From the Center for Stroke Research, Department of Neurology, Henry Ford
Hospital & Health Sciences Center (Detroit Campus of Case Western
University), Detroit, Mich (D.T.); The Computing Center, Bar-ilan University,
Ramat Gan, Israel (S.Y.); and the Department of Epidemiology and Preventive
Medicine, Sackler School of Medicine, Tel-Aviv University and Neufeld Cardiac
Research Institute, Sheba Medical Center, Tel-Hashomer, Israel (U.G.). Dr
Tanne is now at the Department of Neurology, Sheba Medical Center,
Tel-Hashomer, Israel.
Correspondence to U. Goldbourt, PhD, Section of Epidemiology, Neufeld Cardiac Research Institute, Sheba Medical Center, Tel-Hashomer 52621, Israel. E-mail goldbu1{at}ccsg.tau.ac.il
Methods and Results—Civil servants and municipal employees
in Israel (n=9734 men; age,
Conclusions—Assessment of multiple risk factors provides useful
quantitative prediction of long-term ischemic stroke mortality
risk. Regional-ethnic variations are consistent with a
hypothesis that other, undetermined inherent genetic or sociocultural
factors act to increase ischemic stroke mortality rates in
immigrants to Israel from the Mideast and northern Africa over that
predicted by conventional risk factors.
The Israeli Ischemic Heart Disease (IIHD) Project is a
longitudinal investigation of the incidence and risk factors for
cardiovascular disease among about 10 000 male civil
servants and municipal employees in Israel, chosen by stratified
sampling in 6 areas of birth (those born in Israel and those who were
immigrants from 5 other prespecified areas). This cohort provided an
extensive representation of the socioeconomic levels in the
male working population of Israel at the time of inclusion. The
present report deals with the role of regional-ethnic origin in
ischemic stroke mortality, and provides a quantitative
determination of long-term risk based on multiple risk factors. Our
prospective analysis has the advantage of being able to use
repeated measurements of blood pressure (BP) and biochemical attributes
and thus to estimate the regression dilution bias (RDB) and to correct
for it when estimating risks associated with these
factors.9 10
Participants underwent clinical and blood biochemical evaluations in
1963, 1965, and 1968. The response rate to the initial examination was
86.2%, and 98% of those living in 1965 were reexamined. There was no
significant difference between the subjects examined and the
nonresponders with respect to age, area of birth, or socioeconomic
status. Further details of the study (population, sampling procedures,
mortality, follow-up, and analysis) have been described
elsewhere.11 12 The current report includes
mortality follow-up over a 21-year period for the 9734 participants
examined during the second round of examinations in 1965.
The underlying cause of death was documented on the basis of
case-by-case determinations by a review panel until 1970 and by the use
of the International Classification of Diseases
(ICD)13 codes thereafter. Deaths from presumed
ischemic stroke were based on ICD-9 codes 433 to 438. Our data
do not permit separation of cardioembolic from noncardioembolic
mechanisms.
Information on death was derived from the Israeli Mortality Registry.
For all hospital deaths until 1970, comparison of death certificates
with the analyses of hospital records (including physician
notes, autopsy reports, and death certificates) by a study panel
revealed a >90% agreement. A comparison of our physicians'
analyses of a 25% random sample of hospital deaths versus
death certificates showed an agreement of almost 100% for deaths due
to cancer and 84% for deaths due to nonmalignant disease.
BP was measured in the right arm, with the subject in the recumbent
position,
History of myocardial infarction was corroborated by changes on ECG
consistent with an old infarction or by search of the medical
summaries and the ECG tracings at the time of the myocardial infarction
with verification by 2 cardiologists. Definite angina was
diagnosed by use of the World Health Organization (WHO) (Rose) chest
pain questionnaire,14 in which typical presternal
pain was caused by physical exertion and was relieved within 10 minutes
by discontinuation of exertion or by intake of a vasodilating
drug. History of peripheral vascular disease (PVD)
was recorded on the basis of the presence of calf pain induced by
walking that was relieved within 10 minutes by
rest.14 History of diabetes mellitus and smoking
status were recorded by subjects' self-report during the medical
history.
Blood samples were drawn with the subject in a nonfasting state and
were kept refrigerated and shipped daily in ice-cooled containers to a
central laboratory. There, total cholesterol, HDL
cholesterol, uric acid, glucose, and hematocrit levels were
determined.
