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Relationship of Blood Pressure to 25-Year Mortality Due to Coronary Heart Disease, Cardiovascular Diseases, and All Causes in Young Adult Men
The Chicago Heart Association Detection Project in Industry
Katsuyuki Miura, MD, PhD;
Martha L. Daviglus, MD, PhD;
Alan R. Dyer, PhD;
Kiang Liu, PhD;
Daniel B. Garside, MA;
Jeremiah Stamler, MD;
Philip Greenland, MD
Arch Intern Med. 2001;161:1501-1508.
ABSTRACT
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Background Data are limited on blood pressure (BP) in young adults and long-term
mortality. Moreover, screening and hypertension treatment guidelines have
been based mainly on findings for middle-aged and older populations. This
study assesses relationships of BP measured in young adult men to long-term
mortality due to coronary heart disease (CHD), cardiovascular diseases (CVD),
and all causes.
Methods This cohort from the Chicago Heart Association Detection Project in
Industry included 10 874 men aged 18 to 39 years at baseline (1967-1973),
not receiving antihypertensive drugs, and without CHD or diabetes. Relationship
of baseline BP to 25-year CHD, CVD, and all-cause mortality was assessed.
Results Age-adjusted association of systolic BP to CHD mortality was continuous
and graded. Multivariate-adjusted CHD hazard ratios (HRs) for 1 SD higher
systolic BP (15 mm Hg) and diastolic BP (10 mm Hg) were 1.26 (95% confidence
interval [CI], 1.11-1.44) and 1.17 (95% CI, 1.01-1.35), respectively. Compared
with the Sixth Report of the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure stratum with normal BP (and
lowest mortality rates), the large strata with high-normal BP and stage 1
hypertension had 25-year absolute risks for death of 63 and 72 per 1000, respectively,
and absolute excess risks of 10 and 20 per 1000, respectively; accounted for
59.8% of all excess CHD, CVD, and all-cause mortality; and were estimated
to have life expectancy shortened by 2.2 and 4.1 years, respectively.
Conclusions In young adult men, BP above normal was significantly related to increased
long-term mortality due to CHD, CVD, and all causes. Population-wide primary
prevention, early detection, and control of higher BP are indicated from young
adulthood on.
INTRODUCTION
FOR MIDDLE-AGED and older populations worldwide, blood pressure (BP)
has repeatedly been shown to be a significant risk factor for the major cardiovascular
diseases (CVD), including coronary heart disease (CHD) and stroke.1-6
For systolic (SBP) and diastolic BP (DBP), these relationships are continuous,
graded, independent of other risk factors, consistent, predictive, and generally
assessed as etiologically significant. Data indicate that SBP is a stronger
predictor than DBP at these ages.7-10
In contrast, long-term observations of BP and mortality due to CHD and
CVD in young adults are limited. Because major CVD events are rare before
50 years of age in men and 60 years of age in women, studies on risk factors
measured at an average age of about 30 years require long-term follow-up or
large sample sizes to accrue adequate numbers of events. The few reports of
prospective population-based studies are from nested case-control investigations
in former college students11-13
and analyses of life insurance actuarial data.14-16
Other evidence comes from autopsy studies showing that coronary risk factors
relate to early atherosclerotic lesions in young adults.17-19
Although hypertension treatment guidelines are usually considered applicable
for persons aged 18 years and older,20-21
there is limited documentation supporting screening and treatment of young
adults.
This report adds information on this matter. The Chicago Heart Association
Detection Project in Industry (CHA) Study is one of the largest and longest
prospective studies providing CVD mortality data. Approximately 11 000
men aged 18 to 39 years at baseline were followed up for an average of 25
years. The goals of this research were to determine (1) whether SBP, DBP,
and SBP/DBP categories of the Sixth Report of the Joint National Committee
on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure
(JNC-VI)20 predict long-term mortality due
to CHD, CVD, and all causes for young men; (2) whether SBP is a better predictor
than DBP in young men; and (3) long-term absolute risks, absolute excess risks,
and impairment of life expectancy in young men with higher BP, with comparison
of risks in young and middle-aged men.
