American Journal of Epidemiology Vol. 154, No. 8 : 758-764
Copyright © 2001 by The Johns Hopkins University School of Hygiene and Public Health
ORIGINAL CONTRIBUTIONS |
White Blood Cell Count and Incidence of Coronary Heart Disease and Ischemic Stroke and Mortality from Cardiovascular Disease in African-American and White Men and Women: Atherosclerosis Risk in Communities Study
1 Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis, MN.
2 Department of Epidemiology, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, MD.
3 Department of Biostatistics, School of Public Health, University of North Carolina, Chapel Hill, NC.
4 Department of Medicine, School of Medicine, University of Mississippi, and University of Mississippi Medical Center, Jackson, MS.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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The authors examined the association between white blood cell (WBC) count and incidence of coronary heart disease and ischemic stroke and mortality from cardiovascular disease in 13,555 African-American and White men and women from the Atherosclerosis Risk in Communities (ARIC) Study. Blood was drawn at the ARIC baseline examination, beginning in 1987–1989. During an average of 8 years of follow-up (through December 1996), there were 488 incident coronary heart disease events, 220 incident strokes, and 258 deaths from cardiovascular disease. After adjustment for age, sex, ARIC field center, and multiple risk factors, there was a direct association between WBC count and incidence of coronary heart disease (p < 0.001 for trend) and stroke (p for trend < 0.001) and mortality from cardiovascular disease (p for trend < 0.001) in African Americans. The African Americans in the highest quartile of WBC count (
7,000 cells/mm3) had 1.9 times the risk of incident coronary heart disease (95% confidence interval (CI): 1.19, 3.09), 1.9 times the risk of incident ischemic stroke (95% CI: 1.03, 3.34), and 2.3 times the risk of cardiovascular disease mortality (95% CI: 1.38, 3.72) as their counterparts in the lowest quartile of WBC count (<4,800 cells/mm3). These associations were similar in Whites and in never smokers. An elevated WBC count is directly associated with increased incidence of coronary heart disease and ischemic stroke and mortality from cardiovascular disease in African-American and White men and women.
cardiovascular diseases; cerebrovascular accident; coronary disease; leukocyte count; leukocytes; prospective studies
Abbreviations: ARIC, Atherosclerosis Risk in Communities; CI, confidence interval; WBC, white blood cell
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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An elevated total white blood cell (WBC) count is a risk factor for atherosclerotic vascular disease. WBC-derived macrophages and other phagocytes are believed to contribute to vascular injury and atherosclerotic progression (1
, 2). Several prospective studies have shown a positive and independent association between WBC count and coronary heart disease incidence or mortality (3–11). However, little is known about this association in African Americans.
WBC count is associated with several cardiovascular disease risk factors (12–14). WBC count is higher in smokers than in nonsmokers (12–14). Some investigators have reported that elevated WBC count is associated with increased risk of coronary heart disease mortality in both smokers and nonsmokers (9, 10), while other studies have not found an association among never smokers (7). WBC count is inversely associated with physical activity, high density lipoprotein cholesterol, and family income (12–14). Studies consistently report a lower WBC count in African Americans than in Whites, although the reason is unclear. There has been little research on the relation between WBC count and cardiovascular disease incidence or mortality in African Americans (7). Therefore, we investigated the associations between WBC count and incidence of coronary heart disease and ischemic stroke and between WBC count and mortality from cardiovascular disease in African-American and White men and women from the Atherosclerosis Risk in Communities (ARIC) Study.
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MATERIALS AND METHODS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Study population
The ARIC Study is a population-based cohort study designed to investigate the etiology of atherosclerosis in a biracial population. The study population comprises 15,792 men and women aged 45–64 years. Participants were recruited in 1987–1989 from four US communities: Forsyth County, North Carolina; Jackson, Mississippi; Washington County, Maryland; and the northwestern suburbs of Minneapolis, Minnesota. The response rates in these communities were 66 percent, 46 percent, 65 percent, and 67 percent, respectively. All participants from Jackson and 12 percent of the participants from Forsyth County were African-American, whereas 99 percent of participants from the other two communities were White. The complete study design, sampling strategy, and examination techniques used have been described previously (15
).
