(Circulation. 1999;100:354-360.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Is Pulse Pressure Useful in Predicting Risk for Coronary Heart Disease?
The Framingham Heart Study
From the Heart Disease Prevention Program, University of California, Irvine (S.S.F., S.A.K., N.D.W.); The National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Mass (M.G.L., D.L.); and the National Heart, Lung, and Blood Institute, Bethesda, Md (D.L.).
Correspondence to Dr Stanley S. Franklin, UCI Heart Disease Prevention Program, C240 Medical Sciences, University of California Irvine, Irvine, CA 92697. E-mail sfrankln{at}ucla.edu
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Abstract |
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Background—Current definitions of hypertension are based on levels of systolic blood pressure (SBP) and diastolic blood pressure (DBP), but not on pulse pressure (PP). We examined whether PP adds useful information for predicting coronary heart disease (CHD) in the population-based Framingham Heart Study.
Methods and Results—We studied 1924 men and women between 50 and
79 years of age at baseline with no clinical evidence of CHD and not
taking antihypertensive drug therapy. Cox regression, adjusted for age,
sex, and other risk factors, was used to assess the relations between
blood pressure components and CHD risk over a 20-year follow-up. The
association with CHD risk was positive for SBP, DBP, and PP,
considering each pressure individually; of the 3, PP yielded the
largest 
2 statistic. When SBP and DBP were jointly
entered into the multivariable model, the association with CHD risk
was positive for SBP (HR, 1.22; 95% CI, 1.15 to 1.30) and negative for
DBP (HR, 0.86; 95% CI, 0.75 to 0.98). Four subgroups were defined
according to SBP levels (<120, 120 to 139, 140 to 159, and 
160
mm Hg). Within each subgroup, the association with CHD risk was
negative for DBP and positive for PP. A cross-classification of SBP-DBP
levels confirmed these results.
Conclusions—In the middle-aged and elderly, CHD risk increased
with lower DBP at any level of SBP120 mm Hg, suggesting that higher
PP was an important component of risk. Neither SBP nor DBP was superior
to PP in predicting CHD risk.
Key Words: blood pressure • hypertension • coronary disease
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Introduction |
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Current guidelines for the diagnosis and management of hypertension have defined cardiovascular risk by the elevation of systolic blood pressure (SBP) and/or the elevation of diastolic blood pressure (DBP).1 2 3 However, the principal components of blood pressure consist of both a steady component (mean arterial pressure, MAP) and a pulsatile component (pulse pressure, PP). Major determinants of MAP are ventricular ejection and peripheral vascular resistance.4 5 6 PP, the difference between SBP and DBP, is also made up of 2 major components—1 due to ventricular ejection interacting with the viscoelastic properties of the large arteries (direct) and the other due to wave reflection (indirect).4 5 6 The rise in SBP and PP in middle-aged and elderly subjects is due primarily to an increase in large-artery stiffness and an associated increase in wave reflection amplitude.6
Currently, there is increasing evidence that PP, in middle-aged and older subjects, is an independent predictor of risk of coronary heart disease (CHD), compared with MAP.7 8 9 10 11 We recently reported on the age-related change of PP and MAP in persons not receiving antihypertensive therapy and without clinical CHD.12 From age 30 to 50 years, SBP and DBP track together in a nearly parallel manner; however, after age 60 years, DBP decreases, while SBP continues to rise. This age-related phenomenon accounts for the large increase in PP after age 60 years and for the underestimation of peripheral vascular resistance in older persons by the MAP equation.12 Because of the inaccuracy of calculated MAP, it may be preferable to compare PP with SBP or DBP in evaluation of blood pressure predictors of CHD risk.
Therefore, the first goal of the present study, using the previous Framingham Heart Study cohort,12 was to compare various blood pressure components (PP, SBP, and DBP) individually as predictors of risk for CHD. The second goal was to examine the joint influence of any 2 blood pressure components on CHD risk and to determine whether PP adds to the predictive value of either SBP or DBP for CHD events.