MATERIALS AND METHODS
POPULATION
Methods of the CHA study have been described.22-23
Briefly, 39 573 men and women aged 18 years and older underwent screening
from November 1967 through January 1973. All employees at 84 cooperating Chicago-area
companies and organizations, with a labor force of approximately 75 000
people, were invited to participate; volunteer rate was 53%.
SURVEY METHODS
Screening was performed by 2 trained and standardized 4-person field
teams. Data collected at baseline included age, sex, ethnicity, education,
BP, serum total cholesterol level, smoking status, height and weight, resting
electrocardiographic (ECG) findings, medical history, and current treatment
for chronic diseases, including hypertension and diabetes. A single casual
supine BP measurement was obtained by trained staff using a standard mercury
sphygmomanometer. Standardized high-quality methods were used for determination
of total serum cholesterol levels.24 Criteria
of the National Cooperative Pooling Project and the Hypertension Detection
and Follow-up Program were used to code ECG abnormalities.25
MORTALITY END POINTS
Vital status was ascertained through 1995, with average follow-up of
25 years. Deaths were determined before and including 1979 by means of direct
mail, telephone, contact with employer, and matching of cohort records with
Social Security Administration files, and after 1979 by means of matching
of study records with National Death Index records. Multiple causes of death
from death certificates were coded by trained research staff according to
the International Classification of Diseases, Eighth Revision (ICD-8).26
Coding decisions were cross-checked by study team members. All coders were
blinded to baseline data. For this report, underlying cause of death was used.
Mortality due to CHD was defined as ICD-8 codes 410.0
to 414.9; that due to CVD, ICD-8 codes 400.0 to 445.9.
EXCLUSIONS
Men aged 18 to 39 years at baseline numbered 11 248. Of these,
374 were excluded for the following reasons: data missing at baseline or on
follow-up (n = 114); baseline ECG evidence of myocardial infarction (n = 5);
history of myocardial infarction or other CHD (n = 12); antihypertensive drug
treatment at baseline (n = 125); or previously diagnosed diabetes mellitus
(n = 118). Thus, this report is based on 10 874 men.
STATISTICAL ANALYSES
Age-adjusted mortality rates per 10 000 person-years of follow-up
and per 1000 men were computed for CHD, CVD, and all-cause mortality. Mortality
rates were calculated by categories of SBP or DBP and by the following classification
according to the JNC-VI20: optimal (SBP of
<120 mm Hg and DBP of <80 mm Hg); normal not optimal (SBP of 120-129
mm Hg and DBP of <85 mm Hg, or SBP of <130 mm Hg and DBP of 80-84 mm
Hg); high normal (SBP of 130-139 mm Hg and DBP of <90 mm Hg, or SBP of
<140 mm Hg and DBP of 85-89 mm Hg); stage 1 hypertension (SBP of 140-159
mm Hg and DBP of <100 mm Hg, or SBP of <160 mm Hg and DBP of 90-99 mm
Hg); stage 2 hypertension (SBP of 160-179 mm Hg and DBP of <110 mm Hg,
or SBP of <180 mm Hg and DBP of 100-109 mm Hg); and stage 3 hypertension
(SBP of  180 mm Hg or DBP of 110 mm Hg). Rates were age adjusted by
the direct method to the overall cohort age distribution.
Cox proportional hazards regression was used to calculate multivariate-adjusted
hazard ratios (HRs) of death and their 95% confidence intervals (CIs) for
baseline BP categories, and to obtain multivariate-adjusted coefficients for
the relation of BP to mortality. The HRs were adjusted for age (years), race
(African American or not), education (years), serum total cholesterol level
(millimoles per liter [milligrams per deciliter]), cigarette smoking (cigarettes/day),
body mass index (BMI) (weight in kilograms divided by square of height in
meters), BMI2, and any ECG abnormality (no or yes).
Absolute excess death rates per 1000 in 25 years by JNC-VI stratum were
calculated from age-adjusted mortality rates per 1000 in 25 years. The reference
group was the stratum with normal (not optimal) BP. Numbers of excess deaths
for other JNC-VI strata were calculated from these absolute excess rates and
numbers of men in these strata. Percentage of all excess deaths in each stratum
was also calculated.
