JACC
HOME SUBSCRIPTIONS CURRENT ISSUE PAST ISSUES CARDIOSOURCE SEARCH HELP FEEDBACK
QUICK SEARCH:   [advanced]


     

J Am Coll Cardiol, 2005; 46:464-469, doi:10.1016/j.jacc.2005.04.051
© 2005 by the American College of Cardiology Foundation
This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (65)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Khera, A.
Right arrow Articles by de Lemos, J. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Khera, A.
Right arrow Articles by de Lemos, J. A.

CLINICAL RESEARCH: ATHEROSCLEROSIS

Race and Gender Differences in C-Reactive Protein Levels

Amit Khera, MD, MSc*,{dagger},*, Darren K. McGuire, MD, MHSc, FACC*,{dagger}, Sabina A. Murphy, MPH{ddagger}, Harold G. Stanek, MS*, Sandeep R. Das, MD, MPH*,{dagger}, Wanpen Vongpatanasin, MD, FACC*,{dagger}, Frank H. Wians, Jr, PhD§, Scott M. Grundy, MD, PhD*,|| and James A. de Lemos, MD, FACC*,{dagger}

* Donald W. Reynolds Cardiovascular Clinical Research Center, University of Texas Southwestern Medical Center, Dallas, Texas
{dagger} Division of Cardiology, University of Texas Southwestern Medical Center, Dallas, Texas
§ Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas
|| Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas
{ddagger} Brigham and Women’s Hospital, Boston, Massachusetts.

Manuscript received January 10, 2005; revised manuscript received March 22, 2005, accepted April 19, 2005.

* Reprint requests and correspondence: Dr. Amit Khera, Division of Cardiology, UT Southwestern Medical Center, 5909 Harry Hines Boulevard, Room HA9.133, Dallas, Texas 75390-9047. (Email: amit.khera{at}utsouthwestern.edu).


   Abstract
Top
 Abstract
Methods
 Results
 Discussion
 Conclusions
 References
 
OBJECTIVES: This study sought to determine whether there are race and gender differences in the distribution of C-reactive protein (CRP) levels.

BACKGROUND: Few data are available comparing CRP distributions in different race and gender groups. Recent clinical practice recommendations for CRP testing for cardiovascular risk assessment suggest a uniform threshold to define high relative risk (>3 mg/l).

METHODS: We measured CRP in 2,749 white and black subjects ages 30 to 65 participating in the Dallas Heart Study, a multiethnic, population-based, probability sample, and compared levels of CRP between different race and gender groups.

RESULTS: Black subjects had higher CRP levels than white subjects (median, 3.0 vs. 2.3 mg/l; p < 0.001) and women had higher CRP levels than men (median, 3.3 vs. 1.8 mg/l; p < 0.001). The sample-weight adjusted proportion of subjects with CRP levels >3 mg/l was 31%, 40%, 51%, and 58% in white men, black men, white women, and black women, respectively (p < 0.05 for each group vs. white men). After adjustment for traditional cardiovascular risk factors, estrogen and statin use, and body mass index, a CRP level >3 mg/l remained more common in white women (odds ratio [OR] 1.6; 95% confidence interval [CI] 1.1 to 2.5) and black women (OR 1.7; 95% CI 1.2 to 2.6) but not in black men (OR, 1.3; 95% CI, 0.8 to 1.9) when compared with white men.

CONCLUSIONS: Significant race and gender differences exist in the population distribution of CRP. Further research is needed to determine whether race and gender differences in CRP levels contribute to differences in cardiovascular outcomes, and whether thresholds for cardiovascular risk assessment should be adjusted for different race and gender groups.

Abbreviations and Acronyms
  AHA = American Heart Association
  BMI = body mass index
  CDC = Centers for Disease Control and Prevention
  CRP = C-reactive protein
  CV = cardiovascular

C-reactive protein (CRP) is the most extensively studied inflammatory risk marker, and a series of prospective epidemiologic studies have shown that higher levels of CRP are associated with incident cardiac and vascular events in healthy men and women (1–9). Recent clinical practice recommendations from the Centers for Disease Control and Prevention (CDC) and the American Heart Association (AHA) support the use of CRP testing in selected patients to help assess cardiovascular (CV) risk (10), and trials are underway to explore therapeutic strategies based on CRP levels (11).

