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(Circulation. 2003;107:391.)
© 2003 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Center for Cardiovascular Disease Prevention (P.M.R., J.E.B., N.R.C., N.R.), the Divisions of Preventive Medicine (P.M.R., J.E.B., N.R.C.) and Cardiology (P.M.R.), and the LeDucq Center for Cardiovascular Research (P.M.R., N.R.), Brigham and Womens Hospital, and the Department of Laboratory Medicine, Childrens Hospital (N.R.), Harvard Medical School, Boston, Mass.
Correspondence to Paul M Ridker, MD, Center for Cardiovascular Disease Prevention, 900 Commonwealth Ave E, Boston, MA 02215. E-mail pridker{at}partners.org
| Abstract |
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Methods and Results We evaluated interrelationships between CRP, the metabolic syndrome, and incident cardiovascular events among 14 719 apparently healthy women who were followed up for an 8-year period for myocardial infarction, stroke, coronary revascularization, or cardiovascular death; 24% of the cohort had the metabolic syndrome at study entry. At baseline, median CRP levels for those with 0, 1, 2, 3, 4, or 5 characteristics of the metabolic syndrome were 0.68, 1.09, 1.93, 3.01, 3.88, and 5.75 mg/L, respectively (Ptrend <0.0001). Over the 8-year follow-up, cardiovascular event-free survival rates based on CRP levels above or below 3.0 mg/L were similar to survival rates based on having 3 or more characteristics of the metabolic syndrome. At all levels of severity of the metabolic syndrome, however, CRP added prognostic information on subsequent risk. For example, among those with the metabolic syndrome at study entry, age-adjusted incidence rates of future cardiovascular events were 3.4 and 5.9 per 1000 person-years of exposure for those with baseline CRP levels less than or greater than 3.0 mg/L, respectively. Additive effects for CRP were also observed for those with 4 or 5 characteristics of the metabolic syndrome. The use of different definitions of the metabolic syndrome had minimal impact on these findings.
Conclusions These prospective data suggest that measurement of CRP adds clinically important prognostic information to the metabolic syndrome.
Key Words: protein, C-reactive risk factors prognosis diabetes mellitus inflammation
| Introduction |
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| Methods |
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Because recent randomized trial evidence indicates a net hazard in association with hormone replacement therapy (HRT), we elected to increase the generalizability of our data by limiting our analysis to the 15 745 WHS participants not using HRT at study entry. Of these, 14 719 were also free of diabetes at study entry and contributed complete data for all 5 components of the metabolic syndrome. Baseline blood samples from these women were thawed and assayed for CRP by a validated high-sensitivity assay (Denka Seiken), whereas triglyceride and HDL cholesterol levels were ascertained with direct measurement assays (Roche Diagnostics).
Women with 3 or more of the following attributes are typically defined as having the metabolic syndrome: (1) triglycerides
150 mg/dL; (2) HDL cholesterol <50 mg/dL; (3) blood pressure
135/85 mm Hg; (4) obesity as defined by a waist circumference >88 cm; and (5) abnormal glucose metabolism as defined by a fasting glucose
110 mg/dL. In the WHS, triglycerides, HDL cholesterol, and blood pressure were directly ascertained as outlined above. However, waist circumference was not measured until year 6 of follow-up. As such, we elected to use as our cutpoint for obesity a body mass index (BMI) >26.7 kg/m2, a value that corresponded to the same percentile cutpoint for BMI at year 6 as did a waist circumference of 88 cm measured at that time. To address whether this choice of BMI affected our results, we repeated our analyses using a BMI cutpoint of 30 kg/m2 as suggested in recent European guidelines.21 Because fasting glucose levels were not available, we elected to conservatively use the diagnosis of incident type II diabetes during study follow-up as an alternative measure of baseline impairment of glucose metabolism. To address how closely these definitions represented the metabolic syndrome, we compared the proportion of women in the present study categorized according to characteristics of the metabolic syndrome as defined above to that previously published for American women in the National Health and Nutrition Survey (NHANES)22 using categories defined by the ATP-III guideline.
To evaluate for evidence of association between baseline CRP levels and the metabolic syndrome, we first compared the distribution of CRP levels among individuals with or without each of the individual components of the syndrome as defined above. Because levels of CRP are skewed, we evaluated the significance of any differences in median values between groups using the Wilcoxon rank-sum test. We then classified all study subjects as having 0, 1, 2, 3, 4, or 5 components of the metabolic syndrome and assessed for evidence of a relation of median CRP levels across these groups using the Jonckheere-Terpstra test. We then used logistic regression analysis to discern whether elevated CRP levels added prognostic information on risk of subsequent cardiovascular events across the full spectrum of severity of the metabolic syndrome. Consistent with recent recommendations from the Centers for Disease Control and Prevention, a CRP cutpoint of 3 mg/L was used to differentiate high-risk and low-risk groups.23
To directly compare the clinical utility of CRP alone to that of the metabolic syndrome alone, we constructed 8-year cardiovascular event-free survival curves for those with CRP levels above or below 3.0 mg/L and compared these to survival curves based on the presence or absence of 3 or more components of the metabolic syndrome. Age-adjusted c statistics, analogous to the area under the receiver operator characteristic (ROC) curve, were used to assess the discrimination of cardiovascular prediction models based on CRP alone versus those based on having 3 or more characteristics of the metabolic syndrome. These analyses were then repeated with continuous rather than dichotomous definitions used for components of the metabolic syndrome. Finally, in analysis stratified by those with and without the metabolic syndrome, we sought evidence in terms of cardiovascular event-free survival that CRP levels might have additional prognostic value in the prediction of incident cardiovascular end points.