The baseline examination included a home interview and a clinical examination. The home interview assessed participants' health habits, demographic characteristics, and medical histories. The clinical examination included a physical examination, blood pressure measurement, blood tests, collection of anthropometric data, a 12-lead electrocardiogram, and a B-mode ultrasound examination. Details on the examination procedures have been published elsewhere (6, 13, 15, 16).
All participants gave their informed consent for the clinical examination and were asked to fast for the previous 12 hours. Serum, plasma, and whole blood samples were drawn from an antecubital vein (15, 16). WBC count was determined by automated particle counters within 24 hours after venipuncture in local hospital hematology laboratories. The reliability coefficient for the WBC count measurement was greater than 0.96 (13). Levels of plasma total cholesterol and high density lipoprotein cholesterol were measured by an enzymatic method. Seated blood pressure was measured after 5 minutes' rest using a random-zero sphygmomanometer. Diabetes mellitus was defined as a fasting glucose level 126 mg/dl, a nonfasting glucose level 200 mg/dl, use of hypoglycemic agents, or a history of physician-diagnosed diabetes mellitus. Body weight and height were measured with a vertical metal rule and a calibrated scale. Waist girth was measured at the level of the umbilicus with a steel or fiberglass tape measure. Cigarette smoking, alcohol intake, family income, and educational level were assessed by means of standardized questionnaires. Subjects' smoking status was classified as never smoking, formerly smoking, or currently smoking. Alcohol intake status was classified as never drinking, formerly drinking, or currently drinking. Annual family income was classified as low (<$25,000), medium ($25,000–<$50,000), or high ($50,000). Educational level was classified by number of years of education: less than high school, completion of high school, or college graduation or more. Physical activity in sports was assessed by an adaptation of the Baecke et al. (17) physical activity questionnaire, scored from 1 (low) to 5 (high), and was classified as low (<2), moderate (2–<4), or high (4).
Ascertainment of disease incidence or mortality
All participants were followed from the baseline examination to the date of disease incidence/death or loss to follow-up, or through December 31, 1996. ARIC participants were contacted annually by telephone for identification of all hospitalizations and deaths, and lists of discharges from local hospitals were scanned for events. For patients who had been hospitalized with potential myocardial infarction, trained abstractors recorded the presenting signs and symptoms and photocopied up to three 12-lead electrocardiograms for Minnesota coding (18). For assessment of potential stroke, the abstractors recorded relevant signs and symptoms and photocopied neuroimaging and other diagnostic reports. Deaths were identified from death certificates, and potential out-of-hospital fatal coronary heart disease events were investigated by interviewing one or more next of kin and by the completion of a questionnaire by the patient's physician. All coronary heart disease events were validated by a committee of physicians using standardized criteria (19). Incident strokes were validated by a combination of computerized algorithm and physician review (20).
We defined a coronary heart disease event as a definite or probable hospitalized myocardial infarction or definite fatal coronary heart disease. Unstable angina or coronary revascularization was not included, because of concerns about ethnic differences in diagnosis and use of procedures. An ischemic stroke event was defined as a definite or probable hospitalized embolic or thrombotic stroke. Transient ischemic attacks and a small number of undocumented fatal strokes were excluded. Cardiovascular disease death was based only on the death certificate and included any underlying cause of death (codes 390–459) as coded by state health departments according to the International Classification of Diseases, Ninth Revision.
Statistical analysis
We included 13,555 men and women aged 45–64 years who participated in the ARIC baseline examination from 1987 to 1989. Excluded were those with a history of coronary heart disease, stroke, or cancer at baseline; those who had a WBC count of >15,000 cells/mm3 or <2,000 cells/mm3; and those missing baseline WBC counts or other covariate values. Proportional hazards regression was used to examine the overall associations between WBC count and incidence of coronary heart disease and stroke and between WBC count and mortality from cardiovascular disease (21). Race-specific models were used to examine this association in African Americans and Whites separately. We also examined the association between WBC count and disease incidence or mortality by smoking status. WBC counts were grouped into quartiles (<4.8, 4.8–<5.8, 5.8–<7.0, and 7.0 x 1,000 cells/mm3). Relative risks and 95 percent confidence intervals for incidence or mortality were estimated after adjustment for age, sex, and ARIC field center and after further adjustment for family income, education, cigarette smoking, physical activity, alcohol intake, waist girth, high density lipoprotein cholesterol and total cholesterol levels, diabetes, systolic blood pressure, and use of antihypertensive medication. The lowest WBC quartile (<4,800 cells/mm3) was the reference category.