Current recommendations for CRP testing suggest uniform CRP thresholds to characterize the relative risk of CV events based on approximate tertile values in several populations (10). Because these populations predominantly consist of white subjects, it is unclear whether the recommended thresholds appropriately reflect CRP distributions for black men and women. Only limited comparisons of CRP levels between black subjects and white subjects have been performed (12–14), and few data are available regarding the prognostic utility of CRP values in black subjects.

Identical CRP thresholds are also suggested for men and women (10). To date, comparisons of CRP levels between men and women have largely been performed across heterogeneous clinical trial cohorts that may not accurately reflect the general population (15). Only limited data are available directly comparing the distribution of CRP levels between men and women within the same study population (13,16,17).

Given the paucity of available data regarding CRP distributions in different race and gender groups and the increasing interest in CRP for risk prediction, we sought to determine whether race and gender differences exist in the distribution of CRP levels using data from the Dallas Heart Study, a large, multiethnic, population-based sample.


   Methods
Top
 Abstract
 Methods
Results
 Discussion
 Conclusions
 References
 
Study population.   The Dallas Heart Study is a multiethnic, population-based, probability sample of 6,101 subjects in Dallas County, and was designed to study CV disease. Details of the study design and characteristics of the enrolled cohort (18) and variable definitions (19) have been described previously. Briefly, a random probability sample of Dallas County residents ages 18 to 65 years old was obtained from a pool of 841,943 eligible subjects using the U.S. Postal Service Delivery Sequence File, with deliberate oversampling of black subjects. All participants provided informed consent to participate in the study, and the protocol was approved by the Institutional Review Board of the University of Texas Southwestern Medical Center. The initial visit for all 6,101 participants included a detailed in-home interview for demographic and health-related data, as well as measurements of weight, heart rate, and five sequential blood pressure measures. All subjects between the ages of 30 and 65 years who completed the initial visit were invited to participate in a second visit to collect fasting venous blood and urine samples. No significant differences were noted in demographics, medical history, blood pressure, or body mass index (BMI) among subjects participating in the home interview and the phlebotomy visit (18). Sampling weights, reflecting the different probabilities of selection for participants and sample attrition between visits, were constructed to generate unbiased estimates of population frequencies (18). The present analyses were restricted to white and black subjects who completed the second visit (2,749 of 3,398 total subjects completing the second visit) because sample sizes in other race and ethnic groups were limited. Race/ethnicity was determined by subject self-report.

High-sensitivity CRP assay.   Blood samples were obtained after an overnight fast in ethylenediamine tetra-acetic acid tubes and were stored for ≤4 h at 4°C before processing. Plasma aliquots were frozen at –80°C until assays were performed. High-sensitivity CRP measurements were performed on thawed samples using the Roche/Hitachi 912 System, Tina-quant assay (Roche Diagnostics, Indianapolis, Indiana), a latex-enhanced immunoturbidimetric method (20). The minimal detectable range of this assay is 0.1 mg/l, and the upper limit is 20 mg/l. Clinical validation of this assay has been described previously (21).

Statistical analysis.   Categorical data are reported as proportions and continuous data as mean values with standard deviations. Baseline demographic variables and CV risk factors were adjusted for sample weights and compared across categories of CRP using the chi-square trend test for categorical variables and the test for trend across ordered groups for continuous variables. The CRP values were adjusted for sample weights and compared between race and gender groups using the analysis of variance test for four group comparisons and the t test for two group comparisons. The results of these analyses were unchanged when log-transformed CRP values were used, and only the non-transformed data are shown. Log-transformed CRP values were also used in multivariable linear regression models in which CRP was the dependent variable. Subjects were categorized according to the CDC/AHA cut points for CRP into three relative risk groups: low-risk (<1 mg/l), intermediate-risk (1 to 3 mg/l) and high-risk (>3 mg/l) groups. Comparisons of the frequency of high-risk CRP levels for each race and gender group were performed using the chi-square test, with white men as the referent group. Adjusted odds ratios for CRP values >3 mg/l for each race/gender group (compared with white men) were determined using multivariable logistic regression models that included traditional CV risk factors as covariates, and using sampling weights. Analyses were performed using Stata version 8.2 (Stata Corp. LP, College Station, Texas) and SUDAAN version 9 (Research Triangle Institute, Research Triangle Park, North Carolina).