| Results |
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Table 2 presents median CRP values (with interquartile ranges) for those study participants with and without each individual component of the metabolic syndrome. Consistent with prior cross-sectional data, CRP levels were significantly higher among women who had each component of the metabolic syndrome than among women who did not (all P<0.0001).
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Figure 1 displays the distribution of CRP levels after women were classified according to their total number of components of the metabolic syndrome. As shown, there was a strong linear increase in CRP levels as the number of components of the metabolic syndrome increased; median CRP levels for those with 0, 1, 2, 3, 4, or 5 characteristics of the metabolic syndrome were 0.68, 1.09, 1.93, 3.01, 3.88, and 5.75 mg/L, respectively (Ptrend<0.0001).
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As shown in Figure 2, CRP levels >3 mg/L at baseline added prognostic information at all levels of severity of the metabolic syndrome. This additive effect was particularly apparent among those with 3, 4, or 5 characteristics of the metabolic syndrome (all P<0.001).
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Figure 3 presents results of the survival analyses directly comparing CRP with the metabolic syndrome. As shown, the predictive value of CRP levels above or below 3.0 mg/L in terms of the development of first-ever cardiovascular events was quite similar to the predictive value associated with having or not having 3 or more characteristics of the metabolic syndrome. In age-adjusted analyses, the area under the ROC curve associated with CRP alone was 0.77 versus 0.78 for the metabolic syndrome.
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As prespecified, we additionally sought evidence that CRP might have prognostic utility among those with and without the metabolic syndrome. We therefore first performed an analysis limited to the 3597 study participants classified as having 3 or more characteristics of the metabolic syndrome at study entry. Among these women, we observed significant increases in rates of future cardiovascular disease as levels of baseline CRP increased. Specifically, age-adjusted incidence rates were 3.4 and 5.9 events per 1000 person-years of exposure for those with baseline CRP levels less than or greater than 3.0 mg/L, respectively (P<0.001).
To further explore these interrelationships, we divided the study cohort into 4 groups on the basis of the presence or absence of the metabolic syndrome and on the basis of CRP levels less than or greater than 3.0 mg/L. As shown in Figure 4 (left), CRP evaluation provided additional prognostic information both for those with and without the metabolic syndrome. The age-adjusted relative risks of future cardiovascular events for women in the low-CRP/no metabolic syndrome, high-CRP/no metabolic syndrome, low-CRP/yes metabolic syndrome, and high-CRP/yes metabolic syndrome groups were 1.0 (referent), 1.5 (95% CI 1.0 to 2.2), 2.3 (95% CI 1.6 to 3.3), and 4.0 (95% CI 3.0 to 5.4), respectively.
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We performed several additional analyses to address the robustness of these findings. First, because the concept of the metabolic syndrome was developed in part to reflect a secondary target population without hyperlipidemia, we repeated our analyses for the 12 453 women with baseline LDL cholesterol levels <160 mg/dL and for the 8500 women with LDL cholesterol <130 mg/dL. As shown in Figure 4 (middle and right), CRP provided prognostic information in addition to the metabolic syndrome in both of these latter analyses. The relative risks and associated CIs for these analyses are presented in Table 3.
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Second, and as also shown in Table 3, we repeated our analyses using only the end point of coronary heart disease. For this end point, overall effects were, if anything, larger than that observed with the a priori combined end point that also included thromboembolic stroke.
Third, we repeated our analyses using continuous rather than dichotomous variables and found similar effects. In the continuous variable models, the relative risk of future cardiovascular events associated with CRP levels >3.0 mg/L was 1.5 (P=0.006), and the area under the ROC curve was 0.82. By contrast, when dichotomous definitions for each component of the metabolic syndrome were used, the corresponding relative risk was 1.6 (P=0.0003), and the corresponding area under the ROC curve was 0.79.
Fourth, we repeated our primary analyses using a BMI cutpoint of 30 kg/m2 and again found almost identical results in terms of additive predictive value. Use of this cutpoint, however, classified only 17% of the present cohort as obese. By contrast, the use of a BMI cutpoint of 26.7 kg/m2 (as done in our primary analyses) classified 32% of the cohort as obese, a value closer to that observed in the NHANES survey.
