doi: 10.1161/hy0202.104270
(Hypertension. 2002;39:197.)
© 2002 American Heart Association, Inc.
Scientific Contributions |
Association Between Pulse Pressure and C-Reactive Protein Among Apparently Healthy US Adults
From the Department of Medicine, Division of Cardiology, Emory University School of Medicine, Atlanta, Ga.
Correspondence to Jerome L. Abramson, Department of Medicine, Division of Cardiology, Emory University School of Medicine, 1256 Briarcliff Rd, Suite 1 North, Atlanta, GA 30306. E-mail jabram3{at}emory.edu
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Abstract |
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Elevated pulse pressure has been associated with an increased risk of cardiovascular disease, which is increasingly being seen as an inflammatory disease. Thus, the mechanism underlying the link between elevated pulse pressure and cardiovascular disease risk may be inflammation. However, investigators have not examined the relationship between pulse pressure and C-reactive protein, an inflammation marker that has been closely linked to cardiovascular risk. We examined the cross-sectional relationship between pulse pressure and C-reactive protein among 9867 healthy persons 17 years of age or older who participated in the Third National Health and Nutrition Examination Survey. The association between pulse pressure and the odds of having an elevated C-reactive protein level (
0.66 mg/dL) was assessed by logistic regression. In a model that adjusted for systolic blood pressure, demographic factors, cholesterol, measures of obesity, smoking, alcohol consumption, physical activity, and antihypertensive medication use, a 10 mm Hg increase in pulse pressure was associated with a 15% increase in the odds of having an elevated C-reactive protein level (odds ratio, 1.15; 95% confidence interval, 1.01 to 1.31; P=0.04). When the same model was re-run adjusting for diastolic blood pressure instead of systolic blood pressure, a 10 mm Hg rise in pulse pressure was associated with a significant 12% increase in the odds of having an elevated C-reactive protein level. Systolic and diastolic blood pressure were unrelated to C-reactive protein once pulse pressure had been accounted for. Our results suggest that increases in pulse pressure are associated with elevated C-reactive protein levels among apparently healthy US adults, independent of systolic and diastolic blood pressure.
Key Words: blood pressure • hypertension, essential • epidemiology • cross-sectional studies • risk factors
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Introduction |
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During the past few years, several studies have shown that elevations in pulse pressure (PP) are predictive of an increased risk of cardiovascular disease (CVD).1–4 Recent evidence also indicates that elevated levels of inflammation markers, particularly C-reactive protein (CRP), are associated with a higher risk of CVD,5–7 suggesting that inflammation plays a key role in the development of CVD.8 As such, one could hypothesize that one of the mechanisms underlying the link between elevated PP and increased CVD risk may be inflammation. Indeed, there is some evidence to indicate that increases in PP may be capable of stimulating inflammation. In particular, investigators have reported that increases in PP are associated with elevated levels of reactive oxygen species (ROS),9,10 which play a role in stimulating inflammatory signaling pathways.11 Additionally, higher levels of PP are associated with greater flow reversals during diastole,12 and flow reversals can increase the expression of adhesion molecules,13 which would tend to promote the inflammatory process involved in atherosclerosis.
If the link between PP and CVD risk is indeed mediated by inflammation, one would expect to see positive associations between PP and markers of systemic inflammation that are predictive of CVD risk, such as CRP. Prior investigations, however, have not considered the relationship between PP and CRP. In the present study we sought to determine whether increasing PP, independent of systolic blood pressure (SBP) and diastolic blood pressure (DBP), was associated with elevated CRP levels among apparently healthy US adults.
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Methods |
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Study Design and Participants
The current study is based on data from the Third National Health and Nutrition Examination Survey (NHANES III). NHANES III was a cross-sectional study of 33,994 persons conducted from 1988 to 1994 by the National Center for Health Statistics of the US Centers for Disease Control and Prevention. In-home interviews and medical examinations were conducted in order to gather information on participants. We restricted our study to the 9,867 persons in NHANES III who were
17 years of age, who were free of diseases that might substantially affect their CRP levels (cancer, CHD, stroke, diabetes, heart failure, rheumatoid arthritis, asthma, bronchitis, and emphysema), and who had complete data on blood pressure, CRP, and covariates. Additional information on the design of NHANES III has been published elsewhere.14
Study Measures
SBP, DBP, and PP
Physicians obtained 3 sets of blood pressure measurements on each study participant by using a mercury sphygmomanometer. The first and fifth Korotkoff sounds were recorded and used to determine SBP and DBP respectively. The average of the 3 measurements was used as the SBP and DBP values in the present study. Pulse pressure was calculated as SBP minus DBP.
