Download Cardiovascular Risk Assessment Using Pulse

Cardiovascular Risk Assessment Using Pulse Pressure in the
First National Health and Nutrition Examination Survey
(NHANES I)
Michael Domanski, James Norman, Michael Wolz, Gary Mitchell, Marc Pfeffer
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Abstract—Increased stiffness of the conduit arteries has been associated with increased risk of death and cardiovascular
death in a number of populations. None of these populations, however, are fully representative of the US population.
The cohort examined in the First National Health and Nutrition Examination Survey (NHANES I) that was free of overt
cardiovascular disease was selected to be representative of the US population. We assessed and quantified the increased
risk of death associated with elevated pulse pressure in this population. A cohort of 5771 subjects from NHANES I was
used to determine the value of adding pulse pressure to standard cardiovascular disease risk factors for assessment of
the risk of death during a mean follow-up period of 16.5 years. Analyses were performed by use of the SUDAAN
statistical package for performing Cox proportional regression, logistic regression, and other standard methods in
complex, weighted samples. Pulse pressure increased with increasing age, body mass index, cholesterol level, and mean
arterial pressure. With increasing pulse pressure, the percentage of cigarette smokers decreased and the percentage of
diabetics increased. Despite these associations with known risk factors, pulse pressure was independently predictive of
an increased risk of death from cardiovascular disease, coronary heart disease, and all-cause mortality. It provides
independent prognostic information beyond that provided by known risk factors that were evaluated in this study,
including the Sixth Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure hypertension classification. A 10 mm Hg increase in pulse pressure in persons 25 to 45 of age was associated
with a 26% increase in risk of cardiovascular death (95% confidence interval [CI], 5 to 50) and with an 10% increase
(95% CI, 2 to 19) in persons 46 to 77 years of age. In a cohort designed to be representative of the US population,
elevated pulse pressure has been shown to provide independent prognostic information. This variable may be a marker
for the extent of vascular disease and may contribute to the occurrence of clinical events. (Hypertension. 2001;38:793797.)
Key Words: pulse 䡲 arteries 䡲 cardiovascular diseases
I
ncreased arterial stiffness, as indicated by increased pulse
pressure, has been associated with an increased risk for
adverse cardiovascular events, including stroke, myocardial
infarction, heart failure, cardiovascular death, and overall
mortality, in a number of populations.1–11
With aging, there is a gradual stiffening of the conduit
arteries that results from the loss of elastin and deposition of
collagen.12 With stiffening, peak systolic pressure increases
for any given flow wave. Additionally, the pulse wave
velocity of the pressure pulse is increased. This results in
earlier return of reflections from the periphery that, as
stiffening progresses, arrive in the central aorta in late systole
rather than early diastole. This contributes to an augmentation
of peak systolic pressure and a reduction in diastolic pressure
(and consequently an increase in pulse pressure). In addition
to aging, arterial stiffening appears to be hastened by a
number of conditions, including hypertension,12 menopause,13 glucose intolerance,14 elevated homocysteine levels,15 polymorphisms of the angiotensin type I receptor
gene,16 and renal failure.17
Although a number of populations have been studied, none of
them is fully representative of the US population as a whole. The
First National Health and Nutrition Examination Survey
(NHANES I) was a complex, stratified probability sample of the
noninstitutionalized US population between 1 and 77 years of
age.18 –20 We examined individuals in this cohort who were ⱖ25
years to determine and quantify the independent prognostic
significance of pulse pressure and to determine whether pulse
pressure adds prognostic information beyond that supplied by
the classification of the Sixth Joint National Committee on
Prevention, Detection, Evaluation, and Treatment of High Blood
Pressure (JNC VI) on prognosis.21
Received March 6, 2001; first decision March 22, 2001; revision accepted April 23, 2001.
From the Clinical Trials Group, National Heart, Lung, and Blood Institute (M.D., J.N., M.W.), Bethesda, Md; and Cardiovascular Engineering Inc
(G.M.) and Division of Cardiology, Brigham and Women’s Hospital (M.P.), Boston, Mass.
Correspondence to Michael J. Domanski, MD, National Heart, Lung, and Blood Institute, Rockledge II Center, 6701 Rockledge Dr, Room 8146,
Bethesda, MD 20892-7936.
© 2001 American Heart Association, Inc.
Hypertension is available at http://www.hypertensionaha.org
793
794
Hypertension
October 2001
TABLE 1.
