(Hypertension. 1997;30:1410-1415.)
© 1997 American Heart Association, Inc.
Articles |
Pulse Pressure
A Predictor of Long-term Cardiovascular Mortality in a French Male Population
From the Investigations Préventives et Cliniques (A.B., A.R., L.G.), Paris, France; Institut National de la Santé et de la Recherche Médicale (INSERM) U337 (A.B., M.S.) and U258 (J.-L.R., P.D., L.G.), Paris, France; and Department of Medicine (H.S.), State University of New York, Syracuse, NY.
Correspondence to Athanase Benetos, MD, PhD, Investigations Préventives et Cliniques (IPC), 23 rue de Lubeck, 75116 Paris, France.
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Abstract |
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Abstract Studies on the usefulness of blood pressure as a prognostic factor in cardiovascular disease have more often involved investigations of the levels of diastolic or systolic blood pressure. However, blood pressure may be divided into two other components: steady (mean pressure) and pulsatile (pulse pressure). In this study, the relationship of pulse pressure to cardiovascular mortality was investigated in 19 083 men 40 to 69 years old who were undergoing a routine systematic health examination and were being followed up after a mean period of 19.5 years. Subjects were divided into four groups according to age (40 to 54 and 55 to 69 years) and mean arterial pressure (<107 and
107 mm Hg). Each group was further divided into four
subgroups according to the pulse pressure level. A wide pulse pressure
(evaluated according to the quartile group or as a continuous
quantitative variable) was an independent and significant predictor
of all-cause, total cardiovascular, and, especially,
coronary mortality in all age and mean pressure groups. No
significant association between pulse pressure and cerebrvascular
mortality was observed. In conclusion, in a large population of men
with a relatively low cardiovascular risk, a wide pulse
pressure is a significant independent predictor of all-cause,
cardiovascular, and, especially, coronary
mortality.
Key Words: mortality • blood pressure • pulse pressure • cardiovascular disease
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Introduction |
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TopAbstractIntroductionMethodsResultsReferences |
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The standard definition of hypertension includes an elevation of SBP and/or DBP. In adhering to this definition, many epidemiological investigations of the long-term risks of the disease fail to include patients with high SBP but normal or low DBP.1–3 In so doing, patients with the widest PPs were excluded. Despite this systematic entrance bias, these studies have shown increasing cardiovascular risk of higher SBP and PP at the same DBP.4 In 1971, investigators with the Framingham Heart Study5 emphasized the greater risks of an elevated SBP compared with the DBP in patients over the age of 55. Although probably involved, PP was rarely mentioned.6
Although a large PP measured at the brachial artery with use of the cuff method is not an accurate representation of the proximal aortic PP, it does suggest a stiffened aorta. Such stiffening, through a variety of mechanisms,7,8 tends to raise the SBP and lower the DBP. The former, which increases left ventricular pulsatile work, is associated with left ventricular hypertrophy and requires a greater coronary blood flow. The latter reduces the pressure on which coronary flow is dependent, and together they increase the vulnerability of the heart to ischemia. All this suggests that PP itself could be a major predictor of cardiac risk.
Evidence is beginning to accumulate in support of this view. In 1994,
Madhavan et al9 reported a series of 2207 untreated
hypertensive subjects followed for an average of 4.8 years. This study
showed that subjects in the upper tertile of pretreatment PP (63
mm Hg) had a greater mortality than those in the lower tertiles and
that PP, but not SBP or DBP, was an independent predictor of myocardial
infarction. In a later study4 from the same group, an
expanded number of 5730 treated and untreated hypertensive patients
were reported. After adjustment for other risk factors, PP was the only
measure of blood pressure significantly and independently related to
the in-treatment incidence of myocardial infarction.
In 1989, a study from France10 described findings for 18 336 men and 9351 women who had been followed for an average of 9.5 years. These were unselected subjects who volunteered for free medical examinations. Blood pressure data were divided statistically into steady and pulsatile components. There was an association between the pulsatile component and left ventricular hypertrophy in both sexes, as well as a positive correlation with death from coronary artery disease in women. The results in both sexes were weakened by the small number of deaths in each group, which was a consequence of the relatively short duration of follow-up.
The purpose of the present report was to assess the effect of the initial PP on the long-term risks of cardiovascular mortality in the male subjects of this self-selected cohort who had been followed for 10 additional years, to a total follow-up period of 19.5 years.
