Inflammatory Markers and the Risk of Coronary Heart Disease in Men and Women
Jennifer K. Pai, M.H.S., Tobias Pischon, M.D., M.P.H., Jing Ma, M.D., Ph.D., JoAnn E. Manson, M.D., Dr.P.H., Susan E. Hankinson, Sc.D., Kaumudi Joshipura, B.D.S., Sc.D., Gary C. Curhan, M.D., Sc.D., Nader Rifai, Ph.D., Carolyn C. Cannuscio, Sc.D., Meir J. Stampfer, M.D., Dr.P.H., and Eric B. Rimm, Sc.D.
Background Few studies have simultaneously investigated therole of soluble tumor necrosis factor (TNF-) receptors types1 and 2 (sTNF-R1 and sTNF-R2), C-reactive protein, and interleukin-6as predictors of cardiovascular events. The value of these inflammatorymarkers as independent predictors remains controversial.
Methods We examined plasma levels of sTNF-R1, sTNF-R2, interleukin-6,and C-reactive protein as markers of risk for coronary heartdisease among women participating in the Nurses' Health Studyand men participating in the Health Professionals Follow-upStudy in nested case–control analyses. Among participantswho provided a blood sample and who were free of cardiovasculardisease at baseline, 239 women and 265 men had a nonfatal myocardialinfarction or fatal coronary heart disease during eight yearsand six years of follow-up, respectively. Using risk-set sampling,we selected controls in a 2:1 ratio with matching for age, smokingstatus, and date of blood sampling.
Inflammation plays an essential role in the development of insulinresistance and type 2 diabetes mellitus, the initiation andprogression of atherosclerotic lesions, and plaque disruption.1,2Interleukin-6 and tumor necrosis factor (TNF-) are inflammatorycytokines and the main inducers of the secretion of C-reactiveprotein in the liver.3 C-reactive protein is a marker of low-gradeinflammation, and recent studies suggest that this protein hasa role in the pathogenesis of atherosclerotic lesions in humans.4The effects of TNF- are mediated by two receptors, type 1 andtype 2 (TNF-R1 and TNF-R2), which circulate in soluble forms(sTNF-R1 and sTNF-R2, respectively) and can be measured withgreater sensitivity and reliability than can TNF- itself.5 Thesoluble receptors may attenuate the bioactivity of TNF- butmay also serve as slow-release reservoirs and promote inflammationin the absence of free TNF ligand.6
The Nurses' Health Study (NHS) and the Health ProfessionalsFollow-up Study (HPFS) are prospective cohort investigationsrespectively involving 121,700 female U.S. registered nurseswho were 30 to 55 years old at baseline in 1976 and 51,529 U.S.male health professionals who were 40 to 75 years old at baselinein 1986. Information about health and disease is assessed biennially,and information about diet is obtained every four years by meansof self-administered questionnaires.18,19 From 1989 through1990, a blood sample was requested from all participants inthe NHS, and 32,826 women provided one. Similarly, between 1993and 1995, a blood sample was provided as requested by 18,225men in the HPFS. Participants who provided blood samples weresimilar to those who did not, albeit the men who provided sampleswere somewhat younger than those who did not. In the NHS, amongwomen without cardiovascular disease or cancer before 1990,we identified 249 women who had a nonfatal myocardial infarctionor fatal coronary heart disease between the date of blood drawingand June 1998. In the HPFS, we identified 266 men who had anonfatal myocardial infarction or fatal coronary heart diseasebetween the date of blood drawing and the return of the 2000questionnaire. Using risk-set sampling,20 we randomly selectedcontrols in a 2:1 ratio who were matched for age, smoking status,and date of blood sampling from the subgroup of participantswho were free of cardiovascular disease at the time coronarydisease was diagnosed in the case patients. Within the NHS cohort,an additional matching criterion was fasting status at the timeof blood sampling.
