Published online before print April 9, 2007, doi: 10.1161/HYPERTENSIONAHA.106.083592
(Hypertension. 2007;49:1256.)
© 2007 American Heart Association, Inc.
Original Articles |
Predictive Utility of Pulse Pressure and Other Blood Pressure Measures for Cardiovascular Outcomes
From the Bluhm Cardiovascular Institute (D.M.L.-J., P.G.), the Department of Medicine (W.J.M., D.M.L.-J., P.G.), and the Department of Preventive Medicine (D.M.L-J., D.B.G., P.G.), Feinberg School of Medicine, Northwestern University, Chicago, Ill.
Correspondence to Donald M. Lloyd-Jones, Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, 680 N Lake Shore Dr, Suite 1102, Chicago, IL 60611. E-mail dlj{at}northwestern.edu
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Data are sparse regarding the actual predictive utility of pulse pressure and other blood pressure measures for cardiovascular events. We included all of the participants from the Chicago Heart Association Detection Project in Industry who were free of cardiovascular disease and not receiving antihypertensive treatment at baseline (1967–1973). Baseline blood pressure measures were assessed for predictive utility for fatal and nonfatal events over 33 years. Among 36 314 participants (mean age: 39±13 years; 43.4% women), there were 11 452 deaths: 745 were attributed to stroke, 2812 to coronary disease, and 599 to heart failure. Of the 16 393 participants who attained Medicare eligibility, 3050, 1367, and 2207 had
1 hospitalization for stroke, myocardial infarction, or heart failure, respectively. In univariate analyses, hazards ratios for stroke death per SD of pulse, systolic, and diastolic pressure, respectively, were 1.49, 1.75, and 1.71. Likelihood ratio 
2 (134.3, 302.0, and 232.6, respectively), Bayes information criteria values (15 142, 14 974, and 15 044, respectively), and areas under receiver-operating characteristic curves (0.59, 0.64, and 0.63, respectively) all indicated better predictive utility for systolic and diastolic compared with pulse pressure. Results for coronary or heart failure death and stroke, myocardial infarction, or heart failure hospitalization were similar. Pulse pressure had weaker predictive utility at all ages but particularly for those <50 years. In this large cohort study, pulse pressure had predictive utility for cardiovascular events that was inferior to systolic or diastolic pressure. These findings support the approach of current guidelines in the use of systolic and diastolic blood pressure to assess risk and the need for treatment.
Key Words: hypertension • pulse pressure • stroke • coronary heart disease • heart failure • prediction
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Hypertension, currently defined by systolic (SBP) and diastolic (DBP) blood pressure (BP) levels according to Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines, is a major causal risk factor for stroke, coronary heart disease (CHD), and heart failure,1–3 3 of the leading causes of morbidity and mortality in the United States.1 In the last decade there has been controversy regarding the value of pulse pressure (PP), defined as SBP minus DBP, compared with traditional measures of SBP and DBP, for prediction of stroke, CHD, and heart failure outcomes.4–13 However, most studies have merely compared relative risks for single outcomes associated with PP, SBP, and DBP without assessing measures of true predictive utility, such as model fit, informativeness, and areas under receiver-operating characteristic curves.
Thus, although PP has been shown to be associated with stroke, CHD, and heart failure,4–13 it remains controversial whether PP has greater predictive utility than SBP or DBP. Evidence of clear improvements in prediction with use of PP rather than SBP or DBP could change the clinical focus for risk stratification and prevention of these devastating outcomes. Past studies4,5,7,11,12 have been performed mainly in older populations, particularly in those with isolated systolic hypertension. Data are sparse regarding the comparative predictive utility of BP measures for stroke, CHD, and heart failure outcomes from large populations of individual subjects across the age spectrum. For example, the recent large Prospective Studies’ Collaboration2 reported on stroke and ischemic heart disease mortality but not on nonfatal stroke events, CHD, or heart failure outcomes, with limited data on predictive utility. In the current study, we took advantage of the design of the Chicago Heart Association Detection Project in Industry cohort, a large population with a wider age range and longer follow-up period than many previous studies, to compare directly the associations and predictive utility of PP, SBP, and DBP, as well as the summary measures of mean arterial pressure (MAP) and midblood pressure (MidBP), for death or hospitalization because of stroke, CHD, or heart failure. We also examined whether the predictive utility of these measures varied according to the age at which they were measured.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Sample
Between 1967 and 1973, the Chicago Heart Association Detection Project in Industry study recruited 39 522 participants from 84 Chicago-area companies and organizations. Details of the study design and methods have been described.14 Two 4-person research teams trained in standardized methods of data collection performed all of the measurements. Height and weight were measured with participants wearing light indoor clothing; body mass index was calculated as weight in kilograms divided by the square of height in meters. BP was measured as a single supine reading using a standard mercury sphygmomanometer. Nonfasting serum total cholesterol levels were measured by the Levine-Zak method.14 Information on demographics, smoking, medical history, and medication use was collected by questionnaire. All of the participants gave informed consent. The study protocol has received periodic institutional review board approval, and a waiver as described by the Health Insurance Portability and Accountability Act was granted by the institutional review board before commencement of the present project.