CVD Risk Factor Means by Quartiles of Pulse Pressure
Pulse Pressure Quartile, mm Hg
ⱕ36
36 – 44
44 –55
⬎55
1471
1370
1377
1553
Pulse pressure, mm Hg
31.0⫾7.7
40.7⫾3.7
49.4⫾3.7
68.5⫾15.8
Mean arterial pressure, mm Hg
92.3⫾15.3
95.5⫾14.8
98.6⫾3.8
108.9⫾23.6
䡠䡠䡠
⬍0.00001
Systolic pressure, mm Hg
112.9⫾15.3
122.6⫾15.5
131.5⫾17.4
154.5⫾29.5
⬍0.00001
Diastolic pressure, mm Hg
82.0⫾15.3
81.9⫾14.8
82.1⫾17.8
86.0⫾22.8
⬍0.00001
n
P*
Age, y
40.2⫾11.1
42.0⫾15.2
45.4⫾13.7
54.6⫾16.5
⬍0.00001
Body mass index, kg/m2
24.8⫾5.8
25.1⫾5.9
25.5⫾5.9
26.5 ⫾7.1
⬍0.00001
212.4⫾61
215.8⫾59
219.1⫾56
Cholesterol, mg/dL
230.7⫾63
⬍0.00001
Race, % black
10.2
8.5
8.9
11.6
Gender, % women
54.5
49.3
50.6
54.2
䡠 䡠 䡠†
䡠 䡠 䡠†
1.6
3.0
2.5
6.7
⬍0.00001
45.3
42.2
40.2
37.6
⬍0.00001
Diabetes, %
Cigarette smokers, %
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Values are mean⫾SD when appropriate.
*For test of trend.
†Significant curvilinear effect.
Methods
In 1971 to 1975, the National Center for Health Statistics conducted
NHANES I. Data were collected from a complex, stratified probability sample of 23 808 individuals in the civilian noninstitutionalized US population through a variety of questionnaires and a
standardized medical examination administered from mobile hospitals. Starting in 1982, the NHANES Epidemiologic Follow-Up Study
was conducted to provide a database for studies on the relationship
of baseline clinical, nutritional, and behavioral factors to subsequent
morbidity and mortality. The study is described in detail elsewhere.22–24 There were 14 407 examinees in NHANES I who were
25 to 77 years of age at the time of the initial examination (1971 to
1975). Direct information on smoking habits at baseline was available from a subsample of 6903 of the original participants of
NHANES I who were given a detailed examination. After those who
were taking blood pressure medication were eliminated, a subsample
of 5771 persons with all values of the variables of interest was
available for our analyses. The mean length of follow-up was 16.5
years (range, 16 days to 22 years). Mortality data were collected
between 1982 and 1992 by matching with the National Death Index.
Causes of death were coded according to the ninth revision of the
International Classification of Diseases.25 If the decedent’s code was
between 390 and 459, the cause of death coded was attributed to
cardiovascular disease (CVD). Coronary heart disease (CHD) was
coded as 410 through 414. Of the original cohort, 96.2% of those 25
to 77 years of age were successfully traced, and death certificates
were obtained from 4497 (97.7%) of the 4604 decedents.
Statistical Methods
The cohort in this analysis consisted of 5771 adults 25 to 74 years of
age who, when appropriately weighted according to the geographic
and demographic strata from which they were drawn, accurately
represent the US population of the same ages. Analyses were
performed with the SUDAAN statistical package,26 which contains
procedures for performing Cox proportional-hazards regression,
multiple linear regression, logistic regression, and other standard
methods applied to complex, weighted samples. Covariates used in
these analyses were the following risk factors for CVD measured or
observed at baseline: gender, race (specified as black or nonblack on
NHANES I data forms), diabetes, and cigarette smoking (each as
binary variables), as well as age, body mass index, serum cholesterol,
and mean arterial pressure calculated as one third systolic plus two
thirds diastolic blood pressure.
The JNC VI classification of blood pressure for adults ⱖ18 years
of age21 was also used. We assigned ordinal scale values of 1 to 5 to
the respective categories of optimal, normal but not optimal, high
normal, stage 1 hypertension, and stage 2 or higher hypertension.
Quartiles of pulse pressure were calculated with the NHANES
detailed sample weights, which produced unequal numbers of
subjects in the 4 groups of our analysis cohort but represent equal
numbers of persons in the United States. For the same reason, the
approximate median age at baseline of 45 years divides the cohort
into 2 groups of unequal size. Tests for trend in mean risk factor
values across pulse pressure quartiles were made with linear regression for continuous valued factors and logistic regression for the
binary factors (race, gender, smoking, and diabetes). All Cox
proportional-hazards regression survival analyses are reported in
terms of hazard ratios and their 95% confidence intervals (CIs).
