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(Circulation. 2001;103:1245.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Does the Relation of Blood Pressure to Coronary Heart Disease Risk Change With Aging?
The Framingham Heart Study
From the Preventive Cardiology Program, University of California, Irvine (S.S.F., S.A.K., N.D.W.); National Heart, Lung and Blood Institute’s Framingham Heart Study, Framingham, Mass (M.G.L., E.P.L., D.L.); National Heart, Lung and Blood Institute, Bethesda, Md (D.L.); and Department of Epidemiology and Biostatistics, Boston University School of Medicine, Boston, Mass (E.P.L).
Correspondence to Dr Stanley S. Franklin, UCI Heart Disease Prevention Program, C240 Medical Sciences, University of California, Irvine, CA 92697. E-mail sfrankln{at}ucla.edu
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Abstract |
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 Top Abstract IntroductionMethodsResultsDiscussionReferences |
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Background—We examined the relative importance of diastolic (DBP), systolic (SBP) and pulse pressure (PP) as predictors of coronary heart disease (CHD) risk in different age groups of Framingham Heart Study participants.
Methods and Results—We studied 3060 men and 3479 women between 20 and 79 years of age who were free of CHD and were not on antihypertensive drug therapy at baseline. Cox regression adjusted for age, sex, and other risk factors was used to assess the relations of BP indexes to CHD risk over a 20-year follow-up. In the group <50 years of age, DBP was the strongest predictor of CHD risk (hazard ratio [HR] per 10 mm Hg increment, 1.34; 95% CI, 1.18 to 1.51) rather than SBP (HR, 1.14; 95% CI, 1.06 to 1.24) or PP (HR, 1.02; 95% CI, 0.89 to 1.17). In the group 50 to 59 years of age, risks were comparable for all 3 BP indexes. In the older age group, the strongest predictor of CHD risk was PP (HR, 1.24; 95% CI, 1.16 to 1.33). When both SBP and DBP were considered jointly, the former was directly and the latter was inversely related to CHD risk in the oldest age group
Conclusions—With increasing age, there was a gradual shift from DBP to SBP and then to PP as predictors of CHD risk. In patients <50 years of age, DBP was the strongest predictor. Age 50 to 59 years was a transition period when all 3 BP indexes were comparable predictors, and from 60 years of age on, DBP was negatively related to CHD risk so that PP became superior to SBP.
Key Words: blood pressure • hypertension • pulse pressure • coronary disease
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Despite the acknowledged importance of hypertension as a precursor of cardiovascular complications, considerable uncertainty still exists regarding the relative importance of the various components of blood pressure (BP) in predicting cardiovascular disease risk. Since the introduction of the sphygmomanometer at the beginning of the 20th century, the relative importance of diastolic (DBP), systolic (SBP) and pulse pressure (PP) as indicators of hypertensive cardiovascular disease risk has undergone several changes. Initially, DBP was thought to be the best measure of risk,1 2 but in 1971, Kannel et al,3 using early follow-up from the Framingham Heart Study, concluded, "There was a trend of declining relative importance of DBP with a corresponding increase in the importance of SBP with advancing age" as predictors of coronary heart disease (CHD) risk.3 This publication, confirmed subsequently by other studies,4 5 6 has been influential in gradually shaping medical opinion that SBP, in addition to DBP, is a more powerful predictor of CHD risk. Subsequent national7 8 and international9 guidelines for the classification of BP and for the diagnosis and management of hypertension have defined cardiovascular disease risk by the elevation of DBP and/or SBP, with the higher of the 2 establishing severity.
More recently, the relative importance of BP indexes as predictors of CHD risk was reexamined in the original Framingham cohort, with longer follow-up than in the 1971 study and with the use of newer techniques of multivariate Cox regression to eliminate confounding.10 After adjustment for age, sex, and other risk factors, PP was found to be a robust predictor of CHD events10 ; others11 12 13 have noted similar findings. That recent study10 was limited to Framingham subjects between 50 and 79 years of age; the question of which BP component or components best predict CHD risk across a wide age range has not been fully evaluated.
In the present study, we extended the age range of study subjects by combining the original Framingham Heart Study cohort with the Framingham Offspring Study cohort14 ; this provided an age distribution of 20 to 79 years. Furthermore, by combining both Framingham cohorts, the study sample was more than tripled and the number of CHD events was almost doubled compared with our recent publication.10 The goal of the present study was to define the roles of SBP, DBP, and PP as predictors of CHD risk in different age groups.
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Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Overview
The Framingham Heart Study began in 1948 with the enrollment of 5209 men and women, 28 to 62 years of age at entry, with subjects undergoing repeated examinations biennially.15 16 In 1971, 5124 men and women were enrolled in the Framingham Offspring Study14 ; these were the children or the spouses of the children of the original Framingham Heart Study participants. They underwent repeated examinations approximately every 4 years. Each examination included an extensive cardiovascular disease history and physical examination, 12-lead ECG, and various blood chemistries. Morbidity and mortality were continuously monitored by clinic examinations, hospital surveillance, and communication with participants who did not attend a clinic examination. A panel of 3 experienced investigators reviewed all new cardiovascular events. Detailed descriptions of study design have been published elsewhere.16 17
Study Sample
This investigation comprised 2033 subjects from the
original Framingham Heart Study cohort, as described in a previous
publication,10 and 4506
subjects from the Framingham Offspring Study. Baseline examinations for
subjects from the original Framingham Heart cohort were the earliest
examination at which HDL cholesterol was measured; usually this was the
11th biennial examination, but for some it was the 10th or 12th. The
baseline examination for subjects from the Framingham Offspring Study
was the first examination cycle. Study subjects in the original cohort
were between 50 and 79 years of age at baseline to be eligible, and
subjects from the offspring cohort were between 20 and 70 years of age
at baseline. All subjects had no history or clinical evidence of CHD,
and they were not receiving antihypertensive medication at their
baseline examinations. Diabetes mellitus was defined as the presence of
2 casual blood glucose levels of 
150 mg/dL and/or hypoglycemic
medication in the original cohort; the definition was fasting blood
glucose of 140 mg/dL and/or hypoglycemic medication in the offspring
cohort.