Assessment of Coronary Heart Disease
Study physicians who were unaware of the participant's exposurestatus confirmed the diagnosis of myocardial infarction on thebasis of the criteria of the World Health Organization (symptomsplus either diagnostic electrocardiographic changes or elevatedlevels of cardiac enzymes). Deaths were identified from statevital records and the National Death Index or reported by theparticipant's next of kin or the postal system. Fatal coronaryheart disease was confirmed by an examination of hospital orautopsy records, by the listing of coronary heart disease asthe cause of death on the death certificate, if coronary heartdisease was the underlying and most plausible cause, and ifevidence of previous coronary heart disease was available.
Assessment of Other Factors
Anthropometric, lifestyle, and dietary data were derived fromthe questionnaire administered in 1990 to women and 1994 tomen, with missing information substituted from previous questionnaires.Body-mass index was calculated as the weight in kilograms dividedby the square of the height in meters. Average nutrient intakewas computed with the use of a semiquantitative food-frequencyquestionnaire. Physical activity was expressed in terms of metabolicequivalent (MET)–hours. The questionnaires and the validityand reproducibility of measurements have been described previously.18,21
Measurement of Biochemical Variables
Blood samples from women were collected in tubes treated withliquid sodium heparin, and those from men were collected inEDTA-treated tubes. The tubes were then placed on ice packs,stored in Styrofoam containers, returned to our laboratory byovernight courier, centrifuged, and divided into aliquots forstorage in liquid-nitrogen freezers (–130°C or colder).
The levels of C-reactive protein were determined by means ofa highly sensitive immunoturbidimetric assay with the use ofreagents and calibrators from Denka Seiken; this assay has aday-to-day variability of 1 to 2 percent. Levels of sTNF-R1,sTNF-R2, and interleukin-6 were measured by means of enzyme-linkedimmunosorbent assays (R&D Systems), which have a day-to-dayvariability of 3.5 to 9.0 percent. Levels of inflammatory markerswere largely unaffected by transport conditions and reproduciblewithin subjects over time.22,23 Total, high-density lipoprotein(HDL), and directly obtained low-density lipoprotein (LDL) cholesteroland triglycerides were measured according to standard methodswith the use of reagents from Roche Diagnostics and Genzyme.Study samples were sent to the laboratory for analysis in randomlyordered batches, and the laboratory personnel were unaware ofa sample's case–control status.
The study protocol was approved by the institutional reviewboard of the Brigham and Women's Hospital and the Human SubjectsCommittee Review Board of Harvard School of Public Health.
Exclusions
After the exclusion of participants with missing data on biomarkerlevels, our data sets consisted of 708 women (239 patients and469 controls) and 794 men (265 patients and 529 controls). Theassay for interleukin-6 required slightly more plasma than weoriginally reserved for this assay among women. Therefore, analysesinvolving interleukin-6 were restricted to the subgroup of 676women for whom interleukin-6 levels were available.
Statistical Analysis
We analyzed the two cohorts separately. Inflammatory markerswere divided into quintiles, from the lowest to highest levels,on the basis of the sex-specific distributions among the controls.With risk-set sampling, the odds ratio derived from the logisticregression directly estimates the hazard ratio and, thus, therelative risk.20 We analyzed the association between biomarkerlevels and the risk of coronary heart disease using both conditionaland unconditional logistic regression, with adjustment for matchingfactors. Because both analyses provided essentially the sameresults, we present the results of unconditional logistic regression,which parallel the results in the subgroup analyses.
In our multivariable model, we further adjusted for parentalhistory of coronary heart disease before the age of 60 years(yes vs. no), alcohol intake (nondrinker, 0.1 to 4.9 g per day,5.0 to 14.9 g per day, 15.0 to 29.9 g per day, or at least 30.0g per day), body-mass index (less than 20, 20 to 24, 25 to 29,30 to 34, or 35 or more), physical activity (in quintiles fromlowest to highest level), ratio of total to HDL cholesterol(in quintiles from lowest to highest ratio), and use of postmenopausalhormone therapy (yes vs. no — for women only). Finally,we also added a history of diabetes (yes vs. no) and hypertension(yes vs. no) at baseline to the model to assess the effect ofthese potential mediators. Baseline was defined as the yearblood was drawn.