Statistical Methods
To estimate the effect of area of birth, predicted ischemic
stroke mortality rates were calculated by a logistic regression
model18 for the 6 regional-ethnic strata, and
rates were compared with the crude rates observed. To evaluate the
extent to which classification of subjects by their risk factors
discriminates between those destined to die of ischemic stroke
and others, men were ranked according to probability calculated from a
logistic regression model. Comparison of the predicted and observed
rates of events yields an estimate of fit, whereas the gradient of
increase in rates provides a measure of discrimination ability.
Somers' D, Goodman-Kruskal G, and the C statistic
(area under the receiver operating curve) are presented as
measures of rank correlation between the predicted and observed
responses.18 The Hosmer-Lemeshow goodness-of-fit
test was used to test the departure of observed from predicted number
of events within quintiles of probability.
Regression dilution factors were estimated by dividing the difference
in means between the highest and lowest quintiles in 1965 by the same
difference in 1963, based on the 1965 measurements. Corrections for the
RDB, associated with increments in the risk-factor variables, were
made by multiplying the coefficients obtained from the Cox model by the
corresponding regression dilution factors before exponentiation to
obtain the estimated HR.
Predictors of Ischemic Stroke Mortality: Age-Adjusted
Analysis
A strong association was demonstrated between systolic and
diastolic BP and between presence of LVH on ECG and
ischemic stroke mortality (Table 2
Age-adjusted rates were more than doubled among subjects with either
history of angina (29.7 versus 14.4), diabetes mellitus (30.8 versus
13.6), or PVD (31.3 versus 13.6) versus those without
(P<0.01 for each). Rates increased from 12.2 among
nonsmokers to 18.6, 14.1, and 18.7 among men smoking 1 to 10, 11 to 20,
and >20 cigarettes per day on entry, respectively (P=0.01).
Serum glucose levels were positively associated in a dose-response
manner with fatal ischemic stroke rates. Age-adjusted rates
increased from 11.3 to 13.5 and 19.0 for increasing serum glucose
tertiles (P<0.001). A positive trend existed among
nondiabetic subjects also, with rates rising from 11.0 to 12.2 and 14.8
for increasing tertiles (P=0.009). Trends for increasing
rates of ischemic stroke mortality were found with decreasing
tertiles of %HDL and increasing tertiles of uric acid and hematocrit,
but they fell short of a conventional type I error probability.
Predictors of Ischemic Stroke Mortality: Multivariate
Analysis
Separate Cox proportional hazards models performed for each
regional-ethnic group (data not shown) demonstrated interarea
associations between most risk factors and fatal ischemic
stroke that resemble the associations obtained in the entire study
cohort. However, overall lower HRs were noted in subjects born in Asia
or Africa versus those born in Europe for diabetes mellitus (1.4 to 1.7
versus 1.8 to 4.5), PVD (0.6 to 0.7 versus 1.4 to 4.7), and smoking
>20 cigarettes per day (0.6 to 1.4 versus 1.9 to 2.5).
Crude rates of ischemic stroke mortality observed among
subjects immigrating from Asia or Africa (29.4 to 31.2 per 1000
subjects) exceeded the rates predicted on the basis of the individual
risk-factor profiles (21.4 to 24.9). Conversely, the observed rates
among immigrants from Europe were below predicted levels (Table 4
Crude rates were >30-fold greater among subjects at the highest
quintile of probability compared with the lowest quintile, on the basis
of individual risk-factor profiles (81.2 versus 2.6 per 1000 subjects),
as shown in Table 5
To illustrate the incremental significance of risk factors for fatal
ischemic stroke, we have calculated risk as a function of the
number of risk factors identified at baseline separately for subjects
with systolic BP
Regression Dilution Factor
Area of Birth
The relative contribution of genetic, environmental, and behavioral
factors to the differences observed is still unclear. Genetic factors
may affect predisposition and distribution of
atherosclerosis and cardiovascular
disease.21 22 In an autopsy study comparing
cerebral atherosclerosis in Israeli Jewish subjects of
European and Asian or African origin, no differences have been
identified in the severity of atherosclerosis in
arteries of the circle of Willis, but correlations between severity of
cerebral and coronary atherosclerosis were
weaker among those born in Asia or Africa.23
Higher stroke mortality rates were reported among Jewish subjects in
Israel than in Montreal, suggesting additional behavioral or
environmental effects.24 Ethnic variation in
ischemic stroke mortality in our cohort is consistent
with a hypothesis that other, undetermined inherent genetic or
sociocultural differences act to increase the incidence and/or case
fatality from ischemic stroke in immigrants from Africa and
Asia over that predicted from their profiles of conventional risk
factors.