Pulse pressures and mean arterial pressures are expressed in units of
10 mm Hg.
Results
Known risk factors for CVD were assessed as a function of
quartile of pulse pressure (Table 1). Increasing pulse pressure
is associated with increasing age, body mass index, cholesterol level, and mean arterial pressure; an increasing percentage of diabetics; and fewer cigarette smokers. The percentages of blacks and women display significant U-shaped
distributions. A Cox regression analysis, adjusted for the
influence of known CVD risk factors, including mean arterial
pressure level, assessed the effect of pulse pressure on overall
mortality, CVD mortality, and CHD mortality. Tables 2
through 4 display the results of these multivariate analyses.
Pulse pressure is significantly associated with total mortality
in patients above the median age of 45 years and with CVD
and CHD mortality in patients of all ages. Pulse pressure was
most strongly associated with the risk of CHD death (Table
4). Mean arterial pressure is associated with total and CVD
death in all ages and with CHD death in patients ⱖ46 years
of age. Pulse pressure is not associated with an increase in
non-CVD. Compared with persons of other races, blacks are
at increased risk for death from all causes and for death as a
result of CVD but not of CHD. No evidence was found of an
Domanski et al
Pulse Pressure and Cardiovascular Risk Assessment
TABLE 2. Survival Analysis: Hazard Ratios for All Deaths by
Age Group
795
TABLE 4. Survival Analysis: Hazard Ratios for CHD Deaths by
Age Group
Age Group
Age Group
25– 45 y
All
25– 45 y
46 –77 y
People, n
2566
3205
People, n
2566
3205
Deaths, n
174
1319
Deaths, n
38
342
CVD risk factor
CVD risk factor
Age (per 10 y)
1.09 (1.05–1.14)
1.10 (1.09–1.12)
Age (per 10 y)
1.19 (1.09–1.31)
Race (black vs nonblack)
2.01 (1.29–3.16)
1.36 (1.08–1.72)
Race (black vs nonblack)
0.50 (0.18–1.37)
1.11 (1.09–1.14)
0.66 (0.43–1.01)
Gender (women vs men)
0.52 (0.36–0.74)
0.67 (0.58–0.78)
Gender (women vs men)
0.30 (0.12–0.68)
0.45 (0.33–0.62)
Diabetes
3.52 (1.78–6.98)
1.49 (1.01–2.21)
Diabetes
6.89 (2.68–17.71)
1.88 (1.09–3.23)
Cigarette smoking
1.46 (1.18–1.81)
1.51 (1.37–1.67)
Cigarette smoking
1.26 (0.75–2.10)
1.52 (1.29–1.79)
BMI (per kg/m2)
1.01 (0.97–1.06)
1.01 (0.99–1.03)
BMI (per kg/m2)
1.04 (0.96–1.12)
1.07 (1.04–1.09)
Cholesterol (per 10 mg/dL)
1.05 (1.00–1.10)
1.01 (0.99–1.03)
Cholesterol (per 10 mg/dL)
1.08 (0.99–1.17)
1.05 (1.01–1.09)
MAP (per 10 mm Hg)
1.18 (1.01–1.39)
1.12 (1.06–1.20)
MAP (per 10 mm Hg)
1.22 (0.98–1.51)
1.15 (1.02–1.29)
Pulse pressure (per 10 mm Hg)
1.09 (0.95–1.26)
1.07 (1.01–1.13)
Pulse pressure (per 10 mm Hg)
1.44 (1.22–1.70)
1.15 (1.03–1.28)
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BMI indicates body mass index; MAP, mean arterial pressure. Values in
parentheses are 95% CIs.
interaction between pulse pressure and gender or between
pulse pressure and race in the analyses of CVD deaths in the
either age group.
Table 5 presents the results of a Cox regression analysis of
cardiovascular disease mortality with mean arterial pressure
replaced by the JNC VI classification with the 5 levels
described above. It shows that pulse pressure retains its
prognostic significance for cardiovascular death in persons of
all ages. An increase in pulse pressure of 10 mm Hg in
persons ⱕ45 years of age produces an estimated increase in
the risk of CVD death of 24%; the same increase in persons
⬎45 years of age predicts an increase in risk of 12%.