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Methods |
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The Framingham Heart Study is a prospective, population-based cohort study of cardiovascular disease incidence and risk factors, which began in 1948 with the enrollment of 5209 men and women 28 to 62 years old. Participants undergo biennial examinations, which include an extensive cardiovascular history and physical examination, 12-lead ECG, and various blood chemistries. Morbidity and mortality are monitored by biennial clinic examinations and by review of interim hospitalizations. A panel of 3 experienced investigators reviews all new cardiovascular events. Detailed descriptions of the study design have been published.13 14
Study Sample
Subjects selected for this study had measurements of HDL
cholesterol as part of a complete lipid profile. The
earliest examination at which HDL cholesterol was measured
served as the baseline examination for each subject; usually this was
the 10th biennial examination, but for some it was the 11th or
12th. Study subjects were between 50 and 79 years old at baseline to be
eligible. They had no history or clinical evidence of CHD, and they
were not receiving antihypertensive medication. Three hundred
thirty-five subjects were excluded because of concurrent
antihypertensive therapy at baseline, which may have influenced
baseline blood pressure readings and thus their relation to CHD risk.
Ninety-four percent, ie, 1924 of the original 2036 subjects in our
previous study,12 qualified for the present
investigation; 112 subjects were excluded because of missing
covariates.
Blood Pressure Measurement
Readings of SBP and DBP were taken in the supported left arm of
the seated subject, after 5 minutes of quiet rest, with a
mercury-column sphygmomanometer with cuff-size adjustment based on arm
circumference. Readings were recorded to the nearest even number.
SBP was recorded at the first appearance of Korotkoff sounds, and
palpation was used to check auscultatory systolic readings. DBP
was recorded at the disappearance (phase V) of Korotkoff sounds.
Baseline SBP and DBP each were the average of 2 separate measurements
taken by the examining physician; in 2.1% of subjects, only 1 reading
was available at the baseline examination.
End Points
The end point used in this study was incident CHD (fatal or
nonfatal). A subject was considered to have incident CHD if he or she
fulfilled published criteria15 for angina pectoris,
coronary insufficiency (angina pectoris lasting 20 minutes
and accompanied by ischemic ECG changes), myocardial
infarction, or death from CHD occurring since the baseline examination.
Follow-up time was defined from the date of the baseline examination to
the date of the first CHD event or to the date of last contact free of
CHD, up to the date of the 20th biennial examination.
Data Analysis
The relations of CHD hazard ratios (HRs) to single (SBP, DBP, or
PP) and dual (SBP-DBP, PP-SBP, and PP-DBP) blood pressure components,
as continuous variables, were evaluated by Cox proportional hazards
regression.16 HRs, estimated as the exponent
(e) raised to the power of the respective regression
coefficient, were determined, along with 95% confidence limits, for a
10 mm Hg increment in blood pressure component and per 1-SD
increment. Models were adjusted for age, sex, body mass index,
cigarettes smoked per day, glucose intolerance (defined as clinical
diagnosis of diabetes mellitus, definite or trace glycosuria
[Clinitest or Combustix], or casual blood glucose values of 120
mg/dL), and the total cholesterol/HDL ratio. SAS
statistical software (SAS Institute) was used.17
The dual influences of SBP and DBP (model 1) and SBP and PP (model 2)
were also examined by Cox proportional hazards regression with SBP
grouped in 4 discrete categories and PP and DBP plotted as continuous
variables. The SBP groups were based on JNC VI
criteria3 : group 1, <120 mm Hg (optimal
systolic blood pressure); group 2, 120 to 139 mm Hg
(normal and high normal systolic blood pressure); group 3, 140
to 159 mm Hg (stage 1 systolic hypertension); and group
4, 160 mm Hg (stages 2 and 3 systolic
hypertension).
These 2 models were plotted with the middle 90% of the distribution of DBP and PP values for each SBP group used to define the lower and upper limits of DBP and PP. An SBP of 130, DBP of 80, and PP of 50 mm Hg were selected as the reference values having an HR of 1.0.
The relative risks for new CHD events for the 4 SBP categories as
defined above and within specific DBP groupings (<70, 70 to 79, 80 to
89, and 90 mm Hg) were also examined by Cox regression, with
adjustment for age, sex, and the other risk factors as specified above.