Inspection of empirical cumulative hazards plots indicated that the proportional hazards assumption was justified. Trends across WBC counts were tested by treating WBC count categories as an ordinal score. Additionally, we tested WBC count differences between race and sex groups with two-factor analysis of variance. We also examined the relations between differential WBC count and incidence of coronary heart disease and stroke and mortality from cardiovascular disease. All statistical procedures were performed using Statistical Analysis System software (SAS Institute, Inc., Cary, North Carolina).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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During an average of 8 years of follow-up, we identified 488 incident coronary heart disease events, 220 incident ischemic stroke events, and 258 deaths coded as being due to cardiovascular disease. As table 1 shows, White men had a higher WBC count than did White women (p < 0.001), but African-American men had a WBC count similar to that of African-American women (p = 0.15). Both White men and White women had higher WBC counts than did African-American men and women, respectively (p < 0.001). Most other risk factors differed by sex and race in the expected directions and as previously reported by ARIC investigators (13
).
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Overall, there was a direct association of WBC count with incidence of coronary heart disease (p for trend < 0.001) and stroke (p for trend < 0.001) and with cardiovascular disease mortality (p for trend < 0.001), after adjustment for age, sex, race, and ARIC field center. Associations persisted after additional adjustment for other risk factors (figure 1). Individuals in the highest quartile of WBC count (
7,000 cells/mm3) had 1.8 times the risk of incident coronary heart disease (95 percent confidence interval (CI): 1.32, 2.43; p < 0.001), 2.0 times the risk of incident stroke (95 percent CI: 1.29, 2.99; p = 0.002), and 2.3 times the risk of cardiovascular disease mortality (95 percent CI: 1.58, 3.44; p < 0.001) as did individuals in the lowest WBC count category.
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Although there was no significant interaction of WBC count with race (p = 0.37) or sex (p = 0.77), we were interested in examining the race-specific association between WBC count and cardiovascular disease events. Table 2 shows that there was a direct association between WBC count and coronary heart disease incidence in both African Americans (p for trend < 0.001) and Whites (p for trend < 0.001) after adjustment for age, sex, and ARIC field center. After additional adjustment for the covariates, the relative risk for persons in the highest quartile of WBC count versus the lowest was 1.9 among African Americans (95 percent CI: 1.19, 3.09) and 1.7 among Whites (95 percent CI: 1.13, 2.53. Stroke incidence showed trends similar to those of coronary heart disease incidence. An elevated WBC count was positively associated with stroke incidence after adjustment for age, sex, and ARIC field center. The relative risk for the highest quartile of WBC count versus the lowest was 3.0 (95 percent CI: 1.73, 5.23) in African Americans and 2.7 (95 percent CI: 1.55, 4.83) in Whites. This relation remained but was attenuated after further adjustment for other risk factors.
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Figure 2 shows that cardiovascular disease mortality also increased with increasing WBC count in both African Americans and Whites. After adjustment for multivariate risk factors, the relative risks for cardiovascular disease mortality across WBC count categories were 1.00 (referent), 1.15 (95 percent CI: 0.67, 1.98), 1.61 (95 percent CI: 0.95, 2.73), and 2.26 (95 percent CI: 1.38, 3.72) in African Americans (p for trend < 0.001) and 1.00 (referent), 1.00 (95 percent CI: 0.47, 2.10), 1.40 (95 percent CI: 0.70, 2.80), and 2.22 (95 percent CI: 1.13, 4.37) in Whites (p for trend = 0.001).
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We also observed a positive association between WBC count and cardiovascular disease endpoints across categories of smoking status (table 3). After adjustment for all risk factors, there was a direct relation between WBC count and cardiovascular disease mortality among current smokers (p for trend = 0.03) and among individuals who had never smoked (p for trend < 0.001). Similar patterns were observed for incidence of coronary heart disease and stroke (table 3). Among never smokers, the fully adjusted relative risks in the highest quartile of WBC count (versus the lowest) were 1.7 (95 percent CI: 1.08, 2.79) for coronary heart disease incidence and 1.6 (95 percent CI: 0.85, 2.30) for ischemic stroke incidence.