Discussion
This analysis assesses the significance of pulse pressure on
the risk of death in a cohort of patients that is specifically
TABLE 3. Survival Analysis: Hazard Ratios for CVD Deaths by
Age Group
Age Group
25– 45 y
46 –77 y
People, n
2566
3205
Deaths, n
60
613
CVD risk factor
Age (per 10 y)
1.15 (1.08–1.22)
1.11 (1.10–1.13)
Race (black vs nonblack)
1.51 (0.70–3.27)
1.07 (0.81–1.43)
Gender (women vs men)
0.33 (0.17–0.65)
0.61 (0.47–0.78)
Diabetes
5.95 (2.03–17.42)
1.69 (1.11–2.56)
Cigarette smoking
1.49 (1.02–2.18)
1.44 (1.25–1.66)
1.02 (1.00–1.05)
2
BMI (per kg/m )
1.04 (0.98–1.10)
Cholesterol (per 10 mg/dL)
1.12 (1.04–1.22)
1.02 (1.00–1.05)
MAP (per 10 mm Hg)
1.41 (1.15–1.74)
1.23 (1.12–1.35)
Pulse pressure (per 10 mm Hg)
1.26 (1.05–1.50)
1.10 (1.02–1.19)
Abbreviations as in Table 2. Values in parentheses are 95% CIs.
Abbreviations as in Table 2. Values in parentheses are 95% CIs.
designed to be representative of the US population. It demonstrates that pulse pressure is associated with an increased
risk of all-cause, CVD, and CHD death independent of mean
arterial pressure but not with death from noncardiovascular
causes. Furthermore, it provides a quantitative estimate of the
hazard ratios in the US population. Interestingly, blacks are at
greater risk for all-cause mortality than persons of other races,
a finding that appears to be based solely on non-CHD deaths.
In this cohort, they did not appear to be at increased risk for
death from CHD.
By including the JNC VI classification as a covariate in a
Cox regression model with pulse pressure and the other CVD
risk factors, we have demonstrated that pulse pressure has
prognostic significance independent of the JNC VI classification. A general approach to risk assessment in any data set
using blood pressure is improved by including both systolic
and diastolic pressures. Because of the equivalence of the
information conveyed by either mean arterial and pulse
pressures or systolic and diastolic blood pressures, the use of
either pair in any regression model results in identical values
of the statistical measure of fit of the models. Although
systolic blood pressure is a major prognostic determinate, the
inclusion of information from diastolic or pulse pressure
(which is systolic minus diastolic blood pressure) may add
prognostic information, depending on the database examined.
Systolic pressure includes substantial contributions from both
the steady-flow (mean arterial) and pulsatile (pulse pressure)
components of hemodynamic load. Our model includes mean
arterial and pulse pressures, which incorporate systolic and
diastolic pressures.
This analysis suggests that pulse pressure determination
may prove useful in further refining the assessment of
prognosis.
Comparison With Other Studies
A number of studies in diverse cohorts support the notion that
pulse pressure carries important, independent prognostic
information. An analysis of data from the Hypertension
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October 2001
TABLE 5. Survival Analysis: Hazard Ratios for CVD Deaths by
CVD Risk Factor and Age Group with JNC VI Classification of
Blood Pressure for Adults
Age Group
CVD Risk Factor
25– 45 y
46 –77 y
People, n
2566
3205
Deaths, n
60
613
CVD risk factor
Age (per 10 y)
1.16 (1.09–1.23)
1.11 (1.09–1.12)
Race (black vs nonblack)
1.71 (0.87–3.37)
1.16 (0.87–1.55)
Gender (women vs men)
0.37 (0.20–0.71)
0.60 (0.47–0.78)
Diabetes
5.76 (2.00–16.61)
1.65 (1.07–2.56)
Cigarette smoking
1.49 (1.02–2.17)
1.44 (1.24–1.66)
2
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BMI (per kg/m )
1.04 (0.98–1.10)
1.03 (1.01–1.05)
Cholesterol (per 10 mg/dL)
1.12 (1.04–1.20)
1.02 (1.00–1.05)
JNC VI (per unit increase in scale)
1.61 (1.15–2.26)
1.22 (1.08–1.38)
Pulse pressure (per 10 mm Hg)
1.24 (1.06–1.46)
1.12 (1.03–1.21)
Abbreviations as in Table 2. Values in parentheses are 95% CIs. The JNC VI
ordinal scale is as follows: 1 ⫽ optimal; 2 ⫽ normal, not optimal; 3 ⫽ high
normal; 4 ⫽ stage 1 hypertension; and 5 ⫽ stage 2 or higher hypertension.
Detection Follow-Up Program reported by Abernathy et al27
incorporated other available cardiovascular risk factors into a
logistic regression model, demonstrating that pulse pressure
is a significant predictor of mortality in that cohort. In 1989,
Darne et al8 reported their study of 27 000 French subjects in
whom pulse pressure was associated with cardiovascular
death independent of other known risk factors, including
diastolic and mean arterial pressures. Madhavan et al6 studied
2207 hypertensive patients in a union-sponsored hypertension
control program. In this study, an elevated pretreatment pulse
pressure was associated with adverse cardiovascular events.