   Results
Top
 Abstract
 Methods
 Results
Discussion
 Conclusions
 References
 
The baseline characteristics of the four different race and gender groups are shown in Table 1. Compared with white subjects, black men and women had a significantly higher prevalence of diabetes and hypertension. Black women had a higher BMI and used estrogen less often than white women. Black men had the highest prevalence of tobacco use.


View this table:
[in this window]
[in a new window]
  		Table 1. Baseline Clinical Characteristics of Different Race and Gender Groups
 
Subjects were unequally distributed across CRP risk categories (CRP <1 mg/l, n = 546 [20%]; CRP 1 to 3 mg/l, n = 848 [31%]; CRP >3 mg/l, n = 1,355 [49%]) (Table 2). As summarized in Tables 2 and 3, increasing CRP levels were associated with a number of CV risk factors in unadjusted analyses. Importantly, female gender and black race were both associated with higher CRP levels. The correlation between CRP and BMI was stronger than the correlation between CRP and any other continuous variable, including age and all measured lipid risk factors, and was greater in women compared with men (Table 3).


View this table:
[in this window]
[in a new window]
  		Table 2. Association Between C-Reactive Protein Risk Categories and Demographic and Clinical Variables
 

View this table:
[in this window]
[in a new window]
  		Table 3. Correlation Between C-Reactive Protein Levels and Continuous Variables
 
Black subjects had higher CRP levels than white subjects (median, 3.0 vs. 2.3 mg/l; p < 0.001) and women had higher CRP levels than men (median, 3.3 vs. 1.8 mg/l; p < 0.001) (Fig. 1). In multivariate analyses adjusting for traditional CV risk factors, BMI, and estrogen and statin use, race and gender were independently associated with log CRP levels (p < 0.05 for each). Black men, white women, and black women all had higher CRP levels compared with white men, with the highest levels observed among black women (Fig. 2). Excluding users of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) and oral estrogen had little effect on the CRP differences between black and white subjects (median, 2.6 vs. 2.1 mg/l; p < 0.001) or the differences between women and men (median, 2.7 vs. 1.8 mg/l; p < 0.001). In a similar sensitivity analysis, exclusion of these subjects only slightly attenuated the differences in median CRP levels among the four demographic groups (white men, 1.8 mg/l; black men, 2.0 mg/l; white women, 2.6 mg/l; black women, 3.2 mg/l; p < 0.001).



View larger version (14K):
[in this window]
[in a new window]
  		Figure 1 Comparison of C-reactive protein (CRP) levels between white and black subjects, and between men and women. Data are shown as medians (25th and 75th percentiles); p < 0.001 for each comparison.

 


View larger version (14K):
[in this window]
[in a new window]
  		Figure 2 Comparison of C-reactive protein (CRP) levels between different race and gender groups. Data are shown as medians (25th and 75th percentiles); p < 0.001.

 
The proportion of subjects with high-risk CRP levels according to the CDC/AHA practice recommendation was estimated for each race and gender group (Table 4). Black men, white women, and black women were significantly more likely to have CRP values in the high-risk range compared with white men, with almost two-thirds of black women having CRP levels >3 mg/l. These differences persisted after excluding statin and estrogen users and after sample-weight adjustment (Table 4). Adjustment for traditional CV risk factors, BMI, statin and estrogen use, and sampling weights attenuated the differences between race and gender groups, yet an elevated CRP level remained more common in white women and black women than in white men (odds ratio [OR] 1.6, 95% confidence interval [CI] 1.1 to 2.5, p < 0.05; and OR 1.7, 95% CI 1.2 to 2.6, p < 0.05, respectively) (Fig. 3). In contrast, the differences between black men and white men were no longer statistically significant after multivariate adjustment (OR 1.3; 95% CI 0.8 to 1.9).


View this table:
[in this window]
[in a new window]
  		Table 4. Proportion of Subjects with C-Reactive Protein Levels >3 mg/l
 


View larger version (13K):
[in this window]
[in a new window]
  		Figure 3 Adjusted odds ratios and 95% confidence intervals for C-reactive protein (CRP) levels >3 mg/l. White men are the referent group. Filled squares = adjusted for sample weights only; filled diamonds = adjusted for age, diabetes, hypercholesterolemia, high-density lipoprotein cholesterol, hypertension, smoking, body mass index, estrogen use, statin use, creatinine, and sample weights.

 
An increasing BMI was associated with higher CRP levels in each race and gender group (p < 0.001 for each), but the increase in CRP levels with obesity was greater for women than for men (p value for interaction of obesity and gender on log CRP levels <0.001) (Fig. 4).