Exclusions
For the present study, we sought to examine the risks for stroke, CHD, and heart failure outcomes among healthy individuals. From the 39 441 participants in the cohort with known vital status, we excluded those with history of myocardial infarction (n=473) and those who were receiving antihypertensive drug therapy (n=1748) at baseline. We also excluded those with diabetes at baseline (n=749), because duration of diabetes in these individuals was unknown. After 157 additional participants were excluded for missing or incomplete baseline covariate and/or BP data, 36 314 participants were eligible for inclusion in the analyses of stroke, CHD, and heart failure mortality. Among the 18 168 participants who reached Medicare eligibility during follow-up, exclusion using the same algorithm yielded 16 393 participants eligible for inclusion in the analyses of stroke, CHD, and heart failure hospitalization from 1984 to 2002 (details are available in an online data supplement at http://hyper.ahajournals.org).15
Outcomes Ascertainment
Vital status was ascertained through 2003, with an average follow-up of 33 years. Before 1979, follow-up was completed by direct mail, telephone, contact with employer, and matching of records with Social Security Administration files; from 1979 to 1994, the National Death Index was used to identify deaths.16 Death certificates were obtained and coded for multiple causes by trained research staff according to the Eighth Revision of the International Classification of Diseases (ICD-8).17 Later, the National Death Index-plus service was used to obtain ICD Ninth Revision (ICD-9) cause of death coding for 1995–1998 and ICD Tenth Revision (ICD-10) coding from 1999 to 2003.18,19 For this report, the underlying cause of death was used. Mortality from stroke was defined as ICD-8 and ICD-9 codes 430 to 438 and ICD-10 codes I60–I69; CHD mortality was defined as ICD-8 and ICD-9 codes 410 to 414 and ICD-10 codes I20–I25; heart failure mortality was defined as ICD-8 and ICD-9 code 428 and ICD-10 codes I50.1–I50.4. A description of methods used to define hospitalizations is supplied in the data supplement.
Statistical Analyses
All of the statistical analyses were performed using Stata/SE 8.0 statistical software for Windows (StataCorp); P<0.05 was used to determine statistical significance. For the outcomes of stroke, CHD, or heart failure death (separately), Cox proportional hazards regression20 models were constructed to estimate the association and predictive utility of each BP measure in univariate analyses. Two-term models were then constructed with all of the possible combinations of 2 BP measures in the model simultaneously, to examine the associations of the BP measures with the outcomes after adjustment for other BP components. The univariate and 2-term models were then repeated after adjustment for age and sex. Other risk factors, such as lipids and smoking, were also included as covariates but were not included in the results, because they did not change the results materially or improve area under the receiver-operating characteristic curve (AUC). For each model, hazards ratios, 95% CIs, likelihood ratio 2, Akeke information criterion, Bayes’ information criterion, and AUC were determined and compared qualitatively between BP measures. Because of the well-described changes that occur with age in SBP (monotonic increase) and DBP (increase, plateau, and decrease), and the consequent effects on PP, MidBP, and MAP, we next examined univariate Cox models for each BP measure in association with stroke, CHD, or heart failure mortality, stratified by baseline age in 3 groups: <50, 50 to 59, or 60 years. These age groups were chosen a priori. We assessed for differing associations and predictive utilities of the BP measures at these different ages by inclusion of multiplicative interaction terms (BP measurexage group) in models with all of the eligible participants.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Characteristics of the Study Sample
There were 36 314 eligible participants with a mean age of 39±13 years, of whom 15 755 (43.4%) were women. The baseline characteristics of the cohort are shown in Table 1. A high percentage (42%) at baseline was currently smoking, and >80% had graduated high school. Overall, the mean BP was in the prehypertensive range by current Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines.