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We further examined the association between differential WBC count and disease incidence or mortality. As table 4 shows, the associations between WBC count and the study endpoints were strongest for granulocytes, somewhat weaker for monocytes, and weak and not independent of other risk factors for lymphocytes.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
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Although an elevated WBC count is considered a risk marker for cardiovascular disease incidence and mortality (3
–11), there has been little research on this relation in African Americans. Our major finding was that elevated WBC count is directly associated with risk of coronary heart disease and stroke incidence and mortality from cardiovascular disease in African Americans. The incidence of coronary heart disease was 1.9-fold higher in African Americans with WBC counts 7,000 cells/mm3 than in those with counts <4,800 cells/mm3, after adjustment for multiple risk factors. The association was similar in Whites. This finding is consistent with results from the NHANES I Epidemiologic Follow-up Study (7), in which African Americans with WBC counts >7,000 cells/mm3 had twice the incidence of coronary heart disease as those with WBC counts <5,500 cells/mm3. We also observed a positive association between WBC count and ischemic stroke incidence in African Americans, and to our knowledge this is the first prospective report of such an association. This study also showed a direct relation of WBC count to cardiovascular disease mortality in African Americans, with a relative risk of 2.3 for the highest quartile of WBC count after adjustment for multiple risk factors. This finding is somewhat different from that of the NHANES I Epidemiologic Follow-up Study, which showed only a weak association between WBC count and cardiovascular disease mortality in African Americans after adjustment for multiple risk factors (7).
In our study, a dose-response relation between WBC count and cardiovascular disease mortality persisted with and without adjustment or stratification for cigarette smoking. Although cigarette smoking increases WBC count and the pool of phagocytes (1), studies have not consistently observed a positive association between WBC count and coronary heart disease mortality in both smokers and nonsmokers (3, 7, 9, 10). Our finding of strong associations among never smokers suggests that a higher WBC count is a risk factor for cardiovascular disease events independently of smoking.
It is plausible that an elevated WBC count may enhance atherogenesis. Granulocytes and monocytes are believed to be involved in the pathogenesis of atherosclerosis. Monocyte-derived macrophages produce oxidants that can induce endothelial cell injury and subsequent thrombus formation (2). Activated WBCs also reflect the inflammatory activity of atherosclerosis that perpetuates vascular injury and tissue ischemia (1).
Some studies have reported that WBC count is associated with several cardiovascular disease risk factors. These findings include positive associations with body weight, systolic blood pressure, cigarette smoking, fasting glucose level, and fasting insulin level and negative associations with high density lipoprotein cholesterol level, family income, alcohol consumption, and physical activity or physical fitness (12–14). Our data show that although African Americans have less favorable cardiovascular disease risk factor profiles, they have lower WBC counts than Whites (table 1). African Americans have lower neutrophil counts and higher lymphocyte counts than Whites (22). Further studies are needed to determine whether lifestyle differences are related to WBC variability across race and sex groups.
A strength of this study is that African Americans were recruited from two US communities; our study represents the largest cohort study of WBC count and cardiovascular disease in African Americans yet conducted. Our study's biggest drawbacks are that most African Americans were from one community and that we did not have measurements of C-reactive protein, a specific marker of inflammation that is also associated with cardiovascular disease (23, 24). The independent role of WBC count versus C-reactive protein in the prediction of cardiovascular disease must be clarified, and to our knowledge C-reactive protein has not been studied in African Americans.
In conclusion, we found that an elevated WBC count is a risk factor for coronary heart disease and ischemic stroke incidence and cardiovascular disease mortality in African Americans. Despite a lower WBC count among African Americans, our finding suggests that inflammation plays similar roles in atherosclerotic cardiovascular disease for African Americans and Whites.
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ACKNOWLEDGMENTS |
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The Atherosclerosis Risk in Communities (ARIC) Study was supported by National Heart, Lung, and Blood Institute contracts NO1-HC-55015, NO1-HC-55016, NO1-HC-55018, NO1-HC-55019, NO1-HC-55020, NO1-HC-55021, and NO1-HC-55022. Dr. Chong Do Lee was supported by National Institutes of Health training grant HL07779-06.
The authors thank the staff of the ARIC Study for their important contributions.