View larger version (21K):
[in this window]
[in a new window]
  		Figure 4 Relationship between C-reactive protein (CRP) levels and body mass index (BMI) for different race and gender groups (p < 0.001 for association between CRP levels and body mass index categories for each group; p = 0.001 for interaction of body mass index and gender on log CRP levels).

 

   Discussion
Top
 Abstract
 Methods
 Results
 Discussion
Conclusions
 References
 
In a large, multiethnic, population-based sample, we observed that black subjects have significantly higher CRP levels than white subjects, and women have significantly higher CRP levels than men. These findings persisted after exclusion of subjects taking statins and oral estrogen, and after adjustment for traditional CV risk factors and BMI. The associations were robust whether CRP was considered as a continuous or as a categorical variable (CRP >3 mg/l). Given the increasing use of CRP as a component of CV risk prediction, and the potential future use of CRP in clinical decision-making, our findings have important public health implications.

Comparison with other studies.   The potential for important racial and ethnic differences in CRP levels has been shown in studies of other ethnic groups (22–24). However, studies comparing CRP levels between black and white populations are limited (13,14,17,25), and the major studies examining the relationship between CRP levels and CV events have included few if any black subjects (1–9). The National Health and Nutrition Examination Survey 1999 to 2000 compared CRP levels in black and white men age ≥20 years, an age range younger than in the current study (14). Although the investigators concluded that CRP levels were similar between black and white men based on median values, the upper tertiles for black men ages 45 to 64 years and ≥65 years were 5.4 and 7.0 mg/l, respectively, compared with 3.2 and 3.7 mg/l in white men. A similar analysis in women was performed using the same database and showed that the median CRP level in black women was 3.5 mg/l compared with 2.5 mg/l in white women (13). These differences persisted after excluding users of hormone replacement therapy, but data on statin use were not available. Recently, one study explored ethnic differences in CRP levels in women and found that black women had higher CRP levels than white women (25). However, this study consisted of a clinical trial cohort of postmenopausal women with much higher rates of estrogen use, lower BMI measures, and lower CRP values than our population-based sample. The present population-based study showed that in Dallas County, which likely represents a typical multiethnic U.S. urban population, the median CRP level was 30% higher in black subjects than in white subjects.

Previously, CRP levels were thought to be similar between women and men (15,26). However, these conclusions were based on comparisons of CRP levels across different studies with heterogeneous study populations, rather than on direct comparisons between men and women within the same sample. Moreover, these studies were largely performed in volunteers, who may differ from the general population in important ways. No differences in CRP levels between men and women were found in a compilation of European population-based studies (27). However, direct comparisons in U.S. research populations suggest that there may be gender differences in CRP levels (13,16). In our study of a large, contemporary, U.S. population-based sample, we observed that the median CRP level was almost twice as high in women compared with men.

Our contemporary, urban, and unselected cohort has a higher prevalence of overweight and obese subjects than has been reported in previous studies of CRP from more highly selected research populations (4,5,25). We found that increases in BMI were associated with much greater increases in CRP in women than in men (Fig. 4), a finding that may in part explain gender-based differences in CRP levels.

Clinical and public health implications.   The finding of race and gender-based differences in CRP levels has important implications for the clinical use of CRP. Our findings suggest that the CRP risk categories outlined in the CDC/AHA statement, which were derived from selected research populations, may not be reflective of a contemporary, predominantly urban, multiethnic population with very high rates of obesity.

Several different interpretations of our findings are possible. Higher CRP levels in black subjects, and in particular in black women, may portend an increased risk for future CV events. Black subjects have a greater prevalence of CV risk factors than white subjects (28,29), and higher CRP levels may reflect this risk factor burden. Also, racial differences in inflammation may directly contribute to the higher coronary heart disease mortality rates in black subjects (30). On the other hand, it is also possible that reliance on CRP for risk assessment in black subjects may overestimate the risk for cardiac and vascular events, and could lead to overuse of resources. For example, if a CRP value >3 were used as a criterion for initiating a therapeutic intervention, approximately 50% of black subjects between 30 and 65 years of age would be eligible for this intervention in Dallas County. Because our study uses a cross-sectional design, the prognostic implications of the racial differences in CRP distributions cannot be determined: long-term outcome studies in black subjects are needed to determine the implications of these findings and to determine whether the CDC/AHA risk thresholds are appropriate.