|
For the analyses of cause-specific mortality, the 36 314 participants were followed for a total of 1 070 602 person-years, with a mean follow up of 33.1 years. During that time, there were 11 452 total deaths: 745 (2.1% of the cohort and 6.5% of decedents) were attributed to stroke, 2812 (7.7% of cohort and 24.5% of decedents) were attributed to CHD, and 599 (1.7% of the cohort and 5.2% of decedents) were attributed to heart failure. There were 6893 noncardiovascular deaths (3631 because of cancer).
BP Measures and 33-Year Stroke, CHD, and Heart Failure Mortality
For each BP measure, the SDs were as follows: SBP 18.5 mm Hg, DBP 11.6 mm Hg, PP 13.2 mm Hg, MAP 12.8 mm Hg, and MidBP 13.9 mm Hg. In univariate analyses (Table 2), increments of 1 SD in single measures of SBP and DBP and summary measures of MAP and MidBP were associated with similar and highly significant increases in the risk for stroke death with hazard ratios ranging between 1.71 and 1.77. In a clinical scenario, a patient with SBP that is 158 mm Hg compared with one whose SBP is 140 mm Hg would have a 75% higher risk of stroke death. These 4 measures also provided similar statistical information and predictive utility in the prediction of stroke death, as indicated by the values of likelihood ratio 2, Akeke information criterion, and Bayes’ information criterion and similar discrimination, as indicated by AUC. Conversely, a 1-SD increment in PP was associated with a lower hazard ratio (1.49) for stroke death, with less robust statistical information and discrimination.
|
When 2 BP measures were entered into the models for stroke mortality simultaneously (Table 2), SBP had a stronger association with stroke death than either DBP or PP. Of note, in these 2-term models with SBP, DBP retained a significant positive association, and PP, therefore, had a significant inverse association with stroke death. In the 2-component models, as expected, the summary measures MAP and MidBP were more strongly associated with stroke death than the other measures. It should be noted that the statistical and discrimination criteria for the 2-term models are all identical because of the relationships between all of the BP measures; that is, once 2 of the BP components are in the model, the overall association with stroke death is identical regardless of which 2 measures are used. However, there are differences in the magnitude of associations for each of the individual measures in these models.
Adjustment for age and sex attenuated the hazards ratios of all of the BP measures (Table 3); however, the overall patterns of association were the same as in the univariate analyses of stroke death. Because of the importance of age as a predictor of stroke death, the AUCs for all of the models with age, sex, and any BP measure were high, at 0.80.
|
In age- and sex-adjusted analyses (Tables 4 and 5
) for CHD and heart failure death, the hazards ratios for each BP measure were similar in magnitude and overall predictive utility as shown for stroke death. PP continued to have lower hazard ratios per 1-SD increment and poorer predictive utility compared with any of the other BP measures.
|
|
Pairwise correlations between SBP, DBP, MAP, and MidBP all exceeded 0.7 (all P<0.001). PP was correlated variably with the other measures; correlation coefficients were 0.11 for DBP, 0.78 for SBP, 0.44 for MAP, and 0.56 for MidBP (all P<0.001). Findings for the predictive utility of baseline BP measures for stroke, CHD, and heart failure hospitalization were qualitatively similar to those for prediction of death and are provided in the data supplement.