Correlation coefficients were calculated with the use of age-adjustedSpearman partial-correlation coefficients. To test for lineartrend, we used the median levels of inflammatory markers inthe control categories as a continuous variable. To pool theestimates of relative risk for men and women, we used the weightedaverage of estimates according to the random-effects model ofDerSimonian and Laird.24
All P values are two-tailed, and P values below 0.05 were consideredto indicate statistical significance. All analyses were performedwith the use of SAS software, version 8.2 (SAS Institute).
Results
Baseline Characteristics
Women in whom coronary heart disease developed during follow-uphad significantly higher baseline levels of sTNF-R1 and sTNF-R2than did control women; however, the levels did not differ significantlybetween men in whom coronary heart disease developed duringfollow-up and men in the control group (Table 1). In the caseof both men and women, patients had significantly higher baselinelevels of interleukin-6 and C-reactive protein than controls.
Table 2. Age-Adjusted Spearman Partial-Correlation Coefficients between Selected Cardiovascular Risk Factors among 469 Control Women and 529 Control Men.
Main Effects
After adjustment for matching factors, women in the highestquintile of each inflammatory marker, as compared with womenin the lowest quintile, had a significantly increased risk ofcoronary heart disease — by a factor of 1.95 to 2.57 —with significant trends across quintiles (Table 3). After additionaladjustment for the presence or absence of a parental historyof coronary heart disease before the age of 60 years, alcoholintake, level of physical activity, the ratio of total to HDLcholesterol, body-mass index, and the use or nonuse of postmenopausalhormone therapy, these associations were attenuated and no longersignificant, except for C-reactive protein (model 2 in Table 3).Additional adjustment for the presence or absence of diabetesand hypertension, which are potentially in the causal pathway,further reduced the association for all inflammatory markers.
Table 3. Relative Risks of Coronary Heart Disease during Follow-up, According to the Quintile of Plasma Levels of Inflammatory Markers at Baseline.
Among men, we did not find an association between the levelsof soluble TNF- receptors and the risk of coronary heart disease(Table 3). Men in the highest quintile of interleukin-6 hada 57 percent increase in the risk of coronary heart disease,as compared with men in the lowest quintile, after adjustmentfor matching factors, although this association was not significantand was further attenuated after multivariable adjustment. However,we found a significant association between C-reactive proteinlevels and the risk of coronary heart disease. Multivariableadjustment and adjustment for the presence or absence of hypertensionand diabetes moderately attenuated this relationship; afteraccounting for these variables, men in the highest quintileof C-reactive protein, as compared with those in the lowestquintile, had a relative risk of coronary heart disease of 2.55(95 percent confidence interval, 1.40 to 4.65; P for trend =0.02).
For comparison, in the final multivariable-adjusted model (includingthe presence or absence of diabetes and hypertension and C-reactiveprotein levels), the relative risk of coronary heart diseasefor the highest quintile of the ratio of total to HDL cholesterol,as compared with the lowest quintile, was 4.33 (95 percent confidenceinterval, 2.11 to 8.90; P for trend <0.001) in women and3.29 (95 percent confidence interval, 1.84 to 5.90; P for trend<0.001) in men.
Subgroup Analyses
Overall, we found no significant interactions between variouslow and high cardiovascular risk groups and the associationof biomarkers with the risk of coronary heart disease, althoughthe association of C-reactive protein was generally strongerin low-risk subgroups. For example, in the multivariable-adjustedmodel (excluding the presence or absence of hypertension anddiabetes), the relative risk in the highest as compared withthe lowest quintile of C-reactive protein was 2.53 among womenwith a body-mass index of less than 25 (95 percent confidenceinterval, 1.04 to 6.18; P for trend = 0.02) and 6.25 among menwith a body-mass index of less than 25 (95 percent confidenceinterval, 2.28 to 17.1; P for trend = 0.005). Similarly, amongparticipants with LDL cholesterol levels of less than 130 mgper deciliter (3.4 mmol per liter), the corresponding relativerisks were 3.54 (95 percent confidence interval, 1.19 to 10.5;P for trend = 0.01) for women and 2.52 (95 percent confidenceinterval, 1.09 to 5.83; P for trend = 0.04) for men. Among participantswithout hypertension, the corresponding relative risks were1.87 (95 percent confidence interval, 0.77 to 4.56; P for trend= 0.02) for women and 3.01 (95 percent confidence interval,1.41 to 6.44; P for trend = 0.02) for men.