The clinical implications of gender differences in CRP levels also require consideration. Several studies have shown a strong association between CRP levels and CV outcomes in women (4,6). It is not clear, however, that the threshold for defining high-risk CRP levels for research cohorts can be generalized to the population, in which obesity is highly prevalent and more than 50% of women have CRP values >3.


   Conclusions
Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
References
 
In this multiethnic population-based study, we found significant race and gender differences in the distribution of CRP levels, with women and black subjects having higher CRP levels than men and white subjects, respectively. Studies with long-term follow-up will be needed to determine whether these differences in CRP distribution contribute to differences in clinical outcomes and whether CRP risk thresholds should be adjusted for different race and gender groups.


   Acknowledgments
 
The authors thank Jody Balko for performing the CRP measurements and Dr. Helen H. Hobbs for her critical review of the manuscript.


   Footnotes
 
The Dallas Heart Study was funded by the Donald W. Reynolds Foundation (Las Vegas, Nevada). These studies were partially supported by USPHS GCRC grant #M01-RR00633 from NIH/NCRR-CR. The C-reactive protein measurement was supported by Roche Diagnostics (Indianapolis, Indiana). Dr. de Lemos received research grant support from Roche Diagnostics.


   References
Top
 Abstract
 Methods
 Results
 Discussion
 Conclusions
 References
 

  1. Albert CM, Ma J, Rifai N, Stampfer MJ, Ridker PM. Prospective study of C-reactive protein, homocysteine, and plasma lipid levels as predictors of sudden cardiac death Circulation 2002;105:2595-2599.[Abstract/Free Full Text]
  2. Koenig W, Sund M, Frohlich M, et al. C-reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged menresults from the MONICA (Monitoring Trends and Determinants in Cardiovascular Disease) Augsburg Cohort Study, 1984 to 1992. Circulation 1999;99:237-242.[Abstract/Free Full Text]
  3. Kuller LH, Tracy RP, Shaten J, Meilahn EN. Relation of C-reactive protein and coronary heart disease in the MRFIT nested case-control study. Multiple Risk Factor Intervention Trial Am J Epidemiol 1996;144:537-547.[Abstract/Free Full Text]
  4. Pradhan AD, Manson JE, Rossouw JE, et al. Inflammatory biomarkers, hormone replacement therapy, and incident coronary heart diseaseprospective analysis from the Women’s Health Initiative observational study. JAMA 2002;288:980-987.[Abstract/Free Full Text]
  5. Ridker PM, Cushman M, Stampfer MJ, Tracy RP, Hennekens CH. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men N Engl J Med 1997;336:973-979.[Abstract/Free Full Text]
  6. Ridker PM, Buring JE, Shih J, Matias M, Hennekens CH. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women Circulation 1998;98:731-733.[Abstract/Free Full Text]
  7. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women N Engl J Med 2000;342:836-843.[Abstract/Free Full Text]
  8. Ridker PM, Rifai N, Clearfield M, et al. Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events N Engl J Med 2001;344:1959-1965.[Abstract/Free Full Text]
  9. Rost NS, Wolf PA, Kase CS, et al. Plasma concentration of C-reactive protein and risk of ischemic stroke and transient ischemic attackthe Framingham study. Stroke 2001;32:2575-2579.[Abstract/Free Full Text]
  10. Pearson TA, Mensah GA, Alexander RW, 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 2003;107:499-511.[Free Full Text]
  11. Ridker PM. Rosuvastatin in the primary prevention of cardiovascular disease among patients with low levels of low-density lipoprotein cholesterol and elevated high-sensitivity C-reactive proteinrationale and design of the JUPITER trial. Circulation 2003;108:2292-2297.[Free Full Text]
  12. Albert MA, Torres J, Glynn RJ, Ridker PM. Perspective on selected issues in cardiovascular disease research with a focus on black Americans Circulation 2004;110:e7-e12.[Free Full Text]
  13. Ford ES, Giles WH, Mokdad AH, Myers GL. Distribution and correlates of C-reactive protein concentrations among adult U.S. women Clin Chem 2004;50:574-581.[Abstract/Free Full Text]