C-Reactive Protein
Phlebotomists obtained blood samples from study participants as part of the medical examination. The level of C-reactive protein in these sample was determined according to latex-enhanced nephelometry. This method of determining CRP could not detect CRP levels of <0.22 mg/dL. As a result, persons with CRP levels of <0.22 mg/dL were classified as having "undetectable" CRP levels.
Other Study Factors
Other factors included in this study were age, sex, race, education, total and high–density lipoprotein, body mass index (BMI), and waist-to-hip ratio (WHR). Behavioral factors of interest were self-reported smoking status, frequency of alcohol consumption in the prior month, and frequency of physical activity (a count of the total number of times a person had engaged in any physical activity during the preceding month). Information on current use of antihypertensive medications was also obtained.
Statistical Analysis
Analyses were designed to assess the association of blood pressure components (PP, SBP, DBP) with CRP after adjusting for other study factors. In our analyses the blood pressure components and other study factors were independent variables, and CRP was the dependent variable. The distribution of CRP readings was highly skewed, with the most common reading being "undetectable" (<0.22 mg/dL). Thus, we believed it was inappropriate to analyze CRP as a continuous outcome. Instead, we analyzed CRP as a dichotomous outcome (CRP<0.66 mg/dL or CRP< 0.66 mg/dL) in logistic regression models. Individual blood pressure component models assessed the effect of a single blood pressure component (SBP, DBP, or PP) on CRP, without adjustment for other blood pressure components. Dual blood pressure component models assessed the effects of PP on CRP after adjustment for one of the other blood pressure components (SBP or DBP). All statistical tests were two-tailed. SUDAAN (Research Triangle Institute) was used for all analyses in order to account for the complex nature of the NHANES III sample.15
An expanded Methods section can be found in an online data supplement available at http://www.hypertensionaha.org.
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Results |
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The average age of the 9867 participants was 38.1 years. Fifty-one percent of the sample was male. The percentage of persons describing themselves as white, African American, or members of other racial/ethnic groups was 83.9, 10.8, and 5.3, respectively. The average SBP, DBP, and PP of the study population was 118.5 mm Hg, 73.2 mm Hg, and 45.3 mm Hg, respectively. Approximately 9.6% of the sample had a CRP level of 0.66 mg/dL or higher.
Figure 1 shows the percentage of persons with an elevated CRP level, according to quartiles of SBP, DBP, and PP. The percentage of persons with an elevated CRP level tended to increase with higher levels of SBP (P=0.001 according to chi-square test). Similarly, DBP and PP tended to be positively associated with CRP (probability value for 
2 tests for DBP and PP were 0.02 and <0.001 respectively). Table 1 shows the distribution of SBP, DBP, PP, and other study measures according to CRP level. Those with a high CRP level had higher mean SBP, DBP, and PP values. Additionally, compared with those participants with a low CRP level, participants with a high CRP level were older, substantially less likely to be male, more likely to be African American, had higher total cholesterol readings, had a higher average BMI and WHR, and were more likely to be taking antihypertensive medications. Participants with a high CRP level also had a lower frequency of alcohol consumption, lower HDL cholesterol readings, and engaged in physical activity less frequently. The likelihood of having an elevated CRP level did not differ substantially with respect to smoking status.
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Table 2 presents the results of multivariable-adjusted logistic regression models assessing the association of single blood pressure components with elevated CRP. Model 1 shows that after adjustment for other study factors, an increase in SBP was significantly associated with an increase in the odds of having an elevated CRP level. For each 10 mm Hg increase in SBP, the odds of having an elevated CRP level increased by 7% (odds ratio [OR], 1.07; 95% confidence interval [CI], 1.00 to 1.17; P=0.05). In contrast, model 2 shows that, after adjustment for other factors, an increase in DBP could not be shown to be significantly related to elevated CRP. Model 3 shows that, similar to SBP, an increase in PP was significantly associated with an increase in the odds of having an elevated CRP level, independent of other study factors. For each 10 mm Hg increase in PP, the odds of having a high CRP level increased by 13% (OR, 1.13; 95% CI, 1.04 to 1.22; P=0.004).
