Download Is Prehypertension a Risk Factor for Cardiovascular Diseases?

Is Prehypertension a Risk Factor for
Cardiovascular Diseases?
Adnan I. Qureshi, MD; M. Fareed K. Suri, MD; Jawad F. Kirmani, MD;
Afshin A. Divani, PhD; Yousef Mohammad, MD
Downloaded from http://stroke.ahajournals.org/ by guest on May 5, 2017
Background and Purpose—The Joint National Committee on High Blood Pressure identified a new category of blood
pressure in adults termed prehypertension. Our objective was to determine the long-term risk of cardiovascular diseases
associated with this new category in a well-defined cohort of adults.
Methods—We evaluated the association of prehypertension (120 to 139/80 to 89 mm Hg) and hypertension (⬎140/
90 mm Hg) with the incidence of atherothrombotic brain infarction (ABI), all strokes, myocardial infarction (MI), and
coronary artery disease (CAD) using pooled repeated measures and Cox proportional hazards analyses during follow-up
after adjusting for age, gender, obesity, diabetes mellitus, hypercholesterolemia, cigarette smoking, and study period in
a cohort of 5181 persons who participated in the Framingham Study.
Results—Among the 11 116 person observations with a mean follow-up period of 9.9⫾1.0 years, prehypertension was not
associated with an increased risk for ABI (relative risk [RR], 2.2; 95% CI, 0.5 to 9.3). Among the 11 802 person
observations with a mean follow-up period of 9.7⫾1.5 years, prehypertension was associated with an increased risk for
MI (RR, 3.5; 95% CI, 1.6 to 7.5). Prehypertension was also associated with an increased risk of CADs among the 11 570
person observations (RR, 1.7; 95% CI, 1.2 to 2.4).
Conclusions—Prehypertension appears to be associated with an increased risk of MI and CAD but not stroke. Further
studies are required to confirm the anticipated benefits of identifying and intervening in persons with prehypertension.
(Stroke. 2005;36:1859-1863.)
Key Words: cardiovascular diseases 䡲 cerebrovascular disorders 䡲 myocardial infarction 䡲 stroke
A
Measurement of Blood Pressure and Covariates
pproximately 50 million individuals in the United States
are affected by hypertension.1,2 The Seventh Report of
the Joint National Committee on Prevention, Detection,
Evaluation, and Treatment of High Blood Pressure (JNC 7)
designated a new category termed prehypertension and combined stages 2 and 3 of hypertension under 1 category.1
Because screening and treatment efforts are to be directed for
this new category of hypertension in the US population, we
sought to determine the risk of cardiovascular diseases
associated with prehypertension.
At each examination, a physician or nurse using a standard protocol
measured the systolic and diastolic blood pressure (BP) of the seated
subjects. The average of 3 readings was taken as the examination BP
of the participants. Only 1 BP reading was available for 2 examinations (contributed as 3% of total observations), and 2 BP readings
were available for 1 examination (contributed as 0.8% of total
observations). Patients were categorized (based on the JNC 71) as
normal if systolic BP was ⬍120 and diastolic BP was ⬍80 mm Hg;
prehypertension, 120 to 139/80 to 89 mm Hg; or hypertension,
ⱖ140/90 mm Hg. Patients were also classified as hypertensive based
on use of antihypertensive medication at the time of baseline
assessment and recategorization.
The status of BP and other covariates was recategorized every 10
years using the information derived from follow-up evaluation. The
follow-up evaluation was not conducted in the tenth year in a small
proportion of the participants. In those subjects, the next preceding
(year 8), or if not available the next succeeding (year 12), examination was used to acquire pertinent information for recategorization of
the status of BP and other covariates (eg, serum cholesterol).
Methods
We used the data from the well-defined cohort of the Framingham
Study to determine the effect of prehypertension on the long-term
risk of cardiovascular diseases. The study began in 1948, with
recruitment of 2336 men and 2873 women residents of Framingham,
Mass. The participants received a complete physical examination at
baseline, followed by repeat examinations every 2 years during the
course of follow-up, as described previously.3,4 Subjects who were
free of stroke or myocardial infarction (MI) at the baseline evaluation
were included.