Finally, we performed an additional analysis limited to those 3597 participants with the metabolic syndrome at study entry and found that CRP levels <1, 1 to 3, and >3 mg/L stratified the population into 3 risk groups such that those with the metabolic syndrome and the highest CRP levels had a relative risk 2.1 times that of those with the metabolic syndrome who had the lowest CRP levels (95% CI 1.1 to 4.2, P=0.001; Figure 5). In all these analyses, virtually identical results were observed when we excluded incident diabetes as part of the definition of the metabolic syndrome.
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| Discussion |
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That CRP levels correspond with individual components of the metabolic is consistent with work of other investigators1520 and the hypothesized role of inflammation in several processes critical to the development of both diabetes and atherothrombosis.24,25 Indeed, in this cohort, we have previously shown baseline CRP levels to be a strong predictor not only of myocardial infarction and stroke8,10 but also of incident type 2 diabetes.5 Rapidly evolving work now demonstrates that in addition to being a marker of innate immunity, CRP also has several direct effects at the level of the vessel wall.26,27 These observations, along with basic research into the inflammatory mechanisms of both diabetes and vascular dysfunction, provide strong evidence that insulin resistance and atherosclerosis share a common inflammatory basis.28 CRP, however, is also associated with several aspects of the metabolic syndrome not easily ascertained in usual clinical practice, including fasting insulin, hypofibrinolysis, and microalbuminuria.1520 Our finding that CRP measurement adds important prognostic information to clinical definitions of the metabolic syndrome is thus consistent with this hypothesis.
Limitations of this study must be considered. First, the study included only women. We believe, however, that these data are likely to generalize to men because other studies have linked markers of inflammation to individual components of the metabolic syndrome in men, and many cohort studies have already shown CRP to independently predict vascular events in men.7,1114 Second, because we did not have fasting glucose levels in all participants, we elected instead to use the diagnosis of incident diabetes during follow-up as a surrogate for abnormal baseline glucose metabolism. We believe this choice to be valid because other work has shown CRP levels to correlate with fasting glucose level29 and predict incident type 2 diabetes.5,6 Moreover, as shown in Table 1, this choice was, if anything, conservative, because it resulted in only 1.2% of the present cohort being defined as having all 5 characteristics of the metabolic syndrome versus 2.9% in the NHANES survey. We also believe it unlikely that this decision affected validity, because elevated fasting glucose is by far the least common abnormality used to define those with the metabolic syndrome. Finally, these analyses do not make adjustment for other factors that may affect CRP levels, such as smoking status.
We recognize that these data have broad implications for the development of therapies targeting insulin resistance, diabetes, and atherothrombosis. We have previously shown that aspirin and statins are relatively more effective in reducing vascular risk among those with elevated CRP levels,7,9,30 and we have hypothesized on that basis that CRP is likely to have utility in the targeting of therapies for the primary prevention of cardiovascular disease. At the same time, weight reduction and exercise, the first-line therapies stressed by ATP-III for the management of the metabolic syndrome, also reduce CRP levels. Furthermore, a recent report suggests that rosiglitazone directly reduces CRP levels, an intriguing observation because this PPAR-
inhibitor is already established as standard therapy for those with type II diabetes.31
In sum, these data provide clear evidence that the presence of at least 3 of 5 components of the metabolic syndrome predicts incident cardiovascular events in apparently healthy women. However, these data also indicate that among those with and without the metabolic syndrome, baseline CRP levels add clinically relevant prognostic information concerning future vascular risk.
| Acknowledgments |
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| Footnotes |
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Dr Ridker is named as a coinventor on patents filed by the Brigham and Womens Hospital that relate to the use of inflammatory biomarkers in cardiovascular disease and diabetes.
Received December 2, 2002; revision received December 20, 2002; accepted December 20, 2002.
| References |
|---|
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2. Isomaa B, Almgren P, Tuomi T, et al. Cardiovascular morbidity and mortality associated with the metabolic syndrome. Diabetes Care. 2001; 24: 683689.
3. Haffner SM, Valdez RA, Hazuda HP, et al. Prospective analysis of the insulin-resistance syndrome (syndrome X). Diabetes. 1992; 41: 715722.[Abstract]
4. Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults. Executive summary of the Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III). JAMA. 2001; 19: 24862497.
5. Pradhan AD, Manson JE, Rifai N, et al. C-reactive protein, interleukin 6, and the risk of developing type 2 diabetes mellitus. JAMA. 2001; 286: 327334.
6. Freeman DJ, Norrie J, Caslake MJ, et al. C-reactive protein is an independent predictor of risk for the development of diabetes in the West of Scotland Coronary Prevention Study. Diabetes. 2002; 51: 15961600.
7. Ridker PM, Cushman M, Stampfer MJ, et al. Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. N Engl J Med. 1997; 336: 973979.
