(Hypertension. 2000;36:801.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Systolic and Diastolic Blood Pressure, Pulse Pressure, and Mean Arterial Pressure as Predictors of Cardiovascular Disease Risk in Men
From the Division of Preventive Medicine (H.D.S., J.M.G., J.E.M., R.J.G.), Cardiovascular Division (J.M.G.), and Channing Laboratory (M.J.S., B.R., J.E.M.), Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School; Departments of Epidemiology (H.D.S., M.J.S., J.E.M.), Nutrition (M.J.S.), and Biostatistics (R.J.G.), Harvard School of Public Health; and Massachusetts Veterans Epidemiology Research and Information Center, Veterans Affairs Medical Center (J.M.G.), Boston, Mass. Dr Hennekens is currently Visiting Professor of Medicine, Epidemiology, and Public Health at the University of Miami School of Medicine, and his current address is 1415 West Camino Real, Boca Raton, FL 33486.
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Abstract—We compared systolic blood pressure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and mean arterial pressure (MAP) in predicting the risk of cardiovascular disease (CVD), stratifying results at age 60 years, when DBP decreases while SBP continues to increase. We prospectively followed 11 150 male physicians with no history of CVD or antihypertensive treatment through the 2-year questionnaire, after which follow-up began. Reported blood pressure was averaged from both the baseline and 2-year questionnaires. During a median follow-up of 10.8 years, there were 905 cases of incident CVD. For men aged <60 years (n=8743), those in the highest versus lowest quartiles of average SBP (
130 versus <116
mm Hg), DBP (81 versus <73 mm Hg), and MAP (97 versus
<88 mm Hg) had relative risks (RRs) of CVD of 2.16, 2.23, and
2.52, respectively. Models with average MAP and PP did not add
information compared with models with MAP alone
(P>0.05). For men aged 60 years (n=2407), those in
the highest versus lowest quartiles of average SBP (135 versus
<120 mm Hg), PP (55 versus <44 mm Hg), and MAP (99
versus <91 mm Hg) had RRs of CVD of 1.69, 1.83, and 1.43,
respectively. The addition of other blood pressure measures did not add
information compared with average SBP or PP alone (all
P>0.05). These data suggest that average SBP, DBP, and
MAP strongly predict CVD among younger men, whereas either average SBP
or PP predicts CVD among older men. More research should distinguish
whether MAP, highly correlated with SBP and DBP, better predicts
CVD.
Key Words: blood pressure • coronary artery disease • stroke • epidemiology • aging
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Introduction |
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The positive association between either systolic blood pressure (SBP) or diastolic blood pressure (DBP) and the risk of cardiovascular disease (CVD) is well established.1 Blood pressure is also characterized by its pulsatile and steady components.2 3 4 The pulsatile component, estimated by pulse pressure (PP), represents blood pressure variation and is affected by left ventricular ejection fraction, large-artery stiffness, early pulse wave reduction, and heart rate.5 The steady component, estimated by mean arterial pressure (MAP), is a function of left ventricular contractility, heart rate, and vascular resistance and elasticity averaged over time.2 6
It remains unclear which measures of blood pressure, either alone or in combination, best predict the risk of CVD. Data from the Framingham Heart Study5 7 8 and other studies9 10 indicate that SBP increases continuously across all age groups, whereas DBP increases until age 60 years and then begins to decrease steadily. As a result, PP may become a more important blood pressure measure associated with CVD in older individuals.11 In addition, MAP has not been extensively studied, with positive associations in some,12 13 14 but not all,15 studies with CVD.
Therefore, we considered the use of SBP, DBP, PP, and MAP in a large cohort of men aged 40 to 84 years at baseline with no history of antihypertensive treatment. Using self-reported average blood pressure values on the baseline and 2-year questionnaires, we compared the associations of each blood pressure measure with the risk of incident CVD. We further examined potential differences in CVD risk by age dichotomized at 60 years, when DBP levels decrease while SBP continues to increase.3 5
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Methods |
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Study Population and Data Collection
The subjects and methods of the Physicians’ Health Study, a 2x2 factorial trial of aspirin and ß-carotene for the primary prevention of CVD or cancer, have been described previously.16 17 Briefly, 22 071 US male physicians, aged 40 to 84 years at entry, were enrolled and were free from prior myocardial infarction (MI), stroke, transient ischemic attack, cancer (except non-melanoma skin cancer), current renal or liver disease, peptic ulcer, and gout. Among the 22 071 randomized men, subjects were excluded if they had CVD (n=520), any past or current history of antihypertensive medication use (n=3460), or any missing data on blood pressure (n=4540) or antihypertensive medication use (n=2401) on either the baseline or 2-year questionnaires. These exclusions resulted in a study population of 11 150 men.