Risk of Stroke, CHD, and Heart Failure Death at Different Ages
To determine whether BP measures varied in their utility at different ages, we examined each single and summary BP measure among the prespecified age groups of <50 years, 50 to 59 years, and 60 years (Figure). As expected, the absolute 33-year event rates were highest for the oldest age group for stroke, CHD, and heart failure death, at 8.1%, 25.7%, and 9.2%, respectively. The relative risks for stroke, CHD, and heart failure death associated with BP were highest for the youngest age group and declined with greater baseline age. The P values for the interaction between age and SBP were <0.001, <0.001, and 0.005, respectively, for stroke, CHD, and heart failure death as outcomes. These age/BP interactions were observed for each BP measure except PP in heart failure. Hazards ratios for PP associated with CHD and heart failure death were significant and similar across age groups, but PP was not significantly associated with stroke death at ages 60 years. DBP appeared to be associated with the highest hazard ratios for all of the outcomes in the youngest age group, with SBP becoming stronger than DBP at higher baseline ages.
|
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Principal Findings
The principal findings from this 33-year follow-up study of the associations of baseline BP with stroke, CHD, and heart failure are as follows: (1) PP was significantly associated with stroke, CHD, and heart failure outcomes, but PP had less statistical strength and predictive utility than the other measures, and it became inversely associated with outcomes when adjusted for level of SBP; (2) SBP appeared to be the best unadjusted single measure in prediction of stroke, CHD, and heart failure outcomes; (3) there was greater relative risk for stroke, CHD, and heart failure associated with elevated BP in patients <50 years old versus in patients
60 years, although absolute incidence was substantially higher in the older population; (4) when stratified by age groups (<50, 50 to 59, and 60 years old), DBP was associated with the highest relative risk for heart failure, CHD, and stroke death in younger individuals, whereas SBP predominated at higher ages; (5) models with only age, sex, and BP measures provided a high degree of discrimination in predicting stroke, CHD, and heart failure mortality; and (6) among the BP indices, the summary measures of MAP and particularly MidBP provided the greatest predictive utility for these outcomes.
Implications
It is well known that hypertension plays a significant role in the pathogenesis of stroke, CHD, and heart failure,1–3,7 and treatment of hypertension yields marked decreases in the incidence of these outcomes.21–24 In recent literature, PP has been shown to be associated significantly with incident CHD, heart failure, and stroke,4–13,25–27 especially in older individuals. There has been significant discussion of whether PP is a better marker of risk than SBP. However, much of the literature has been limited by a focus solely on measures of association (eg, hazards ratios) rather than on predictive utility. Consistent with some of the previous literature, we observed, in our large population with an extended follow-up period of both death and hospitalization, that PP was a weaker predictor of stroke, CHD, and heart failure outcomes than SBP and other BP measures. Our results highlight a major limitation of PP. Like MAP and MidBP, PP incorporates information from 2 BP components (SBP and DBP) and should, therefore, improve classification and risk stratification. However, unlike MAP and MidBP, PP is "floating"; it has no relation to an absolute BP level. For example, a PP of 60 mm Hg could be associated with BP of 180/120 mm Hg or one of 120/60 mm Hg.
These data, therefore, support the approach taken by the National High Blood Pressure Education Program28 and the Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines29 in recommending that SBP be the main focus for staging and treatment of hypertension, especially in older individuals. This information also adds importantly to the findings of the large Prospective Studies Collaboration,2 which examined predictive utility of BP measures for stroke and ischemic heart disease death, by including nonfatal stroke, CHD, and heart failure events (including hospitalizations) and by examining the significance of several BP measures.
Aging and Vascular Changes
With age, the incidence of stroke, CHD, and heart failure all increase substantially. PP, a measure of central arterial stiffness and pulsatile load, tends to increase after age 55 to 60 years when SBP and DBP tend to increase and decrease, respectively.30–32 Increased arterial stiffness affects central pressures both directly and indirectly. The direct effect appears to be because of decreased elastic capacity and diminished elastic recoil of the capacitance arteries, causing quicker runoff of stroke volume and lower central blood volume and pressure at the beginning of diastole. The indirect effect is an amplified pulse wave velocity, causing early return of pulse waves in late systole rather than in diastole. These changes thereby cause an increase in SBP with elevation of aortic and left ventricular pressures, increased myocardial oxygen consumption, and promotion of left ventricular hypertrophy.30,31
Current Study in Context
Miura et al26 reported previously that PP was independently associated with incident CHD mortality in the Chicago Heart Association cohorts, but they also observed that SBP was associated with higher hazard ratios and 2 values. In this study, in addition to CHD, we examined stroke and heart failure mortality, as well as hospitalization rates for CHD, stroke, and heart failure, using the same cohort, and expanded the examination of the predictive utility of BP measures for these outcomes. As expected, our results using the same cohort as Miura et al26 further support their conclusion associating SBP with greater predictive value than PP for CHD.