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NOTES |
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Reprint requests to Dr. Aaron Folsom, Division of Epidemiology, University of Minnesota School of Public Health, 1300 South 2nd Street, Suite 300, Minneapolis, MN 55454-1015 (e-mail: Folsom{at}epi.umn.edu).
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REFERENCES |
|---|
|
TOPABSTRACTINTRODUCTIONMATERIALS AND METHODSRESULTSDISCUSSIONREFERENCES |
|---|
-
Ernst E, Hammerschmidt DE, Bagge U, et al. Leukocytes and the risk of ischemic diseases. JAMA 1987;257:2318–24.
[Abstract/Free Full Text] -
Fuster V, Lewis A. Mechanisms leading to myocardial infarction--insights from studies of vascular biology. Circulation 1994;90:2126–46.
[Abstract/Free Full Text] -
Kannel WB, Anderson K, Wilson PW. White blood cell count and cardiovascular disease: insights from the Framingham Study. JAMA 1992;267:1253–6.
[Abstract/Free Full Text] - Zalokar JB, Richard JL, Claude JR. Leukocyte count, smoking, and myocardial infarction. N Engl J Med 1981;304:465–8.[Web of Science][Medline]
-
Prentice RL, Szatrowski TP, Fujikura T, et al. Leukocyte counts and coronary heart disease in a Japanese cohort. Am J Epidemiol 1982;116:496–509.
[Abstract/Free Full Text] -
Folsom AR, Wu KK, Rosamond WD, et al. Prospective study of hemostatic factors and incidence of coronary heart disease: The Atherosclerosis Risk in Communities (ARIC) Study. Circulation 1997;96:1102–8.
[Abstract/Free Full Text] - Gillum RF, Ingram DD, Makuc DM. White blood cell count, coronary heart disease, and death: The NHANES I Epidemiologic Follow-up Study. Am Heart J 1993;125:855–63.[Web of Science][Medline]
- Friedman GD, Klatsky AL, Siegelaub AB. The leukocyte count as a predictor of myocardial infarction. N Engl J Med 1974;290:1275–8.
-
Grimm RH, Neaton JD, Ludwig W. Prognostic importance of the white blood cell count for coronary, cancer, and all-cause mortality. JAMA 1985;254:1932–7.
[Abstract/Free Full Text] -
Weijenberg MP, Feskens EJ, Kromhout D. White blood cell count and the risk of coronary heart disease and all-cause mortality in elderly men. Arterioscler Thromb Vasc Biol 1996;16:499–503.
[Abstract/Free Full Text] - De Labry LO, Campion EW, Glynn RJ, et al. White blood cell count as a predictor of mortality: results over 18 years from the Normative Aging Study. J Clin Epidemiol 1990;43:153–7.[Web of Science][Medline]
-
Hansen LK, Grimm RH, Neaton JD. The relationship of white blood cell count to other cardiovascular risk factors. Int J Epidemiol 1990;19:881–8.
[Abstract/Free Full Text] -
Nieto FJ, Szklo M, Folsom AR, et al. Leukocyte count correlates in middle-aged adults: The Atherosclerosis Risk in Communities (ARIC) Study. Am J Epidemiol 1992;136:525–37.
[Abstract/Free Full Text] -
Friedman GD, Tekawa I, Grimm RH, et al. The leukocyte count: correlates and relationship to coronary risk factors. The CARDIA Study. Int J Epidemiol 1990;19:889–93.
[Abstract/Free Full Text] -
The ARIC Investigators. The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. Am J Epidemiol 1989;129:687–702.
[Abstract/Free Full Text] - Papp AC, Hatzakis H, Bracey A, et al. ARIC hemostasis study. I. Development of a blood collection and processing system suitable for multicenter hemostatic studies. Thromb Haemost 1989;61:15–19.[Web of Science][Medline]
-
Baecke JA, Burema J, Frijters JE. A short questionnaire for the measurement of habitual physical activity in epidemiological studies. Am J Clin Nutr 1982;36:936–42.
[Abstract/Free Full Text] - Prineas RJ, Crow RS, Blackburn H. The Minnesota Code manual of electrocardiographic findings: standards and procedures for measurement and classification. Littleton, MA: John Wright-PSG, Inc, 1982.