8. Ridker PM, Hennekens CH, Buring JE, et al. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000; 342: 836843.
9. Ridker PM, Rifai N, Clearfield M, et al, for the Air Force/Texas Coronary Atherosclerosis Prevention Study Investigators. 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: 19591965.
10. Ridker PM, Rifai N, Rose L, et al. Comparison of C-reactive protein and low-density lipoprotein cholesterol in the prediction of first cardiovascular events. N Engl J Med. 2002; 347: 15571565.
11. Tracy RP, Lemaitre RN, Psaty BM, et al. 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: 11211127.
12. Koenig W, Sund M, Froelich M, et al. C-reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men: results from the MONICA (Monitoring trends and determinants in cardiovascular disease) Augsberg Cohort Study, 1984 to 1992. Circulation. 1999; 99: 237242.
13. Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis: a comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein(a), and standard cholesterol screening as predictors of peripheral arterial disease. JAMA. 2001; 285: 24812485.
14. Danesh J, Whincup P, Wlaker M, et al. Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses. BMJ. 2000; 321: 199204.
15. Yudkin JS, Stehouwer CDA, Emeis JJ, et al. C-reactive protein in healthy subjects: associations with obesity, insulin resistance, and endothelial dysfunction: a potential role of cytokines originating from adipose tissue? Arterioscler Thromb Vasc Biol. 1999; 19: 972978.
16. Festa A, DAgostino R, Howard G, et al. Chronic subclinical inflammation as part of the insulin resistance syndrome: the Insulin Resistance Atherosclerosis Study (IRAS). Circulation. 2000; 102: 4247.
17. Frohlich M, Imhof A, Berg C, et al. Association between C-reactive protein and features of the metabolic syndrome: a population based study. Diabetes Care. 2000; 23: 18351839.
18. Festa A, DAgostino R, Howard G, et al. Inflammation and microalbuminuria in nondiabetic and type 2 diabetic subjects: the Insulin Resistance Atherosclerosis Study. Kidney Int. 2000; 58: 17031710.[CrossRef][Medline] [Order article via Infotrieve]
19. Stehouwer CD, Gall MA, Twisk JW, et al. Increased urinary albumin excretion, endothelial dysfunction, and chronic low-grade inflammation in type 2 diabetes: progressive, interrelated, and independently associated with risk of death. Diabetes. 2002; 51: 11571165.
20. Festa A, DAgostino R, Tracy RP, et al. Elevated levels of acute-phase proteins and plasminogen activator inhibitor-1 predict the development of type 2 diabetes: the Insulin Resistance Atherosclerosis Study. Diabetes. 2002; 51: 11311137.
21. Alberti KG, Zimmet PZ. Definition, diagnosis and classification of diabetes and its complications, part 1: diagnosis and classification of diabetes provisional report of a WHO consultation. Diabetic Med. 1998; 15: 539553.[CrossRef][Medline] [Order article via Infotrieve]
22. Ford ES, Giles WH, Dietz WH. Prevalence of the metabolic syndrome among US adults: findings from the Third National Health and Nutrition Examination Survey. JAMA. 2002; 287: 356359.
23. Centers for Disease Control/American Heart Association Workshop on Inflammatory Markers, and Cardiovascular Disease: application to clinical and public health practice: Atlanta, March 1415, 2002. Atlanta, Ga: Centers for Disease Control and Prevention; 2002.
24. Fernandez-Real JM, Ricart W. Insulin resistance and inflammation in an evolutionary perspective: the contribution of cytokine genotype/phenotype to thriftiness. Diabetologia. 1999; 42: 13671374.[CrossRef][Medline] [Order article via Infotrieve]
25. Pickup JC, Crook MA. Is type II diabetes mellitus a disease of the innate immune system? Diabetologia. 1998; 41: 12411248.[CrossRef][Medline] [Order article via Infotrieve]
26. Pasceri V, Willerson JT, Yeh ET. Direct proinflammatory effect of C-reactive protein on human endothelial cells. Circulation. 2000; 102: 21652168.
27. Pasceri V, Chang J, Willerson JT, et al. Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs. Circulation. 2001; 103: 25312534.
28. Pradhan A, Ridker PM. Do atherosclerosis and type 2 diabetes share a common inflammatory basis? Eur Heart J. 2002; 23: 831834.
29. Mendall MA, Patel P, Ballam L, et al. C reactive protein and its relation to cardiovascular risk factors: a population based cross sectional study. BMJ. 1996; 312: 10611065.
30. Ridker PM, Rifai N, Pfeffer MA, et al. Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Circulation. 1998; 98: 839844.
31. Haffner SM, Greenberg AS, Weston WM, et al. Effect of rosiglitazone treatment on nontraditional markers of cardiovascular disease in patients with type 2 diabetes mellitus. Circulation. 2002; 106: 679684.