Age and Clinical Determinants
LVH on ECG
Blood Lipids
Multiple Risk Factors
Limitations
In summary, our data facilitate the estimation of risk for long-term
ischemic stroke mortality in an immigrant working male
population of marked ethnic and cultural background in Israel and
provide a quantitative determination of risk based on multiple risk
factors. Ethnic variations observed in ischemic stroke
mortality are consistent with a hypothesis that other,
undetermined inherent genetic or sociocultural differences act to
increase ischemic stroke mortality rates in immigrants to
Israel from Asia and Africa over that predicted from their profile of
risk factors. Further studies assessing genetic, environmental, and
behavioral factors on stroke risk among different populations are
warranted.
Received February 12, 1998;
revision received May 20, 1998;
accepted May 28, 1998.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Risk Profile and Prediction of Long-Term Ischemic Stroke Mortality
A 21-Year Follow-up in the Israeli Ischemic Heart Disease (IIHD) Project
Abstract
Top
Abstract
Introduction
Methods
Results
Discussion
References
Background—Multinational
comparisons demonstrate marked ethnic and regional variation in stroke
mortality and risk-factor distribution. We assessed the role of
ethnicity and estimated the cumulative effect of multiple risk factors
on long-term ischemic stroke mortality. 
42 years), chosen by stratified sampling
in 6 prespecified areas of birth (those born in Israel and those who
were immigrants from 5 other regional-ethnic strata), were included in
the Israeli Ischemic Heart Disease (IIHD) Project. Over a
21-year follow-up period, age-adjusted mortality rates per 10 000
person-years attributed to ischemic stroke (n=282;
International Classification of Diseases [ICD]-9 codes 433 to 438)
were higher among immigrants to Israel from northern Africa and the
Mideast (17.1 to 19.0), than from 3 parts of Europe (11.3 to 12.4).
Crude rates per 1000 subjects observed in those born in Asia or Africa
(29.4 to 31.2) exceeded rates predicted by risk-factor profiles (21.4
to 24.9). Adjusted hazard ratios were 3.00 for age (per 10 years), 2.15
for left ventricular hypertrophy, 1.69 for
systolic blood pressure (BP, per 20 mm Hg), 1.86 for
diabetes mellitus, 1.83 for peripheral vascular disease,
1.79 for smoking (>20 cigarettes per day), 1.51 for coronary
heart disease, 1.16 for percent cholesterol contained in
the HDL fraction (%HDL, per 5% decrease), and 1.88 for
diastolic BP (per 12 mm Hg; assessed in an
alternative model). Accounting for regression dilution bias and
assessed from repeat measurements, we found that hazard ratio estimates
associated with diastolic BP, systolic BP, and
percent HDL (per increments described) increased to 3.22, 2.23, and
1.23, respectively. Ischemic stroke mortality rates were
30-fold greater among subjects at the highest versus the lowest
quintile of predicted probability according to risk-factor profiles
(81.2 versus 2.6 per 1000 subjects).
Key Words: cerebrovascular disorders • risk factors • epidemiology • mortality
Introduction
Top
Abstract
Introduction
Methods
Results
Discussion
References
Multinational comparisons demonstrate marked ethnic and
regional variation in stroke mortality rates.1 2 3
The relative importance of different predictors of fatal
ischemic stroke varies among
populations.4 5 6 7 8 A considerable proportion of the
Israeli population was formed by immigration from Europe, the Mideast,
and northern Africa. The diversity in ethnic background and lifestyle
provides an unusual opportunity for evaluating the role of ethnic
origin and enhancing generalizability of risk-factor assessment for
stroke.