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Methods |
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Subjects
The French Public Health System (Securité Sociale–CNAM) offers to all working and retired persons and their families free health examinations every 5 years. The IPC is one of the largest medical centers in France; since 1970,
15 000 examinations of
persons living in the Paris area have been performed annually. In the
present study, we present data that describe a population
composed of all 19 083 men aged 40 to 69 years who underwent a
systematic health check-up in the center IPC during the period of May
1972 through May 1977. These subjects were selected from the 39 495
men examined during this period at the Center IPC. Clerks and working
executives represented 88% of the studied
population. Supine blood pressure was measured by a nurse in the right arm with the use of a manual sphygmomanometer. After a 10-minute rest period, pressure was measured three times, and the mean of the last two measurements was calculated. The first and the fifth Korotkoff's phases were used to define SBP and DBP. Smoking status was assessed with a self-administered questionnaire with dichotomic (yes or no) questions regarding tobacco use. Plasma cholesterol was measured with a Technicon SMA 12.
The follow-up study period ended on December 1994 (mean follow-up, 19.5 years). Deceased subjects were identified from the mortality records of the Institut National de Statistiques et d'Etudes Economiques. A patient of our cohort was considered to be deceased when he had the same first name, last name, sex, and date of birth as a person recorded in the Institut National de Statistiques et d'Etudes Economiques mortality records during the period of the follow-up. Through the use of this matching procedure, the identification error was <1%. Only subjects fulfilling all four of these criteria were considered to be deceased. Individuals matching for sex, last name, and only one of the other two criteria were excluded from the study. All other subjects were considered to be alive at the end of the follow-up period. On the basis of this procedure, 3653 subjects of our cohort were considered to have 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 the INSERM (Unit SC 8). Causes of death were codified according to the International Classification of Disease (eighth revision until 1978 and ninth revision after 1979).
Data Analysis
Subjects were divided into four groups according to age (young,
40 to 54 years; older, 55 to 69 years) and MBP
(MBP=2/3DBP+1/3SBP; low MBP, <107 mm Hg; high MBP,
107 mm Hg). In each of the four groups identified according to
age and MBP, the role of PP was studied either as a qualitative
parameter (separation according to the four 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 quartiles distribution in the whole population by steps of 5
mm Hg.
For comparisons among the PP groups within each of the four original
groups (defined according to age and MBP), mean values of morphometric
parameters, blood pressure, and total
cholesterol were compared with the use of a one-way
analysis of variance and a 
2 test for tobacco
status; deaths for the different causes of mortality were compared with
the use of a trend 2 test; and the difference in
survival probability for the different causes of mortality were tested
by using a Cox analysis with adjustments for age, total
cholesterol, and tobacco consumption.
We also assessed (in a multiple logistic regression) the respective roles of MBP and PP, both of which are considered to be continuous quantitative variables. To test whether the effects of one variable was affected by the other, we introduced the interactive term. In the case of significant interaction MBPxPP, we reconstructed the effect of each variable in the hypothetical populations corresponding to selected levels (mean, first, and third quartiles) of the other variable.
All statistical analyses were performed with SAS software.
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Results |
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Table 1
provides a summary of the
mean values of morphometric parameters, blood pressure,
total cholesterol, and tobacco consumption among the
different groups according to the PP level. In both groups of young
patients (Table 1A), age, weight, height, BMI, and tobacco consumption
did not show any clinically significant differences among the four PP
subgroups. SBP levels progressively increased from the first PP group
to the higher PP groups, whereas mean values of DBP were significantly
lower in the subgroups with the higher PP. Total
cholesterol was increased from groups PP1 to
PP4. In the two groups of older patients (Table 1B), age
was higher in the subgroups with the higher PP values. For the other
parameters, the same trends were observed as for younger
patients.
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Table 2 shows death rates for the
different causes of mortality. All-cause,
cardiovascular, and coronary heart disease
mortality rates were constantly higher as PP increased. This
association was observed in all groups (young versus old and low MBP
versus high MBP). However, no significant association was observed
between PP and cerebrovascular mortality.
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Fig 1 shows survival probabilities for
cardiovascular mortality, with adjustments for age,
total cholesterol, and tobacco consumption. In the four
groups of subjects, lower survival probabilities were observed in
subjects with higher PP, especially in the subgroup with PP values of
65 mm Hg. The differences among PP subgroups progressively
increased throughout the follow-up period. These differences become
significant after 10 years of follow-up. Similar patterns were observed
in survival probabilities for all-cause and coronary heart
mortality but not for cerebrovascular mortality (data not shown).