Cox multivariate proportional hazards regression coefficients for the
relation of JNC-VI strata to all-cause mortality were used to estimate years
of shorter life expectancy for men with higher baseline BP levels compared
with men with normal BP. Detailed methods for these calculations have been
described elsewhere.23, 27
RESULTS
BASELINE FINDINGS
Table 1 presents data on
baseline variables. At baseline, 8.6% of the cohort had optimal BP (JNC-VI
criteria); 20.2%, normal (not optimal) BP; 25.5%, high-normal BP; and 36.4%,
stage 1 hypertension.
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Table 1. Baseline Characteristics of Men Aged 18-39 Years*
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BASELINE SBP AND DBP AND MORTALITY
During follow-up, 197 men died of CHD; 257 of CVD; and 759 of all causes.
Age-Adjusted Mortality Rates
With higher SBP, age-adjusted mortality due to CHD and CVD increased
continuously and markedly (Table 2).
For DBP, mortality due to CHD and CVD was lower for men with DBP of 70 to
79 mm Hg than for those with DBP of less than 70 mm Hg. For strata with DBP
of greater than 70 to 79 mm Hg, mortality rates were progressively and markedly
higher.
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Table 2. Relationship of Baseline Blood Pressure (BP) to 25-Year Mortality
From Coronary Heart Disease, Cardiovascular Diseases, and All Causes
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For all-cause mortality, rates were lowest in men with SBP of 120 to
129 mm Hg and with DBP of 70 to 79 mm Hg; for strata with higher levels, rates
were generally progressively higher.
Multivariate-Adjusted HRs
With SBP of 120 to 129 mm Hg and DBP of 70 to 79 mm Hg as the references,
HRs for CHD, CVD, and all-cause mortality generally increased with higher
SBP and DBP level (Table 2).
For men with DBP of less than 70 mm Hg, HRs were nonsignificantly higher
for all 3 end points (1.63, 1.32, and 1.22 for CHD, CVD, and all-cause mortality,
respectively) compared with men with DBP of 70 to 79 mm Hg.
Cox Multivariate-Adjusted Coefficients
For SBP and DBP, Cox coefficients were statistically significant for
all 3 mortality end points (Table 2).
For CHD deaths, these coefficients yielded HRs—for 1-SD higher SBP (15.2
mm Hg) and DBP (10.4 mm Hg)—of 1.26 (95% CI, 1.11-1.44) for SBP and
1.17 (95% CI, 1.01-1.35) for DBP. For comparison, these estimates for the
CHA cohort of middle-aged men (aged 40-59 years) were 1.23 (95% CI, 1.15-1.32)
for SBP and 1.29 (95% CI, 1.21-1.38) for DBP (coefficients 0.0108 and 0.0223;
1 SD, 19.3 mm Hg and 11.5 mm Hg).
BASELINE SBP/DBP (JNC-VI CRITERIA) AND LONG-TERM MORTALITY
Overall Findings
Age-adjusted death rates and multivariate-adjusted HRs were lowest for
the normal (but not optimal) stratum (Table
3). Adjusted rates and HRs increased progressively for strata above
normal BP, eg, CHD HRs of 1.37 for the high-normal stratum and of 1.62, 2.51,
and 3.60 for hypertension stages 1, 2, and 3 strata, respectively, compared
with the normal stratum.
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Table 3. Relationship of Baseline JNC-VI Classification to 25-Year
Mortality Due to Coronary Heart Disease, Cardiovascular Diseases, and All
Causes*
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HRs in Men With Optimal BP
For men with optimal BP, risks were relatively (nonsignificantly) higher
for CHD, CVD, and all causes than for those with normal BP (Table 3). As mentioned in JNC-V and JNC-VI guidelines on optimal
BP, unusually low BP readings need clinical evaluation.20, 28
For men with optimal BP in this cohort, 45 deaths (of 59 due to all causes)
were attributed to noncardiovascular causes, and about half of these deaths
were due to neoplasms (Table 4). In a further analysis, age-adjusted rates for CHD and CVD for men with optimal
BP were equal to or lower than those for men with normal BP (Table 5). Multivariate-adjusted HRs, particularly for CHD and CVD,
were lower than those in Table 3,
ie, 1.08 (CHD), 1.06 (CVD), and 1.24 (all causes). With exclusion also of
men with DBP of 60 to 64 mm Hg, HR for all causes was reduced to 1.15 (95%
CI, 0.79-1.68) (detailed data not shown).