Follow-Up and Outcome Events
All study subjects were under continuous surveillance for the
development of cardiovascular events and death. The primary
Received March 18, 2005; accepted April 6, 2005.
From the Zeenat Qureshi Stroke Research Center, Department of Neurology and Neurosciences (A.I.Q., M.F.K.S., J.F.K., A.A.D.), University of
Medicine and Dentistry of New Jersey, Newark; and Department of Neurology (Y.M.), Ohio State University, Columbus.
Reprint requests to Adnan I. Qureshi, MD, Neurological Institute of New Jersey, 90 Beren St, DOC 8100, Newark, NJ 07103. E-mail
[email protected]
© 2005 American Heart Association, Inc.
Stroke is available at http://www.strokeaha.org
DOI: 10.1161/01.STR.0000177495.45580.f1
1859
1860
Stroke
September 2005
outcomes were atherothrombotic brain infarction (ABI), all strokes,
MI, and coronary artery disease (CAD). CAD was defined by
occurrence of angina pectoralis, MI, coronary insufficiency, or death
from coronary heart disease. Criteria for these end points have been
described previously.5,6
Statistical Methods
Downloaded from http://stroke.ahajournals.org/ by guest on May 5, 2017
We used the technique of pooled repeated measures, an approach
that allows individuals to contribute multiple person observations to
the analysis as long as they meet the inclusion criteria at the
beginning of each observation interval.7,8 Specifically, persons free
of the specific cardiovascular disease at an examination were eligible
for the next period of observation for that incident event. For
example, patients who had not experienced MI during the first period
of observation were included in the screening during the second
observation interval for incident MI. Because the BP status varies
over time, the pooled repeated measures method was used to account
for time-dependent covariates. The technique is a generalized
person-years approach in that it treats each observation interval (of
equal length) as a mini–follow-up study in which the current risk
factor measurements are used to predict an event in the specified
interval. Observations over multiple intervals are pooled into a single
sample to predict the intermediate-term risk of an event.
Cox proportional hazards regression analyses were performed to
examine the association of BP measures with the incidence of a first
ABI, all strokes, MI, and CAD over a follow-up period of 10 years
after adjusting for established risk factors defined at the baseline
examination (age, gender, cigarette smoking, obesity, hypercholesterolemia, diabetes mellitus, and study period) and interaction
between BP measures and baseline covariates. Hypercholesterolemia
was defined by serum cholesterol concentration ⬎200 mg/dL.
Kaplan–Meier analysis was performed to estimate the risk of
developing hypertension among persons with normal BP or prehypertension at baseline evaluation during the 50-year follow-up
period. We determined the population-attributable risk (PAR)9 for
prehypertension. PAR% expresses the proportion of disease (such as
MI or ischemic stroke) in the study population that is attributable to
the exposure (prehypertension) and could be eliminated if the
exposure was eliminated. The PAR% was calculated as
PAR%⫽(Pe)(RR⫺1)/[(Pe)(RR⫺1)⫹1)]䡠100, where Pe is the proportion of the population exposed to the risk factor (prehypertension), and RR indicates relative risk (multivariate adjusted). We also
determined the effect of age (⬍45 years, between 45 and 64 years,
and ⱖ65 years), gender, cigarette smoking, obesity, hypercholesterolemia, and diabetes mellitus among prehypertensive person observations on the risk of developing events of interest.
TABLE 1. Baseline Demographic and Clinical Characteristics
of the Participants in the Framingham Study
Characteristics
Hypertension Prehypertension Normotension
(n⫽2042)
(n⫽2127)
(n⫽1012)
Mean age, years⫾SD
47.4⫾8.2*
42.9⫾8.2*
39.6⫾7.4
Men
997 (49%)
997 (47%)
320 (32%)
692 (68%)
Women
1045 (51%)*
1130 (53%)*
Mean systolic BP, mm Hg⫾SD
155⫾20*
128⫾6*
Mean diastolic BP, mm Hg⫾SD
95⫾10*
80⫾5*
72⫾5
28.2⫾4.7*
25.7⫾3.6*
24.0⫾3.0
Body mass index
Obesity, body mass index ⱖ30
112⫾6
597 (29%)*
321 (15%)*
35 (4%)
1057 (52%)*
1291 (61%)
621 (61%)
Previous cigarette smoker
136 (7%)
115 (5%)
52 (5%)
Nonsmoker
849 (42%)
721 (34%)
339 (33%)
Current cigarette smoker
Diabetes mellitus
Serum cholesterol, mg/dL⫾SD
64 (3%)*
24 (1%)
10 (1%)
232⫾47*
217⫾43*
205⫾41
Means and frequencies are compared using ANOVA and ␹2 methods,
respectively.