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, 45<PP
, 50<PP<65; and 
, PP
Finally, the respective roles of MBP and PP, considered in this
analysis as continuous quantitative variables, were
evaluated after adjustment for age (Table 3 and Fig 2). In younger patients, when MBP and PP
were used together in the model (model 3 in Table 3A), both are highly
significant predictors for all-cause,
noncardiovascular, total
cardiovascular, and coronary heart disease
mortality. The effects of the MBP and PP were additive (no interaction
MBPxPP was observed). For cerebrovascular mortality, MBP but not PP
was a strong predictor. In the older subjects, MBP and PP were both
predictors for the different causes of mortality (Table 3B). However,
difference from what we observed in younger subjects, a significant
negative interaction was observed in older individuals between PP and
MBP for total cardiovascular (P=.012) and
coronary heart disease (P=.013) mortality. After
that, we evaluated the effect of PP at three different levels of MBP
(mean, first, and third quartiles) (Fig 2, top) and the effect of MBP
at the same three levels of the PP (Fig 2, bottom). This
analysis showed that both PP and MBP were significant
predictors for total cardiovascular and
coronary heart disease mortality, with the more pronounced
effects of each parameter when values of the other
parameter were lower.
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Comments
Therapeutic decision making and management in patients with
mild-to-moderate hypertension are complicated by the wide variation in
their clinical characteristics. Clinicians therefore have sought more
precise means to describe the outlook for individual patients. One
approach has been to use different measures of baseline blood pressure,
such as 24-hour recordings and variability of blood pressure to
prognostically stratify patients. Our study is the first to clearly
show that in a large male unselected population with a relatively low
risk (volunteers for free medical examinations), PP measurement may
help in the evaluation of the individual risk and therefore in the
therapeutic decision making. Although the use of a single blood
pressure measurement reduced statistical power, our results demonstrate
that increased PP is a predictor of global mortality and
cardiovascular mortality, independent of other known
cardiovascular factors such as age, mean blood
pressure, total cholesterol, and smoking. Interestingly,
increased PP was a predictor of coronary heart disease
mortality, whereas its predictive value was not significant for
cerebrovascular mortality.
A previous analysis of the same cohort was not able to
establish a significant relationship between PP and
cardiovascular mortality in male subjects. We believe
that this was due to the fact that in this low-risk population, the
duration of the follow-up of the previous analysis was too
short (9 years) to evaluate the role of PP. As shown from the
survival curves in the present study (Fig 1
) differences among the
four subgroups according to the PP levels, only become clear after the
10th year of follow-up.
Physiologically, PP describes the oscillation around the mean arterial pressure (calculated as DBP+1/3PP) 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.7,8 Although 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 slight 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, that is, the viscoelastic properties of the arterial wall and timing of the reflected waves. Increased stiffness and earlier wave reflections within the thoracic aorta increase the PP due to an increase in SBP and a decrease in DBP.7,11 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 showed that the widest PPs were due to both an increase in SBP and a decrease in DBP. Thus, the changes in PP may be considered as markers of increased arterial stiffness, with consequences for the cardiovascular mortality.
In the present study, in the younger individuals (40 to 54 years),
PP and MBP have additive effects in the evaluation of the risk for the
different causes of mortality (except for cerebrovascular, for which
MBP but not PP is a strong predictor). Interestingly, in older
individuals (55 to 70 years), a negative interaction was observed
between MBP and PP, suggesting that the effect of PP in total
cardiovascular and, especially, coronary heart
disease mortality is enhanced in individuals with low MBP (Table 3b and
Fig 2). Taken together, these results show that increased PP was a
major predictor of coronary mortality even in the presence of
values of MBPs conventionally accepted as being within the normal range
(MBP <107 mm Hg). Indeed, the coronary circulation is
the only circulation with volume flow that is governed by the DBP
rather than the SBP.12 Thus, any decrease in DBP as a
consequence of increased arterial stiffness may limit
coronary blood flow, particularly in the presence of associated
stenosis of the coronary arteries.11 In
addition to a decrease in DBP, increased arterial stiffness
is responsible for an increase in SBP, which, through increased
end-systolic stress, promotes cardiac hypertrophy.