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Table 4. Underlying Cause for 45 Noncardiovascular Deaths With Optimal
Blood Pressure at Baseline
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Table 5. Relationship of Baseline JNC-VI Classification to 25-Year
Mortality From Coronary Heart Disease, Cardiovascular Diseases, and All Causes*
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ABSOLUTE EXCESS RISKS AND EXCESS DEATHS BY JNC-VI BP CLASSIFICATION
Absolute excess risks for CVD death were 6.3, 10.8, 33.1, and 74.1 per
1000 in 25 years for men with high-normal BP and stages 1, 2, and 3 hypertension,
respectively (Table 6). For all-cause
death, absolute excess risks ranged from 10.1 to 107.6 per 1000 in 25 years.
For men with higher BP levels, ie, high-normal BP and stages 1, 2, and 3
hypertension, estimated life expectancy was shorter by 2.2, 4.1, 8.4, and 12.2 years, respectively,
compared with men with normal BP.23, 27
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Table 6. Absolute Excess Risk per 1000 in 25 Years and Percentage of
All Excess Deaths in Strata of JNC-VI Classification*
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For each mortality end point, the highest proportion of all excess deaths—41.6%
to 45.6%—was in the large stratum (3963 of the 10 874 men) with
stage 1 hypertension (Table 6). Of all excess deaths, 15.6% to 16.9% were in the sizable high-normal stratum
(2773 men), more than in the small stratum (161 men) with stage 3 hypertension.
Together, the high-normal and stage 1 hypertensive strata accounted for 58.5%
of excess CVD deaths and 59.4% of excess deaths due to all causes.
COMMENT
The main findings on this cohort of young adult employed men are as
follows. (1) Even at their age (average, 30 years), SBP/DBP at optimal or
normal levels prevailed in only 28.8% (8.6% + 20.2%), whereas (2) SBP/DBP
was high-normal or stage 1 hypertension in 61.9% (25.5% + 36.4%). These findings
almost certainly reflect the adverse impact of dietary and other lifestyle
traits leading to BP rise from youth onward in most people (eg, on average
the cohort was overweight [BMI, 26.0]). (3) Blood pressure measured in young
adulthood predicted long-term risks for CHD, CVD, and all-cause mortality.
As in middle-aged and older persons,1-6
relationships of SBP, DBP, and SBP/DBP (JNC-VI strata) to mortality were generally
graded, strong, and independent. (4) Multivariate-adjusted HRs tended to be
greater for SBP than DBP, and similar in size to those for middle-aged men.
(5) For the 2 large strata with high-normal BP and stage 1 hypertension, 25-year
absolute risks and absolute excess risks for mortality—for the years
from average ages of 30 to 55 years—were substantial, eg, all-cause
mortality rates of 63 and 72 per 1000 and absolute excess rates of 10 and
20 per 1000, translating into estimated shorter life expectancy of 2.2 and
4.1 years. These 2 strata accounted for 59.4% of all excess deaths attributable
to above-normal SBP/DBP.
Observations on BP and CHD or total CVD mortality in young adults are
limited, mainly because elucidation of this matter requires large sample sizes
and long-term follow-up to accrue sufficient events for statistical analysis.
In the 1960s, Paffenbarger et al11-13
reported nested case-control investigations of 45 000 college entrants
(average age, 19 years) from the University of Pennsylvania and Harvard University
examined from 1921 through 1950. They demonstrated that higher percentages
of those who died of CHD and stroke had higher SBP (130 mm Hg) at entry
examination. However, analyses of BP and mortality were not multivariate adjusted,
and detailed relations by BP strata were not investigated. Other long-term
cohort studies have investigated cardiovascular risk factors in young adults
on a smaller scale. Thirty-year follow-up data on Framingham Study participants
aged 31 to 39 years at baseline did not provide results on blood pressure29; 14- and 18-year follow-up reports on Framingham
young adults combined participants aged 30 to 49 years.7, 30
The Johns Hopkins Precursors Study on almost 1000 young male medical students
(mean age, 22 years) reported 30-year CVD mortality in relation to serum cholesterol
levels31 and vascular reactivity,32
but these reports gave no data on blood pressure and subsequent CVD events.