Methods
Top
Abstract
Introduction
Methods
Results
Discussion
References
Subjects
The participants of the IIHD Project were chosen by
stratified sampling of civil servants and municipal employees in 1963
based on (1) men aged 40 years on inclusion, (2) place of work
confined to the 3 largest urban areas in Israel (Tel-Aviv, Jerusalem,
and Haifa), and (3) sampling fractions aimed at obtaining numbers of
study subjects from 6 areas of birth (central Europe, eastern Europe,
the Balkan countries, the Mideast, northern Africa, and Israel)
proportional to the Israeli male population of this age. The sampling
frame consisted of 24 330 eligible men, and the sampling ratios used
were 1:4 for eastern Europe, 5:7 for central Europe, 5:6 for the Balkan
countries, and 1:1 each for Israel, the Mideast, and northern
Africa. 
30 to 45 minutes after arrival at the clinic and again 15
to 30 minutes later. Left ventricular
hypertrophy (LVH) on ECG was diagnosed by R wave in lead
aVF 2.0 mV or lead aVL 1.3 mV, S wave in V1
plus R wave in lead V5 or
V6 4.6 mV, or S wave in
V2 plus R wave in lead V5
or V6 4.6 mV.
Direct age-adjusted ischemic stroke mortality rates were
calculated in person-years, taking into account the shifting age of the
study population over the long follow-up
period.15 Testing trend of increasing rates in
tertiles or quintiles of risk factors was performed by use of the TREND
utility.16 Multivariate
analysis of ischemic stroke mortality was performed by
use of the Cox proportional hazards model within the whole study
cohort.17 The model incorporated age, area of
birth (by introducing 5 indicator variables to account for the 6
regional-ethnic strata), diabetes mellitus, systolic BP, LVH on
ECG, history of coronary heart disease (CHD) (myocardial
infarction or angina), cigarette smoking status, PVD, body mass index,
serum glucose, uric acid, percentage of serum cholesterol
contained in the HDL fraction (%HDL), and hematocrit. In an
alternative model, diastolic BP was included instead of
systolic (because of the high intercorrelation between these 2
variables). Separate models were also performed within each area of
birth. Adjusted hazard ratios (HR) and 95% CIs are
presented.
Results
Top
Abstract
Introduction
Methods
Results
Discussion
References
Over a 21-year follow-up, a total of 3276 (33.7%) deaths
were recorded among the 9734 participants. Deaths attributed to
ischemic stroke (282 cases) accounted for 8.6% of the total
mortality.
Ischemic stroke mortality rates varied 1.7-fold between
highest and lowest according to area of birth (Table 1
). Immigrants to Israel from Asia and
Africa had higher age-adjusted rates (17.1 to 19.0 per 10 000
person-years) than counterparts born in the 3 parts of Europe (11.3 to
12.4).
View this table:
[in a new window]
Table 1. Age-Adjusted Ischemic Stroke Mortality Rates in 6
Regional-Ethnic Strata Defined by Area-of-Birth Immigration to
Israel ). Age-adjusted rates rose almost 6-fold
from the lowest to the highest quintile for systolic BP (5.4 to
31.0, respectively) and >4-fold for diastolic BP (7.3 to
30.7). Subjects with LVH on ECG exhibited a 2.5-fold increased risk of
fatal ischemic stroke compared with those without (35.0 versus
13.8, P<0.001).
View this table:
[in a new window]
Table 2. Age-Adjusted Ischemic Stroke Mortality Rates by
Baseline BP and ECG Evidence for LVH
Age, the strongest independent predictor of ischemic
stroke mortality, was associated with tripling of risk per 10-year
increment (Table 3). LVH on ECG was
independently associated with more than doubling of risk. An increase
of 1 SD in systolic BP (20 mm Hg) was associated with
a 1.69-fold greater risk, whereas a corresponding change in
diastolic BP (12 mm Hg), assessed in an alternative
model, conferred a 1.88-fold greater risk. Diabetes mellitus, history
of PVD, and CHD on entry were each associated with excess risk of
>50%, and cigarette smoking (>20 cigarettes per day) was associated
with excess of approximately 80%. A 5% relative decrease in the %HDL
was associated with 16% excess risk of fatal ischemic stroke.
Compared with subjects born in northern Africa, the adjusted HR
associated with the other regional-ethnic strata were as follows: the
Mideast 0.94 (95% CI, 0.58 to 1.52), Israel 0.76 (95% CI, 0.45 to
1.29), eastern Europe 0.63 (95% CI, 0.39 to 1.04), central Europe 0.62
(95% CI, 0.35 to 1.09), and the Balkan countries 0.56 (95% CI, 0.33
to 0.94).