In hypertensive subjects, a positive and significant association has
been previously observed between increased PP and increased cardiac
mass independent of mean arterial pressure.13
Therefore, it is reasonable to suggest that an increased PP, through
both these mechanisms, increases coronary risk.
In the present study, no comparable risk was observed for PP in the cerebral circulation. This finding may be in part due to a loss of statistical power as a consequence of the relatively small number of cerebrovascular deaths compared with coronary ischemic deaths. However, in our cohort, MBP was the most significant predictor of cerebrovascular mortality, and mean arterial pressure (but not PP) is the perfusion pressure of the cerebral circulation.
In conclusion, the present study has shown that in male subjects with normal or elevated mean arterial pressure, increased PP is a strong predictor of general and cardiovascular mortality, affecting especially the coronary but not the cerebrovascular circulation.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was performed with the help of INSERM (Paris). We thank the Caisse Nationale d'Assurance Maladie (CNAM) for support of this study. The authors are grateful to Jean-François Morcet and Jean Pierre Huby for their help and advice in analysis of the data. We thank Dr Anne Safar for help in preparing the manuscript.
Received April 8, 1997; first decision April 24, 1997; accepted June 25, 1997.
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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. T. Powell, R. J. Turner, M. Sian, R. Debasso, and T. Lanne Influence of fibrillin-1 genotype on the aortic stiffness in men J Appl Physiol, September 1, 2005; 99(3): 1036 - 1040. [Abstract] [Full Text] [PDF]
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A. A. Voors, C. J. Petrie, M. C. Petrie, A. Charlesworth, H. L. Hillege, F. Zijlstra, J. J. McMurray, and D. J. van Veldhuisen Low pulse pressure is independently related to elevated natriuretic peptides and increased mortality in advanced chronic heart failure Eur. Heart J., September 1, 2005; 26(17): 1759 - 1764. [Abstract] [Full Text] [PDF]
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C. Williams, B. A Kingwell, K. Burke, J. McPherson, and A. M Dart Folic acid supplementation for 3 wk reduces pulse pressure and large artery stiffness independent of MTHFR genotype Am. J. Clinical Nutrition, July 1, 2005; 82(1): 26 - 31. [Abstract] [Full Text] [PDF]
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F. Verbeke, P. Segers, S. Heireman, R. Vanholder, P. Verdonck, and L. M. Van Bortel Noninvasive Assessment of Local Pulse Pressure: Importance of Brachial-to-Radial Pressure Amplification Hypertension, July 1, 2005; 46(1): 244 - 248. [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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C. Vlachopoulos, D. Panagiotakos, N. Ioakeimidis, I. Dima, and C. Stefanadis Chronic coffee consumption has a detrimental effect on aortic stiffness and wave reflections Am. J. Clinical Nutrition, June 1, 2005; 81(6): 1307 - 1312. [Abstract] [Full Text] [PDF]
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 H. O. Ventura and M. R. Mehra The Interaction of Vascular Stiffness and Cardiovascular Events in Women: Insights From the Heart and Estrogen/Progestin Replacement Study Chest, May 1, 2005; 127(5): 1477 - 1480. [Full Text] [PDF]
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S. J. Zieman, V. Melenovsky, and D. A. Kass Mechanisms, Pathophysiology, and Therapy of Arterial Stiffness Arterioscler Thromb Vasc Biol, May 1, 2005; 25(5): 932 - 943. [Abstract] [Full Text] [PDF]
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J. A. Chirinos, J. P. Zambrano, S. Chakko, A. Veerani, A. Schob, H. J. Willens, G. Perez, and A. J. Mendez Aortic Pressure Augmentation Predicts Adverse Cardiovascular Events in Patients With Established Coronary Artery Disease Hypertension, May 1, 2005; 45(5): 980 - 985. [Abstract] [Full Text] [PDF]