Each group pairing of SBP and DBP was compared with a reference group
with SBP <120 mm Hg and DBP <70 mm Hg with an HR of
1.0.
Secondary analyses were done to examine for sex differences and for potential bias that could affect the prediction of CHD risk from baseline blood pressure components: (1) an interaction term for sex was added to the model to test for sex differences; (2) subjects excluded from the study because of previous antihypertensive therapy at baseline were added to the study cohort to test for hypertension selection bias; and (3) postbaseline hypertension treatment was added as a time-dependent covariate to test for possible influence on the prediction of CHD risk from baseline blood pressure.
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Results |
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Demographic and Clinical Characteristics
The sample comprised 830 men and 1094 women (Table 1
). The mean follow-up time was
14.3 years, during which 433 subjects developed CHD. Of the initial CHD
events, 187 were angina pectoris or coronary insufficiency, 182
were myocardial infarction with survival beyond 1 day, and 64 were CHD
deaths. Subjects who developed new CHD events had higher levels of
total serum cholesterol, lower levels of serum HDL
cholesterol, and a higher prevalence of glucose intolerance
(women only) at baseline than those who did not experience CHD. All
blood pressure components (SBP, DBP, and PP) were higher in subjects
who experienced new CHD events than in those free of such events.
Correlations among blood pressure components were r=0.87 for
SBP-PP, r=0.66 for SBP-DBP, and r=0.21 for
PP-DBP.
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Single Blood Pressure Component Models
The HRs associated with a 10 mm Hg increment in blood
pressure were as follows: PP, 1.23 (P<0.001); SBP, 1.16
(P<0.001); and DBP, 1.14 (P<0.05),
respectively, after adjustment for other risk factors. The HRs per 1 SD
were PP, 1.38; SBP, 1.35; and DBP, 1.14 (Table 2).
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Dual Blood Pressure Component Models
The combination of SBP (positive) and DBP (negative) (model 1)
showed a modest incremental contribution from DBP
(2=5.2, P<0.05) above and beyond
SBP, but the combination of SBP and PP (model 2) or PP and DBP (model
3) showed no incremental value of SBP or DBP, respectively, in
predicting CHD once PP was included in the model. These conclusions
were unaltered when standardized HRs were considered (Table 2
).
Table 3 shows CHD HRs for blood pressure
components within the 4 SBP groups. Model 1 demonstrated that the slope
of the inverse relation of DBP (HR per 10 mm Hg, 0.84 to 0.87;
P<0.05), as a continuous variable, to CHD risk was
similar (Wald 2=5.6, 3 df,
P=0.13) across all categories of SBP. In this model, SBP
provided further contribution to CHD risk (HR per 10 mm Hg, 1.25;
95% CI, 1.11 to 1.41) over and above DBP. Likewise, model 2 indicated
that the positive slope of the relations of PP (HR, 1.12 to 1.20;
P<0.05), as a continuous variable, to CHD risk was
similar (Wald 2=5.6, 3 df,
P=0.13) across all categories of SBP. In this model, there
was no added value of SBP in predicting CHD risk over and above PP (HR,
1.05; 95% CI, 0.90 to 1.23). These findings remained similar when
standardized HRs were calculated.
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The joint influences of SBP and DBP on CHD risk are plotted in Figure 1. For any level of SBP, subjects with
lower DBP, ie, higher PP (moving leftward along each line) had greater
CHD risk; alternatively, for any level of DBP, those with higher SBP
and PP (moving upward from line to line) had greater risk. Figure 2 shows the joint influences of SBP and PP on CHD risk. For any
given level of SBP 130 mm Hg (group 2, 3, or 4), subjects with
higher PP, ie, lower DBP (moving rightward along each line) had a
considerable increase in CHD risk. By contrast, for any given level of
PP 50 mm Hg, subjects with a parallel increase in SBP and DBP
(moving upward from line to line) had only a minimal increase in CHD
risk. For example, a 20 mm Hg increment in PP for SBP group 2, 3,
or 4 was associated with a much greater increase in CHD risk than a
20 mm Hg parallel increment in SBP and DBP (moving upward from 1
SBP line to the next) for any given level of PP 50 mm Hg.