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H. M. Lee, T. V. Le, V. A. Lopez, and N. D. Wong Association of C-Reactive Protein With Reduced Forced Vital Capacity in a Nonsmoking U.S. Population With Metabolic Syndrome and Diabetes Diabetes Care, October 1, 2008; 31(10): 2000 - 2002. [Abstract] [Full Text] [PDF] |
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R. L. Pande, T. S. Perlstein, J. A. Beckman, and M. A. Creager Association of Insulin Resistance and Inflammation With Peripheral Arterial Disease: The National Health and Nutrition Examination Survey, 1999 to 2004 Circulation, July 1, 2008; 118(1): 33 - 41. [Abstract] [Full Text] [PDF] |
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K. Chen, J. B Lindsey, A. Khera, J. A. D. Lemos, C. R Ayers, A. Goyal, G. L Vega, S. A Murphy, S. M Grundy, and D. K Mcguire Independent associations between metabolic syndrome, diabetes mellitus and atherosclerosis: observations from the Dallas Heart Study Diabetes and Vascular Disease Research, June 1, 2008; 5(2): 96 - 101. [Abstract] [PDF] |
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M K Baum, C Rafie, S Sales, S Lai, R Duan, D T Jayaweera, J B Page, and A Campa C-reactive protein: a poor marker of cardiovascular disease risk in HIV+ populations with a high prevalence of elevated serum transaminases Int J STD AIDS, June 1, 2008; 19(6): 410 - 413. [Abstract] [Full Text] [PDF] |
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V. M. Miller and S. P. Duckles Vascular Actions of Estrogens: Functional Implications Pharmacol. Rev., June 1, 2008; 60(2): 210 - 241. [Abstract] [Full Text] [PDF] |
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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] |
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F. Tabassum, M. Kumari, A. Rumley, G. Lowe, C. Power, and D. P. Strachan Effects of Socioeconomic Position on Inflammatory and Hemostatic Markers: A Life-Course Analysis in the 1958 British Birth Cohort Am. J. Epidemiol., June 1, 2008; 167(11): 1332 - 1341. [Abstract] [Full Text] [PDF] |
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T. You, B. J. Nicklas, J. Ding, B. W. J. H. Penninx, B. H. Goodpaster, D. C. Bauer, F. A. Tylavsky, T. B. Harris, S. B. Kritchevsky, and for the Health, Aging and Body Composition Study The Metabolic Syndrome Is Associated With Circulating Adipokines in Older Adults Across a Wide Range of Adiposity J Gerontol A Biol Sci Med Sci, April 1, 2008; 63(4): 414 - 419. [Abstract] [Full Text] [PDF] |
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D. Conen, P. M. Ridker, S. Mora, J. E. Buring, and R. J. Glynn Risk of type 2 diabetes mellitus in those with hypertension: reply Eur. Heart J., April 1, 2008; 29(7): 953 - 954. [Full Text] [PDF] |
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H. Watanabe, N. Tanabe, T. Watanabe, D. Darbar, D. M. Roden, S. Sasaki, and Y. Aizawa Metabolic Syndrome and Risk of Development of Atrial Fibrillation: The Niigata Preventive Medicine Study Circulation, March 11, 2008; 117(10): 1255 - 1260. [Abstract] [Full Text] [PDF] |
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V. Stangl, V. Witzel, G. Baumann, and K. Stangl Current diagnostic concepts to detect coronary artery disease in women Eur. Heart J., March 2, 2008; 29(6): 707 - 717. [Abstract] [Full Text] [PDF] |
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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] |
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C. Cuaz-Perolin, L. Billiet, E. Bauge, C. Copin, D. Scott-Algara, F. Genze, B. Buchele, T. Syrovets, T. Simmet, and M. Rouis Antiinflammatory and Antiatherogenic Effects of the NF-{kappa}B Inhibitor Acetyl-11-Keto-{beta}-Boswellic Acid in LPS-Challenged ApoE-/- Mice Arterioscler Thromb Vasc Biol, February 1, 2008; 28(2): 272 - 277. [Abstract] [Full Text] [PDF] |
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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] |
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J. M. Moreno-Navarrete, F. J. Ortega, J. Bassols, A. Castro, W. Ricart, and J. M. Fernandez-Real Association of Circulating Lactoferrin Concentration and 2 Nonsynonymous LTF Gene Polymorphisms with Dyslipidemia in Men Depends on Glucose-Tolerance Status Clin. Chem., February 1, 2008; 54(2): 301 - 309. [Abstract] [Full Text] [PDF] |
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R. R. S. Packard and P. Libby Inflammation in Atherosclerosis: From Vascular Biology to Biomarker Discovery and Risk Prediction Clin. Chem., January 1, 2008; 54(1): 24 - 38. [Abstract] [Full Text] [PDF] |