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J. C. Verhave, P. Fesler, G. du Cailar, J. Ribstein, M. E. Safar, and A. Mimran Elevated Pulse Pressure Is Associated With Low Renal Function in Elderly Patients With Isolated Systolic Hypertension Hypertension, April 1, 2005; 45(4): 586 - 591. [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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 C. Vlachopoulos, F. Kosmopoulou, D. Panagiotakos, N. Ioakeimidis, N. Alexopoulos, C. Pitsavos, and C. Stefanadis Smoking and caffeine have a synergistic detrimental effect on aortic stiffness and wave reflections J. Am. Coll. Cardiol., November 2, 2004; 44(9): 1911 - 1917. [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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S. Mustata, C. Chan, V. Lai, and J. A. Miller Impact of an Exercise Program on Arterial Stiffness and Insulin Resistance in Hemodialysis Patients J. Am. Soc. Nephrol., October 1, 2004; 15(10): 2713 - 2718. [Abstract] [Full Text] [PDF]
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T. L. Medley, T. J. Cole, A. M. Dart, C. D. Gatzka, and B. A. Kingwell Matrix Metalloproteinase-9 Genotype Influences Large Artery Stiffness Through Effects on Aortic Gene and Protein Expression Arterioscler Thromb Vasc Biol, August 1, 2004; 24(8): 1479 - 1484. [Abstract] [Full Text] [PDF]
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J. N. Cohn, A. A. Quyyumi, N. K. Hollenberg, and K. A. Jamerson Surrogate Markers for Cardiovascular Disease: Functional Markers Circulation, June 29, 2004; 109(25_suppl_1): IV-31 - IV-46. [Full Text] [PDF]
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X.-F. Zhang, J. Attia, C. D'Este, and X.-H. Yu Prevalence and Magnitude of Classical Risk Factors for Stroke in a Cohort of 5092 Chinese Steelworkers Over 13.5 Years of Follow-up Stroke, May 1, 2004; 35(5): 1052 - 1056. [Abstract] [Full Text] [PDF]
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M. Domanski and M. Proschan The metabolic syndrome J. Am. Coll. Cardiol., April 21, 2004; 43(8): 1396 - 1398. [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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A. A. Mangoni Diastolic and Pulse Pressure: The Old and the New? Hypertension, March 1, 2004; 43(3): 531 - 532. [Full Text] [PDF]
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T. Weber, J. Auer, M. F. O'Rourke, E. Kvas, E. Lassnig, R. Berent, and B. Eber Arterial Stiffness, Wave Reflections, and the Risk of Coronary Artery Disease Circulation, January 20, 2004; 109(2): 184 - 189. [Abstract] [Full Text] [PDF]
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P. Verdecchia, F. Angeli, and R. Gattobigio Clinical Usefulness of Ambulatory Blood Pressure Monitoring J. Am. Soc. Nephrol., January 1, 2004; 15(90010): S30 - 33. [Abstract] [Full Text]
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 C. Vlachopoulos, K. Hirata, and M. F O'Rourke Effect of sildenafil on arterial stiffness and wave reflection Vascular Medicine, November 1, 2003; 8(4): 243 - 248. [Abstract] [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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J. D. Cameron, C. J. Bulpitt, E. S. Pinto, and C. Rajkumar The Aging of Elastic and Muscular Arteries: A comparison of diabetic and nondiabetic subjects Diabetes Care, July 1, 2003; 26(7): 2133 - 2138. [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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K. K. Naka, A. C. Tweddel, D. Parthimos, A. Henderson, J. Goodfellow, and M. P. Frenneaux Arterial distensibility: acute changes following dynamic exercise in normal subjects Am J Physiol Heart Circ Physiol, March 1, 2003; 284(3): H970 - H978. [Abstract] [Full Text] [PDF]
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 T. S. Hiles and P. M. Moriarty Pulse Pressure and Risk of Cardiovascular Disease JAMA, January 8, 2003; 289(2): 174 - 175. [Full Text] [PDF]
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 A. W. Haider, M. G. Larson, S. S. Franklin, and D. Levy 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, January 7, 2003; 138(1): 10 - 16. [Abstract] [Full Text] [PDF]
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J Amar, B Chamontin, J Ferrieres, N Danchin, O Grenier, C Cantet, and J-P Cambou Hypertension control at hospital discharge after acute coronary event: influence on cardiovascular prognosis--the PREVENIR study Heart, December 1, 2002; 88(6): 587 - 591. [Abstract] [Full Text] [PDF]
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J. H. Young, M. J. Klag, P. Muntner, J. L. Whyte, M. Pahor, and J. Coresh Blood Pressure and Decline in Kidney Function: Findings from the Systolic Hypertension in the Elderly Program (SHEP) J. Am. Soc. Nephrol., November 1, 2002; 13(11): 2776 - 2782. [Abstract] [Full Text] [PDF]