Self-reported blood pressure is expected to be reliable and valid, since a single measurement of self-reported blood pressure in a different study of physicians was highly correlated with measured SBP (r=0.72) and DBP (r=0.60).18 Another study of the agreement of measured and self-reported blood pressure found a correlation similar to that for 2 measurements of blood pressure within a year.19 We considered 2 other blood pressure measurements besides SBP and DBP. First, we calculated the PP, defined as SBP minus DBP. Second, we calculated the MAP as 1/3(SBP)+2/3(DBP). The average of the baseline and 2-year blood pressure values was used to further minimize any potential misclassification in self-reported blood pressure. On the baseline questionnaire, participants reported other coronary risk factors, including age, smoking status, alcohol use, frequency of vigorous exercise, history of diabetes mellitus, and parental history of MI at <60 years. Body mass index (in kg/m2) was calculated from height and weight.
Follow-up of the 11 150 participants began after completion of the 2-year questionnaire. On annual follow-up questionnaires, participants were asked whether they had experienced any CVD event since the return of the last questionnaire. CVD events included MI, angina pectoris, coronary artery bypass graft surgery, percutaneous transluminal coronary angioplasty, stroke, and cardiovascular death. For men reporting MI or stroke and for reported deaths, relevant medical records were obtained from >95% of the participants. Nonfatal MI was diagnosed with the use of World Health Organization criteria.20 Nonfatal stroke was defined as a typical neurological deficit, sudden or rapid in onset, lasting >24 hours. CVD death was documented by convincing evidence of a cardiovascular mechanism from death certificates and medical records. All analyses are based on the first CVD event. At the end of follow-up, 99.2% of men still provided morbidity information; mortality follow-up was 99.99% complete.17 In all, 905 incident CVD cases occurred over a median follow-up of 10.8 years (maximum, 11.2 years).
Data Analysis
All analyses were stratified a priori by baseline
ages of <60 years (n=8743) and 60 years (n=2407). We first
determined the mean values or proportions of baseline coronary
risk factors according to each group of men. Next, we examined the
blood pressure distributions in each subgroup of men. Stratum-specific
Spearman correlation coefficients were also computed among the 4
measures of blood pressure.
Two separate analysis strategies sought to determine which
measures of average blood pressure predicted the risk of CVD. We first
compared equivalent multivariate Cox proportional
hazards models that only differed by the measures of average blood
pressure used. Seven main models were compared, including SBP only, DBP
only, both SBP and DBP, PP only, both PP and DBP, MAP only, and both PP
and MAP. Other joint models included SBP and PP, SBP and MAP, and DBP
and MAP. Models included terms for age (years), body mass index
(kg/m2), randomized aspirin treatment (yes, no),
randomized ß-carotene treatment (yes, no), smoking status (never,
past, current <1 pack/d, current 1 packs/d), vigorous exercise
1/wk (yes, no), alcohol consumption (<1 drink/wk, 1 to 6 drinks/wk,
1 drink/d), parental history of MI at <60 years (yes, no), and
history of diabetes mellitus (yes, no). Use of finer categories of
physical activity did not appreciably change the results. Although we
did not control for self-reported lipid levels because data were
missing in >10% of participants,21 additional control
for history of hyperlipidemia (self-reported or
measured cholesterol >260 mg/dL) had little effect on the
results. We calculated relative risks (RRs) and 95% CIs, assuming a
10-mm Hg increase in each blood pressure measure. All probability
values were 2-tailed 
=0.05. Nested blood pressure models were
compared with the 
2 test statistic from
likelihood ratio tests.
Our second analysis strategy examined the individual effects of
average SBP, DBP, PP, and MAP. Each blood pressure measure was
categorized into quartiles for each subgroup of men. Cox proportional
hazards models were used to calculate the RR of CVD, with the first
quartile as the reference group. We also compared the 95th versus
<25th percentiles. Multivariate models adjusted for
the same coronary risk factors as before. The assumption of
proportional hazards was confirmed in all models (all
P>0.05) by Wald tests for the interaction of time with each
measure of blood pressure. A linear trend across quartiles of blood
pressure was tested with an ordinal variable, using median blood
pressure levels within each quartile.