View this table:
[in a new window]
Table 3. Cox Proportional Hazards Model for Ischemic Stroke
Mortality Over a 21-Year Follow-Up Period Among 9734 Men in the IIHD
Project1 ). There are important age differences
between subjects from the different areas of birth, and thus the
area-of-birth order in the observed crude rates is not fully maintained
in the age-adjusted analysis.
View this table:
[in a new window]
Table 4. Predicted Ischemic Stroke Mortality Rates in 6
Regional-Ethnic Strata Based on Risk-Factor Profiles and Crude Rates
Observed . Nearly 60% of
events were observed among subjects in the highest quintile of
probability. The rank correlations between the observed and predicted
responses assessed by Somers' D (0.55), Goodman-Kruskal G
(0.56), and the C statistic (0.77) are consistent with a
satisfactory agreement between predicted and observed rates. The
Hosmer-Lemeshow goodness-of-fit test (P=0.28) does not point
to a meaningful departure of the model from the observed data.
View this table:
[in a new window]
Table 5. Predicted Ischemic Stroke Mortality Rates by
Quintile of Probability Based on a Logistic Regression Model and Crude
Rates Observed 160 mm Hg or diastolic BP
105 mm Hg versus counterparts with lower baseline BP
measurements (Figure 1). Crude rates were
3-fold greater among subjects with higher BP than among counterparts
with lower baseline BP and increased with an increasing number of
additional risk factors (rate range per 1000 subjects, 42 to 91 for men
with higher BP versus 12 to 41 for men with lower BP, for 0, 1, or 2
additional risk factors).
View larger version (23K):
[in a new window]
Figure 1. Crude rates of ischemic stroke mortality
per 1000 subjects by increasing number of baseline risk factors (age
>60 years, diabetes mellitus, coronary heart disease,
peripheral vascular disease, or smoking >20 cigarettes per
day) in subjects with baseline systolic blood pressure (SBP)
160 mm Hg or diastolic blood pressure (DBP)
105 mm Hg, and in counterparts with lower blood pressure
measurements.
Regression dilution factors estimated from repeated measurements
on 2 rounds of examination were highest for diastolic BP
(1.85) and systolic BP (1.53) and <1.5 for %HDL, serum
glucose, and uric acid. Age-adjusted ischemic stroke mortality
rates by quintiles of baseline BP measurements versus by quintiles of
an estimation of an individual's average BP (usual BP) are depicted in
Figure 2. Both diastolic and
systolic BP measurements displayed a curvilinear relationship
with ischemic stroke mortality with an increase in rates that
occurred predominantly above the second quintile. Estimated HR after
correction for the corresponding RDB increased for
diastolic BP from 1.88 to 3.22, for systolic BP
from 1.69 to 2.23, and for %HDL from 1.16 to 1.23 (Table 6).
View larger version (29K):
[in a new window]
Figure 2. Age-adjusted ischemic stroke mortality
rates per 10 000 person-years by quintiles of baseline (top) and usual
(bottom), systolic (left), and diastolic (right)
blood pressure measurements. Abbreviations as in Figure 1 
.
View this table:
[in a new window]
Table 6. HR Associated With BP and %HDL Before and After
Correction for RDB
Discussion
Top
Abstract
Introduction
Methods
Results
Discussion
References
The 21-year follow-up of almost 10 000 participants included in
the IIHD Project cohort provided nearly 200 000 person-years of
follow-up of a working male population in Israel of marked ethnic,
cultural, and occupational diversity, representing
immigrants from >20 countries on 3 continents.
Stroke mortality is known to vary markedly among regions and
ethnic groups.1 2 3 19 20 Data, however, are
derived mainly from multinational comparisons and are limited from
areas such as the Mideast and northern Africa. Subjects born in
Asia or Africa exhibited higher age-adjusted ischemic stroke
mortality rates than those born in Europe, as shown also in a
population-based study from northern Israel.19
The trends in risks of ischemic stroke mortality observed among
areas of birth after adjustment are consistent with a role for
attributes specific to areas of birth beyond the conventional stroke
risk factors. Although subjects born in Europe exhibited lower
ischemic mortality rates than predicted by their risk-factor
profile, those born in Asia or Africa exhibited higher rates than
predicted. Opposite trends were found for CHD in the same
cohort,21 suggesting possible effects of
additional factors involved in predilection to end-organ damage.