- White AD, Folsom AR, Chambless LE, et al. Community surveillance of coronary heart disease in the Atherosclerosis Risk in Communities (ARIC) Study: methods and initial two years' experience. J Clin Epidemiol 1996;49:223–33.[Web of Science][Medline]
-
Rosamond WD, Folsom AR, Chambless LE, et al. Stroke incidence and survival among middle-aged adults: 9-year follow-up of the Atherosclerosis Risk in Communities (ARIC) cohort. Stroke 1999;30:736–43.
[Abstract/Free Full Text] - Cox DR. Regression models and life tables (with discussion). J R Stat Soc B 1972;34:187–220.
- McGrath CR, Hitchcock DC, Van Assendelft OW. Total white blood cell counts for persons ages 1–74 years with differential leukocyte counts for adults ages 25–74 years. (Vital and health statistics, series 11, no. 220). Hyattsville, MD: National Center for Health Statistics, 1982.
-
Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and risk of cardiovascular disease in apparently healthy men. N Engl J Med 1997;336:973–9.
[Abstract/Free Full Text] -
Ridker PM, Buring JE, Shih J, et al. Prospective study of C-reactive protein and the risk of future cardiovascular events among apparently healthy women. Circulation 1998;98:731–3.
[Abstract/Free Full Text]
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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]
|
|
|
|
 |
|
 F. Orio Jr., S. Palomba, T. Cascella, S. Di Biase, F. Manguso, L. Tauchmanova, L. G. Nardo, D. Labella, S. Savastano, T. Russo, et al. The Increase of Leukocytes as a New Putative Marker of Low-Grade Chronic Inflammation and Early Cardiovascular Risk in Polycystic Ovary Syndrome J. Clin. Endocrinol. Metab., January 1, 2005; 90(1): 2 - 5. [Abstract] [Full Text] [PDF]
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|
|
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M. Madjid, I. Awan, J. T. Willerson, and S. W. Casscells Leukocyte count and coronary heart disease: Implications for risk assessment J. Am. Coll. Cardiol., November 16, 2004; 44(10): 1945 - 1956. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Sans In search of the grail: the never-ending story of biomarkers for coronary risk prediction Eur. Heart J., August 1, 2004; 25(15): 1271 - 1273. [Full Text] [PDF]
|
|
|
|
|
|
J. G Wheeler, M. E Mussolino, R. F Gillum, and J. Danesh Associations between differential leucocyte count and incident coronary heart disease: 1764 incident cases from seven prospective studies of 30 374 individuals Eur. Heart J., August 1, 2004; 25(15): 1287 - 1292. [Abstract] [Full Text] [PDF]
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R. A Boyajian, S. M Otis, F. W Hall, and P. A Higginbottom Cardiovascular disease, periodontitis, and the monocyte relationship Eur. Heart J., August 1, 2004; 25(15): 1365 - 1366. [Full Text] [PDF]
|
|
|
|
|
|
K. Buhlin, A. Gustafsson, J. Frostegard, B. Klinge, and A Graham Pockley Cardiovascular disease, periodontitis and the monocyte relationship: Reply Eur. Heart J., August 1, 2004; 25(15): 1366 - 1366. [Full Text] [PDF]
|
|
|
|
|
|
L. E. Chambless, G. Heiss, E. Shahar, M. J. Earp, and J. Toole Prediction of Ischemic Stroke Risk in the Atherosclerosis Risk in Communities Study Am. J. Epidemiol., August 1, 2004; 160(3): 259 - 269. [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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P. C. Tong, K.-F. Lee, W.-Y. So, M. H. Ng, W.-B. Chan, M. K. Lo, N. N. Chan, and J. C. Chan White Blood Cell Count Is Associated With Macro- and Microvascular Complications in Chinese Patients With Type 2 Diabetes Diabetes Care, January 1, 2004; 27(1): 216 - 222. [Abstract] [Full Text] [PDF]
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|
 C. T. Jurkovitz, J. L. Abramson, L. V. Vaccarino, W. S. Weintraub, and W. M. McClellan Association of High Serum Creatinine and Anemia Increases the Risk of Coronary Events: Results from the Prospective Community-Based Atherosclerosis Risk in Communities (ARIC) Study J. Am. Soc. Nephrol., November 1, 2003; 14(11): 2919 - 2925. [Abstract] [Full Text] [PDF]
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