  14. Ford ES, Giles WH, Myers GL, Mannino DM. Population distribution of high-sensitivity C-reactive protein among U.S. menfindings from National Health and Nutrition Examination Survey 1999–2000. Clin Chem 2003;49:686-690.[Free Full Text]
  15. Rifai N, Ridker PM. Population distributions of C-reactive protein in apparently healthy men and women in the United Statesimplication for clinical interpretation. Clin Chem 2003;49:666-669.[Free Full Text]
  16. McConnell JP, Branum EL, Ballman KV, Lagerstedt SA, Katzmann JA, Jaffe AS. Gender differences in C-reactive protein concentrations—confirmation with two sensitive methods Clin Chem Lab Med 2002;40:56-59.[CrossRef][ISI][Medline]
  17. Wener MH, Daum PR, McQuillan GM. The influence of age, gender, and race on the upper reference limit of serum C-reactive protein concentration J Rheumatol 2000;27:2351-2359.[ISI][Medline]
  18. Victor RG, Haley RW, Willett DL, et al. The Dallas Heart studya population-based probability sample for the multidisciplinary study of ethnic differences in cardiovascular health. Am J Cardiol 2004;93:1473-1480.[CrossRef][ISI][Medline]
  19. Deo R, Khera A, McGuire DK, et al. Association among plasma levels of monocyte chemoattractant protein-1, traditional cardiovascular risk factors, and subclinical atherosclerosis J Am Coll Cardiol 2004;44:1812-1818.[Abstract/Free Full Text]
  20. Roberts WL, Moulton L, Law TC, et al. Evaluation of nine automated high-sensitivity C-reactive protein methods: implications for clinical and epidemiological applications. Part 2 Clin Chem 2001;47:418-425.[Abstract/Free Full Text]
  21. Danesh J, Wheeler JG, Hirschfield GM, et al. C-reactive protein and other circulating markers of inflammation in the prediction of coronary heart disease N Engl J Med 2004;350:1387-1397.[Abstract/Free Full Text]
  22. Lear SA, Chen MM, Birmingham CL, Frohlich JJ. The relationship between simple anthropometric indices and C-reactive proteinethnic and gender differences. Metabolism 2003;52:1542-1546.[CrossRef][ISI][Medline]
  23. Chambers JC, Eda S, Bassett P, et al. C-reactive protein, insulin resistance, central obesity, and coronary heart disease risk in Indian Asians from the United Kingdom compared with European white subjects Circulation 2001;104:145-150.[Abstract/Free Full Text]
  24. Anand SS, Razak F, Yi Q, et al. C-reactive protein as a screening test for cardiovascular risk in a multiethnic population Arterioscler Thromb Vasc Biol 2004;24:1509-1515.[Abstract/Free Full Text]
  25. Albert MA, Glynn RJ, Buring J, Ridker PM. C-reactive protein levels among women of various ethnic groups living in the United States (from the Women’s Health Study) Am J Cardiol 2004;93:1238-1242.[CrossRef][ISI][Medline]
  26. Ridker PM. Clinical application of C-reactive protein for cardiovascular disease detection and prevention Circulation 2003;107:363-369.[Free Full Text]
  27. Imhof A, Frohlich M, Loewel H, et al. Distributions of C-reactive protein measured by high-sensitivity assays in apparently healthy men and women from different populations in Europe Clin Chem 2003;49:669-672.[Free Full Text]
  28. Potts JL, Thomas J. Traditional coronary risk factors in African Americans Am J Med Sci 1999;317:189-192.[CrossRef][ISI][Medline]
  29. Watkins LO. Perspectives on coronary heart disease in African Americans Rev Cardiovasc Med 2004;5(Suppl 3):S3-S13.
  30. Albert MA, Ridker PM. Inflammatory biomarkers in African Americansa potential link to accelerated atherosclerosis. Rev Cardiovasc Med 2004;5(Suppl 3):S22-S27.



This article has been cited by other articles:


Home page
 Clin. Chem.Home page
A. Kelley-Hedgepeth, D. M. Lloyd-Jones, A. Colvin, K. A. Matthews, J. Johnston, M. R. Sowers, B. Sternfeld, R. C. Pasternak, C. U. Chae, and for the SWAN Investigators
Ethnic Differences in C-Reactive Protein Concentrations
Clin. Chem., June 1, 2008; 54(6): 1027 - 1037.
[Abstract] [Full Text] [PDF]

Home page
 NEJMHome page
J. A. de Lemos and D. M. Lloyd-Jones
Multiple Biomarker Panels for Cardiovascular Risk Assessment
N. Engl. J. Med., May 15, 2008; 358(20): 2172 - 2174.
[Full Text] [PDF]