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Next, we ran dual-component blood pressure models that assessed the association between PP and CRP after adjustment for SBP or DBP and other study factors (Table 3). In model 1 the dual effects of SBP and PP were considered. This model showed that SBP was no longer associated with elevated CRP, whereas a 10 mm Hg rise in PP significantly increased the odds of an elevated CRP level by 15% (P=0.04). In model 2 the dual effects of DBP and PP were considered. A 10 mm Hg increase in DBP was not related to CRP levels, but each 10 mm Hg increase in PP was associated with a significant 12% increase (P=0.006) in the odds of an elevated CRP. We then added quadratic and cubic terms for PP to our models. These terms proved to be less significant predictors of elevated CRP than was the linear term for PP, suggesting that the association between PP and elevated CRP tended to follow a fairly linear "dose-response" pattern.
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In order to check whether our results were applicable to a different definition of "elevated" CRP, we repeated the analyses with an elevated CRP level defined as 0.22 mg/dL, ie, any CRP value large enough to be in the "detectable" range. This level has been considered indicative of low-grade inflammation in previous studies.16 In a model that included PP, SBP, and other study factors, we found that a 10 mm Hg increase in PP was associated with a significant increase in the odds of having a CRP 0.22 mg/dL (OR, 1.14; 95% CI, 1.03 to 1.27; P=0.017). In contrast, SBP was not associated with CRP in this model. When this model was refitted with adjustment for DBP instead of SBP, a 10 mm Hg increase in PP was again associated with an increased odds of having a CRP level 0.22 mg/dL (OR, 1.13; 95% CI, 1.05 to 1.21; P=0.002). As was the case with SBP, DBP was not associated with elevated CRP.
We then ran 2 subgroup analyses. First, we examined the association between PP and CRP in the group not taking antihypertensive medications. We found that in this group the association between PP and CRP was strengthened somewhat. Among those not taking antihypertensive medications, each 10 mm Hg increase in PP was associated with a significant 17% increase (P=0.03) in the odds of having an elevated CRP after adjustment for SBP and other study factors. When this model was reconstructed controlling for DBP instead of SBP, a 10 mm Hg increase in PP increased the odds of an elevated CRP by 13% (P=0.006).
Second, it has been reported that the association of increasing PP with higher CVD risk is stronger in older populations.17 Therefore, we sought to determine whether the association between PP and elevated CRP (0.66 mg/dL) differed according to age by constructing separate models among persons <45, 45 to 64, and 65 years of age. When controlling for SBP and other study factors, there was some indication that the association between PP and CRP was strongest among older persons; a 10 mm Hg increase in PP among those <45, 45 to 64, and 65 years of age was associated with an 11, 6, and 23% increase respectively in the odds of having an elevated CRP level. None of these results was significant, however, in part because of the reduced sample size in each age subgroup. When controlling for DBP and other study factors, there was only limited indication that PP was more strongly related to CRP in the older age groups; a 10 mm Hg increase in PP among those <45, 45 to 64, and 65 years of age was associated with an 10, 13, and 12% increase respectively in the odds of having an elevated CRP level. When a term representing the interaction between continuous age and PP was included in models controlling for SBP or DBP as well as other study factors, it was found not to be significant (P=0.44).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The primary finding of the present study was that an increasing PP was associated with increased odds of having an elevated CRP level (
0.66 mg/dL) among apparently healthy adults who were representative of the general US population. This association was independent of SBP, DBP, and a number of other factors including demographic factors, cholesterol levels, obesity, smoking status, alcohol consumption, and physical activity. The result persisted even when an alternative definition of "elevated" CRP (0.22 mg/dL) was employed. Of note is that SBP and DBP did not show significant associations with CRP once PP was taken into account. A prior study had reported an association between hypertension (defined as either a SBP >140 mm Hg, a DBP >90 mm Hg, or use of antihypertensive medications) and higher CRP levels,18 but this study did not consider whether PP was associated with CRP. Other investigators had reported that PP is positively associated with two inflammatory markers, intercellular adhesion molecule-1 and interleukin-6,19 but did not establish whether this association was independent of SBP or DBP and did not examine PP’s association with CRP, an inflammation marker which has been especially predictive of CHD risk. To the best of our knowledge, the present study is the first to show that an increasing PP is associated with an elevated CRP level in the general population, independent of SBP or DBP. The present study also found some indication that the association between an increasing PP and elevated CRP was stronger in older compared with younger persons, but the interaction between PP and age was not significant. Evidence indicates that there are plausible mechanisms by which PP could increase inflammation levels. Investigators have reported that elevated levels of PP are associated with impaired acetylcholine induced endothelium-dependent relaxation, and that this impaired relaxation is prevented by administration of the antioxidant superoxide dismutase.10 This has led some to believe that a high PP may impair endothelium-dependent relaxation by generating reactive oxygen species (ROS).10 Indeed, there is evidence that in humans, PP is positively associated with increased production of the ROS hydrogen peroxide and that this association is stronger than the association of SBP or DBP with hydrogen peroxide production.9 Increased ROS levels, in turn, can stimulate inflammatory signaling pathways.11 A wide PP also tends to be associated with greater flow reversals during diastole.12 It has been demonstrated that oscillatory shear with flow reversals increases adhesion molecule expression,13 which would tend to promote the inflammatory process involved in atherosclerosis. Along these lines, investigators have shown recently that increases in PP are associated with increased adhesion of monocytes.20 While the evidence noted above provides some plausible biologic mechanisms which could explain why increases in PP might have been associated with elevated levels of the inflammatory marker CRP in this study, it is important to note that we had no information on ROS or adhesion molecules in the present investigation. As such, explaining our results in terms of these mechanisms is necessarily speculative.