Fang et al7 examined data on 5730 participants who entered
a hypertension control program between 1973 and 1992.
After 5.4 years of follow-up, an elevated pulse pressure was
identified as the most important predictor of a subsequent
myocardial infarction. Domanski et al5 showed an association
between pulse pressure and the risk of stroke in patients
entered in the Systolic Hypertension in the Elderly Program
(SHEP). Using a proportional-hazards model, they demonstrated an 11% increase in the risk of stroke and a 16%
increase in total mortality for each 10 mm Hg increase in
pulse pressure.
Patients entered in the Survival and Ventricular Enlargement (SAVE) trial were also studied.2 For the 2231 post–
myocardial infarction patients in the trial (left ventricular
ejection fraction ⱕ0.40), multivariate analysis showed pulse
pressure to be an independent predictor of all-cause mortality
and myocardial infarction.
Patients entered in the Studies of Left Ventricular Dysfunction (SOLVD) study, who had left ventricular ejection fraction ⱕ0.35, were shown on multivariate analysis to have a
strong association of all-cause mortality and cardiovascular
death with pulse pressure.1 In fact, in this study, an increase
in mean arterial pressure was associated with reduced mortality, whereas an increase in pulse pressure was associated
with increased mortality. Across a wide spectrum of diseases
from severe hypertension to heart failure with lowered mean
arterial pressure, an elevated pulse pressure was found to be
an indicator of heightened CVD risk.
Chae et al3 followed 1621 healthy elderly subjects with no
history of heart failure and a mean age of 77.9 years for an
average of 3.8 years. After adjustment for other CVD risk
factors, pulse pressure was shown to be independently associated with the risk of developing heart failure.
Data from 50 years of follow-up of participants in the
Framingham study demonstrated that pulse pressure, rather
than systolic or diastolic pressure, had the strongest association with mortality.4 Although Framingham comprises an
initially healthy cohort of adults in an eastern Massachusetts
city, the design of NHANES I provides a population that is
representative of the US population.
Pathophysiology Associated With Increased
Conduit Vessel Stiffness
There are a number of potential mechanisms by which
increased arterial stiffness could worsen prognosis. The
loading caused by increased vascular stiffness has been
shown to be associated with increased left ventricular
mass.28 –30 Increased pulse pressure is also associated with
increased intimal and medial thickness of the carotid artery.31–33 Data from animal studies suggest that the ventricle
is more susceptible to ischemia when the aorta is stiff34,35 and
that coronary occlusion results in greater ventricular
damage.36
Although the presence of atherosclerosis may increase
arterial stiffness, increased stiffening occurs even in populations in which atherosclerosis is unusual, as demonstrated by
the work of Avolio et al11 in China. It is possible that aortic
stiffening may be atherogenic. In a primate model, atherosclerosis severity was found to increase with an increase in
pulsatile strain.37 In addition, increased pulse pressure has
been associated with reduced NO production by the endothelium,38 which has been shown to be atherogenic.39 It should
be added that pulse pressure changes may occur with changes
in stroke volume. Thus, an elevated pulse pressure should be
viewed as both a marker of vascular disease and a contributor
to disease progression.
Study Limitations
Caution must be exercised in the interpretation of models of
mortality in survey data based on death certificates. The
causes of death listed on death certificates are not always
accurate.40 However, they are useful in establishing trends
and have been shown to track well with studies of mortality
that used more accurate methods of ascertainment.41
Because the white-coat effect may raise initial blood
pressures measured in the office setting,42 a single measurement can overestimate blood pressure levels. Multiple measurements reduce the variability of the measurements.43
Clinical Implications and Conclusions
This study demonstrates and quantifies the prognostic importance of pulse pressure in a cohort that is representative of the
US population. Because there is a functional component of
Domanski et al
Pulse Pressure and Cardiovascular Risk Assessment
arterial stiffening, conduit vessel stiffening is a potential
therapeutic target. The demonstration that pulse pressure adds
prognostic information beyond that of known CVD risk
factors, including the JNC VI classification, suggests that it
may be useful as an additional factor in risk assessment for
future therapeutic decision making.
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Cardiovascular Risk Assessment Using Pulse Pressure in the First National Health and
Nutrition Examination Survey (NHANES I)
Michael Domanski, James Norman, Michael Wolz, Gary Mitchell and Marc Pfeffer
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Hypertension. 2001;38:793-797
doi: 10.1161/hy1001.092966
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