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Y Yamada, S Ichihara, K Kato, T Yoshida, K Yokoi, H Matsuo, S Watanabe, N Metoki, H Yoshida, K Satoh, et al. Genetic risk for metabolic syndrome: examination of candidate gene polymorphisms related to lipid metabolism in Japanese people J. Med. Genet., January 1, 2008; 45(1): 22 - 28. [Abstract] [Full Text] [PDF] |
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D. Conen, P. M. Ridker, S. Mora, J. E. Buring, and R. J. Glynn Blood pressure and risk of developing type 2 diabetes mellitus: The Women's Health Study Eur. Heart J., December 1, 2007; 28(23): 2937 - 2943. [Abstract] [Full Text] [PDF] |
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C A Daly, P Hildebrandt, M Bertrand, R Ferrari, W Remme, M Simoons, K M Fox, and on behalf of the EUROPA investigators Adverse prognosis associated with the metabolic syndrome in established coronary artery disease: data from the EUROPA trial Heart, November 1, 2007; 93(11): 1406 - 1411. [Abstract] [Full Text] [PDF] |
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D. H St-Pierre, J.-P. Bastard, L. Coderre, M. Brochu, A. D Karelis, M.-E. Lavoie, F. Malita, J. Fontaine, D. Mignault, K. Cianflone, et al. Association of acylated ghrelin profiles with chronic inflammatory markers in overweight and obese postmenopausal women: a MONET study Eur. J. Endocrinol., October 1, 2007; 157(4): 419 - 426. [Abstract] [Full Text] [PDF] |
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A. Kotronen, J. Westerbacka, R. Bergholm, K. H. Pietilainen, and H. Yki-Jarvinen Liver Fat in the Metabolic Syndrome J. Clin. Endocrinol. Metab., September 1, 2007; 92(9): 3490 - 3497. [Abstract] [Full Text] [PDF] |
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A. Muscari, S. Antonelli, G. Bianchi, G. Cavrini, S. Dapporto, A. Ligabue, C. Ludovico, D. Magalotti, G. Poggiopollini, M. Zoli, et al. Serum C3 Is a Stronger Inflammatory Marker of Insulin Resistance Than C-Reactive Protein, Leukocyte Count, and Erythrocyte Sedimentation Rate: Comparison study in an elderly population Diabetes Care, September 1, 2007; 30(9): 2362 - 2368. [Abstract] [Full Text] [PDF] |
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E. Ingelsson, M. J. Pencina, G. H. Tofler, E. J. Benjamin, K. J. Lanier, P. F. Jacques, C. S. Fox, J. B. Meigs, D. Levy, M. G. Larson, et al. Multimarker Approach to Evaluate the Incidence of the Metabolic Syndrome and Longitudinal Changes in Metabolic Risk Factors: The Framingham Offspring Study Circulation, August 28, 2007; 116(9): 984 - 992. [Abstract] [Full Text] [PDF] |
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S. Liu, L. Tinker, Y. Song, N. Rifai, D. E. Bonds, N. R. Cook, G. Heiss, B. V. Howard, G. S. Hotamisligil, F. B. Hu, et al. A Prospective Study of Inflammatory Cytokines and Diabetes Mellitus in a Multiethnic Cohort of Postmenopausal Women Arch Intern Med, August 13, 2007; 167(15): 1676 - 1685. [Abstract] [Full Text] [PDF] |
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S. Cicala, G. de Simone, M. J. Roman, L. G. Best, E. T. Lee, W. Wang, T. K. Welty, J. M. Galloway, B. V. Howard, and R. B. Devereux Prevalence and Prognostic Significance of Wall-Motion Abnormalities in Adults Without Clinically Recognized Cardiovascular Disease: The Strong Heart Study Circulation, July 10, 2007; 116(2): 143 - 150. [Abstract] [Full Text] [PDF] |
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D.-F. Dai, J.-W. Lin, J.-H. Kao, C.-N. Hsu, F.-T. Chiang, J.-L. Lin, Y.-H. Chou, K.-L. Hsu, C.-D. Tseng, Y.-Z. Tseng, et al. The Effects of Metabolic Syndrome Versus Infectious Burden on Inflammation, Severity of Coronary Atherosclerosis, and Major Adverse Cardiovascular Events J. Clin. Endocrinol. Metab., July 1, 2007; 92(7): 2532 - 2537. [Abstract] [Full Text] [PDF] |
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Authors/Task Force Members:, G. Mancia, G. De Backer, A. Dominiczak, R. Cifkova, R. Fagard, G. Germano, G. Grassi, A. M. Heagerty, S. E. Kjeldsen, et al. 2007 Guidelines for the Management of Arterial Hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC) Eur. Heart J., June 11, 2007; (2007) ehm236v1. [Full Text] [PDF] |