We also considered joint models of average SBP and DBP. Average SBP was
categorized into <120, 120 to <130, 130 to <140, and 140
mm Hg, and average DBP was categorized into <70, 70 to <80, 80 to
<90, and 90 mm Hg. The reference group included men with
average SBP <120 mm Hg and average DBP <70 mm Hg. In
sensitivity analyses, we considered other age cut points
besides age 60 years. Separate multivariate models for
each blood pressure measure were considered for men aged 40 to 49, 50
to 59, 60 to 69, and 70 years. Effect modification by age was
assessed by examining the interaction between age (classified as an
ordinal variable using median values from categories of 40 to 49,
50 to 59, 60 to 69, and 70 years) and each average blood pressure
measure in multivariate models. We then examined
whether the association between blood pressure and risk of CVD was
similar for men with any history of hypertension treatment. Finally,
the RRs for stroke (200 cases) were compared with the overall results
for CVD.
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Results |
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The mean (±SD) levels of average SBP, DBP, PP, and MAP for all 11 150 men (mean age, 52.3 years) were 124.1±11.1, 77.5±7.1, 46.6±8.8, and 93.0±7.6 mm Hg, respectively. Table 1 compares the blood pressure parameters and other baseline characteristics of men aged <60 and
60 years. As expected, men aged 60 years had higher levels
of average SBP, PP, and MAP than men aged <60 years. Average DBP in
men aged 60 years was similar to that in men aged <60 years. There
were 5.3% and 16.8% of men aged <60 and 60 years, respectively,
who had an average SBP 140 mm Hg or DBP 90 mm Hg
despite reporting no history of antihypertensive treatment.
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Spearman correlations between average SBP and DBP were 0.70 and 0.61 in
men aged <60 and 60 years (both P<0.001). Average SBP
and DBP were each highly correlated with MAP, with Spearman
correlations ranging from 0.88 to 0.94 (all P<0.001) in all
men. Average DBP was weakly correlated with PP, with Spearman
correlations of 0.03 and 0.06 in men aged <60 and 60 years,
respectively. All other combinations of blood pressure measures were
highly correlated.
During 112 384 person-years of follow-up (median follow-up, 10.8
years), we identified 905 total cases (<60 years, 509 cases; 60
years, 396 cases) of incident CVD. To reduce any potential bias due to
underlying illnesses that may have affected their blood pressure
levels, the exclusion of men with CVD during the first 3 years of
follow-up did not materially alter the results. Additional adjustment
for coronary risk factors other than age had a small relative
impact on the RRs for blood pressure. There were 204 men (22 cases of
CVD) who were excluded from multivariate models because
of missing coronary risk factor data besides age; however, a
comparison of age-adjusted models with and without these subjects did
not affect the RRs. For all Cox proportional hazards models in Tables 2 and 3,
adjustment for coronary risk factors introduced 12 degrees of
freedom (df). Average blood pressure measures were then
added to the multivariate model as follows: model 1,
SBP; model 2, DBP; model 3, SBP and DBP; model 4, PP; model 5, DBP and
PP; model 6, MAP; and model 7, PP and MAP.
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Among men aged <60 years, the addition of any single measure of blood
pressure added significantly to the multivariate model
(all P<0.05 with 1 df) (Table 2). An
increase of 10 mm Hg in average SBP, DBP, PP, and MAP had
corresponding RRs of 1.31, 1.46, 1.23, and 1.48, respectively. In model
3, including both SBP and DBP did not add information compared with SBP
alone (2=2.96, 1 df,
P=0.09) but did add information compared with DBP alone
(2=8.53, 1 df, P=0.003).
Finally, a model with average MAP alone was virtually as good as models
with MAP and either SBP, DBP, or PP (all P>0.05). In model
5, including both DBP and PP did add information compared with either
DBP or PP alone (both P<0.05).
Among men aged 60 years, the addition of average SBP, PP, and MAP
added significantly to the multivariate model (all
P<0.05 with 1 df) (Table 3), with
corresponding RRs for 10-mm Hg increases in average SBP, PP, and MAP
of 1.21, 1.24, and 1.28, respectively. Average DBP was not
significantly associated with the risk of CVD in men aged 60 years.
In model 3, including both SBP and DBP did not add significantly to the
model 1 with SBP alone (2=0.57, 1
df, P=0.45). In addition, the
parameter estimate for average DBP was essentially zero.