BP Measurement
SBP and DBP readings were taken in the supported left
arm of the resting seated subject, 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 were
based on the average of 2 separate measurements taken by the examining
physician.
End Points
The primary end point was incident CHD (fatal or
nonfatal). A subject was considered to have incident CHD if he or she
fulfilled published
criteria17 for angina
pectoris, coronary insufficiency (angina pectoris lasting 20 minutes
and accompanied by ischemic ECG changes), myocardial infarction
(recognized and unrecognized), or death resulting from CHD occurring
after the baseline examination. In addition, secondary analyses were
done for hard CHD end points, which consisted of recognized myocardial
infarction, coronary insufficiency, or death resulting from CHD.
Follow-up time was defined as the time 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 in
the original cohort, and up to the 5th examination cycle in the
offspring cohort.
Data Analysis
The relations of CHD hazard ratios (HRs) to single
(SBP, DBP, or PP) and dual (SBP and DBP) BP components as continuous
variables were evaluated by Cox proportional-hazards
regression18 separately for
the 3 age groups (<50, 50 to 59, and 60 years). HRs were estimated,
along with 95% CIs, for a 10 mm Hg increase in BP. Models were
adjusted for age, sex, body mass index, cigarette smoking (yes/no),
diabetes mellitus (yes/no), and ratio of total to HDL cholesterol. SAS
statistical software (SAS Institute) was
used.19
We also assessed whether, across ages, there was
constancy of the risk contributed by SBP relative to DBP. Cox models
with both SBP and DBP were fitted by age groups (i=1 to 5 for groups
<40, 40 to 49, 50 to 59, 60 to 69, and 70 to 79 years of age,
respectively). The difference between SBP and DBP coefficients, ie,
i=ß(SBP)i-ß(DBP)i,
and the corresponding variance, Var(i), were
estimated for each age group. Also, the mean age for subjects in each
age group, Xi, was computed. Weighted regression
was used for the model
i=
0+1xXi,,
with weights equal to inverse variances,
Wi=1/Var(i). The test
statistic,
t=i/se(i), was
referred to as the t distribution with 3
df. Finally, a simulation
procedure was done to validate the probability value. For this, 10 000
replicates of the data were generated under the null hypothesis of no
age-related change in ß(SBP)-ß(DBP). In each replicate, Cox
models and weighted regressions were run as outlined above. Across
replicates, we counted the number of times the test statistic was
obtained as large in absolute value as found in the real
data.
In secondary analyses, we introduced a time-dependent antihypertensive treatment variable to incorporate treatment status after the baseline examination. We also tested for a difference in regression coefficients between men and women. Further analyses were performed for hard CHD end points.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Demographic and Clinical Characteristics
The sample comprised 3060 men and 3479 women (Table 1
). The mean follow-up time was 17 years,
during which 807 subjects developed CHD (532 men and 275 women). Of the
initial CHD events, 374 were angina pectoris or coronary insufficiency,
336 were myocardial infarction with survival >1 day, and 97 were CHD
deaths. Older subjects at baseline had higher ratios of total to HDL
cholesterol, higher body mass index, higher prevalence of diabetes, but
a lower rate of cigarette smoking than did younger subjects. SBP and PP
were higher in older subjects. The correlation coefficients between SBP
and DBP were r=0.79 for age
<50 years, r=0.77 for age 50
to 59 years, and r=0.61 for age
60 years.
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Single BP Component Models by Age
HRs associated with a 10 mm Hg increase in BP in the
group <50 years of age were 1.34 for DBP
(P<0.0001), 1.14 for SBP
(P=0.001), and 1.02 for PP
(P=0.79)
(Table 2). In the group 50 to 59 years of age, HRs were
comparable for all 3 indexes: SBP, 1.08
(P=0.01); DBP, 1.14
(P=0.09); and PP, 1.11
(P=0.02). In the group 60,
HRs were 1.24 for PP
(P<0.001), 1.17 for SBP
(P<0.001), and 1.12 for DBP
(P=0.08). HRs tended to
decrease with increasing age for DBP, whereas they increased with
increasing age for PP.
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Dual BP Component Models by Age
The combination of SBP and DBP in the same model is
shown in
Table 3. In the group <50 years of age, DBP was predictive
of CHD risk and SBP was not; HRs were 1.42
(P=0.001) and 0.95
(P=0.49), respectively. In the
group 50 to 59 years of age, neither SBP
(P=0.07) nor DBP
(P=0.74) predicted CHD risk,
possibly because of collinearity. In the group 60 years, the
combination of SBP (HR, 1.24;
P<0.0001) and DBP (HR, 0.83;
P=0.02) showed a modest
improvement over SBP alone.
|
Plots of ß(SBP)-ß(DBP) for the 5 age groups, along
with their 95% CIs, are shown in the
Figure.
