. van der Kuip, A. Hofman, and J. C. M. Witteman The Value of C-Reactive Protein in Cardiovascular Risk Prediction: The Rotterdam Study Arch Intern Med, June 9, 2003; 163(11): 1323 - 1328. [Abstract] [Full Text] [PDF]
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 W. Koenig C-reactive protein and cardiovascular risk: an update on what is going on in cardiology Nephrol. Dial. Transplant., June 1, 2003; 18(6): 1039 - 1041. [Full Text] [PDF]
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D. E. King, A. G. Mainous III, T. A. Buchanan, and W. S. Pearson C-Reactive Protein and Glycemic Control in Adults With Diabetes Diabetes Care, May 1, 2003; 26(5): 1535 - 1539. [Abstract] [Full Text] [PDF]
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Z. T. Bloomgarden Inflammation and Insulin Resistance Diabetes Care, May 1, 2003; 26(5): 1619 - 1623. [Full Text] [PDF]
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A. W. Chan, D. L. Bhatt, D. P. Chew, J. Reginelli, J. P. Schneider, E. J. Topol, and S. G. Ellis Relation of Inflammation and Benefit of Statins After Percutaneous Coronary Interventions Circulation, April 8, 2003; 107(13): 1750 - 1756. [Abstract] [Full Text] [PDF]
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M. M. Kimberly, H. W. Vesper, S. P. Caudill, G. R. Cooper, N. Rifai, F. Dati, and G. L. Myers Standardization of Immunoassays for Measurement of High-Sensitivity C-reactive Protein. Phase I: Evaluation of Secondary Reference Materials Clin. Chem., April 1, 2003; 49(4): 611 - 616. [Abstract] [Full Text] [PDF]
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G. J. Blake and P. M. Ridker C-reactive protein and other inflammatory risk markers in acute coronary syndromes J. Am. Coll. Cardiol., February 19, 2003; 41(4_Suppl_S): 37S - 42S. [Abstract] [Full Text] [PDF]
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P.O Bonetti, L.O Lerman, C Napoli, and A Lerman Statin effects beyond lipid lowering--are they clinically relevant? Eur. Heart J., February 1, 2003; 24(3): 225 - 248. [Full Text] [PDF]
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P. M Ridker Clinical Application of C-Reactive Protein for Cardiovascular Disease Detection and Prevention Circulation, January 28, 2003; 107(3): 363 - 369. [Full Text] [PDF]
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T. A. Pearson, G. A. Mensah, R. W. Alexander, J. L. Anderson, R. O. Cannon III, M. Criqui, Y. Y. Fadl, S. P. Fortmann, Y. Hong, G. L. Myers, et al. Markers of Inflammation and Cardiovascular Disease: Application to Clinical and Public Health Practice: A Statement for Healthcare Professionals From the Centers for Disease Control and Prevention and the American Heart Association Circulation, January 28, 2003; 107(3): 499 - 511. [Full Text] [PDF]
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References Circulation, December 17, 2002; 106(25): 3373 - 3421. [Full Text]
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T. McLaughlin, F. Abbasi, C. Lamendola, L. Liang, G. Reaven, P. Schaaf, and P. Reaven Differentiation Between Obesity and Insulin Resistance in the Association With C-Reactive Protein Circulation, December 3, 2002; 106(23): 2908 - 2912. [Abstract] [Full Text] [PDF]
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P. Di Napoli, A.A. Taccardi, M. Oliver, and R. De Caterina Statins and stroke: evidence for cholesterol-independent effects Eur. Heart J., December 2, 2002; 23(24): 1908 - 1921. [PDF]
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I. M. van der Meer, M. P.M. de Maat, A. E. Hak, A. J. Kiliaan, A. I. del Sol, D. A.M. van der Kuip, R. L.G. Nijhuis, A. Hofman, and J. C.M. Witteman C-Reactive Protein Predicts Progression of Atherosclerosis Measured at Various Sites in the Arterial Tree: The Rotterdam Study Stroke, December 1, 2002; 33(12): 2750 - 2755. [Abstract] [Full Text] [PDF]
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P. M. Ridker, N. Rifai, L. Rose, J. E. Buring, and N. R. Cook Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events N. Engl. J. Med., November 14, 2002; 347(20): 1557 - 1565. [Abstract] [Full Text] [PDF]
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R. Park, R. Detrano, M. Xiang, P. Fu, Y. Ibrahim, L. LaBree, and S. Azen Combined Use of Computed Tomography Coronary Calcium Scores and C-Reactive Protein Levels in Predicting Cardiovascular Events in Nondiabetic Individuals Circulation, October 15, 2002; 106(16): 2073 - 2077. [Abstract] [Full Text] [PDF]