Models with SBP or PP alone were not improved with the addition of any
other blood pressure measure (all P>0.05). The RRs for a
model with both SBP and MAP were 1.29 and 0.89, respectively.
We next examined similar multivariate models in
Table 4 but based on quartiles of average
SBP, DBP, PP, and MAP. In men <60 years, average SBP, DBP, and MAP all
had strong associations with CVD risk. Men in the highest versus lowest
quartiles of average SBP (130 versus <116 mm Hg), DBP (81
versus <73 mm Hg), and MAP (97 versus <88 mm Hg) had
RRs of CVD of 2.16, 2.23, and 2.52, respectively. An increased risk of
CVD was evident in men aged <60 years in the second quartile of
SBP, DBP, and MAP. In men aged 60 years, increasing quartiles of SBP
and PP were strongly associated with the risk of CVD. Comparing the
highest versus lowest quartiles of average SBP (135 versus <120
mm Hg) and PP (55 versus <44 mm Hg), the corresponding RRs
were 1.69 and 1.83. MAP was also associated with the risk of CVD, but
with RRs of lower magnitude.
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Finally, we examined the joint effect of average SBP and DBP with the
CVD risk in men aged <60 and 60 years after adjustment for
coronary risk factors. In men aged <60 years, single category
increases in average SBP (from <120 to the category 120 to <130
mm Hg) or DBP (from <70 to the category 70 to <80 mm Hg)
resulted in a 2- or 3-fold increase in CVD risk. In men aged 60
years, there were similar patterns of an increased CVD risk but of a
lower magnitude. Older men with greater PPs (average SBP 130 to <140
and DBP <70 mm Hg) had the highest RR of CVD.
In sensitivity analyses, we also considered age stratified into
4 age groups (<50, 50 to 59, 60 to 69, and 70 years) and compared
the age-specific, multivariate RRs of CVD for 10-mm Hg
increases in individual blood pressure measures (Figure
). There was a pattern of declining RRs
with age for average SBP, DBP, and MAP but not for average PP. These
results were further supported by significant interactions found
between categories of age and either SBP (P=0.004), DBP
(P=0.013), or MAP (P=0.01). The largest
reductions in effect sizes with age were for average DBP and MAP, which
primarily occurred from ages 50 to 59 to 60 to 69 years. Among other
subanalyses, the association between blood pressure and stroke
(205 cases) yielded RRs similar to those for CVD, although the smaller
number of strokes greatly diminished power. We then considered the
associations between blood pressure measures and CVD among men with any
past or present history of antihypertensive treatment at baseline.
The RRs of CVD for 10-mm Hg increases in SBP (men <60 years, 1.18;
men 60 years, 1.28), DBP (men <60 years, 1.12; men 60 years,
1.24), PP (men <60 years, 1.19; men 60 years, 1.20), and MAP (men
<60 years, 1.21; men 60 years, 1.44) were somewhat different than
the results in Tables 2 and 3.
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Discussion |
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We found modest differences according to age for the relationship between blood pressure and CVD risk in men with no history of antihypertensive treatment after comparing models with 4 different blood pressure measures. Average SBP, DBP, and MAP were all strongly associated with an increased CVD risk in younger men. However, average DBP was not associated with CVD risk in men aged
60 years. Average PP
was associated with the risk of CVD in both younger and older men.
This study of middle-aged and older men was sufficiently powered to
examine the association between various blood pressure measures and
risk of CVD. Because we excluded men with any history of
antihypertensive treatment, these male physicians had a lower
distribution of blood pressure values compared with other
community-based cohorts.5 22 Still, in men aged <60
years, we found an increased CVD risk among men starting in the second
quartile of average SBP (116 mm Hg), DBP (73 mm Hg),
and MAP (88 mm Hg). In addition to average SBP, PP emerged with
a strong positive association with the risk of CVD in men aged 60
years. Despite somewhat lower but elevated RRs in men aged 60 years,
their greater incidence of CVD underscores the potentially large public
health impact of elevated yet untreated blood pressure in the
elderly.