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Authors/Task Force Members, L. Ryden, E. Standl, M. Bartnik, G. V. d. Berghe, J. Betteridge, M.-J. de Boer, F. Cosentino, B. Jonsson, M. Laakso, et al. Guidelines on diabetes, pre-diabetes, and cardiovascular diseases: full text: The Task Force on Diabetes and Cardiovascular Diseases of the European Society of Cardiology (ESC) and of the European Association for the Study of Diabetes (EASD) Eur. Heart J. Suppl., June 1, 2007; 9(suppl_C): C3 - C74. [Full Text] [PDF] |
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M. Persson, B. Hedblad, J. J. Nelson, and G. Berglund Elevated Lp-PLA2 Levels Add Prognostic Information to the Metabolic Syndrome on Incidence of Cardiovascular Events Among Middle-Aged Nondiabetic Subjects Arterioscler Thromb Vasc Biol, June 1, 2007; 27(6): 1411 - 1416. [Abstract] [Full Text] [PDF] |
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A. W Fogarty, S. Jones, J. R Britton, S. A Lewis, and T. M McKeever Systemic inflammation and decline in lung function in a general population: a prospective study Thorax, June 1, 2007; 62(6): 515 - 520. [Abstract] [Full Text] [PDF] |
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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] |
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P. M. Ridker C-Reactive Protein and the Prediction of Cardiovascular Events Among Those at Intermediate Risk: Moving an Inflammatory Hypothesis Toward Consensus J. Am. Coll. Cardiol., May 29, 2007; 49(21): 2129 - 2138. [Abstract] [Full Text] [PDF] |
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P. E. Szmitko and S. Verma C-Reactive Protein and Reendothelialization: NO Involvement Circ. Res., May 25, 2007; 100(10): 1405 - 1407. [Full Text] [PDF] |
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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] |
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I. M. Wahba and R. H. Mak Obesity and Obesity-Initiated Metabolic Syndrome: Mechanistic Links to Chronic Kidney Disease Clin. J. Am. Soc. Nephrol., May 1, 2007; 2(3): 550 - 562. [Abstract] [Full Text] [PDF] |
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A. Lopez-Bermejo, B. Chico-Julia, A. Castro, M. Recasens, E. Esteve, J. Biarnes, R. Casamitjana, W. Ricart, and J.-M. Fernandez-Real Alpha Defensins 1, 2, and 3: Potential Roles in Dyslipidemia and Vascular Dysfunction in Humans Arterioscler Thromb Vasc Biol, May 1, 2007; 27(5): 1166 - 1171. [Abstract] [Full Text] [PDF] |
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A. I. Kakafika, D. P. Mikhailidis, A. Karagiannis, and V. G. Athyros The Role of Endocannabinoid System Blockade in the Treatment of the Metabolic Syndrome J. Clin. Pharmacol., May 1, 2007; 47(5): 642 - 652. [Abstract] [Full Text] [PDF] |
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C. Pitsavos, D. B. Panagiotakos, N. Tzima, Y. Lentzas, C. Chrysohoou, U. N. Das, and C. Stefanadis Diet, Exercise, and C-Reactive Protein Levels in People With Abdominal Obesity: The ATTICA Epidemiological Study Angiology, April 1, 2007; 58(2): 225 - 233. [Abstract] [PDF] |
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J. Wang, S. Ruotsalainen, L. Moilanen, P. Lepisto, M. Laakso, and J. Kuusisto The metabolic syndrome predicts cardiovascular mortality: a 13-year follow-up study in elderly non-diabetic Finns Eur. Heart J., April 1, 2007; 28(7): 857 - 864. [Abstract] [Full Text] [PDF] |
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O. Schlager, M. Exner, W. Mlekusch, S. Sabeti, J. Amighi, P. Dick, O. Wagner, R. Koppensteiner, E. Minar, and M. Schillinger C-Reactive Protein Predicts Future Cardiovascular Events in Patients With Carotid Stenosis Stroke, April 1, 2007; 38(4): 1263 - 1268. [Abstract] [Full Text] [PDF] |
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J. Jose Diaz, J. Arguelles, I. Malaga, C. Perillan, A. Dieguez, M. Vijande, and S. Malaga C-reactive protein is elevated in the offspring of parents with essential hypertension Arch. Dis. Child., April 1, 2007; 92(4): 304 - 308. [Abstract] [Full Text] [PDF] |
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D. E. King, B. M. Egan, R. F. Woolson, A. G. Mainous III, Y. Al-Solaiman, and A. Jesri Effect of a High-Fiber Diet vs a Fiber-Supplemented Diet on C-Reactive Protein Level Arch Intern Med, March 12, 2007; 167(5): 502 - 506. [Abstract] [Full Text] [PDF] |
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C. Ay, T. Tengler, R. Vormittag, R. Simanek, W. Dorda, T. Vukovich, and I. Pabinger Venous thromboembolism a manifestation of the metabolic syndrome Haematologica, March 1, 2007; 92(3): 374 - 380. [Abstract] [Full Text] [PDF] |