Investigations by the Society of Actuaries yielded detailed findings on BP
levels at entry and all-cause mortality among approximately 4 million entrants
aged 15 to 69 years.14-16
These large-scale data showed continuous and graded relationships of SBP/DBP
to mortality in entrants aged 20 to 29 and 30 to 39 years, but the data were
not multivariate adjusted and may have limitations related to accuracy of
BP measurement in insurance examinations. Recently, a study from Glasgow,
Scotland, briefly reported a significant relationship between SBP in university
students and subsequent CVD mortality, but detailed relations by BP strata
were not given.33 Thus, our data go beyond
the few previous findings and constitute, to our knowledge, the first detailed
report from a large, long-term study of young adults from the general population
showing a significant independent association of BP level and CHD or CVD mortality.
Advanced coronary atherosclerosis was seen in most young American men
undergoing autopsy during the Korean and Vietnam wars.34-35
Other studies of the natural history of atherosclerosis indicate that in populations
with high rates of premature coronary artery disease, advanced lesions appear
with increasing frequency during the years of childhood and young adulthood.36 In autopsy studies from the Bogalusa Heart Study,
among children and young adults who died prematurely of noncardiac causes,
the extent of involvement of aortic and coronary artery wall with fatty streaks
and fibrous plaques was associated with major coronary risk factors, including
BP.17-18 Another autopsy study
of youth showed a relation of coronary atherosclerosis to an index of mean
arterial pressure based on findings in small renal arteries.19
Correspondingly, a recent report on electron-beam computed tomography showed
that, in young adults, BP related to presence of coronary artery calcification.37 It is reasonable to interpret our data as concordant,
ie, indicating that such BP-related early atherosclerotic lesions lead to
greater risk for fatal CVD during the decades from young adulthood through
middle age.
Our data indicate that SBP may be more useful in predicting future CHD
and CVD deaths than DBP. Risk generally increased throughout the range of
SBP from 120 to 180 mm Hg and above. This finding for young adults lends support
to recent assessments, based on data for older adults, that SBP might be more
important than DBP and that both (SBP/DBP) merit consideration in assessment
of CVD risk.7-10
Although not statistically significant, our data on low DBP (<70
mm Hg) suggest it may be related to increased long-term CHD, CVD, and all-cause
mortality and that low SBP (<120 mm Hg) may be related to increased all-cause
mortality. These results should be interpreted with caution for several reasons.
First, HRs were not significant and 95% CIs were wide, given small numbers
of CHD and CVD deaths in these categories. Second, as footnoted in the BP
classification of JNC-V and JNC-VI,20, 28
people with very low BP, especially very low DBP, may have medical abnormalities,
eg, aortic insufficiency or preclinical neoplastic disease, hence needing
medical evaluation. We could not completely exclude men with medical conditions.
After exclusion of those with low DBP (<60 mm Hg, also <65 mm Hg), risks
for CHD and CVD mortality in the optimal and normal BP strata were almost
identical. Therefore, it is reasonable to infer that these data do not critically
bring into question the conclusion that the relationship between SBP/DBP and
CVD risks is generally continuous (monotonic), and that for healthy adults,
including young as well as older adults, SBP/DBP of less than 120/80 mm Hg
(<120/<80 mm Hg) or of less than or equal to 120/80 mm Hg ( 120/80
mm Hg) is optimal.
A limitation of the present study is that results were based on a single
measurement of blood pressure, hence, they probably underestimate true associations
because of regression dilution bias.1 Nonetheless,
as shown here and in many other prospective population studies, a single BP
reading is strongly predictive of future CVD events. Since this cohort was
identified at employment sites, the role of the "healthy worker effect" should
be considered, ie, because working populations tend to be healthier than general
populations, the mortality rate of the CHA cohort was about 30% lower than
that expected for a similar sample of the general population. However, this
phenomenon has little or no bearing qualitatively on the relation of baseline
risk factors (including BP) to long-term mortality, as shown by many prospective
studies with similar qualitative results on this matter for workplace-based
and community-based populations samples.1-2
It is possible that because of this phenomenon, our study quantitatively underestimates
absolute risk and absolute excess risks of adverse blood pressure levels for
young adult men. Thus, it is a reasonable inference, supported by the limited
data available from other studies of young adults, that these findings are
generalizable.