Clinical Cutoff Points for C-Reactive Protein
We further categorized the study participants, on the basisof recently proposed cutoff points for C-reactive protein, ashaving low levels (less than 1.0 mg per liter), moderate levels(1.0 to 2.9 mg per liter), and high levels (at least 3.0 mgper liter).25 In these analyses, participants with high levelsof C-reactive protein, as compared with those with low levels,had a relative risk of coronary heart disease of approximately1.8 after adjustment for covariates (including body-mass indexand lipid levels) (Table 4). When we pooled the risk estimatesfor men and women, the final multivariable-adjusted relativerisk (including adjustment for the presence or absence of diabetesand hypertension) was 1.68 in the group with high levels ofC-reactive protein, as compared with the group with low levels(95 percent confidence interval, 1.18 to 2.38; P for trend =0.008) (Table 4). This is similar to the pooled estimate (relativerisk, 1.48; 95 percent confidence interval, 1.08 to 2.04; Pfor trend = 0.03) after we controlled for covariates from theFramingham risk score,26 including age, presence or absenceof hypertension and diabetes, ratio of total to HDL cholesterol,and smoking status.
Table 4. Relative Risks of Coronary Heart Disease during Follow-up According to the Baseline Level of C-Reactive Protein.
We found a gradient of risk of coronary heart disease withineach increasing category of C-reactive protein and ratio oftotal to HDL cholesterol (Figure 1). This finding supports thehypothesis that the levels of C-reactive protein may predictrisk beyond the information afforded by lipid levels. However,despite the independent associations, the gradient of risk associatedwith lipid levels was greater than that for C-reactive proteinlevels.
Figure 1. Multivariable-Adjusted Relative Risk of Coronary Heart Disease among Women (Panel A) and Men (Panel B), According to the Baseline Level of C-Reactive Protein (CRP) and the Quintile of the Ratio of Total to HDL Cholesterol.
Data on women are from the Nurses' Health Study and include eight years of follow-up, and data on men are from the Health Professionals Follow-up Study and include six years of follow-up. The model was adjusted for age, smoking status, date of blood sampling, presence or absence of a parental history of coronary heart disease before the age of 60 years, alcohol intake, level of physical activity, and body-mass index. Among women, the multivariable model was also adjusted for fasting status at the time of blood sampling and the use or nonuse of postmenopausal hormone therapy. In each panel, the subjects in quintile 1 who had a CRP level of less than 1.0 mg per liter served as the reference group.
Additional Analyses
When we stratified our analysis according to the time to anevent in two-year intervals, the relative risk of coronary heartdisease associated with C-reactive protein levels remained relativelystable over time (data not shown). When we repeated our mainanalyses after excluding participants with C-reactive proteinlevels of at least 10.0 mg per liter, we found essentially thesame results. C-reactive protein levels may be affected by hormonetherapy.10 However, results were similar when we used quintilesof C-reactive protein based on levels in women in the controlgroup who reported never using hormones.
Discussion
In these two nested case–control studies, we found thathigh plasma levels of C-reactive protein were associated withan increased risk of coronary heart disease among women andmen without previous cardiovascular disease. Elevated plasmalevels of sTNF-R1 and sTNF-R2 were related to an increased riskamong women, but not men. We found only a moderate suggestionof increased risk associated with elevated levels of interleukin-6.For all markers, associations were substantially attenuatedand — with the exception of C-reactive protein —no longer significant after adjustment for cardiovascular riskfactors, particularly body-mass index and the presence or absenceof diabetes and hypertension. These findings are consistentwith a role of these inflammatory markers in the elevated riskof cardiovascular events that is associated with type 2 diabetesand hypertension.