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R. Kelishadi, M. Sharifi, A. Khosravi, and K. Adeli Relationship Between C-Reactive Protein and Atherosclerotic Risk Factors and Oxidative Stress Markers Among Young Persons 10-18 Years Old Clin. Chem., March 1, 2007; 53(3): 456 - 464. [Abstract] [Full Text] [PDF] |
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V. Jeevanantham, N. Singh, K. Izuora, J. P. D'souza, and D. H. Hsi Correlation of High Sensitivity C-Reactive Protein and Calcific Aortic Valve Disease Mayo Clin. Proc., February 1, 2007; 82(2): 171 - 174. [Abstract] [Full Text] [PDF] |
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H. Koyama, T. Shoji, S. Fukumoto, K. Shinohara, T. Shoji, M. Emoto, K. Mori, H. Tahara, E. Ishimura, R. Kakiya, et al. Low Circulating Endogenous Secretory Receptor for AGEs Predicts Cardiovascular Mortality in Patients With End-Stage Renal Disease Arterioscler Thromb Vasc Biol, January 1, 2007; 27(1): 147 - 153. [Abstract] [Full Text] [PDF] |
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E K Iliodromitis, S Kyrzopoulos, I A Paraskevaidis, K G Kolocassides, S Adamopoulos, G Karavolias, and D T Kremastinos Increased C reactive protein and cardiac enzyme levels after coronary stent implantation. Is there protection by remote ischaemic preconditioning? Heart, December 1, 2006; 92(12): 1821 - 1826. [Abstract] [Full Text] [PDF] |
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S. Bo, M. Durazzo, S. Guidi, M. Carello, C. Sacerdote, B. Silli, R. Rosato, M. Cassader, L. Gentile, and G. Pagano Dietary magnesium and fiber intakes and inflammatory and metabolic indicators in middle-aged subjects from a population-based cohort. Am. J. Clinical Nutrition, November 1, 2006; 84(5): 1062 - 1069. [Abstract] [Full Text] [PDF] |
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S. Devaraj, E. Chan, and I. Jialal Direct Demonstration of an Antiinflammatory Effect of Simvastatin in Subjects with the Metabolic Syndrome J. Clin. Endocrinol. Metab., November 1, 2006; 91(11): 4489 - 4496. [Abstract] [Full Text] [PDF] |
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P. Libby and P. M. Ridker Inflammation and Atherothrombosis: From Population Biology and Bench Research to Clinical Practice J. Am. Coll. Cardiol., October 27, 2006; 48(9_Suppl_A): A33 - A46. [Abstract] [Full Text] [PDF] |
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J. V. Solis, J. L. Portero, J. Diaz, R. Garcia, J. M. Ligero, E. Vazquez, C. Lodeiro, and L. Ballesteros Iron Deficiency in the Acute-Phase Reaction After Open Aortic Surgery Vascular and Endovascular Surgery, October 1, 2006; 40(5): 392 - 398. [Abstract] [PDF] |
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E Ingelsson, J Arnlov, L Lind, and J Sundstrom Metabolic syndrome and risk for heart failure in middle-aged men Heart, October 1, 2006; 92(10): 1409 - 1413. [Abstract] [Full Text] [PDF] |
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S. Zarich, C. Luciano, J. Hulford, and A. Abdullah Prevalence of metabolic syndrome in young patients with acute MI: does the Framingham Risk Score underestimate cardiovascular risk in this population? Diabetes and Vascular Disease Research, September 1, 2006; 3(2): 103 - 107. [Abstract] [PDF] |
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S. E. Kahn, B. Zinman, S. M. Haffner, M. C. O'Neill, B. G. Kravitz, D. Yu, M. I. Freed, W. H. Herman, R. R. Holman, N. P. Jones, et al. Obesity is a major determinant of the association of C-reactive protein levels and the metabolic syndrome in type 2 diabetes. Diabetes, August 1, 2006; 55(8): 2357 - 2364. [Abstract] [Full Text] [PDF] |
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M. A. Mittleman A 39-year-old woman with hypercholesterolemia. JAMA, July 19, 2006; 296(3): 319 - 326. [Abstract] [Full Text] [PDF] |
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N. R. Cook, J. E. Buring, and P. M Ridker The Effect of Including C-Reactive Protein in Cardiovascular Risk Prediction Models for Women Ann Intern Med, July 4, 2006; 145(1): 21 - 29. [Abstract] [Full Text] [PDF] |
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S. D. de Ferranti, K. Gauvreau, D. S. Ludwig, J. W. Newburger, and N. Rifai Inflammation and Changes in Metabolic Syndrome Abnormalities in US Adolescents: Findings from the 1988-1994 and 1999-2000 National Health and Nutrition Examination Surveys Clin. Chem., July 1, 2006; 52(7): 1325 - 1330. [Abstract] [Full Text] [PDF] |
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