The estimated slope per decade of age from the weighted regression
procedure was 0.29 (SE=0.046, t=6.27,
P=0.008). The validation
probability value also was 0.008 from 10 000 simulations under the
null hypothesis of no age-related slope. The differences in ß
coefficients for predicting CHD risk favored DBP over SBP in subjects
<50 years of age and SBP over DBP in patients >60 years of age, with
the transition occurring roughly between the ages of 50 and 59
years.
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Secondary Analyses
During follow-up, 1728 subjects (26.4%) began
antihypertensive treatment: 17.5% of subjects <50 years of age at
baseline, 39.4% of subjects 50 to 59 years of age, and 42.8% of
subjects 60 years. Analyses were repeated with postbaseline
antihypertensive treatment entered as a time-dependent variable.
Similar results were obtained with slight attenuation of the
coefficients and probability value for the BP variables.
Analysis by sex showed DBP predominance in predicting CHD
risk in the group <50 years of age and SBP and PP predominance in the
group 60 years of age for both sexes. There were no statistically
significant sex differences in BP coefficients in any age group for any
BP component.
The analyses for
Tables 2
and 3 were rerun with hard CHD end points, which
reduced the total end points from 807 to 505. The findings remained
generally the same: For
Table 2, each HR for hard CHD was within 10% of the
corresponding estimate for total CHD; for
Table 3, a similar pattern of HRs was observed, but with
fewer events, only 1 was significant (SBP at 60 years of age).
Finally, adjustment for heart rate in
Tables 2 and 3 had no discernible effect on BP
coefficients.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrated that with advancing age there was a gradual shift from DBP to SBP and eventually to PP as predictors of CHD risk. In patients <50 years of age, DBP was a stronger predictor of CHD risk than SBP or PP. Age 50 to 59 was a transition state when all 3 indexes were comparable, and from age 60 years on, when considered together with SBP, DBP was negatively related to CHD risk and PP emerged as the best predictor.
Hemodynamic Mechanisms of Risk
The finding that SBP and DBP both predicted CHD risk in
the group <50 years of age is consistent with increased peripheral
resistance being dominant in determining CHD risk in young
hypertensives.10 20 21 22 23
Similarly, the finding that PP and SBP dominate as predictors of CHD
risk in the group 60 years of age is consistent with large artery
stiffness contributing to CHD risk in older
hypertensives.10 20 21 22 23
The finding that DBP was a stronger predictor of CHD risk than SBP in patients <50 years of age is not consistent with increased small vessel resistance alone20 21 and therefore suggests the additional effect of pulse wave reflection on the recording of BP in the upper limb.23 24 25 In young normotensive adults, when the body is fully grown but the aorta is still very distensible, peripheral amplification of the arterial pulse wave will result in considerably higher brachial artery peak SBP compared with SBP values in the ascending aorta.23 24 25 In young adult hypertensives, however, there is a functional increase in large artery stiffness secondary to increased vascular resistance with a resulting decrease in brachial artery pulse wave amplification. This may partially offset the peripheral rise in SBP without affecting the rise in DBP; thus, peripheral DBP becomes superior to SBP as a predictor of CHD risk.
Age-related differences favoring DBP over SBP in predicting CHD risk in young adults were noted in some3 26 27 28 but not in all previous studies.29 The finding that there was a preference for DBP over SBP for the group <50 years of age in an early Framingham report3 and in the present study was confirmed in the Whitehall British male civil servants study26 and in a Norwegian study of men.27 Follow-up of middle-aged men screened for the Multiple Risk Factor Intervention Trial28 revealed a superiority of DBP for subjects 35 to 39 years of age, whereas SBP was a better predictor of CHD mortality for subjects 40 to 57 years of age. In contrast, in the Western Collaborative Study of Californian Male Employees,29 SBP was the superior predictor for men 39 to 59 years of age. The observed differences in BP predictors of CHD risk in these studies may be due to differences in population characteristics or differences in BP measurements.
Middle-Aged and Elderly Hypertensive
Subjects
With aging and the development of structural arterial
stiffening, there is a gradual reduction in peripheral
amplification.23 25
In addition, there is as an increase in amplitude and velocity of
incident waves, so left ventricular ejection becomes affected by early
wave reflection during systole rather than diastole, further increasing
aortic SBP and adding to
afterload.30 Given the same
stroke volume and ejection rate, increased central arterial stiffness
and early wave reflection will produce a higher brachial artery SBP, a
lower DBP, and a wider PP (ie, isolated systolic hypertension). The
increased CHD risk of isolated systolic hypertension may be due not
only to elevated peak SBP in the aorta (ie, increased afterload) but
also to low DBP (ie, decreased coronary blood
flow).23
Predictive Role of BP Indexes Across the
Age Spectrum
The changing contribution of SBP relative to DBP
in the diagnosis of CHD risk is continuous and graded over an extended
adult age range
(theFigure).
Because peak SBP at the ascending aorta largely determines cardiac
afterload, distortion of the peripheral SBP by wave reflection most
likely accounts for the age-related change in BP indexes that predict
CHD risk. In young hypertensive individuals, diminished peripheral
amplification of SBP by altered wave reflection results in a greater
peripheral increase in DBP than in SBP despite a parallel rise in
central SBP and DBP. Consequently, elevated peripheral DBP is superior
to SBP in predicting CHD risks. However, with age-dependent increases
in large artery stiffness, there is a narrowing of differences between
central and peripheral SBP as a result of both diminished peripheral
amplification and early wave reflection, thereby gradually improving
the utility of peripheral SBP while diminishing that of DBP in the
prediction of CHD risk. From age 60 years on, with central and
peripheral PPs approximating each other, PP becomes the dominant
predictor of CHD risk by incorporating both the positive predictive
role of SBP and the negative predictive role of
DBP.