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R. Pini, M. C. Cavallini, F. Bencini, G. Silvestrini, E. Tonon, W. De Alfieri, N. Marchionni, M. Di Bari, R. B. Devereux, G. Masotti, et al. Cardiovascular remodeling is greater in isolated systolic hypertension than in diastolic hypertension in older adults: the Insufficienza Cardiaca negli Anziani Residenti (ICARE) a Dicomano Study J. Am. Coll. Cardiol., October 2, 2002; 40(7): 1283 - 1289. [Abstract] [Full Text] [PDF]
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 G. M. London, S. J. Marchais, A. P. Guerin, F. Metivier, and H. Adda Arterial structure and function in end-stage renal disease Nephrol. Dial. Transplant., October 1, 2002; 17(10): 1713 - 1724. [Full Text] [PDF]
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P. Henry, F. Thomas, A. Benetos, and L. Guize Impaired Fasting Glucose, Blood Pressure and Cardiovascular Disease Mortality Hypertension, October 1, 2002; 40(4): 458 - 463. [Abstract] [Full Text] [PDF]
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 R. Asmar, P. Gosse, J. Topouchian, G. N'tela, A. Dudley, and G. L Shepherd Effects of telmisartan on arterial stiffness in Type 2 diabetes patients with essential hypertension Journal of Renin-Angiotensin-Aldosterone System, September 1, 2002; 3(3): 176 - 180. [Abstract] [PDF]
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B. A. Kingwell, T. K. Waddell, T. L. Medley, J. D. Cameron, and A. M. Dart Large artery stiffness predicts ischemic threshold in patients with coronary artery disease J. Am. Coll. Cardiol., August 21, 2002; 40(4): 773 - 779. [Abstract] [Full Text] [PDF]
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D. Goldsmith, R. MacGinley, A. Smith, and A. Covic How important and how treatable is vascular stiffness as a cardiovascular risk factor in renal failure? Nephrol. Dial. Transplant., June 1, 2002; 17(6): 965 - 969. [Full Text] [PDF]
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J. R Chiong and A. B Miller Review: Renin-angiotensin system antagonism and lipid-lowering therapy in cardiovascular risk management Journal of Renin-Angiotensin-Aldosterone System, June 1, 2002; 3(2): 96 - 102. [Abstract] [PDF]
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P. Lantelme, C. Mestre, M. Lievre, A. Gressard, and H. Milon Heart Rate: An Important Confounder of Pulse Wave Velocity Assessment Hypertension, June 1, 2002; 39(6): 1083 - 1087. [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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C. Dekkers, F. A. Treiber, G. Kapuku, E. J.C.G. van den Oord, and H. Snieder Growth of Left Ventricular Mass in African American and European American Youth Hypertension, May 1, 2002; 39(5): 943 - 951. [Abstract] [Full Text] [PDF]
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T. S. Manning, B. E. Shykoff, and J. L. Izzo Jr Validity and Reliability of Diastolic Pulse Contour Analysis (Windkessel Model) in Humans Hypertension, May 1, 2002; 39(5): 963 - 968. [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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G. Bobrie and J. F Potter The elderly hypertensive population: what lies ahead of us? Journal of Renin-Angiotensin-Aldosterone System, March 1, 2002; 3(1_suppl): S4 - S9. [PDF]
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J. Blacher and M. Safar Specific aspects of high blood pressure in the elderly Journal of Renin-Angiotensin-Aldosterone System, March 1, 2002; 3(1_suppl): S10 - S15. [PDF]
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 I.S. Mackenzie, I.B. Wilkinson, and J.R. Cockcroft Assessment of arterial stiffness in clinical practice QJM, February 1, 2002; 95(2): 67 - 74. [Full Text] [PDF]
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J. L. Abramson, W. S. Weintraub, and V. Vaccarino Association Between Pulse Pressure and C-Reactive Protein Among Apparently Healthy US Adults Hypertension, February 1, 2002; 39(2): 197 - 202. [Abstract] [Full Text] [PDF]
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 E. Nicolaides and C. J. Jones Review: Type 2 diabetes -- implications for macrovascular mechanics and disease The British Journal of Diabetes & Vascular Disease, January 1, 2002; 2(1): 9 - 12. [Abstract] [PDF]
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P. Boutouyrie, A. I. Tropeano, R. Asmar, I. Gautier, A. Benetos, P. Lacolley, and S. Laurent Aortic Stiffness Is an Independent Predictor of Primary Coronary Events in Hypertensive Patients: A Longitudinal Study Hypertension, January 1, 2002; 39(1): 10 - 15. [Abstract] [Full Text] [PDF]