Home page
 Ann Fam MedHome page
D. E. King, A. G. Mainous III, B. M. Egan, R. F. Woolson, and M. E. Geesey
Effect of Psyllium Fiber Supplementation on C-Reactive Protein: The Trial to Reduce Inflammatory Markers (TRIM)
Ann. Fam. Med, March 1, 2008; 6(2): 100 - 106.
[Abstract] [Full Text] [PDF]

Home page
 LupusHome page
S-S. Lee, S. Singh, L. Magder, and M. Petri
Predictors of high sensitivity C-reactive protein levels in patients with systemic lupus erythematosus
Lupus, February 1, 2008; 17(2): 114 - 123.
[Abstract] [PDF]

Home page
 Clin. Chem.Home page
C. Marsik, L. Kazemi-Shirazi, T. Schickbauer, S. Winkler, C. Joukhadar, O. F. Wagner, and G. Endler
C-Reactive Protein and All-Cause Mortality in a Large Hospital-Based Cohort
Clin. Chem., February 1, 2008; 54(2): 343 - 349.
[Abstract] [Full Text] [PDF]

Home page
 Endocr. Rev.Home page
D. P. Rose, S. M. Haffner, and J. Baillargeon
Adiposity, the Metabolic Syndrome, and Breast Cancer in African-American and White American Women
Endocr. Rev., December 1, 2007; 28(7): 763 - 777.
[Abstract] [Full Text] [PDF]

Home page
 StrokeHome page
K. Sander, C. Schulze Horn, C. Briesenick, and D. Sander
High-Sensitivity C-Reactive Protein Is Independently Associated With Early Carotid Artery Progression in Women But Not in Men: The INVADE Study
Stroke, November 1, 2007; 38(11): 2881 - 2886.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
T. Liukkonen, P. Rasanen, A. Ruokonen, J. Laitinen, J. Jokelainen, M. Leinonen, V. B. Meyer-Rochow, and M. Timonen
C-reactive protein Levels and Sleep Disturbances: Observations Based on The Northern Finland 1966 Birth Cohort Study
Psychosom Med, October 1, 2007; 69(8): 756 - 761.
[Abstract] [Full Text] [PDF]

Home page
 HypertensionHome page
S. K. Mehta, J. E. Rame, A. Khera, S. A. Murphy, R. M. Canham, R. M. Peshock, J. A. de Lemos, and M. H. Drazner
Left Ventricular Hypertrophy, Subclinical Atherosclerosis, and Inflammation
Hypertension, June 1, 2007; 49(6): 1385 - 1391.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
O. Ben-Yehuda
High-Sensitivity C-Reactive Protein in Every Chart?: The Use of Biomarkers in Individual Patients
J. Am. Coll. Cardiol., May 29, 2007; 49(21): 2139 - 2141.
[Abstract] [Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
X. Ye, Z. Yu, H. Li, O. H. Franco, Y. Liu, and X. Lin
Distributions of C-Reactive Protein and its Association With Metabolic Syndrome in Middle-Aged and Older Chinese People
J. Am. Coll. Cardiol., May 1, 2007; 49(17): 1798 - 1805.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, and R. H. Christenson
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes
Circulation, April 3, 2007; 115(13): e356 - e375.
[Full Text] [PDF]

Home page
 Clin. Chem.Home page
NACB WRITING GROUP MEMBERS, D. A. Morrow, C. P. Cannon, R. L. Jesse, L. K. Newby, J. Ravkilde, A. B. Storrow, A. H.B. Wu, R. H. Christenson, NACB COMMITTEE MEMBERS, et al.
National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: Clinical Characteristics and Utilization of Biochemical Markers in Acute Coronary Syndromes
Clin. Chem., April 1, 2007; 53(4): 552 - 574.
[Full Text] [PDF]

Home page
 CirculationHome page
W. Vongpatanasin, G. D. Thomas, R. Schwartz, L. A. Cassis, S. Osborne-Lawrence, L. Hahner, L. L. Gibson, S. Black, D. Samols, and P. W. Shaul
C-Reactive Protein Causes Downregulation of Vascular Angiotensin Subtype 2 Receptors and Systolic Hypertension in Mice
Circulation, February 27, 2007; 115(8): 1020 - 1028.
[Abstract] [Full Text] [PDF]