Clinical Implications
The finding in the present study that BP measured
in young and middle-aged adults is positively related to CHD risk in
later life implies that the risk of cardiovascular disease starts early
in adult life. These findings are confirmatory of the University of
Glasgow Student Study, which showed that BPs in men at a mean age of
20.5 years—a time when most youths were not yet
hypertensive—predicted future cardiovascular
disease.31 Thus, the onset
of CHD risk begins long before middle age, and primary preventive
measures may be more effective if applied earlier in the course of the
disease.
The finding that DBP is stronger than SBP as a predictor of CHD risk in young adults, whereas the opposite is true in older persons, emphasizes the importance of the roles of both DBP and SBP in the staging of hypertension.7 9 The favoring of diastolic over systolic hypertension by earlier generations of physicians may have been due to the emphasis of hypertension as a young person’s disease.32 We must also recognize, however, that hypertension has become largely a disease of older people and that inadequate control of systolic rather than diastolic hypertension is by far the more pressing public health problem.8 Furthermore, the greatest burden of hypertension-related cardiovascular disease at present occurs in the middle-aged and elderly, in whom systolic hypertension predominates.8
Study Strengths and Limitations
This study confirms earlier findings from Framingham
and extends them to a larger, younger cohort free of clinical CHD and
not on antihypertensive therapy at baseline. There are potential
limitations regarding the interpretation of these data. Because few
women in the youngest age group subsequently developed CHD, our
findings in this group require confirmation.
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, the magnitude of coefficients for BP components was reduced slightly but did not affect the pattern of age-related indexes for predicting CHD risk.
Because the study sample consisted almost exclusively of whites, most of whom were middle class, results may not apply to other ethnic or socioeconomic groups. Indeed, there is evidence of an even greater BP-dependent increase in aortic stiffness in blacks than in whites.33 Finally, the inferences as to underlying hemodynamic mechanisms in this study are not based on direct physiological measurements. Studies now underway in Framingham and elsewhere that include pulse-wave velocity measurements and applanation tonometry for recording high-fidelity central pulse-wave forms may eventually clarify these issues.
In conclusion, aging plays an important role in influencing the relation of BP indexes to CHD risk. In patients <50 years of age, DBP is a stronger predictor of CHD risk than SBP or PP, suggesting that increased peripheral resistance and altered peripheral pulse-wave amplification are dominant in determining CHD risk. Between the ages of 50 and 59 years, all 3 BP indexes are similarly predictive of CHD risk, suggesting a balance between small vessel resistance and large artery stiffness. From age 60 years on, there is a shift in favor of PP and SBP as predictors of CHD risk, suggesting that large artery stiffness with early wave reflection are the dominant hemodynamic determinants of risk. Although DBP predominates over SBP in young adults, the greatest burden of cardiovascular disease occurs in older subjects with isolated systolic hypertension and a wide PP.
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Acknowledgments |
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The Framingham Heart Study is funded by NIH/NHLBI contract NO1-HC- 38038. This project was supported in part by an educational grant from Bristol-Myers Squibb Company, Princeton, NJ.
Received September 8, 2000; revision received November 10, 2000; accepted November 14, 2000.
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 R. B. Goldberg, M. Temprosa, S. Haffner, T. J. Orchard, R. E. Ratner, S. E. Fowler, K. Mather, S. Marcovina, C. Saudek, M. J. Matulik, et al. Effect of Progression From Impaired Glucose Tolerance to Diabetes on Cardiovascular Risk Factors and Its Amelioration by Lifestyle and Metformin Intervention: The Diabetes Prevention Program randomized trial by the Diabetes Prevention Program Research Group Diabetes Care, April 1, 2009; 32(4): 726 - 732. [Abstract] [Full Text] [PDF]
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 R. Agarwal Blood Pressure Components and the Risk for End-Stage Renal Disease and Death in Chronic Kidney Disease Clin. J. Am. Soc. Nephrol., April 1, 2009; 4(4): 830 - 837. [Abstract] [Full Text] [PDF]
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 J. A. Chirinos, S. S. Franklin, R. R. Townsend, and L. Raij Body Mass Index and Hypertension Hemodynamic Subtypes in the Adult US Population Arch Intern Med, March 23, 2009; 169(6): 580 - 586. [Abstract] [Full Text] [PDF]
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 W. Fang, X. Yang, J. M. Bargman, and D. G. Oreopoulos ASSOCIATION BETWEEN PULSE PRESSURE AND MORTALITY IN PATIENTS UNDERGOING PERITONEAL DIALYSIS Perit. Dial. Int., March 1, 2009; 29(2): 163 - 170. [Abstract] [Full Text] [PDF]
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 T. Adragao, A. Pires, R. Birne, J. D. Curto, C. Lucas, M. Goncalves, and A. P. Negrao A plain X-ray vascular calcification score is associated with arterial stiffness and mortality in dialysis patients Nephrol. Dial. Transplant., March 1, 2009; 24(3): 997 - 1002. [Abstract] [Full Text] [PDF]