Although the findings of the present study suggest that increases in PP may increase the odds of having an elevated CRP level, other explanations are possible. First, the present study was based on observational data, and confounding from factors that were not controlled for, and/or residual confounding from factors that we did control for, but that were imperfectly measured, may be an alternative explanation for our results. Second, the present study was based on cross-sectional data, making it impossible to determine the temporal ordering of the association that we observed between PP and CRP. Although the evidence noted above suggests that increases in PP would enhance inflammation, the cross-sectional nature of our data leaves open the possibility that increases in inflammation lead to higher PP levels. Indeed, some investigators who have noted associations between inflammation markers and blood pressure have argued that it is inflammation which is a precursor to increased blood pressure.18 Third, one cannot definitively rule out chance as an explanation for the findings of this study. In fact, although we observed that PP was significantly associated with CRP in models that adjusted for SBP, the probability values were between 0.05 and 0.01. However, the consistency of the association between PP and CRP across different models and different definitions of CRP elevation indicates that our results may not simply be due to chance. Fourth, the measure of CRP used in this study was not high-sensitivity CRP, and this probably led to some misclassification of CRP levels which could have biased our results. Such misclassification would probably have been random though, and would have tended to attenuate associations between PP and CRP. Thus, misclassification in CRP measurements may have actually led us to underestimate the strength of the association between PP and CRP.
Growing evidence suggests that elevated PP may be an important predictor of CVD, independent of SBP and DBP.2,3,17 Several theories have been offered as to why an elevated PP may be a predictor of CVD. Elevated PP, which is often a manifestation of increased arterial stiffness, can lead to adverse cardiovascular effects such as increased myocardial work,21 impaired ventricular relaxation,22 and ischemia.23 These effects could, in turn, increase CVD risk. However, the present study suggests another explanation as to why PP may be predictive of CVD incidence. By showing that increasing levels of PP were associated with higher odds of having an elevated CRP level, the present study suggests that a higher PP may induce or facilitate an inflammatory response, which could promote the development of atherosclerosis and, eventually, CVD. Given the observational and cross-sectional nature of our study, however, our results should not be taken as evidence of a causal relationship leading from PP to CRP and should therefore be interpreted with caution. Future studies need to use a prospective cohort design to clarify whether or not an elevated PP leads to increased inflammation, whether this effect is more or less pronounced in certain subgroups such as the elderly, and whether the association between PP and inflammation helps to explain why PP has been associated with CVD risk.
Received September 13, 2001; first decision October 8, 2001; accepted December 7, 2001.
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References |
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1. Benetos A, Safar M, Rudnichi A, Smulyan H, Richard JL, Ducimetieere P, Guize L. Pulse pressure: a predictor of long-term cardiovascular mortality in a French male population. Hypertension. 1997; 30: 1410–1415.
2. Vaccarino V, Holford TR, Krumholz HM. Pulse pressure and risk for myocardial infarction and heart failure in the elderly. J Am Coll Cardiol. 2000; 36: 130–138.
3. Franklin SS, Khan SA, Wong ND, Larson MG, Levy D. Is pulse pressure useful in predicting risk for coronary heart disease? The Framingham heart study. Circulation. 1999; 100: 354–360.