TNF- and interleukin-6 are the main inducers of hepatic productionof acute-phase proteins, including C-reactive protein.3 Theseinflammatory markers are associated with biologic and environmentalrisk factors for cardiovascular events, including componentsof the metabolic syndrome (obesity, insulin resistance, diabetes,hypertension, and low HDL cholesterol levels), and lifestylefactors, such as smoking, abstinence from alcohol, and physicalinactivity.27,28,29
Compelling evidence suggests that inflammation causally contributesto several precursors of cardiovascular disease. TNF- and interleukin-6can cause insulin resistance in animal models, and plasma levelsof C-reactive protein and interleukin-6 have been shown to predicttype 2 diabetes in humans.30,31 The increased cytokine synthesisin obesity may promote insulin resistance and impaired glucoseuptake, type 2 diabetes, and ultimately, coronary heart disease.30In line with these hypotheses, we found that plasma levels ofinterleukin-6 and C-reactive protein, in particular, were relatedto the risk of coronary heart disease and that the risks wereattenuated after adjustment for the presence or absence of diabetesand hypertension.
TNF- has a limited half-life and is difficult to measure inlarge-scale epidemiologic studies.5,6 In a nested case–controlstudy, Ridker et al. reported a multivariable-adjusted relativerisk of recurrent coronary events of 2.5 (95 percent confidenceinterval, 1.3 to 5.1) among men whose TNF- levels exceeded the95th percentile, as compared with men with lower levels.32 Cesariet al. reported a relative risk of of coronary events of 1.79(95 percent confidence interval, 1.18 to 2.71) among elderlyparticipants without cardiovascular disease who had the highestof three levels of TNF-, as compared with those who had thelowest levels.8 The value of assessing circulating levels ofTNF- is unknown, since such levels can be very low and unstable.The levels of soluble TNF- receptors may be more stable andmay better reflect longer-term average circulating levels ofTNF-, although data on the role of soluble TNF- receptors incoronary heart disease are scarce.7,33 It is unclear why wefound a difference in risk between men and women associatedwith elevated levels of soluble TNF- receptors; however, othersalso have found differences between women and men with respectto lipids34 and in the overall prediction of risk.35 Similarly,mechanisms of insulin sensitivity, rather than inflammation,may contribute more to the risk of coronary heart disease inwomen than men.
Findings of an association between interleukin-6 levels andthe risk of coronary heart disease have been inconsistent.8,10,36In our study, this association was substantially reduced andno longer significant after multivariable adjustment.
C-reactive protein is the most extensively studied inflammatorymarker in prospective settings. In an early meta-analysis of11 prospective studies, the relative risk of coronary heartdisease in subjects with the highest of three C-reactive proteinlevels, as compared with those with the lowest levels, was 2.0(95 percent confidence interval, 1.6 to 2.5) among population-basedstudies.37 Eleven other prospective studies have since beenpublished. In an updated meta-analysis, Danesh et al. reportedan overall odds ratio of 1.58 (95 percent confidence interval,1.48 to 1.68) among subjects with the highest of three levelsof C-reactive protein, as compared with subjects with the lowestlevel.16 This risk estimate is similar to that in our comparisonsof C-reactive protein levels of at least 3.0 mg per liter withthose of less than 1.0 mg per liter. However, the degree ofadjustment for traditional cardiovascular risk factors differedmarkedly among the studies included in the meta-analysis.
An important question is whether knowing the level of C-reactiveprotein adds materially to risk prediction. In the Women's HealthStudy, Ridker et al. reported that the level of C-reactive proteinwas a stronger predictor than the LDL cholesterol level andthat it added to the information provided by the Framinghamrisk score.12,38 Comparing C-reactive protein levels of at least3.0 mg per liter with those of less than 1.0 mg per liter, theyreported a relative risk of 1.5 (95 percent confidence interval,1.2 to 1.9) after adjustment for the Framingham risk score andthe presence or absence of diabetes.38
In our analysis, the pooled relative risk among men and womenclassified according to clinical cutoff points for the levelsof C-reactive protein was 1.48 (95 percent confidence interval,1.08 to 2.04; P for trend = 0.03) after we accounted for covariatesin the Framingham risk score, including the presence or absenceof diabetes. Our results are similar to those of Ridker et al.38and Ballantyne et al.,14 as well as those of the recent meta-analysisby Danesh et al.,16 a fact that suggests that after adjustmentfor the Framingham risk score, the relative risk associatedwith a clinical cutoff point of at least 3.0 mg per liter, ascompared with a cutoff of less than 1.0 mg per liter, is probablymoderately less than previously suggested in the guidelinesfor the clinical assessment of inflammatory markers issued bythe American Heart Association and the Centers for Disease Controland Prevention (relative risk, 1.5 vs. approximately 2.0).25Nevertheless, our findings support the theory that the levelof C-reactive protein provides an additional measure of therisk of coronary heart disease beyond that afforded by the Framinghamrisk score.