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 G. Schillaci, M. Pirro, and E. Mannarino Assessing Cardiovascular Risk: Should We Discard Diastolic Blood Pressure? Circulation, January 20, 2009; 119(2): 210 - 212. [Full Text] [PDF]
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S. S. Franklin, V. A. Lopez, N. D. Wong, G. F. Mitchell, M. G. Larson, R. S. Vasan, and D. Levy Single Versus Combined Blood Pressure Components and Risk for Cardiovascular Disease: The Framingham Heart Study Circulation, January 20, 2009; 119(2): 243 - 250. [Abstract] [Full Text] [PDF]
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 M. L. Fontes, S. Aronson, J. P. Mathew, Y. Miao, B. Drenger, P. G. Barash, D. T. Mangano, For the Multicenter Study of Perioperative Ischemi, and the Ischemia Research and Education Foundation (IR Pulse Pressure and Risk of Adverse Outcome in Coronary Bypass Surgery Anesth. Analg., October 1, 2008; 107(4): 1122 - 1129. [Abstract] [Full Text] [PDF]
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E. Ingelsson, P. Gona, M. G. Larson, D. M. Lloyd-Jones, W. B. Kannel, R. S. Vasan, and D. Levy Altered Blood Pressure Progression in the Community and Its Relation to Clinical Events Arch Intern Med, July 14, 2008; 168(13): 1450 - 1457. [Abstract] [Full Text] [PDF]
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M. Coylewright, J. F. Reckelhoff, and P. Ouyang Menopause and Hypertension: An Age-Old Debate Hypertension, April 1, 2008; 51(4): 952 - 959. [Full Text] [PDF]
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P. Jankowski, K. Kawecka-Jaszcz, D. Czarnecka, M. Brzozowska-Kiszka, K. Styczkiewicz, M. Loster, M. Kloch-Badelek, J. Wilinski, A. M. Curylo, D. Dudek, et al. Pulsatile but Not Steady Component of Blood Pressure Predicts Cardiovascular Events in Coronary Patients Hypertension, April 1, 2008; 51(4): 848 - 855. [Abstract] [Full Text] [PDF]
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 M. L. Burr, E. Dolan, E. W. O'Brien, E. T. O'Brien, and P. McCormack The value of ambulatory blood pressure in older adults: the Dublin outcome study Age Ageing, March 1, 2008; 37(2): 201 - 206. [Abstract] [Full Text] [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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 A. Coca, F. H. Messerli, A. Benetos, Q. Zhou, A. Champion, R. M. Cooper-DeHoff, and C. J. Pepine Predicting Stroke Risk in Hypertensive Patients With Coronary Artery Disease: A Report From the INVEST Stroke, February 1, 2008; 39(2): 343 - 348. [Abstract] [Full Text] [PDF]
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C. Rosendorff, H. R. Black, C. P. Cannon, B. J. Gersh, J. Gore, J. L. Izzo Jr, N. M. Kaplan, C. M. O'Connor, P. T. O'Gara, and S. Oparil REPRINT Treatment of Hypertension in the Prevention and Management of Ischemic Heart Disease: A Scientific Statement From the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention Hypertension, August 1, 2007; 50(2): e28 - e55. [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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S. M.L. Wallace, Yasmin, C. M. McEniery, K. M. Maki-Petaja, A. D. Booth, J. R. Cockcroft, and I. B. Wilkinson Isolated Systolic Hypertension Is Characterized by Increased Aortic Stiffness and Endothelial Dysfunction Hypertension, July 1, 2007; 50(1): 228 - 233. [Abstract] [Full Text] [PDF]
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A. D. Protogerou, M. E. Safar, P. Iaria, H. Safar, K. Le Dudal, J. Filipovsky, O. Henry, P. Ducimetiere, and J. Blacher Diastolic Blood Pressure and Mortality in the Elderly With Cardiovascular Disease Hypertension, July 1, 2007; 50(1): 172 - 180. [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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C. Rosendorff, H. R. Black, C. P. Cannon, B. J. Gersh, J. Gore, J. L. Izzo Jr, N. M. Kaplan, C. M. O'Connor, P. T. O'Gara, and S. Oparil Treatment of Hypertension in the Prevention and Management of Ischemic Heart Disease: A Scientific Statement From the American Heart Association Council for High Blood Pressure Research and the Councils on Clinical Cardiology and Epidemiology and Prevention Circulation, May 29, 2007; 115(21): 2761 - 2788. [Full Text] [PDF]
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S. Javaheri, R. Shukla, H. Zeigler, and L. Wexler Central Sleep Apnea, Right Ventricular Dysfunction, and Low Diastolic Blood Pressure Are Predictors of Mortality in Systolic Heart Failure J. Am. Coll. Cardiol., May 22, 2007; 49(20): 2028 - 2034. [Abstract] [Full Text] [PDF]
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 S. Riou, B. Mees, B. Esposito, R. Merval, J. Vilar, D. Stengel, E. Ninio, R. van Haperen, R. de Crom, A. Tedgui, et al. High Pressure Promotes Monocyte Adhesion to the Vascular Wall Circ. Res., April 27, 2007; 100(8): 1226 - 1233. [Abstract] [Full Text] [PDF]
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 G. Fernandez-Fresnedo, E. Rodrigo, A. L. M. de Francisco, S. S. de Castro, O. Castaneda, and M. Arias Role of Pulse Pressure on Cardiovascular Risk in Chronic Kidney Disease Patients J. Am. Soc. Nephrol., December 1, 2006; 17(12_suppl_3): S246 - S249. [Abstract] [Full Text] [PDF]