The major risk factors identified in our cohort (older age,
high BP, history of diabetes mellitus, PVD, CHD, and cigarette smoking)
are in agreement with a large body of
evidence.4 5 6 7 8 25 26 27 The risk of ischemic
stroke mortality increased directly with elevations in BP, whether
systolic or diastolic, with rates increasing
steeply from above the second quintile. Corrections for the RDB gave
more reliable estimates of risk with a more than tripling of the risk
for diastolic BP and more than doubling for
systolic BP, associated with increments of 1 SD.
LVH detected by ECG was identified in our cohort to be a strong
determinant for ischemic stroke mortality, independent of
conventional BP measurements and other atherogenic risk factors. These
data support prior reports on the association between LVH or left
ventricular mass and stroke.28 LVH is
associated with extracranial carotid atherosclerosis,
thus also predisposing individuals to ischemic stroke, although
the mechanisms underlying this association are not
clear.29
There are conflicting data regarding the association between serum
lipid levels and ischemic strokes. Recent reports, however,
show that treatment of dyslipidemia reduces the risk of
stroke and total mortality.30 In our cohort, HDL
cholesterol levels were inversely associated with fatal
ischemic strokes, and total cholesterol positively
was associated. Low HDL cholesterol emerged, adjusting for
multiple risk factors, as an independent predictor of ischemic
stroke mortality.31
Risk factors interact to increase the probability of stroke in
subjects with multiple risk factors. Analyses of data from the
Framingham study have described a general cerebrovascular risk profile
that can be used to identify 10% of the population that will have at
least one third of the strokes.27 Subjects at the
highest quintile of probability in our cohort exhibited a >30-fold
greater risk of ischemic stroke mortality than those at the
lowest quintile. Risk increased substantially with the number of risk
factors present. It is notable that variables, readily
determined on routine examination, have such a predictive power on
ischemic stroke mortality rates measure over >20 years,
irrespective of interventions and treatment during follow-up. Stroke
prevention strategies are gradually improving. Quantitative estimates
of the magnitude of increased risk for ischemic stroke
mortality in the presence of multiple risk factors may help both
patient and physician to more fully appreciate the need for measures to
limit risk factors and for aggressive risk-factor management.
Long-term mortality data were obtained from death certificates,
known for their potential inaccuracies. A validation study suggested
that deaths from stroke could be grouped fairly into hemorrhagic and
ischemic strokes by death certificate
diagnosis.32 In our study design, we do not have
data regarding interventions and treatment during long-term follow-up.
These limitations represent analytical shortcomings that may
lead to underestimation of true risks identified in the present
analysis. Finally, risks associated with prior stroke,
congestive heart failure, or atrial fibrillation, all extremely rare on
inclusion in our working male population, as well as risk profiles
applicable for women, could not be assessed in this study.
Acknowledgments
Data collection, analysis, baseline, and 2 incidence
examinations (1963, 1965, and 1968) were part of a collaborative study
by the National Institute of Health, the Ministry of Health, Israel;
and the Hadassah medical organization, supported by PL 480 counterpart
funds, research agreement No. 375106. The Israeli Academy of Sciences,
Fund for Basic Research, supported the mortality follow-up from 1970
to 1978.
References
Top
Abstract
Introduction
Methods
Results
Discussion
References
S, Nissinen A, Toshima H. Serum total
cholesterol and long-term coronary heart disease
mortality in different cultures. JAMA. 1995;274:131–136.[Abstract]
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D. Tanne, M. J. Gorman, V. E. Bates, S. E. Kasner, P. Scott, P. Verro, J. R. Binder, J. M. Dayno, L. R. Schultz, and S. R. Levine Intravenous Tissue Plasminogen Activator for Acute Ischemic Stroke in Patients Aged 80 Years and Older : The tPA Stroke Survey Experience Stroke, February 1, 2000; 31(2): 370 - 375. [Abstract] [Full Text] [PDF]
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C. L. Hart, D. J. Hole, and G. D. Smith Risk Factors and 20-Year Stroke Mortality in Men and Women in the Renfrew/Paisley Study in Scotland Stroke, October 1, 1999; 30(10): 1999 - 2007. [Abstract] [Full Text] [PDF]
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