Concerning stroke, some of the literature has shown that those patients who have isolated systolic hypertension (and, therefore, have increased PP) may have a greater risk of stroke compared with those with dual diastolic and systolic hypertension or isolated diastolic hypertension.9,10 However, we did not observe this phenomenon. As noted by Psaty at al,11 although PP provides some predictive information, it has not consistently been shown to be stronger than SBP for the prediction of stroke. In addition to a large population and extended follow-up, our study examined the additional statistical measures to point out the greater utility of SBP compared with PP. Adding these additional measures, particularly AUC, also highlights the potency of age as a risk factor, suggesting that age and BP account for a large degree of the risk for stroke mortality.
Contrary to stroke, previously published data support the concept that PP is similar to if not better than SBP in predicting heart failure.4,6,7,12 These studies all examined older populations and combined heart failure hospitalization and mortality as one end point. In contrast, we examined a larger population with a wider age range and longer duration of follow-up and examined hospitalization and death separately. Differing from the previous studies, we observed that SBP was a stronger predictor than PP for both heart failure hospitalization and death. This finding was independent of age and sex and was also seen when we stratified by age to examine the older subset of individuals who were more likely to have an elevated PP. Indeed, PP is significantly associated with heart failure, but it does not appear to be superior to SBP for heart failure risk prediction. Similar to stroke, age adjustment provided a high degree of discrimination affirming the dominance of age and BP as risk factors for heart failure.3
The increased relative risks for stroke, CHD, and heart failure outcomes associated with BP elevation in younger as compared with older individuals likely have several explanations. First, there is a very low incidence of outcomes in younger patients with lower BP (the referent group). With higher baseline age, there are more outcomes in patients with both normal and elevated BP likely secondary to age-related changes and accumulating comorbidities; thus, the relative risks diminish with age. In addition, elderly patients with elevated BP are also more likely to receive treatment during follow-up, thereby reducing their risk.23,24,33
Limitations
There are several limitations that should be noted. First, BP values were obtained from a single baseline measurement, with the possibility of misclassification and regression–dilution bias. Current Seventh Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure guidelines29 recommend 2 BP readings on separate occasions for appropriate classification of BP. As mentioned by Miura et al,26 there is a likely "healthy worker effect" in this cohort, enabling them to work. It is conceivable that this healthier population may have "successfully aged,"30 putting them at lower risk for detrimental vascular changes that cause increased arterial stiffness and magnify the PP. Consistent with this hypothesis, Franklin et al34 have noted that DBP was not substantially lower among the older individuals in this cohort. Nonetheless, because the vast majority of the US population is employed, these findings should be broadly generalizable.
Perspectives
In our population of >36 000 working men and women without history of antihypertensive treatment, PP was significantly associated with increased risk for stroke, CHD, and heart failure but failed to show greater predictive value than SBP, DBP, MAP, or MidBP. We were able to demonstrate this with several advantages over many of the previous studies, including the size and age range of the cohort, duration and completeness of follow-up, ascertainment of fatal and nonfatal events, numbers of events, and examination with measures of predictive utility, not just measures of association (ie, relative risks). Of the summary measures, MidBP and MAP were associated with the highest relative risks and predictive utilitys, but these measures may be difficult to incorporate into clinical practice, and they were not markedly better than SBP and DBP in risk prediction. We conclude that SBP and DBP should continue to be the primary focus for risk stratification and therapy for the prevention of CHD, heart failure, and stroke.
|
Acknowledgments |
|---|
A list of colleagues who contributed to earlier aspects of this work has been published.14
Sources of Funding
We acknowledge support by the American Heart Association (Dallas, Tex) and its Chicago and Illinois affiliates; the National Heart, Lung, and Blood Institute (Bethesda, Md) grants R01-HL 15174, R01-HL 21010, and R01-HL 03387; the Chicago Health Research Foundation (Chicago, Ill); Northwestern Memorial Foundation; and the Goldberg Family Charitable Trust.
Disclosures
None.