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Table 4 shows the hazards for CHD
by cross-classification of SBP and DBP, using SBP <120 mm Hg and
DBP <70 mm Hg as the reference group. At all levels of DBP, the
hazards for CHD rose with increasing SBP groups. Conversely, for all
SBP groups 120 mm Hg, the hazards for CHD rose with decreasing
DBP (with the sole exception of the group SBP 140 to 159 and DBP 80 to
89 mm Hg).
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Secondary Analyses
When an interaction term for sex was introduced into the model,
there was no significant difference in predicting CHD risk for men
compared with women (P=0.29 for PP, P=0.23 for
SBP, and P=0.81 for DBP). None of the blood pressure
components were predictive of CHD risk in the subjects (n=303) excluded
from the study because of concurrent antihypertensive therapy at
baseline examination (P=0.45 for PP, P=0.63 for
SBP, and P=0.73 for DBP). When treated and untreated
subjects were combined (n=1924+303= 2227), PP and SBP remained
predictors of CHD risk (2=36.0 and 31.6,
respectively) and DBP was of borderline significance
(2=4.3). When postbaseline antihypertensive
therapy was added as a time-dependent covariate, the magnitude of the
prediction of CHD risk did not change significantly for baseline PP and
SBP (ß-coefficients of 0.19 for PP and 0.14 for SBP, both adjusted
per 10 mm Hg) or for the baseline dual model of SBP-DBP
(ß-coefficients of 0.19 for SBP and –0.17 for DBP, both adjusted per
10 mm Hg), similar to the ß-coefficients estimated earlier
(Table 2).
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Discussion |
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The principal new information provided by this study was that in middle-aged and older individuals, CHD risk was inversely related to DBP at any given SBP of
120 mm Hg, consistent with the
hypothesis that higher PP is an important component of risk. Moreover,
neither SBP nor DBP was superior to PP in predicting CHD risk. There
was a far greater increase in CHD risk with increments in PP without a
change in SBP than with increments in SBP without a change in PP. An
increase in PP with fixed SBP occurs solely as a function of declining
DBP; this is a consequence of a rise in large-artery
stiffness.18 An increase in SBP with fixed PP occurs when
there are parallel increases in SBP and DBP; this is a consequence of a
rise in peripheral vascular resistance.18 An elevated DBP has long been associated with increased CHD risk.1 2 3 A negative association of DBP with CHD risk has been recognized only recently.7 8 9 10 11 Most of the early studies assessing blood pressure as a risk factor for CHD were based on young individuals, in whom SBP and DBP tend to track together and in whom both are strongly associated with CHD risk.19 With advancing age, there is a decline in DBP12 and in the role of DBP in predicting CHD risk.20 In the present sample, however, with a mean age of 61.2 years, DBP when considered alone remained positively (but weakly) associated with CHD risk. In contrast, when DBP and SBP were considered jointly, an inverse relation between DBP and CHD risk became apparent. Similar trends for the association of PP with CHD events were reported in 3 previous publications, with mean sample ages of 51.6, 53.1, and 59.5 years, respectively.9 10 11
Hemodynamic Implications
As large-artery stiffness increases in middle-aged and elderly
subjects, SBP rises and DBP falls, with a resulting increase in
PP.18 The normally present higher gradient of
peripheral to central arterial PP
(amplification) found in young subjects gradually decreases with aging
as a result of the augmentation of central PP by early wave
reflection.21 22 Therefore, brachial artery cuff
measurement of PP in the elderly, in contrast to the young, becomes a
more accurate indicator of central PP and an improved predictor of CHD
risk.
As vascular resistance rises, there is a proportional increase in SBP and DBP in young individuals. With the onset of middle age, however, SBP rises more than DBP, resulting in elevation of PP.12 18 Thus, DBP rises with increased peripheral arterial resistance and falls with increased central artery stiffness; the relative contributions of these 2 opposing forces determine DBP and ultimately PP.
Normally, PP and SBP are highly correlated because both blood pressure components rise with increases in vascular resistance and large-artery stiffness. When assessed individually, however, increments in PP at a fixed SBP were associated with a greater risk for CHD than were increments in SBP at a fixed PP. From these findings, we can hypothesize that CHD risk is related more to the pulsatile stress caused by large-artery stiffness during systole than to the steady-state stress due to small-vessel resistance during diastole.23 24 25 Similarly, our data show that not all hypertensive subjects with the same elevation in SBP have the same CHD risk; those with lower DBP, and therefore wider PP, have greater CHD risk, possibly due to greater pulsatile stress.
This concept also explains the paradox of CHD risk being directly related to DBP when considered alone and inversely related to DBP when SBP and DBP were jointly entered into the model. Considered alone, DBP is a measure of vascular resistance (although an underestimate because of the counteracting influence of large-artery stiffness). In individuals <50 years old, elevations of SBP and DBP are concordant, strongly supporting the major influence of increased vascular resistance and minimizing the importance of large-artery stiffness in young adults.18 In our middle-aged and older cohort, PP, which is an indicator of large-artery stiffness, became the dominant factor predicting CHD risk. Therefore, despite the high correlation of PP with SBP (r=0.87), PP predominates in predicting CHD risk because of the contribution of the strong pulsatile stress in a minority of subjects with discordantly low DBP values.
Clinical Implications
Our analysis showed only slight favoring of PP over SBP in
predicting CHD risk, presumably because of the overall strong
concordance of SBP with DBP. In dual-component models, however, neither
SBP nor DBP had additional value in predicting CHD risk over and above
the contribution of PP. Further support favoring PP over SBP in
subjects with discordantly low DBP was provided by a
cross-classification matrix of SBP and DBP using 4 discrete levels of
SBP. This approach enabled us to examine the effect of discordant
SBP-DBP pairings on CHD risk. At any SBP 120 mm Hg, with only 1
exception, DBP was inversely associated with CHD risk.
These results support the conclusion that in subjects with identical levels of SBP, those with isolated systolic hypertension are at greater risk for CHD than those with combined systolic-diastolic hypertension. This may have important public health implications, because isolated systolic hypertension is the most common type of hypertension among untreated adults >50 years old.26
From these findings, we cannot determine whether the association between PP and CHD events is causal or whether elevated PP is a marker for the underlying vascular disease, which predisposes to CHD. It is premature to suggest that current treatment recommendations1 2 3 be modified on the basis of our observational data. Our study, however, may be useful in generating hypotheses that can be tested directly in clinical trials and in identifying high-risk hypertensive subjects who may benefit from more aggressive control of their blood pressure.
Study Strengths and Limitations
In this study, we quantified the contributions of PP and SBP to
CHD risk in both normotensive and hypertensive subjects followed up for
up to 20 years. These findings were established in a cohort of subjects
who were free of clinical CHD at baseline and who were not receiving
antihypertensive therapy.
There are potential limitations regarding the interpretation of our data. There may have been a selection bias resulting from the exclusion of 335 subjects receiving antihypertensive therapy at baseline, which represented 30% of the hypertensive population in this cohort. When treated and untreated subjects were combined, however, SBP and PP remained significant predictors of CHD risk, and DBP was of borderline significance. These results are consistent with a previous study of combined treated and untreated hypertensive patients that showed a positive association between PP and myocardial infarction.9
Because elevated DBP was the main criterion for treating hypertension
until the early 1980s, this may have resulted in a higher prevalence of
isolated systolic hypertension in the present study.
However, our selection process, which may have eliminated the most
severe hypertensives on treatment, would presumably result in a more
representative population of normotensives, those with
borderline blood pressure, and predominantly untreated stage 1 and 2
hypertensives. Stages 1 and 2 compose 
94% of the hypertensive
population.27 Furthermore, the results of this study have
no bearing on accelerated or malignant hypertension, an acute or
subacute process with an entirely different pathophysiology and
clinical course.
Although a postbaseline treatment bias is possible, we found little evidence to support this conclusion. When a time-dependent covariate term for antihypertensive therapy was used in the model, there was no evidence that postbaseline treatment diminished the prediction of CHD events by baseline PP, SBP, or by baseline dual components of SBP and DBP. Any follow-up treatment effect in our study should bias results toward the null, because a previous Framingham Heart Study publication28 has shown a substantial reduction in CHD mortality with long-term hypertension therapy. Therefore, our findings may underestimate the utility of PP in predicting CHD risk.
The value of the single office PP, shown in this study to be predictive of CHD risk, may not be accurate in the individual subject. The averaging of multiple blood pressure readings taken on several visits or the use of ambulatory monitoring29 will improve accuracy and precision. Last, because the original Framingham sample consisted almost exclusively of whites, the majority of whom were middle class, results may not apply to other ethnic or socioeconomic groups.
In summary, PP provides important predictive value for CHD events in normotensive and untreated hypertensive middle-aged and elderly adults. PP may be the most reliable blood pressure indicator of risk when high-normal SBP or systolic hypertension is accompanied by normal or low DBP. Our data suggest that CHD events are more related to the pulsatile stress of large-artery stiffness during systole (as reflected in a rise of PP) than the steady-state stress of resistance during diastole (as reflected in a parallel rise in SBP and DBP). Indeed, at similar elevations of SBP, subjects with isolated systolic hypertension are at greater risk for CHD events than those with combined systolic-diastolic hypertension. For middle-aged and older persons, these new findings call into question the prevailing belief that elevations of SBP and DBP contribute equally to CHD risk.
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Acknowledgments |
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The Framingham Heart Study is supported by NIH/NHLBI contract N01-HC-38038. This project was supported, in part, by an educational grant from Bristol-Myers Squibb Co, Princeton, NJ.
Received February 1, 1999; revision received April 12, 1999; accepted April 30, 1999.
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 R. Pini, M. C. Cavallini, V. Palmieri, N. Marchionni, M. Di Bari, R. B. Devereux, G. Masotti, and M. J. Roman Central but not brachial blood pressure predicts cardiovascular events in an unselected geriatric population: the ICARe Dicomano Study. J. Am. Coll. Cardiol., June 24, 2008; 51(25): 2432 - 2439. [Abstract] [Full Text] [PDF]
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 C. M. McEniery, Yasmin, B. McDonnell, M. Munnery, S. M. Wallace, C. V. Rowe, J. R. Cockcroft, I. B. Wilkinson, and on Behalf of the Anglo-Cardiff Collaborative Trial Central Pressure: Variability and Impact of Cardiovascular Risk Factors: The Anglo-Cardiff Collaborative Trial II Hypertension, June 1, 2008; 51(6): 1476 - 1482. [Abstract] [Full Text] [PDF]
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 V. F. Panoulas, G. S. Metsios, A. V. Pace, H. John, G. J. Treharne, M. J. Banks, and G. D. Kitas Hypertension in rheumatoid arthritis Rheumatology, May 29, 2008; (2008) ken159v2. [Abstract] [Full Text] [PDF]
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E. S. Schaeffner, T. Kurth, T. S. Bowman, R. P. Gelber, and J. M. Gaziano Blood pressure measures and risk of chronic kidney disease in men Nephrol. Dial. Transplant., April 1, 2008; 23(4): 1246 - 1251. [Abstract] [Full Text] [PDF]
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A. M. Dart, B. A. Kingwell, C. D. Gatzka, K. Willson, Y.-L. Liang, K. L. Berry, L. M.H. Wing, C. M. Reid, P. Ryan, L. J. Beilin, et al. Smaller Aortic Dimensions Do Not Fully Account for the Greater Pulse Pressure in Elderly Female Hypertensives Hypertension, April 1, 2008; 51(4): 1129 - 1134. [Abstract] [Full Text] [PDF]
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G. F. Mitchell, V. Gudnason, L. J. Launer, T. Aspelund, and T. B. Harris Hemodynamics of Increased Pulse Pressure in Older Women in the Community-Based Age, Gene/Environment Susceptibility-Reykjavik Study Hypertension, April 1, 2008; 51(4): 1123 - 1128. [Abstract] [Full Text] [PDF]
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 H. Moriya, M. Oka, K. Maesato, T. Mano, R. Ikee, T. Ohtake, and S. Kobayashi Weekly Averaged Blood Pressure Is More Important than a Single-Point Blood Pressure Measurement in the Risk Stratification of Dialysis Patients Clin. J. Am. Soc. Nephrol., March 1, 2008; 3(2): 416 - 422. [Abstract] [Full Text] [PDF]
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 C. M. Schooling, C. Q. Jiang, T. H. Lam, W. S. Zhang, K. K. Cheng, and G. M. Leung Life-Course Origins of Social Inequalities in Metabolic Risk in the Population of a Developing Country Am. J. Epidemiol., February 15, 2008; 167(4): 419 - 428. [Abstract] [Full Text] [PDF]
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 M. E. Safar Review: Pulse pressure, arterial stiffness and wave reflections (augmentation index) as cardiovascular risk factors in hypertension Therapeutic Advances in Cardiovascular Disease, February 1, 2008; 2(1): 13 - 24. [Abstract] [PDF]
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 J.-C. Philips, M. Marchand, and A. J. Scheen Squatting Amplifies Pulse Pressure Increase With Disease Duration in Patients With Type 1 Diabetes Diabetes Care, February 1, 2008; 31(2): 322 - 324. [Abstract] [Full Text] [PDF]
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E. Osher and N. Stern Diastolic Pressure in Type 2 Diabetes: Can target systolic pressure be reached without "diastolic hypotension"? Diabetes Care, February 1, 2008; 31(Supplement_2): S249 - S254. [Abstract] [Full Text] [PDF]
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 B. Kirkpatrick, E. Messias, P. D. Harvey, E. Fernandez-Egea, and C. R. Bowie Is Schizophrenia a Syndrome of Accelerated Aging? Schizophr Bull, December 21, 2007; (2007) sbm140v1. [Abstract] [Full Text] [PDF]
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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]
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 C. M. Schooling, C. Jiang, T. H. Lam, G. N. Thomas, M. Heys, Bmbs, X. Lao, W. Zhang, P. Adab, K. K. Cheng, et al. Height, Its Components, and Cardiovascular Risk Among Older Chinese: A Cross-Sectional Analysis of the Guangzhou Biobank Cohort Study Am J Public Health, October 1, 2007; 97(10): 1834 - 1841. [Abstract] [Full Text] [PDF]
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F. Mzayek, S. Hassig, R. Sherwin, J. Hughes, W. Chen, S. Srinivasan, and G. Berenson The Association of Birth Weight with Developmental Trends in Blood Pressure from Childhood through Mid-Adulthood: The Bogalusa Heart Study Am. J. Epidemiol., August 15, 2007; 166(4): 413 - 420. [Abstract] [Full Text] [PDF]
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M. J. Roman, R. B. Devereux, J. R. Kizer, E. T. Lee, J. M. Galloway, T. Ali, J. G. Umans, and B. V. Howard Central Pressure More Strongly Relates to Vascular Disease and Outcome Than Does Brachial Pressure: The Strong Heart Study Hypertension, July 1, 2007; 50(1): 197 - 203. [Abstract] [Full Text] [PDF]
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D. Levy, S.-J. Hwang, A. Kayalar, E. J. Benjamin, R. S. Vasan, H. Parise, M. G. Larson, T. J. Wang, J. Selhub, P. F. Jacques, et al. Associations of Plasma Natriuretic Peptide, Adrenomedullin, and Homocysteine Levels With Alterations in Arterial Stiffness: The Framingham Heart Study Circulation, June 19, 2007; 115(24): 3079 - 3085. [Abstract] [Full Text] [PDF]
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W. J. Mosley II, P. Greenland, D. B. Garside, and D. M. Lloyd-Jones Predictive Utility of Pulse Pressure and Other Blood Pressure Measures for Cardiovascular Outcomes Hypertension, June 1, 2007; 49(6): 1256 - 1264. [Abstract] [Full Text] [PDF]
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G. F. Mitchell, C.-Y. Guo, E. J. Benjamin, M. G. Larson, M. J. Keyes, J. A. Vita, R. S. Vasan, and D. Levy Cross-Sectional Correlates of Increased Aortic Stiffness in the Community: The Framingham Heart Study Circulation, May 22, 2007; 115(20): 2628 - 2636. [Abstract] [Full Text] [PDF]
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