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R. P. Tracy Inflammation in Cardiovascular Disease: Cart, Horse or Both-Revisited Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1514 - 1515. [Full Text] [PDF]
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E. A. Bermudez, N. Rifai, J. Buring, J. E. Manson, and P. M. Ridker Interrelationships Among Circulating Interleukin-6, C-Reactive Protein, and Traditional Cardiovascular Risk Factors in Women Arterioscler. Thromb. Vasc. Biol., October 1, 2002; 22(10): 1668 - 1673. [Abstract] [Full Text] [PDF]
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J. K. Plenge, T. L. Hernandez, K. M. Weil, P. Poirier, G. K. Grunwald, S. M. Marcovina, and R. H. Eckel Simvastatin Lowers C-Reactive Protein Within 14 Days: An Effect Independent of Low-Density Lipoprotein Cholesterol Reduction Circulation, September 17, 2002; 106(12): 1447 - 1452. [Abstract] [Full Text] [PDF]
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A. R. Brasier, A. Recinos III, and M. S. Eledrisi Vascular Inflammation and the Renin-Angiotensin System Arterioscler. Thromb. Vasc. Biol., August 1, 2002; 22(8): 1257 - 1266. [Abstract] [Full Text] [PDF]
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G. Engstrom, P. Lind, B. Hedblad, L. Stavenow, L. Janzon, and F. Lindgarde Effects of Cholesterol and Inflammation-Sensitive Plasma Proteins on Incidence of Myocardial Infarction and Stroke in Men Circulation, June 4, 2002; 105(22): 2632 - 2637. [Abstract] [Full Text] [PDF]
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A.D. Pradhan and P.M. Ridker Do atherosclerosis and type 2 diabetes share a common inflammatory basis? Eur. Heart J., June 1, 2002; 23(11): 831 - 834. [Full Text] [PDF]
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J.-J. Li, H. Jiang, C.-X. Huang, C.-H. Fang, Q.-Z. Tang, H. Xia, J. Liu, and G.-S. Li Elevated Level of Plasma C-reactive Protein in Patients with Unstable Angina: Its Relations with Coronary Stenosis and Lipid Profile Angiology, May 1, 2002; 53(3): 265 - 272. [Abstract] [PDF]
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E. Rizos, A. Kostoula, M. Elisaf, and D. P. Mikhailidis Effect of Ciprofibrate on C-Reactive Protein and Fibrinogen Levels Angiology, May 1, 2002; 53(3): 273 - 277. [Abstract] [PDF]
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W. Koenig and M. B. Pepys C-Reactive Protein Risk Prediction: Low Specificity, High Sensitivity Ann Intern Med, April 2, 2002; 136(7): 550 - 552. [Full Text] [PDF]
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 E. J. Corwin, L. C. Klein, and K. Rickelman Predictors of Fatigue in Healthy Young Adults: Moderating Effects of Cigarette Smoking and Gender Biol Res Nurs, April 1, 2002; 3(4): 222 - 233. [Abstract] [PDF]
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G. Sesmilo, W. P. Fairfield, L. Katznelson, K. Pulaski, P. U. Freda, V. Bonert, E. Dimaraki, S. Stavrou, M. L. Vance, D. Hayden, et al. Cardiovascular Risk Factors in Acromegaly before and after Normalization of Serum IGF-I Levels with the GH Antagonist Pegvisomant J. Clin. Endocrinol. Metab., April 1, 2002; 87(4): 1692 - 1699. [Abstract] [Full Text] [PDF]
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G. R Thompson Screening relatives of patients with premature coronary heart disease Heart, April 1, 2002; 87(4): 390 - 394. [Full Text] [PDF]
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P. Libby, P. M. Ridker, and A. Maseri Inflammation and Atherosclerosis Circulation, March 5, 2002; 105(9): 1135 - 1143. [Abstract] [Full Text] [PDF]
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R. S. Eidelman, G. A. Lamas, C. H. Hennekens, and P. M. Ridker Aspirin, Postmenopausal Hormones, and C-Reactive Protein Arch Intern Med, February 25, 2002; 162(4): 480 - 481. [Full Text] [PDF]
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A. Tchernof, A. Nolan, C. K. Sites, P. A. Ades, and E. T. Poehlman Weight Loss Reduces C-Reactive Protein Levels in Obese Postmenopausal Women Circulation, February 5, 2002; 105(5): 564 - 569. [Abstract] [Full Text] [PDF]
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