Received October 24, 2006; first decision November 17, 2006; accepted March 16, 2007.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Rosamond W, Flegal K, Friday G, Furie K, Go A, Greenlund K, Haase N, Ho M, Howard V, Kissela B, Kittner S, Lloyd-Jones D, McDermott M, Meigs J, Moy C, Nichol G, O’Donnell CJ, Roger V, Rumsfeld J, Sorlie P, Steinberger J, Thom T, Wasserthiel-Smoller S, Hong Y. Heart disease and stroke statistics–2007 update. A report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2007; 115: e69–e171.
2. Prospective Studies’ Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002; 360: 1903–1913.[CrossRef][Medline] [Order article via Infotrieve]
3. Levy D, Larson MG, Vasan RS, Kannel WB, Ho KK. The progression from hypertension to congestive heart failure. JAMA. 1996; 275: 1557–1562.
4. Chae CU, Pfeffer MA, Glynn RJ, Mitchell GF, Taylor JO, Hennekens CH. Increased pulse pressure and risk of heart failure in the elderly. JAMA. 1999; 281: 634–639.
5. Domanski MJ, Davis BR, Pfeffer MA, Kastantin M, Mitchell GF. Isolated systolic hypertension: prognostic information provided by pulse pressure. Hypertension. 1999; 34: 375–380.
6. Haider AW, Larson MG, Franklin SS, Levy D. Systolic blood pressure, diastolic blood pressure, and pulse pressure as predictors of risk for congestive heart failure in the Framingham Heart Study. Ann Intern Med. 2003; 138: 10–16.
7. Kostis JB, Lawrence-Nelson J, Ranjan R, Wilson AC, Kostis WJ, Lacy CR. Association of increased pulse pressure with the development of heart failure in SHEP. Am J Hypertens. 2001; 14: 798–803.[CrossRef][Medline] [Order article via Infotrieve]
8. Mattace-Raso FUS, van der Cammen TJM, van Popele NM, van der Kuip DAM, Schalekamp MADH, Hofman A, Breteler MMB, Witteman JCM. Blood pressure components and cardiovascular events in older adults: the Rotterdam study. J Am Geriatr Soc. 2004; 52: 1538–1542.[CrossRef][Medline] [Order article via Infotrieve]
9. Nielsen WB, Lindenstrom E, Vestbo J, Jensen GB. Is diastolic hypertension an independent risk factor for stroke in the presence of normal systolic blood pressure in the middle-aged and elderly? Am J Hypertens. 1997; 10: 634–639.[CrossRef][Medline] [Order article via Infotrieve]
10. Paultre F, Mosca L. Association of blood pressure indices and stroke mortality in isolated systolic hypertension. Stroke. 2005; 36: 1288–1290.
11. Psaty BM, Furberg CD, Kuller LH, Cushman M, Savage PJ, Levine D, O’Leary DH, Bryan RN, Anderson M, Lumley T. Association between blood pressure level and the risk of myocardial infarction, stroke, and total mortality. Arch Intern Med. 2001; 161: 1183–1192.
12. 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.
13. Weitzman D, Goldbourt U. The significance of various blood pressure indices for long-term stroke, coronary heart disease, and all-cause mortality in men: The Israeli Ischemic Heart Disease study. Stroke. 2006; 37: 358–363.
14. Stamler J, Dyer AR, Shekelle RB, Neaton JD, Stamler R. Relationship of baseline major risk factors to coronary and all-cause mortality, and to longevity: findings from long-term follow-up of Chicago cohorts. Cardiology. 1993; 82: 191–222.[Medline] [Order article via Infotrieve]
15. Yan LL, Daviglus ML, Liu K, Stamler J, Wang R, Pirzada A, Garside DB, Dyer AR, Van Horn L, Liao Y, Fries JF, Greenland P. Midlife body mass index and hospitalization and mortality in older age. JAMA. 2006; 295: 190–198.
16. Public Health Service. National Death Index User’s Manual. Hyattsville, MD: Public Health Service; 2000.
17. World Health Organization. International Classification of Diseases, Eighth Revision (ICD-8). Geneva, Switzerland: World Health Organization; 1967.
18. Department of Health and Human Services. The International Classification of Diseases. 9th Revision, Clinical Modification: ICD-9-CM. Washington, DC: Department of Health and Human Services; 1980.