Our study has some limitations. As with any observational studydesign, there is the possibility of unmeasured confounding.However, we controlled for most known cardiovascular risk factors.Though we obtained only a single blood sample at baseline, previousstudies have shown the levels of biomarkers to be relativelystable over time.22,23 Since the ranges of anthropometric variablesin our cohorts were quite broad, the biologic relationshipsfound should be widely generalizable. Though we excluded menand women with missing data on blood levels, generalizabilityshould be minimally affected because the participants were similarto those who did not provide blood samples.
Although the Framingham risk score is a tool for estimatingthe 10-year risk of coronary heart disease among healthy subjects,26it does not include other well-established risk factors, suchas body-mass index, alcohol intake, level of physical activity,or the presence or absence of a parental history of coronaryheart disease.40 Therefore, to examine the role of inflammatorymarkers in coronary heart disease, we used an etiologic approachin our main analyses, to take into account the pathophysiologyof coronary heart disease and include the major cardiovascularrisk factors, beyond those included in the Framingham risk score,for comparison.
Our questionnaires did not include questions on the use of hydroxymethylglutarylcoenzymeA reductase inhibitors (statins) because these drugs were notwidely used at time of blood sampling. However, the reporteduse of cholesterol-lowering drugs was generally low in bothcohorts.
Supported by grants (HL35464, CA55075, AA11181, and HL34594)from the National Institutes of Health and by a grant from MerckResearch Laboratories. Dr. Pischon is a Jetson Lincoln fellow,supported in part by an unrestricted gift from Mr. Lincoln.Ms. Pai is supported by an institutional training grant (HL07575)from the National Heart, Lung, and Blood Institute.
Dr. Cannuscio was an employee of Merck at the time the researchwas conducted. Dr. Manson is listed as a coinventor of a patentfiled by Brigham and Women's Hospital related to inflammatorymarkers and diabetes mellitus. Dr. Rimm reports having receivedgrant support from Merck.
We are indebted to Alan Paciorek, Helena Ellis, and Jeanne Sparrowfor coordinating the collection of samples and for laboratorymanagement, and to Lydia Liu for programming review.
Source Information
From the Departments of Epidemiology (J.K.P., T.P., J.E.M., S.E.H., K.J., G.C.C., M.J.S., E.B.R.) and Nutrition (T.P., M.J.S., E.B.R.), Harvard School of Public Health; the Division of Preventive Medicine (J.K.P., J.E.M.) and Channing Laboratory (T.P., J.M., S.E.H., G.C.C., M.J.S., E.B.R.), Department of Medicine, Brigham and Women's Hospital and Harvard Medical School; the Department of Oral Health Policy and Epidemiology, Harvard School of Dental Medicine (K.J.); the Department of Laboratory Medicine, Children's Hospital (N.R.); and the Department of Pathology, Harvard Medical School (N.R.) — all in Boston; the Department of Epidemiology, German Institute of Human Nutrition, Potsdam-Rehbruecke, Germany (T.P.); and Merck Research Laboratories, West Point, Pa. (C.C.C.). Ms. Pai and Dr. Pischon contributed equally to this article.
Address reprint requests to Dr. Rimm at the Departments of Epidemiology and Nutrition, Harvard School of Public Health, 665 Huntington Ave., Boston, MA 02115, or at erimm{at}hsph.harvard.edu.
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