Our results indicate that levels of blood pressure above normal in young
adults is a large unsolved problem for medical care and public health. Long-term
absolute risks and absolute excess risks, ie, from average age of 30 years
at baseline to 55 years, were substantial for these young adult men, making
up 61.9% of this cohort, with 59.4% of all excess deaths in men with high-normal
BP and stage 1 hypertension.
These data lend strong support to 2 strategic concepts. First population-wide
primary prevention by safe nutritional-hygienic means of adverse BP levels,
highly prevalent at present in middle-aged and older people, is important.
With such primary prevention, a substantial increase can be achieved in the
proportion of people in the population who throughout life have favorable
levels of BP (and other risk factors). Second, population-wide efforts should
be made for early detection of children, teenagers, young adults, and others
with unfavorable BP levels, so that therapeutic efforts can be instituted
early, first and foremost to improve lifestyles. Initial lifestyle recommendations
to prevent and treat high BP involved avoidance of high levels of salt intake,
inadequate potassium intake, excess alcohol use, overweight, and sedentary
habit.38-40 Based
on recent research advances, these recommendations have been expanded to include
high intake of fruits, vegetables, whole grains, and legumes; fat-free and
low-fat protein sources; and low intake of lipid-rich foods (ie, reduced dietary
total fat, saturated fat, and cholesterol) and sweets.20, 41-43
Our results also support recommendations by JNC-VI on dealing with risks
for persons aged 18 years and older with high BP. Because our study was observational,
not interventional, it yielded no direct data related to treatment of high
BP in young adults by lifestyle and (as indicated) pharmacological means.
For hypertensive men of this age, there are no clinical trial data, no trials
on-going, and to the best of our knowledge none planned, because sample size
and duration are forbidding. Therefore, use of drugs for this age group must
rely on judgment concerning the likely mix of benefit and risk with decades-long
treatment. Our data are important evidence on risks; they reinforce JNC-VI
recommendations to base drug (along with lifestyle) treatment on BP levels,
findings for other risk factors and for target organ damage, and response
to initial lifestyle intervention, and not on age.
In conclusion, the data of this study on young adult men underscore
the soundness of recommendations for population-wide lifestyle modifications
to prevent adverse BP levels, population-wide efforts for early detection
and lifestyle counseling for those who already have unfavorable BP levels,
and, for those with frank high BP at any adult age, implementation of JNC-VI
guidelines for treatment.
AUTHOR INFORMATION
Accepted for publication November 7, 2000.
The Chicago Heart Association Detection Project in Industry has been
supported by the American Heart Association and its Chicago and Illinois affiliates,
Chicago, Ill; the Illinois Regional Medical Program, Chicago; grant HL21010
from the National Heart, Lung, and Blood Institute, Bethesda, Md; the Chicago
Health Research Foundation, Chicago; and private donors.
Presented at the 18th Scientific Meeting of the International Society
of Hypertension, Chicago, Ill, August 23, 2000.
The work of the Chicago Heart Association Detection Project in Industry
Study was accomplished thanks to the invaluable cooperation of 84 Chicago
companies and organizations and their officers, staff, and employees, whose
volunteer efforts made the project possible. Acknowledgment is also gratefully
extended to all those in the Chicago Heart Association—staff and volunteers—serving
the project. Many of these individuals are cited by name in Stamler et al.22-23
Corresponding author and reprints: Martha L. Daviglus, MD, PhD, Northwestern
University Medical School, Department of Preventive Medicine, 680 N Lake Shore
Dr, Suite 1102, Chicago, IL 60611-4402 (e-mail: daviglus{at}nwu.edu).
From the Department of Preventive Medicine, Northwestern University
Medical School, Chicago, Ill (Drs Miura, Daviglus, Dyer, Liu, Stamler, and
Greenland and Mr Garside), and the Department of Public Health, Kanazawa Medical
University, Ishikawa, Japan (Dr Miura).
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