19. World Health Organization. International Statistical Classification of Diseases and Related Health Problems, 10th ed. Geneva, Switzerland: World Health Organization; 1992.
20. Cox DR. Regression models and life tables (with discussions). J R Stat Soc B. 1972; 34: 187–220.
21. Psaty BM, Lumley T, Furberg CD, Schellenbaum G, Pahor M, Alderman MH, Weiss NS. Health outcomes associated with various antihypertensive therapies used as first-line agents: a network meta-analysis. JAMA. 2003; 289 2534–2544.
22. Psaty BM, Smith NL, Siscovick DS, Koepsell TD, Weiss NS, Heckbert SR, Lemaitre RN, Wagner EH, Furberg CD. Health outcomes associated with antihypertensive therapies used as first-line agents. A systematic review and meta-analysis. JAMA. 1997; 277: 739–745.
23. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program (SHEP). JAMA. 1991; 265: 3255–3264.
24. Staessen JA, Fagard R, Thijs L, Celis H, Arabidze GG, Birkenhager WH, Bulpitt CJ, de Leeuw PW, Dollery CT, Fletcher AE, Forette F, Leonetti G, Nachev C, O’Brien ET, Rosenfeld J, Rodicio JL, Tuomilehto J, Zanchetti A. Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. the Systolic Hypertension in Europe (Syst-Eur) Trial investigators. Lancet. 1997; 350: 757–764.[CrossRef][Medline] [Order article via Infotrieve]
25. 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.
26. Miura K, Dyer AR, Greenland P, Daviglus ML, Hill M, Liu K, Garside DB, Stamler J. Pulse pressure compared with other blood pressure indexes in the prediction of 25-year cardiovascular and all-cause mortality rates: the Chicago Heart Association Detection Project in Industry Study. Hypertension. 2001; 38: 232–237.
27. Benetos A, Rudnichi A, Safar M, Guize L. Pulse pressure and cardiovascular mortality in normotensive and hypertensive subjects. Hypertension. 1998; 32: 560–564.
28. Izzo JL, Levy D, Black HR. Importance of systolic blood pressure in older Americans. Hypertension. 2000; 35: 1021–1024.
29. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL Jr, Jones DW, Materson BJ, Oparil S, Wright JT Jr, Roccella EJ, the National High Blood Pressure Education Program Coordinating Committee. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Hypertension. 2003; 42: 1206–1252.
30. Lakatta EG, Levy D. Arterial and cardiac aging: major shareholders in cardiovascular disease enterprises: part I: aging arteries: a "set up" for vascular disease. Circulation. 2003; 107: 139–146.
31. O’Rourke M. Arterial stiffness and hypertension. In: Izzo JL, Black HR, eds. Hypertension Primer, 2nd ed. Dallas, TX: American Heart Association; 1999: 160–162.
32. Franklin SS, Gustin W, Wong ND, Larson MG, Weber MA, Kannel WB, Levy D. Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation. 1997; 96: 308–315.
33. Lloyd-Jones DM, Evans JC, Levy D. Hypertension in adults across the age spectrum: Current outcomes and control in the community. JAMA. 2005; 294: 466–472.
34. Franklin SS, Wong ND, Larson MG, Kannel WB, Levy D. How important is pulse pressure as a predictor of cardiovascular risk? Hypertension. 2002; 39: e12–e13.[Medline] [Order article via Infotrieve]
This article has been cited by other articles:
 |
|
 |
|
  S. S. Franklin, V. A. Lopez, N. D. Wong, G. F. Mitchell, M. G. Larson, R. S. Vasan, and D. Levy Single Versus Combined Blood Pressure Components and Risk for Cardiovascular Disease: The Framingham Heart Study Circulation, January 20, 2009; 119(2): 243 - 250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. Blacher, M. E. Safar, C. Vesin, and A. Rudnichi Brachial Pulse Pressure and Cardiovascular Risk Hypertension, November 1, 2007; 50(5): e161 - e161. [Full Text] [PDF]
|
|
|
|
|
|
W. J. Mosley II, P. Greenland, D. B. Garside, and D. M. Lloyd-Jones Response to Brachial Pulse Pressure and Cardiovascular Risk Hypertension, November 1, 2007; 50(5): e162 - e162. [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||