4. Madhavan S, Ooi WL, Cohen H, Alderman MH. Relation of pulse pressure and blood pressure reduction to the incidence of myocardial infarction. Hypertension. 1994; 23: 395–401.
5. Ridker PM, Hennekens CH, Buring JE, Rifai N. C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. N Engl J Med. 2000; 342: 836–843.
6. Ridker PM. High-sensitivity C-reactive protein: potential adjunct for global risk assessment in the primary prevention of cardiovascular disease. Circulation. 2001; 103: 1813–1818.
7. Koenig W, Sund M, Frohlich M, Fischer HG, Lowel H, Doring A, Hutchinson WL, Pepys MB. 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) Augsburg Cohort Study, 1984 to 1992. Circulation. 1999; 99: 237–242.
8. Weissberg PL, Bennett MR. Atherosclerosis—an inflammatory disease. N Engl J Med. 1999; 340: 1928–1929.
9. Lacy F, Kailasam MT, O’Connor DT, Schmid-Schonbein GW, Parmer RJ. Plasma hydrogen peroxide production in human essential hypertension: role of heredity, gender, and ethnicity. Hypertension. 2000; 36: 878–884.
10. Ryan SM, Waack BJ, Weno BL, Heistad DD. Increases in pulse pressure impair acetylcholine-induced vascular relaxation. Am J Physiol. 1995; 268: H359–H363.[Medline] [Order article via Infotrieve]
11. Hensley K, Robinson KA, Gabbita SP, Salsman S, Floyd RA. Reactive oxygen species, cell signaling, and cell injury. Free Radic Biol Med. 2000; 28: 1456–1462.[CrossRef][Medline] [Order article via Infotrieve]
12. Mitchell GF, Pfeffer MA. Pulsatile hemodynamics in hypertension. Curr Opin Cardiol. 1999; 14: 361–369.[CrossRef][Medline] [Order article via Infotrieve]
13. Chappell DC, Varner SE, Nerem RM, Medford RM, Alexander RW. Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ Res. 1998; 82: 532–539.
14. Plan and Operation of the Third Health and Nutrition Examination Survey, 1988–1994. National Center for Health Statistics. Vital Health Stat. 1(32). 1994.
15. Analytic reporting guidelines. The Third National Health and Nutrition Examination Survey, NHANES III (1988–1994). Hyattsville, MD: National Center for Health Statistics Centers for Disease Control and Prevention; 1996.
16. Visser M, Bouter LM, McQuillan GM, Wener MH, Harris TB. Elevated C-reactive protein levels in overweight and obese adults. JAMA. 1999; 282: 2131–2135.
17. Franklin SS, Larson MG, Khan SA, Wong ND, Leip EP, Kannel WB, Levy D. Does the relation of blood pressure to coronary heart disease risk change with aging? The Framingham Heart Study. Circulation. 2001; 103: 1245–1249.
18. Bautista LE, Lopez-Jaramillo P, Vera LM, Casas JP, Otero AP, Guaracao AI. Is C-reactive protein an independent risk factor for essential hypertension? J Hypertens. 2001; 19: 857–861.[CrossRef][Medline] [Order article via Infotrieve]
19. Chae CU, Lee RT, Rifai N, Ridker PM. Blood pressure and inflammation in apparently healthy men. Hypertension. 2001; 38: 399–403.
20. Williams JC, Fotherby MD, Forster LA, Tull SP, Ferns GA. Mononuclear cell adhesion to collagen ex vivo is related to pulse pressure in elderly subjects. Atherosclerosis. 2000; 151: 463–469.[CrossRef][Medline] [Order article via Infotrieve]
21. Kelly RP, Tunin R, Kass DA. Effect of reduced aortic compliance on cardiac efficiency and contractile function of in situ canine left ventricle. Circ Res. 1992; 71: 490–502.
22. Kohno F, Kumada T, Kambayashi M, Hayashida W, Ishikawa N, Sasayama S. Change in aortic end-systolic pressure by alterations in loading sequence and its relation to left ventricular isovolumic relaxation. Circulation. 1996; 93: 2080–2087.
23. Kass DA, Saeki A, Tunin RS, Recchia FA. Adverse influence of systemic vascular stiffening on cardiac dysfunction and adaptation to acute coronary occlusion. Circulation. 1996; 93: 1533–1541.
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