When we considered SBP and DBP simultaneously, only SBP
remained significant in multivariate models for men
aged <60 and 60 years. During the seventh decade of life,
age-specific SBP levels continue to increase, while DBP levels begin to
decline.5 7 8 9 10 We found no independent association
between average DBP and CVD risk in men aged 60 years. This loss of
predictive value for average DBP may be due to an increasing number of
men with underlying illnesses23 ; however, we would have
expected fewer such men in our cohort of apparently healthy male
physicians. Isolated systolic hypertension becomes more
prevalent with age and has been associated with a significant,
increased risk of CVD.21 24
Increases in PP are associated with aging, particularly after age 60 years.5 10 Higher levels of PP have been associated with carotid stenosis,15 left ventricular hypertrophy,25 MI,3 26 27 28 CVD death,12 29 and congestive heart failure30 in both normotensive and hypertensive populations. Studies in older men and women have found that PP remains important even after controlling for either SBP or DBP.11 15 30 Our results for average PP in older, but not younger, men were consistent with these findings.
Few studies have prospectively addressed the effect of MAP in relation to CVD.12 13 14 28 Dyer et al13 found that the steady component of blood pressure (highly correlated with MAP) was more strongly associated with CVD risk than PP in 4 Chicago epidemiological studies. Among subjects with a history of MI, one study indicated a significant 12% increase in recurrent MI for each 10-mm Hg increase in MAP.28 However, MAP was a weaker predictor than PP and was not associated with CVD mortality. We found that MAP may be strongly associated with CVD risk in men aged <60 years, with a RR of CVD for a 10-mm Hg increase in average MAP of 1.48. This RR was greater than a RR of 1.33 for a comparable 10-mm Hg increase among French men aged 40 to 54 years.12
Any clinical advantage for MAP, which is a function of SBP and DBP, for
the evaluation of CVD risk among younger men remains unclear. Models
with any 2 blood pressure parameters yielded identical -2
log likelihoods for men <60 and 60 years because of the linear
relationship between blood pressure variables. In this regard, MAP
when used in combination with other blood pressure
parameters offers no additional ability to predict the risk
of CVD. However, among models with single blood pressure
parameters in men aged <60 years, MAP was a slightly
stronger predictor of CVD than SBP based on -2 log likelihoods.
Therefore, in younger men, either MAP or SBP may best predict the risk
of CVD when individual blood pressure parameters are
considered.
Biologically, the magnitude of RRs of CVD for average SBP in men aged
<60 and 60 years reflects the strength of its continuous, graded
relationship with CVD risk.1 Higher SBP levels may reflect
the progressive stiffening of the arterial wall, changes in
the vascular structure, and the development of
atherosclerosis.31 Decreased DBP may
indicate poor coronary flow reserve and coronary
perfusion of the myocardium.32 Increases in PP
reflect the stiffening of the conduit vessels. Such vessel stiffening
increases pulse-wave velocity, which ultimately increases systemic load
while decreasing coronary perfusion pressure.28
MAP is the steady flow of blood through the aorta and its arteries and
equals the cardiac output multiplied by vascular
resistance.2
Some limitations should also be considered in light of these results.
First, our use of self-reported blood pressure may be subject to
misclassification. For example, the weak association between DBP and
CVD in men aged 60 years may be explained by an underreporting of DBP
due to individual differences in recording fourth or fifth
Korotkoff sounds. By averaging self-reported blood pressure on the
baseline and 2-year questionnaires, we sought to further minimize any
misclassification. We excluded men with any history of antihypertensive
treatment to reduce any potential confounding by antihypertensive
treatment on blood pressure values, although data from Framingham
suggest that antihypertensive treatment may not confound the
association between blood pressure and coronary heart
disease.11 Next, our findings may not apply to women,
lower socioeconomic groups, and non-white populations, who may be more
or less susceptible to hypertension and responsive to changes in blood
pressure. Finally, unaccounted biochemical, clinical, and genetic
markers for the risk of CVD may introduce residual confounding.
In conclusion, among men with no history of antihypertensive treatment,
SBP may be best utilized in men aged <60 years, whereas either SBP or
PP may be best suited for men aged 60 years. DBP was a strong
predictor of CVD in younger, but not older, men. Finally, more research
must distinguish whether MAP, which is highly correlated with either
SBP or DBP, may be an important predictor of CVD in younger men.
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Acknowledgments |
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This research was supported by research grants CA-40360, CA-34944, HL-26490, and HL-34595; institutional training grant HL-07575 from the National Institutes of Health; and a grant from Bristol-Myers Squibb.
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Footnotes |
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Reprint requests to Howard D. Sesso, ScD, MPH, Brigham and Women’s Hospital, 900 Commonwealth Ave E, Boston MA 02215-1204.
Received May 8, 2000; first decision May 24, 2000; accepted May 31, 2000.
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