Home page
 StrokeHome page
C. D. Bushnell, P. Hurn, C. Colton, V. M. Miller, G. del Zoppo, M. S.V. Elkind, B. Stern, D. Herrington, G. Ford-Lynch, P. Gorelick, et al.
Advancing the Study of Stroke in Women: Summary and Recommendations for Future Research From an NINDS-Sponsored Multidisciplinary Working Group
Stroke, September 1, 2006; 37(9): 2387 - 2399.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
M. A. Albert and P. M Ridker
C-Reactive Protein as a Risk Predictor: Do Race/Ethnicity and Gender Make a Difference?
Circulation, August 1, 2006; 114(5): e67 - e74.
[Full Text] [PDF]

Home page
 Arch Intern MedHome page
D. M. Lloyd-Jones and L. Tian
Predicting cardiovascular risk: so what do we do now?
Arch Intern Med, July 10, 2006; 166(13): 1342 - 1344.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
A. S. Jaffe, L. Babuin, and F. S. Apple
Biomarkers in Acute Cardiac Disease: The Present and the Future
J. Am. Coll. Cardiol., July 4, 2006; 48(1): 1 - 11.
[Abstract] [Full Text] [PDF]

Home page
 ANN INTERN MEDHome page
D. M. Lloyd-Jones, K. Liu, L. Tian, and P. Greenland
Narrative Review: Assessment of C-Reactive Protein in Risk Prediction for Cardiovascular Disease
Ann Intern Med, July 4, 2006; 145(1): 35 - 42.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
K. Niu, A. Hozawa, S. Kuriyama, K. Ohmori-Matsuda, T. Shimazu, N. Nakaya, K. Fujita, I. Tsuji, and R. Nagatomi
Dietary long-chain n-3 fatty acids of marine origin and serum C-reactive protein concentrations are associated in a population with a diet rich in marine products
Am. J. Clinical Nutrition, July 1, 2006; 84(1): 223 - 229.
[Abstract] [Full Text] [PDF]

Home page
 Ann. Thorac. Surg.Home page
C. W. Hogue Jr, C. A. Palin, R. Kailasam, J. S. Lawton, A. Nassief, V. G. Davila-Roman, B. Thomas, and R. Damiano
C-reactive protein levels and atrial fibrillation after cardiac surgery in women.
Ann. Thorac. Surg., July 1, 2006; 82(1): 97 - 102.
[Abstract] [Full Text] [PDF]

Home page
 Anesth. Analg.Home page
C. W. Hogue Jr, T. Hershey, D. Dixon, R. Fucetola, A. Nassief, K. E. Freedland, B. Thomas, and K. Schechtman
Preexisting cognitive impairment in women before cardiac surgery and its relationship with C-reactive protein concentrations.
Anesth. Analg., June 1, 2006; 102(6): 1602 - 1608.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
T. W. Wallace, S. M. Abdullah, M. H. Drazner, S. R. Das, A. Khera, D. K. McGuire, F. Wians, M. S. Sabatine, D. A. Morrow, and J. A. de Lemos
Prevalence and Determinants of Troponin T Elevation in the General Population
Circulation, April 25, 2006; 113(16): 1958 - 1965.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Clin. Nutr.Home page
Y. Ma, J. A Griffith, L. Chasan-Taber, B. C Olendzki, E. Jackson, E. J Stanek III, W. Li, S. L Pagoto, A. R Hafner, and I. S Ockene
Association between dietary fiber and serum C-reactive protein.
Am. J. Clinical Nutrition, April 1, 2006; 83(4): 760 - 766.
[Abstract] [Full Text] [PDF]

Home page
 Nephrol Dial TransplantHome page
M. Hermann and F. Ruschitzka
Novel anti-inflammatory drugs in hypertension
Nephrol. Dial. Transplant., April 1, 2006; 21(4): 859 - 864.
[Full Text] [PDF]

Home page
 Journal Watch CardiologyHome page
CRP Levels Vary by Sex and Race
Journal Watch Cardiology, September 16, 2005; 2005(916): 4 - 4.
[Full Text]

Home page
 JWatch GeneralHome page
C-Reactive Protein Levels -- Do Race and Sex Matter?
Journal Watch (General), September 13, 2005; 2005(913): 2 - 2.
[Full Text]

This Article
Right arrow Abstract Freely available
Right arrow Figures Only
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager