From Investigations Préventives et Cliniques (IPC) (A.B., A.R.,
L.G.) and INSERM U337 (A.B., M.S.), Paris, France.
Correspondence to Athanase Benetos, MD, PhD, Investigations Préventives et Cliniques (IPC), 23 rue de Lubeck, 75116 Paris, France.
Abstract
Abstract—There is now increasing
evidence that high pulse pressure, which is an indicator of large
artery stiffness, is an independent risk factor for
cardiovascular mortality, especially coronary
mortality, in different populations. We have recently shown in a large
French population that in male subjects aged 40 to 69 years, increased
pulse pressure was a strong predictor of cardiovascular
mortality, especially coronary mortality. In the present
report, we analyzed the effect of pulse pressure in men and
women of the same cohort after classifying them as normotensive
(systolic blood pressure [SBP] <140 mm Hg and DBP
<90 mm Hg) or hypertensive (SBP
Aging and
environmental and genetic factors are responsible for structural and
functional changes of the arterial wall media leading to
decreased elasticity and increased stiffness.1 2
The alteration of large artery elasticity has deleterious effects on
the heart and is responsible for an inadequate increase in
systolic pressure and a relative decrease in aortic
diastolic pressure at any given value of mean
arterial blood pressure (MBP).
We have recently shown in a large French population that in male
subjects aged 40 to 69 years, increased pulse pressure (PP) was a
strong predictor of general and cardiovascular
mortality, especially coronary
mortality.3 An analysis of the Survival
and Ventricular Enlargement (SAVE) study showed that PP
measured at the site of the brachial artery was a powerful independent
predictor of recurrent events after myocardial infarction in patients
with impaired left ventricular
function.4 These data, in addition to data from
previous studies in hypertensives,5 suggest that
PP itself could be a major predictor of cardiac risk in different
populations.
Compared with our previous analysis, the purpose of this study
was to evaluate whether the role of PP on
cardiovascular mortality is significant in normotensive
and hypertensive subjects of both genders. We therefore
analyzed the effect of PP in men and women after classifying
them as normotensive (systolic blood pressure [SBP]
<140 mm Hg and diastolic blood pressure [DBP]
<90 mm Hg) and hypertensive (SBP
Methods
Subjects
In the present analysis, we included male and female
subjects defined as normotensive or hypertensive. Normotensives were
subjects with SBP <140 mm Hg and DBP <90 mm Hg and
without any antihypertensive treatment (5503 women and 7128 men).
Hypertensives were subjects with SBP
A nurse measured supine blood pressure in the right arm using a manual
sphygmomanometer. After a 10-minute rest period, blood pressure was
measured 3 times, and the mean of the last 2 measurements was
calculated. The first and fifth Korotkoff phases were used to define
SBP and DBP. Smoking status and physical activity were assessed using a
self-administered questionnaire containing dichotomic (yes or no)
questions regarding tobacco use. Plasma cholesterol was
measured with a Technicon SMA-12.
The follow-up study period ended in December 1994 (mean follow-up was
19.5 years). Deceased subjects were identified through the mortality
records of the Institut National de Statistiques et d'Etudes
Economiques (INSEE) following the procedure previously
detailed.3 Following this procedure, it was
determined that 3135 subjects of our cohort had died during the
follow-up period. Causes of mortality were taken from the death
certificates. These data were provided by the Department of Mortality
of INSERM (Unit SC 8). Causes of death were codified according to the
International Classification of Disease (8th revision until
1978 and 9th revision after 1979).
Data Analysis
The following statistical tests were used for comparisons among the PP
groups: (1) After adjustment for age, mean values of body mass index
(BMI), blood pressure, and total cholesterol were compared
using a 1-way ANOVA. (2) Deaths for the different causes of mortality
were compared using a trend
Results
Tables 1
All-cause and total cardiovascular mortality were
consistently more elevated in the higher PP groups both in
normotensive men (Table 3
In men, an elevation in PP of 10 mm Hg significantly increased
the RR of cardiovascular mortality by 20% in
normotensives and by 9% in hypertensives (Table 5
Comments
There is now increasing evidence that high PP reflecting large artery
stiffness is a significant independent risk factor for
cardiovascular, especially coronary, mortality
in different populations. Madhavan et al5
reported that untreated hypertensive subjects with a PP >63
mm Hg had an increased risk of cardiovascular
complications. In addition, they found that these subjects were at
greater risk of myocardial infarction when there was too great a fall
in DBP after treatment. The same group later reported that in a larger
population of treated and untreated hypertensive subjects, PP was the
only blood pressure measurement independently related to the
in-treatment incidence of myocardial infarction.7
The link between PP and cardiovascular complications
has also been shown in subjects who had myocardial infarction with left
ventricular dysfunction.4 In this
population, a single measurement of PP 3 to 16 days after myocardial
infarction was a significant predictor of recurrent
cardiovascular events. We recently reported that PP is
a significant predictor of cardiovascular mortality in
a general male population aged 40 to 69 years. The present study
shows that the evaluation of PP is of interest even in individuals with
normal values of SBP (<140 mm Hg) and DBP (<90 mm Hg).
Our results presented in Table 5
As expected, hypertensive individuals globally showed higher mortality
levels than normotensive men (Tables 3
Thus, according to our results, normotensive men that are in the higher
PP group (mean values of SBP, 131 mm Hg; DBP, 73 mm Hg;
MBP, 92 mm Hg; PP, 58 mm Hg) have (1) an increased relative
cardiovascular risk of 40% compared with normotensives
who belong in the lower PP group (SBP, 120 mm Hg; DBP, 78
mm Hg; MBP, 92 mm Hg; PP, 42 mm Hg), and (2) a similar
cardiovascular risk as hypertensive subjects who belong
in the lower PP group (SBP, 145 mm Hg; DBP, 105 mm Hg; MBP,
118 mm Hg; PP, 40 mm Hg).
Interestingly, increased PP was a predictor of coronary heart
disease mortality, whereas its predictive value was not significant for
cerebrovascular mortality. Physiologically, PP
describes the oscillation around the mean
arterial pressure (calculated as DBP plus one third PP) and
is influenced by hemodynamic mechanisms that differ
from those controlling mean arterial pressure. MBP is the
pressure that would be present in the aorta and its major arteries
during a given cardiac cycle if the cardiac output was
nonpulsatile.1 2 While mean arterial
pressure remains nearly constant along the arterial tree,
PP increases markedly from central to peripheral arteries
as a consequence of a substantial increase in SBP and a small lowering
of DBP. At a given stroke volume and velocity of
ventricular ejection, the mechanisms influencing PP are
related to the status of conduit arteries, ie, the viscoelastic
properties of the arterial wall and the timing of the
reflected waves. Increased stiffness and earlier wave reflections
within the thoracic aorta increase the PP because of an increase in SBP
and a decrease in DBP.1 8 Alternatively,
increased stroke volume or ventricular ejection rate may be
responsible for an increase in SBP with no change in DBP. In the
present study, we found that the highest PPs were due both
to higher SBP and lower DBP. Thus, the changes in PP may be considered
as markers of increased arterial stiffness, with
consequences for cardiovascular mortality, especially
coronary mortality.9 10 The elevation in
SBP causes a disproportionate increase in end-systolic stress,
which is the principal hemodynamic factor that promotes
the development of cardiac hypertrophy, increased
ventricular oxygen consumption, and left
ventricular
hypertrophy,11 and can compromise
capacity for coronary perfusion.10 These
hemodynamic changes could explain why
arterial stiffness and PP are related mainly to
coronary and not cerebrovascular circulation. In our cohort,
MBP was the most significant predictor of cerebrovascular mortality,
and mean arterial pressure (but not PP) is the perfusion
pressure of cerebral circulation.
In conclusion, this study showed that in both normotensive and
hypertensive males, increased PP is an independent predictor of
cardiovascular mortality. The lack of such an
association in women could be partially explained by the lower
cardiovascular mortality rates in this population.
Acknowledgments
This study was carried out with the help of INSERM (Institut
National de la Santé et de la Recherche Médicale, Paris,
France). We would like to thank the Caisse Nationale d'Assurance
Maladie (CNAM) for supporting this study. The authors are grateful to
Jean-François Morcet, Jean-Pierre Huby, Frederique Thomas,
and Kathy Bean for their help in the analysis of the data and
the writing of the article.
Received January 24, 1998;
first decision March 5, 1998;
accepted April 13, 1998.
References
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Safar ME. Pulse pressure in essential hypertension:
clinical and therapeutical implications. J Hypertens. 1989;7:769–776.[Medline]
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Benetos A, Safar M, Rudnichi A, Smulyan H, Richard
J-L, Ducimetiere P, Guize L. Pulse pressure: a predictor of long-term
mortality in a French male population. Hypertension. 1997;30:1410–1415.
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Mitchell GF, Moye LA, Braunwald E, Rouleau J-L,
Bernstein V, Geltman EM, Flaker GC, Pfeffer M, for the SAVE
Investigators. Sphygmomanometric determined pulse pressure is a
powerful independent predictor of recurrent events after myocardial
infarction in patients with impaired left ventricular
function. Circulation. 1997;96:4254–4260.
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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.
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Mensink GBM, Hoffmeister H. The relationship between
resting heart rate and all-cause, cardiovascular and
cancer mortality. Eur Heart J. 1997;18:1404–1410.
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Fang J, Madhavan S, Cohen H, Alderman MH. Measures of
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patients. J Hypertens. 1995;13:413–419.[Medline]
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Kelly R, Tunin R, Kass D. Effect of reduced aortic
compliance on left ventricular contractile function and
energetics in vivo. Circ Res. 1992;71:490–502.
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Hoffman JIE. A critical view of coronary
reserve. Circulation. 1987;75(suppl I):I-6– I-11.
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Watanabe H, Ohtsuka S, Kakihana M, Sugishita Y.
Coronary circulation in dogs with experimental decrease in
aortic compliance. J Am Coll Cardiol. 1993;21:1497–1506.[Abstract]
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ME. Pulse pressure and echocardiographic findings in
essential hypertension. J Hypertens. 1989;7:127–129.[Medline]
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© 1998 American Heart Association, Inc.
Third Workshop on Structure and Function of Large
Arteries: Part III
Pulse Pressure and Cardiovascular Mortality in Normotensive and Hypertensive Subjects
160 mm Hg or DBP
95 mm Hg). After adjustment for age, mean blood pressure, and
other risk factors, the relative risk (95% confidence limits) for
cardiovascular mortality for an increase of 10
mm Hg of pulse pressure was 1.20 (1.01 to 1.44) in normotensives and
1.09 (1.03 to 1.14) in hypertensives. Cardiovascular
and coronary death rates were similar in the group of
normotensive men with a pulse pressure >50 mm Hg and in the
group of hypertensive men with a pulse pressure <45 mm Hg. No
association between cardiovascular mortality and pulse
pressure was observed in either normotensive or hypertensive women
(0.85 [0.60 to 1.21] and 1.0 [0.91 to 1.11], respectively). Low
mortality rates could explain this observation in normotensive but not
in hypertensive women, in whom cardiovascular mortality
rates were relatively high. Because a high pulse pressure in men is an
independent predictor of cardiovascular mortality in
both hypertensives and in those considered as having normal blood
pressure, this parameter could aid in evaluating
cardiovascular risk.
Key Words: cardiovascular diseases • coronary artery disease • mortality • blood pressure • normotension • hypertension, essential160 mm Hg or DBP
95 mm Hg).
The French public healthcare system (Securité
Sociale–Caisse Nationale d'Assurance Maladie [CNAM]) provides all
working and retired persons and their families with a free health
examination every 5 years. The Centre d'Investigations
Préventives et Cliniques (IPC) is one of the largest medical
centers of this kind in France, having performed approximately 15 000
examinations per year since 1970 for persons living in the Paris area.
In this study, we present data of the normotensive and hypertensive
men and women aged 40 to 69 years who had a health checkup at the IPC
Center during the period of May 1972 through May 1977. The general
characteristics of this population have been described
previously.3 160 mm Hg or DBP
95 mm Hg (1945 women and 5379 men). All other subjects with
intermediate blood pressure values were excluded from the present
analysis.
In each of the 4 groups identified according to gender and
presence or absence of hypertension, the role of PP was studied either
as a qualitative parameter (separation according to the 4
quartiles of PP defined in the whole population) or as a continuous
quantitative parameter. The qualitative separation was
accomplished by dividing each group into PP quartiles defined as
PP1
45; 45<PP250;
50<PP3<65; and
PP465 mm Hg. This classification is the
closest to the quartile distribution in the whole population by steps
of 5 mm Hg. However, in normotensives the number of
PP4 was too low, leading us to regroup
PP3 and PP4. 
2 test. (3) The
role of PP as a quantitative or qualitative variable for the
different causes of mortality was tested using a
multivariate Cox regression controlling for age, MBP,
total cholesterol, and tobacco consumption. 
and 2 summarize the mean values of age, BMI,
blood pressure, and total cholesterol (values were adjusted
for age) in the different groups according to the PP level. In all
groups, age and SBP increased progressively from the first to the
fourth PP group, whereas DBP was significantly lower in the subgroups
with the higher PP. BMI was slightly but significantly higher in the
higher PP groups.
View this table:
[in a new window]
Table 1. Description of Population According to PP:
Normotensive Subjects (SBP <140 and DBP <90
mm Hg)
View this table:
[in a new window]
Table 2. Description of Population According to PP:
Hypertensive Subjects (SBP 160 or DBP 95
mm Hg)) and in
hypertensive men and women (Table 4).
However, the multivariate Cox regression
analysis controlling for age alone (Table
5a) or age and other risk factors such as
MBP, total cholesterol, and tobacco consumption (Table 5b)
showed that the association between cardiovascular
mortality and PP was significant in the 2 groups of men but not in
women. The Cox analysis showed that in hypertensive women, MBP
was a significant determinant for cardiovascular
mortality with a relative risk (RR) for an increase in 10 mm Hg
of 1.16 (95% confidence limits, 1.02 to 1.32). In normotensive women,
undoubtedly due to the low mortality rates, only age had a predictive
value in the different causes of mortality.
View this table:
[in a new window]
Table 3. Mortality Rates in Normotensive Subjects (SBP <140
and DBP <90 mm Hg) According to PP
Levels
View this table:
[in a new window]
Table 4. Mortality Rates in Hypertensive Subjects (SBP 160
or DBP 95 mm Hg) According to PP
Levels). Comparing this
with the effects of MBP, we observed that an elevation in MBP of
10 mm Hg significantly increased the RR of
cardiovascular mortality in hypertensive (RR, 1.14
[95% confidence limits, 1.07 to 1.21]) but not in normotensive men
(1.10 [0.88 to 1.40]). The effects of PP on the
cardiovascular mortality were related to its influence
on coronary mortality but not cerebrovascular mortality. The
latter was influenced by MBP levels (data not shown) but not by PP
levels (Table 5). When PP was considered as a qualitative
parameter, the RR for cardiovascular
mortality in male subjects with a PP >50 mm Hg versus those with
a PP 50 mm Hg was increased by 40% in normotensives and 48%
in hypertensives (Figure). This
association was related to an increase in coronary mortality
but not in cerebrovascular mortality in both normotensive and
hypertensive men.
View this table:
[in a new window]
Table 5. Relative Risks and 95% Confidence Limits of
Mortality Corresponding to an Increase of 10 mm Hg of
PP
View larger version (11K):
[in a new window]
Figure 1. Relative risk and 95% confidence limits for total
cardiovascular mortality in subjects with PP >50
mm Hg compared with subjects with PP 50 mm Hg in the 4 groups
of subjects according to gender and presence of hypertension.
The main finding of this study is that in a large unselected
population, PP is an independent predictor of
cardiovascular mortality in both normotensive and
hypertensive men. Therefore, PP measurement may help in the evaluation
of individual risk and therefore in therapeutic decision-making. In
women, the same association between PP and
cardiovascular mortality was observed in those with
hypertension. The higher the PP, the higher the
cardiovascular mortality. However, after adjustment for
age alone or age and other risk factors, this association lost its
significance. This lack of association can be explained only partially
by the low statistical power of our analysis. In normotensive
women, we are unable to draw any conclusions because
cardiovascular mortality rates are very low in this
particular subpopulation. However, in hypertensive women, we observed
that mortality rates from cardiovascular disease,
especially coronary heart disease, were higher than in
normotensive men. In this latter subpopulation, PP is a strong
predictor of cardiovascular and coronary
mortality. Moreover, in hypertensive women, MBP was a predictor of the
different causes of mortality. Interestingly, several
studies,6 showed similar gender differences concerning
heart rate; for example, increased heart rate was a significant
predictor of cardiovascular mortality, especially
coronary mortality, in men but not in women. Larger studies are
needed to evaluate whether gender can influence the role of cyclic
stress (depending on PP and heart rate) on the
cardiovascular system. 
show that evaluation of PP
could be of even more interest for normotensives than hypertensives,
since the odds ratios for cardiovascular and
coronary mortality corresponding to the increase of 10
mm Hg of PP are higher than those for hypertensives. The lack of such
a difference between normotensive and hypertensive subjects in the
qualitative analysis (presented in the Figure) is
explained by a larger difference in PP levels between "low" and
"high" PP individuals in the hypertensive group. and 4). However,
cardiovascular, especially coronary, death
rates were similar in normotensive men with a PP >50 mm Hg and
in hypertensive men with PP <45 mm Hg. This result was unchanged
using a multivariate Cox regression analysis
after adjustment for age and other risk factors.
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G. Assmann, P. Cullen, T. Evers, D. Petzinna, and H. Schulte Importance of arterial pulse pressure as a predictor of coronary heart disease risk in PROCAM Eur. Heart J., October 2, 2005; 26(20): 2120 - 2126. [Abstract] [Full Text] [PDF]
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J. Ruiz, D. Monbaron, G. Parati, S. Perret, E. Haesler, C. Danzeisen, and D. Hayoz Diabetic Neuropathy Is a More Important Determinant of Baroreflex Sensitivity Than Carotid Elasticity in Type 2 Diabetes Hypertension, July 1, 2005; 46(1): 162 - 167. [Abstract] [Full Text] [PDF]
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J. Amar, J.-B. Ruidavets, J.-C. Peyrieux, J.-M. Mallion, J. Ferrieres, M. E. Safar, and B. Chamontin C-Reactive Protein Elevation Predicts Pulse Pressure Reduction in Hypertensive Subjects Hypertension, July 1, 2005; 46(1): 151 - 155. [Abstract] [Full Text] [PDF]
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K. Sutton-Tyrrell, S. S. Najjar, R. M. Boudreau, L. Venkitachalam, V. Kupelian, E. M. Simonsick, R. Havlik, E. G. Lakatta, H. Spurgeon, S. Kritchevsky, et al. Elevated Aortic Pulse Wave Velocity, a Marker of Arterial Stiffness, Predicts Cardiovascular Events in Well-Functioning Older Adults Circulation, June 28, 2005; 111(25): 3384 - 3390. [Abstract] [Full Text] [PDF]
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 D. G Brillante, M. T Johnstone, and L. G Howes Effects of Intravenous PD 123319 on Haemodynamic and Arterial Stiffness Indices in Healthy Volunteers Journal of Renin-Angiotensin-Aldosterone System, June 1, 2005; 6(2): 102 - 106. [Abstract] [PDF]
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 G. V. Nair, L. A. Chaput, E. Vittinghoff, D. M. Herrington, and for the Heart and Estrogen/Progestin Replacement S Pulse Pressure and Cardiovascular Events in Postmenopausal Women With Coronary Heart Disease Chest, May 1, 2005; 127(5): 1498 - 1506. [Abstract] [Full Text] [PDF]
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 H. H. Dao, R. Essalihi, C. Bouvet, and P. Moreau Evolution and modulation of age-related medial elastocalcinosis: Impact on large artery stiffness and isolated systolic hypertension Cardiovasc Res, May 1, 2005; 66(2): 307 - 317. [Abstract] [Full Text] [PDF]
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F. Fyhrquist, B. Dahlof, R. B. Devereux, S. E. Kjeldsen, S. Julius, G. Beevers, U. de Faire, H. Ibsen, K. Kristianson, O. Lederballe-Pedersen, et al. Pulse Pressure and Effects of Losartan or Atenolol in Patients With Hypertension and Left Ventricular Hypertrophy Hypertension, April 1, 2005; 45(4): 580 - 585. [Abstract] [Full Text] [PDF]
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 S. Nakano, K. Konishi, K. Furuya, K. Uehara, M. Nishizawa, A. Nakagawa, T. Kigoshi, and K. Uchida A Prognostic Role of Mean 24-h Pulse Pressure Level for Cardiovascular Events in Type 2 Diabetic Subjects Under 60 Years of Age Diabetes Care, January 1, 2005; 28(1): 95 - 100. [Abstract] [Full Text] [PDF]
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K. Miura, Y. Soyama, Y. Morikawa, M. Nishijo, Y. Nakanishi, Y. Naruse, K. Yoshita, S. Kagamimori, and H. Nakagawa Comparison of Four Blood Pressure Indexes for the Prediction of 10-Year Stroke Risk in Middle-Aged and Older Asians Hypertension, November 1, 2004; 44(5): 715 - 720. [Abstract] [Full Text] [PDF]
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J. Amar, J. P. Cambou, E. Touze, V. Bongard, G. Jullien, A. Vahanian, G. Coppe, J. L. Mas, and on behalf of ECLAT1 Study Investigators Comparison of Hypertension Management After Stroke and Myocardial Infarction: Results From ECLAT1--A French Nationwide Study Stroke, July 1, 2004; 35(7): 1579 - 1583. [Abstract] [Full Text] [PDF]
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H. Hashimoto, K. Kitagawa, H. Hougaku, H. Etani, and M. Hori Relationship Between C-Reactive Protein and Progression of Early Carotid Atherosclerosis in Hypertensive Subjects Stroke, July 1, 2004; 35(7): 1625 - 1630. [Abstract] [Full Text] [PDF]
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M. E. Safar, M. Lajemi, A. Rudnichi, R. Asmar, and A. Benetos Angiotensin-Converting Enzyme D/I Gene Polymorphism and Age-Related Changes in Pulse Pressure in Subjects with Hypertension Arterioscler Thromb Vasc Biol, April 1, 2004; 24(4): 782 - 786. [Abstract] [Full Text] [PDF]
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 V. Fonseca, C. Desouza, S. Asnani, and I. Jialal Nontraditional Risk Factors for Cardiovascular Disease in Diabetes Endocr. Rev., February 1, 2004; 25(1): 153 - 175. [Abstract] [Full Text] [PDF]
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N. J. Camp, P. N. Hopkins, S. J. Hasstedt, H. Coon, A. Malhotra, R. M. Cawthon, and S. C. Hunt Genome-Wide Multipoint Parametric Linkage Analysis of Pulse Pressure in Large, Extended Utah Pedigrees Hypertension, September 1, 2003; 42(3): 322 - 328. [Abstract] [Full Text] [PDF]
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G. Mancia, G. Parati, P. Castiglioni, R. Tordi, E. Tortorici, F. Glavina, and M. Di Rienzo Daily Life Blood Pressure Changes Are Steeper in Hypertensive Than in Normotensive Subjects Hypertension, September 1, 2003; 42(3): 277 - 282. [Abstract] [Full Text] [PDF]
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S. Laurent, S. Katsahian, C. Fassot, A.-I. Tropeano, I. Gautier, B. Laloux, and P. Boutouyrie Aortic Stiffness Is an Independent Predictor of Fatal Stroke in Essential Hypertension Stroke, May 1, 2003; 34(5): 1203 - 1206. [Abstract] [Full Text] [PDF]
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F. Viazzi, G. Leoncini, D. Parodi, M. Ravera, E. Ratto, S. Vettoretti, C. Tomolillo, M. D. Sette, G. P. Bezante, G. Deferrari, et al. Pulse pressure and subclinical cardiovascular damage in primary hypertension Nephrol. Dial. Transplant., October 1, 2002; 17(10): 1779 - 1785. [Abstract] [Full Text] [PDF]
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 P. Nestel, H. Shige, S. Pomeroy, M. Cehun, M. Abbey, and D. Raederstorff The n-3 fatty acids eicosapentaenoic acid and docosahexaenoic acid increase systemic arterial compliance in humans Am. J. Clinical Nutrition, August 1, 2002; 76(2): 326 - 330. [Abstract] [Full Text] [PDF]
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G. F. Mitchell, J. L. Izzo Jr, Y. Lacourciere, J.-P. Ouellet, J. Neutel, C. Qian, L. J. Kerwin, A. J. Block, and M. A. Pfeffer Omapatrilat Reduces Pulse Pressure and Proximal Aortic Stiffness in Patients With Systolic Hypertension: Results of the Conduit Hemodynamics of Omapatrilat International Research Study Circulation, June 25, 2002; 105(25): 2955 - 2961. [Abstract] [Full Text] [PDF]
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 M. Domanski, G. Mitchell, M. Pfeffer, J. D. Neaton, J. Norman, K. Svendsen, R. Grimm, J. Cohen, J. Stamler, and for the MRFIT Research Group Pulse Pressure and Cardiovascular Disease-Related Mortality: Follow-up Study of the Multiple Risk Factor Intervention Trial (MRFIT) JAMA, May 22, 2002; 287(20): 2677 - 2683. [Abstract] [Full Text] [PDF]
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P. S. Klassen, E. G. Lowrie, D. N. Reddan, E. R. DeLong, J. A. Coladonato, L. A. Szczech, J. M. Lazarus, and W. F. Owen Jr Association Between Pulse Pressure and Mortality in Patients Undergoing Maintenance Hemodialysis JAMA, March 27, 2002; 287(12): 1548 - 1555. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, K. Prasad, I. R. Hall, A. Thomas, H. MacCallum, D. J. Webb, M. P. Frenneaux, and J. R. Cockcroft Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia J. Am. Coll. Cardiol., March 20, 2002; 39(6): 1005 - 1011. [Abstract] [Full Text] [PDF]
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 P. C. Deedwania The Changing Face of Hypertension: Is Systolic Blood Pressure the Final Answer? Arch Intern Med, March 11, 2002; 162(5): 506 - 508. [Full Text] [PDF]
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A. Benetos, F. Thomas, K. Bean, S. Gautier, H. Smulyan, and L. Guize Prognostic Value of Systolic and Diastolic Blood Pressure in Treated Hypertensive Men Arch Intern Med, March 11, 2002; 162(5): 577 - 581. [Abstract] [Full Text] [PDF]
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R. A.J.M. van Dijk, J. A. Rauwerda, M. Steyn, J. W.R. Twisk, and C. D.A. Stehouwer Long-Term Homocysteine-Lowering Treatment With Folic Acid Plus Pyridoxine Is Associated With Decreased Blood Pressure but Not With Improved Brachial Artery Endothelium-Dependent Vasodilation or Carotid Artery Stiffness: A 2-Year, Randomized, Placebo-Controlled Trial Arterioscler Thromb Vasc Biol, December 1, 2001; 21(12): 2072 - 2079. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, S. S. Franklin, I. R. Hall, S. Tyrrell, and J. R. Cockcroft Pressure Amplification Explains Why Pulse Pressure Is Unrelated to Risk in Young Subjects Hypertension, December 1, 2001; 38(6): 1461 - 1466. [Abstract] [Full Text] [PDF]
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S. Kinlay, M. A. Creager, M. Fukumoto, H. Hikita, J. C. Fang, A. P. Selwyn, and P. Ganz Endothelium-Derived Nitric Oxide Regulates Arterial Elasticity in Human Arteries In Vivo Hypertension, November 1, 2001; 38(5): 1049 - 1053. [Abstract] [Full Text] [PDF]
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M. Domanski, J. Norman, M. Wolz, G. Mitchell, and M. Pfeffer Cardiovascular Risk Assessment Using Pulse Pressure in the First National Health and Nutrition Examination Survey (NHANES I) Hypertension, October 1, 2001; 38(4): 793 - 797. [Abstract] [Full Text] [PDF]
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A. L. Pauca, M. F. O'Rourke, and N. D. Kon Prospective Evaluation of a Method for Estimating Ascending Aortic Pressure From the Radial Artery Pressure Waveform Hypertension, October 1, 2001; 38(4): 932 - 937. [Abstract] [Full Text] [PDF]
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M. F. O'Rourke Diastolic heart failure, diastolic left ventricular dysfunction and exercise intolerance J. Am. Coll. Cardiol., September 1, 2001; 38(3): 803 - 805. [Full Text] [PDF]
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R. S. Khattar, J. D. Swales, C. Dore, R. Senior, and A. Lahiri Effect of Aging on the Prognostic Significance of Ambulatory Systolic, Diastolic, and Pulse Pressure in Essential Hypertension Circulation, August 14, 2001; 104(7): 783 - 789. [Abstract] [Full Text] [PDF]
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K. Miura, A. R. Dyer, P. Greenland, M. L. Daviglus, M. Hill, K. Liu, D. B. Garside, and J. Stamler 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, August 1, 2001; 38(2): 232 - 237. [Abstract] [Full Text] [PDF]
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R. H. Fagard, K. Pardaens, J. A. Staessen, and L. Thijs The pulse pressure-to-stroke index ratio predicts cardiovascular events and death in uncomplicated hypertension J. Am. Coll. Cardiol., July 1, 2001; 38(1): 227 - 231. [Abstract] [Full Text] [PDF]
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R. S KHATTAR and J. D SWALES Pulse pressure and prognosis Heart, May 1, 2001; 85(5): 484 - 486. [Full Text]
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S. Laurent, P. Boutouyrie, R. Asmar, I. Gautier, B. Laloux, L. Guize, P. Ducimetiere, and A. Benetos Aortic Stiffness Is an Independent Predictor of All-Cause and Cardiovascular Mortality in Hypertensive Patients Hypertension, May 1, 2001; 37(5): 1236 - 1241. [Abstract] [Full Text] [PDF]
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A. Aviv Hypothesis : Pulse Pressure and Human Longevity Hypertension, April 1, 2001; 37(4): 1060 - 1066. [Abstract] [Full Text] [PDF]
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 I. B Wilkinson, H. MacCallum, P. C Hupperetz, C. J van Thoor, J. R Cockcroft, and D. J Webb Changes in the derived central pressure waveform and pulse pressure in response to angiotensin II and noradrenaline in man J. Physiol., February 1, 2001; 530(3): 541 - 550. [Abstract] [Full Text] [PDF]
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A. Benetos, K. Okuda, M. Lajemi, M. Kimura, F. Thomas, J. Skurnick, C. Labat, K. Bean, and A. Aviv Telomere Length as an Indicator of Biological Aging : The Gender Effect and Relation With Pulse Pressure and Pulse Wave Velocity Hypertension, February 1, 2001; 37(2): 381 - 385. [Abstract] [Full Text] [PDF]
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L. D. Atwood, P. B. Samollow, J. E. Hixson, M. P. Stern, and J. W. MacCluer Genome-Wide Linkage Analysis of Pulse Pressure in Mexican Americans Hypertension, February 1, 2001; 37(2): 425 - 428. [Abstract] [Full Text] [PDF]
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A. Benetos, F. Thomas, M. E. Safar, K. E. Bean, and L. Guize Should diastolic and systolic blood pressure be considered for cardiovascular risk evaluation: a study in middle-aged men and women J. Am. Coll. Cardiol., January 1, 2001; 37(1): 163 - 168. [Abstract] [Full Text] [PDF]
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D. M. Lloyd-Jones, J. C. Evans, M. G. Larson, C. J. O'Donnell, E. J. Roccella, and D. Levy Differential Control of Systolic and Diastolic Blood Pressure : Factors Associated With Lack of Blood Pressure Control in the Community Hypertension, October 1, 2000; 36(4): 594 - 599. [Abstract] [Full Text] [PDF]
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E. Jeanclos, N. J. Schork, K. O. Kyvik, M. Kimura, J. H. Skurnick, and A. Aviv Telomere Length Inversely Correlates With Pulse Pressure and Is Highly Familial Hypertension, August 1, 2000; 36(2): 195 - 200. [Abstract] [Full Text] [PDF]
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V. Vaccarino, T. R. Holford, and H. M. Krumholz Pulse pressure and risk for myocardial infarction and heart failure in the elderly J. Am. Coll. Cardiol., July 1, 2000; 36(1): 130 - 138. [Abstract] [Full Text] [PDF]
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R. Pedrinelli, G. Dell'Omo, G. Penno, S. Bandinelli, A. Bertini, V. Di Bello, and M. Mariani Microalbuminuria and Pulse Pressure in Hypertensive and Atherosclerotic Men Hypertension, January 1, 2000; 35(1): 48 - 54. [Abstract] [Full Text] [PDF]
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K. Narkiewicz and V. K. Somers Interactive Effect of Heart Rate and Muscle Sympathetic Nerve Activity on Blood Pressure Circulation, December 21, 1999; 100(25): 2514 - 2518. [Abstract] [Full Text] [PDF]
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M. O'Rourke and E. D. Frohlich Pulse Pressure : Is This a Clinically Useful Risk Factor? Hypertension, September 1, 1999; 34(3): 372 - 374. [Full Text] [PDF]
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