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B. Llamas, C. Lau, W. A. Cupples, M.-L. Rainville, E. Souzeau, and C. F. Deschepper Genetic Determinants of Systolic and Pulse Pressure in an Intercross Between Normotensive Inbred Rats Hypertension, November 1, 2006; 48(5): 921 - 926. [Abstract] [Full Text] [PDF]
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I. Sipahi, E. M. Tuzcu, P. Schoenhagen, K. E. Wolski, S. J. Nicholls, C. Balog, T. D. Crowe, and S. E. Nissen Effects of Normal, Pre-Hypertensive, and Hypertensive Blood Pressure Levels on Progression of Coronary Atherosclerosis J. Am. Coll. Cardiol., August 15, 2006; 48(4): 833 - 838. [Abstract] [Full Text] [PDF]
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 M. F. O'Rourke and J. B. Seward Central Arterial Pressure and Arterial Pressure Pulse: New Views Entering the Second Century After Korotkov Mayo Clin. Proc., August 1, 2006; 81(8): 1057 - 1068. [Abstract] [Full Text] [PDF]
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W. Palmas, A. Moran, T. Pickering, J. P. Eimicke, J. Teresi, J. E. Schwartz, L. Field, R. S. Weinstock, and S. Shea Ambulatory Pulse Pressure and Progression of Urinary Albumin Excretion in Older Patients With Type 2 Diabetes Mellitus Hypertension, August 1, 2006; 48(2): 301 - 308. [Abstract] [Full Text] [PDF]
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 A. Stang, S. Moebus, S. Mohlenkamp, N. Dragano, A. Schmermund, E.-M. Beck, J. Siegrist, R. Erbel, K.-H. Jockel, and on behalf of the Heinz Nixdorf Recall Study Invest Algorithms for Converting Random-Zero to Automated Oscillometric Blood Pressure Values, and Vice Versa Am. J. Epidemiol., July 1, 2006; 164(1): 85 - 94. [Abstract] [Full Text] [PDF]
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P Collins Risk factors for cardiovascular disease and hormone therapy in women Heart, May 1, 2006; 92(suppl_3): iii24 - iii28. [Full Text] [PDF]
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A. M. Dart, C. D. Gatzka, B. A. Kingwell, K. Willson, J. D. Cameron, Y.-L. Liang, K. L. Berry, L. M.H. Wing, C. M. Reid, P. Ryan, et al. Brachial Blood Pressure But Not Carotid Arterial Waveforms Predict Cardiovascular Events in Elderly Female Hypertensives Hypertension, April 1, 2006; 47(4): 785 - 790. [Abstract] [Full Text] [PDF]
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E. Dolan, L. Thijs, Y. Li, N. Atkins, P. McCormack, S. McClory, E. O'Brien, J. A. Staessen, and A. V. Stanton Ambulatory Arterial Stiffness Index as a Predictor of Cardiovascular Mortality in the Dublin Outcome Study Hypertension, March 1, 2006; 47(3): 365 - 370. [Abstract] [Full Text] [PDF]
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A. Benetos and P. Lacolley From 24-Hour Blood Pressure Measurements to Arterial Stiffness: A Valid Short Cut? Hypertension, March 1, 2006; 47(3): 327 - 328. [Full Text] [PDF]
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G. L. Gierach, B. D. Johnson, C. N. Bairey Merz, S. F. Kelsey, V. Bittner, M. B. Olson, L. J. Shaw, S. Mankad, C. J. Pepine, S. E. Reis, et al. Hypertension, Menopause, and Coronary Artery Disease Risk in the Women's Ischemia Syndrome Evaluation (WISE) Study J. Am. Coll. Cardiol., February 7, 2006; 47(3_Suppl_S): S50 - S58. [Abstract] [Full Text] [PDF]
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F. U.S. Mattace-Raso, T. J.M. van der Cammen, A. Hofman, N. M. van Popele, M. L. Bos, M. A.D.H. Schalekamp, R. Asmar, R. S. Reneman, A. P.G. Hoeks, M. M.B. Breteler, et al. Arterial Stiffness and Risk of Coronary Heart Disease and Stroke: The Rotterdam Study Circulation, February 7, 2006; 113(5): 657 - 663. [Abstract] [Full Text] [PDF]
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T. Willum Hansen, J. A. Staessen, C. Torp-Pedersen, S. Rasmussen, L. Thijs, H. Ibsen, and J. Jeppesen Prognostic Value of Aortic Pulse Wave Velocity as Index of Arterial Stiffness in the General Population Circulation, February 7, 2006; 113(5): 664 - 670. [Abstract] [Full Text] [PDF]
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M. H. Freitag, R. Peila, K. Masaki, H. Petrovitch, G. W. Ross, L. R. White, and L. J. Launer Midlife Pulse Pressure and Incidence of Dementia: The Honolulu-Asia Aging Study Stroke, January 1, 2006; 37(1): 33 - 37. [Abstract] [Full Text] [PDF]
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 J M Gonzalez-Clemente, G Gimenez-Perez, C Richart, M Broch, A Caixas, A Megia, O Gimenez-Palop, I Simon, D Mauricio, and J Vendrell The tumour necrosis factor (TNF)-{alpha} system is activated in accordance with pulse pressure in normotensive subjects with type 1 diabetes mellitus Eur. J. Endocrinol., November 1, 2005; 153(5): 687 - 691. [Abstract] [Full Text] [PDF]
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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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 K. Okazaki, K.-i. Iwasaki, A. Prasad, M. D. Palmer, E. R. Martini, Q. Fu, A. Arbab-Zadeh, R. Zhang, and B. D. Levine Dose-response relationship of endurance training for autonomic circulatory control in healthy seniors J Appl Physiol, September 1, 2005; 99(3): 1041 - 1049. [Abstract] [Full Text] [PDF]
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 J. M. Seubert, F. Xu, J. P. Graves, J. B. Collins, S. O. Sieber, R. S. Paules, D. L. Kroetz, and D. C. Zeldin Differential renal gene expression in prehypertensive and hypertensive spontaneously hypertensive rats Am J Physiol Renal Physiol, September 1, 2005; 289(3): F552 - F561. [Abstract] [Full Text] [PDF]