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 M. ZUREIK, A. BENETOS, C. NEUKIRCH, D. COURBON, K. BEAN, F. THOMAS, and P. DUCIMETIERE Reduced Pulmonary Function Is Associated with Central Arterial Stiffness in Men Am. J. Respir. Crit. Care Med., December 15, 2001; 164(12): 2181 - 2185. [Abstract] [Full Text] [PDF]
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G. M. London, B. Pannier, A. P. Guerin, J. Blacher, S. J. Marchais, B. Darne, F. Metivier, H. Adda, and M. E. Safar Alterations of Left Ventricular Hypertrophy in and Survival of Patients Receiving Hemodialysis: Follow-up of an Interventional Study J. Am. Soc. Nephrol., December 1, 2001; 12(12): 2759 - 2767. [Abstract] [Full Text] [PDF]
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C. Vlachopoulos, K. Hirata, and M. F. O'Rourke Pressure-Altering Agents Affect Central Aortic Pressures More Than Is Apparent From Upper Limb Measurements in Hypertensive Patients: The Role of Arterial Wave Reflections Hypertension, December 1, 2001; 38(6): 1456 - 1460. [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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J. L. Izzo Jr, T. S. Manning, and B. E. Shykoff Office Blood Pressures, Arterial Compliance Characteristics, and Estimated Cardiac Load Hypertension, December 1, 2001; 38(6): 1467 - 1470. [Abstract] [Full Text] [PDF]
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 J. Westerbacka, A. Seppala-Lindroos, and H. Yki-Jarvinen Resistance to Acute Insulin Induced Decreases in Large Artery Stiffness Accompanies the Insulin Resistance Syndrome J. Clin. Endocrinol. Metab., November 1, 2001; 86(11): 5262 - 5268. [Abstract] [Full Text] [PDF]
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T. SHOJI, M. EMOTO, K. SHINOHARA, R. KAKIYA, Y. TSUJIMOTO, H. KISHIMOTO, E. ISHIMURA, T. TABATA, and Y. NISHIZAWA Diabetes Mellitus, Aortic Stiffness, and Cardiovascular Mortality in End-Stage Renal Disease J. Am. Soc. Nephrol., October 1, 2001; 12(10): 2117 - 2124. [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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L. M.A.B. Van Bortel, H. A.J. Struijker-Boudier, and M. E. Safar Pulse Pressure, Arterial Stiffness, and Drug Treatment of Hypertension Hypertension, October 1, 2001; 38(4): 914 - 921. [Abstract] [Full Text] [PDF]
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T. K. Waddell, A. M. Dart, T. L. Medley, J. D. Cameron, and B. A. Kingwell Carotid Pressure Is a Better Predictor of Coronary Artery Disease Severity Than Brachial Pressure Hypertension, October 1, 2001; 38(4): 927 - 931. [Abstract] [Full Text] [PDF]
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W. C. Cushman, B. J. Materson, D. W. Williams, and D. J. Reda Pulse Pressure Changes With Six Classes of Antihypertensive Agents in a Randomized, Controlled Trial Hypertension, October 1, 2001; 38(4): 953 - 957. [Abstract] [Full Text] [PDF]
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G. M. London, J. Blacher, B. Pannier, A. P. Guerin, S. J. Marchais, and M. E. Safar Arterial Wave Reflections and Survival in End-Stage Renal Failure Hypertension, September 1, 2001; 38(3): 434 - 438. [Abstract] [Full Text] [PDF]
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C. Labat, P. Lacolley, M. Lajemi, M. de Gasparo, M. E. Safar, and A. Benetos Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet Hypertension, September 1, 2001; 38(3): 439 - 443. [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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E.-R. Rietzschel, E. Boeykens, M. L. De Buyzere, D. A. Duprez, and D. L. Clement A Comparison Between Systolic and Diastolic Pulse Contour Analysis in the Evaluation of Arterial Stiffness Hypertension, June 1, 2001; 37 (6): e15 - e22. [Abstract] [Full Text] [PDF]
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P. Verdecchia, G. Schillaci, G. Reboldi, S. S. Franklin, and C. Porcellati Different Prognostic Impact of 24-Hour Mean Blood Pressure and Pulse Pressure on Stroke and Coronary Artery Disease in Essential Hypertension Circulation, May 29, 2001; 103(21): 2579 - 2584. [Abstract] [Full Text] [PDF]
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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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