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F. J. He, N. D. Markandu, and G. A. MacGregor Modest Salt Reduction Lowers Blood Pressure in Isolated Systolic Hypertension and Combined Hypertension Hypertension, July 1, 2005; 46(1): 66 - 70. [Abstract] [Full Text] [PDF]
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Y. Ichigi, H. Takano, K. Umetani, K. Kawabata, J.-e. Obata, Y. Kitta, Y. Kodama, A. Mende, T. Nakamura, D. Fujioka, et al. Increased Ambulatory Pulse Pressure Is a Strong Risk Factor for Coronary Endothelial Vasomotor Dysfunction J. Am. Coll. Cardiol., May 3, 2005; 45(9): 1461 - 1466. [Abstract] [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.-G. Wang, J. A. Staessen, S. S. Franklin, R. Fagard, and F. Gueyffier Systolic and Diastolic Blood Pressure Lowering as Determinants of Cardiovascular Outcome Hypertension, May 1, 2005; 45(5): 907 - 913. [Abstract] [Full Text] [PDF]
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R. Boynton-Jarrett, J. Rich-Edwards, S. Malspeis, S. A. Missmer, and R. Wright A Prospective Study of Hypertension and Risk of Uterine Leiomyomata Am. J. Epidemiol., April 1, 2005; 161(7): 628 - 638. [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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T. W. Hansen, J. Jeppesen, S. Rasmussen, H. Ibsen, and C. Torp-Pedersen Ambulatory Blood Pressure and Mortality: A Population-Based Study Hypertension, April 1, 2005; 45(4): 499 - 504. [Abstract] [Full Text] [PDF]
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T. G. Pickering, J. E. Hall, L. J. Appel, B. E. Falkner, J. Graves, M. N. Hill, D. W. Jones, T. Kurtz, S. G. Sheps, and E. J. Roccella Recommendations for Blood Pressure Measurement in Humans and Experimental Animals: Part 1: Blood Pressure Measurement in Humans: A Statement for Professionals From the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research Circulation, February 8, 2005; 111(5): 697 - 716. [Abstract] [Full Text] [PDF]
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T. G. Pickering, J. E. Hall, L. J. Appel, B. E. Falkner, J. Graves, M. N. Hill, D. W. Jones, T. Kurtz, S. G. Sheps, and E. J. Roccella Recommendations for Blood Pressure Measurement in Humans and Experimental Animals: Part 1: Blood Pressure Measurement in Humans: A Statement for Professionals From the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research Hypertension, January 1, 2005; 45(1): 142 - 161. [Abstract] [Full Text] [PDF]
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I. Karp, M. Abrahamowicz, G. Bartlett, and L. Pilote Updated Risk Factor Values and the Ability of the Multivariable Risk Score to Predict Coronary Heart Disease Am. J. Epidemiol., October 1, 2004; 160(7): 707 - 716. [Abstract] [Full Text] [PDF]
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M. Ronnback, J. Fagerudd, C. Forsblom, K. Pettersson-Fernholm, A. Reunanen, P.-H. Groop, and on behalf of the Finnish Diabetic Nephropathy Stu Altered Age-Related Blood Pressure Pattern in Type 1 Diabetes Circulation, August 31, 2004; 110(9): 1076 - 1082. [Abstract] [Full Text] [PDF]
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V. Franco, S. Oparil, and O. A. Carretero Hypertensive Therapy: Part I Circulation, June 22, 2004; 109(24): 2953 - 2958. [Full Text] [PDF]
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A. Taguchi, M. Sanada, Y. Suei, M. Ohtsuka, K. Lee, K. Tanimoto, M. Tsuda, K. Ohama, M. Yoshizumi, and Y. Higashi Tooth Loss Is Associated With an Increased Risk of Hypertension in Postmenopausal Women Hypertension, June 1, 2004; 43(6): 1297 - 1300. [Abstract] [Full Text] [PDF]
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 R. H. Samson Hypertension and the Vascular Patient Vascular and Endovascular Surgery, March 1, 2004; 38(2): 103 - 119. [Abstract] [PDF]
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 J. A. Staessen, E. Den Hond, H. Celis, R. Fagard, L. Keary, G. Vandenhoven, and E. T. O'Brien Antihypertensive Treatment Based on Blood Pressure Measurement at Home or in the Physician's Office: A Randomized Controlled Trial JAMA, February 25, 2004; 291(8): 955 - 964. [Abstract] [Full Text] [PDF]
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P. J. O'Connor Overcome Clinical Inertia to Control Systolic Blood Pressure Arch Intern Med, December 8, 2003; 163(22): 2677 - 2678. [Full Text] [PDF]
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A. V. Chobanian, G. L. Bakris, H. R. Black, W. C. Cushman, L. A. Green, J. L. Izzo Jr, D. W. Jones, B. J. Materson, S. Oparil, J. T. Wright Jr, et al. Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure Hypertension, December 1, 2003; 42(6): 1206 - 1252. [Abstract] [Full Text] [PDF]
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 R. Pastor-Barriuso, J. R. Banegas, J. Damian, L. J. Appel, and E. Guallar Systolic Blood Pressure, Diastolic Blood Pressure, and Pulse Pressure: An Evaluation of Their Joint Effect on Mortality Ann Intern Med, November 4, 2003; 139(9): 731 - 739. [Abstract] [Full Text] [PDF]
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 O. O. Aalami, T. D. Fang, H. M. Song, and R. P. Nacamuli Physiological Features of Aging Persons Arch Surg, October 1, 2003; 138(10): 1068 - 1076. [Full Text] [PDF]
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W. B. Kannel, R. S. Vasan, and D. Levy Is the Relation of Systolic Blood Pressure to Risk of Cardiovascular Disease Continuous and Graded, or Are There Critical Values? Hypertension, October 1, 2003; 42(4): 453 - 456. [Full Text] [PDF]
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Asia Pacific Cohort Studies Collaboration Blood Pressure Indices and Cardiovascular Disease in the Asia Pacific Region: A Pooled Analysis Hypertension, July 1, 2003; 42(1): 69 - 75. [Abstract] [Full Text] [PDF]
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C. Lenfant, A. V. Chobanian, D. W. Jones, and E. J. Roccella Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7): Resetting the Hypertension Sails Circulation, June 24, 2003; 107(24): 2993 - 2994. [Full Text] [PDF]
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C. Lenfant, A. V. Chobanian, D. W. Jones, and E. J. Roccella Seventh Report of the Joint National Committee on the Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC 7): Resetting the Hypertension Sails Hypertension, June 1, 2003; 41(6): 1178 - 1179. [Full Text] [PDF]
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J. J. Oliver and D. J. Webb Noninvasive Assessment of Arterial Stiffness and Risk of Atherosclerotic Events Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 554 - 566. [Abstract] [Full Text] [PDF]
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J. A Staessen, J.-G. Wang, and W. H Birkenhager Outcome beyond blood pressure control? Eur. Heart J., March 2, 2003; 24(6): 504 - 514. [Full Text] [PDF]
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E. G. Lakatta and D. Levy Arterial and Cardiac Aging: Major Shareholders in Cardiovascular Disease Enterprises: Part I: Aging Arteries: A "Set Up" for Vascular Disease Circulation, January 7, 2003; 107(1): 139 - 146. [Full Text] [PDF]
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C-K Wong and H D White Relation between blood pressure after an acute coronary event and subsequent cardiovascular risk Heart, December 1, 2002; 88(6): 555 - 558. [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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H. W. Hense, W. Maziak, and J. Heidrich Why is blood pressure control unsatisfactory--or is it? Nephrol. Dial. Transplant., September 1, 2002; 17(9): 1547 - 1550. [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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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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J.-H. Wu, J. Hagaman, S. Kim, R. L. Reddick, and N. Maeda Aortic Constriction Exacerbates Atherosclerosis and Induces Cardiac Dysfunction in Mice Lacking Apolipoprotein E Arterioscler Thromb Vasc Biol, March 1, 2002; 22(3): 469 - 475. [Abstract] [Full Text] [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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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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S. S. Franklin, N. D. Wong, M. G. Larson, W. B. Kannel, D. Levy, P. Greenland, A. R. Dyer, J. Stamler, and K. Miura How Important Is Pulse Pressure as a Predictor of Cardiovascular Risk? * Response Hypertension, February 1, 2002; 39 (2): e12 - e13. [Full Text] [PDF]
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R. S. Vasan, J. M. Massaro, P. W.F. Wilson, S. Seshadri, P. A. Wolf, D. Levy, and R. B. D'Agostino Antecedent Blood Pressure and Risk of Cardiovascular Disease: The Framingham Heart Study Circulation, January 1, 2002; 105(1): 48 - 53. [Abstract] [Full Text] [PDF]
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S. Meaume, A. Benetos, O.F. Henry, A. Rudnichi, and M.E. Safar Aortic Pulse Wave Velocity Predicts Cardiovascular Mortality in Subjects >70 Years of Age Arterioscler Thromb Vasc Biol, December 1, 2001; 21(12): 2046 - 2050. [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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K. W. Davidson, T. G. Pickering, B. S. Jonas, S. S. Franklin, S. A. Khan, N. D. Wong, M. G. Larson, E. P. Leip, W. B. Kannel, and D. Levy Cautionary Note on the Use of Pulse Pressure as a Risk Factor for Coronary Heart Disease Response Circulation, November 27, 2001; 104 (22): e128 - e129. [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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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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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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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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 Age Affects How BP Indicators Relate to Heart Disease Risk Journal Watch Cardiology, May 4, 2001; 2001(504): 7 - 7. [Full Text]
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M. E. Safar Epidemiological Findings Imply That Goals for Drug Treatment of Hypertension Need to Be Revised Circulation, March 6, 2001; 103(9): 1188 - 1190. [Full Text] [PDF]
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D. A. Kass, E. P. Shapiro, M. Kawaguchi, A. R. Capriotti, A. Scuteri, R. C. deGroof, and E. G. Lakatta Improved Arterial Compliance by a Novel Advanced Glycation End-Product Crosslink Breaker Circulation, September 25, 2001; 104(13): 1464 - 1470. [Abstract] [Full Text] [PDF]
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