*P value of ⬍0.05 for comparison with normotensive participants.
change in BP status over time, the data were converted into
person observations.
Prehypertension and Risk of ABI and All Strokes
A total of 11 116 person observations with a mean follow-up
period of 9.9⫾1.0 years were categorized as hypertensive
(n⫽5712), prehypertensive (n⫽4163), and normotensive
(n⫽1241). The observed events rate for ABI was 24 (0.6%)
and 207 (3.6%) for prehypertensive and hypertensive person
observations, respectively. After adjusting for potential confounders, prehypertension was not associated with an increased risk for ABI (RR, 2.2; 95% CI, 0.5 to 9.3; Table 2).
The risk of all strokes was not higher among person with
Results
Baseline Characteristics of Participants
Ten persons with previous history of ABI and 18 persons
with history of MI at baseline evaluation were excluded from
analysis. A total of 5181 persons were included in the
analysis. The mean age (⫾SD) was 44.0⫾8.6 years; 2314
(45%) were men. The participants were followed for a period
of 31⫾13 years. The baseline demographic and clinical
characteristics of participants according to BP status are
provided in Table 1.
Risk of Developing Hypertension
The Figure demonstrates the cumulative risk of developing
hypertension over the duration of the follow-up period for
prehypertensive and normotensive participants. The risk of
developing hypertension over time was significantly higher
for persons with prehypertension (RR, 2.0; 95% CI, 1.9 to
2.2) compared with normotensive participants. To adjust for
Hypertension-free survival among persons with prehypertension
and normotension in the Framingham Study using Kaplan–Meier
analysis. The solid black line represents persons with normotension, and the dotted black line represents persons with
prehypertension.
Qureshi et al
Prehypertension and Cardiovascular Diseases
1861
TABLE 2. Risk of Cardiovascular Events Associated With Various BP Categories
in the Framingham Study
BP Categories
Person
Observations
Event
Rate
Age- and SexAdjusted
Risk (95% CI)
MultivariateAdjusted
Risk (95% CI)
Atherothrombotic brain infarction
Normotension
1241
2 (0.2%)
Reference
Reference
Prehypertension
4163
24 (0.6%)
2.0 (0.5–8.6)
2.2 (0.5–9.3)
Hypertension
5712
207 (3.6%)
8.0 (2.0–33)
9.0 (2.2–37)
All strokes
Normotension
1254
4 (0.3%)
Reference
Reference
Prehypertension
4280
56 (1.3%)
2.1 (0.7–5.7)
2.3 (0.8–6.3)
Hypertension
6307
439 (7.0%)
6.4 (2.4–17)
7.1 (2.6–19)
Normotension
1257
7 (0.6%)
Reference
Reference
Prehypertension
4253
138(3.2%)
3.3 (1.5–7.0)
3.5 (1.6–7.5)
Hypertension
6292
647(10.3%)
7.2 (3.5–15)
7.4 (3.5–16)
MI
Downloaded from http://stroke.ahajournals.org/ by guest on May 5, 2017
CAD
Normotension
1249
33 (2.6%)
Reference
Reference
Prehypertension
4219
285 (6.8%)
1.6 (1.1–2.3)
1.7 (1.2–2.4)
Hypertension
6102
1083 (17.7%)
3.2 (2.3–4.6)
3.2 (2.2–4.5)
The multivariate analysis adjusted for age, gender, cigarette smoking, obesity, diabetes mellitus,
hypercholesterolemia, and study period.
prehypertension (RR, 2.3; 95% CI, 0.8 to 6.3) compared with
normotensive persons. Hypertension was associated with an
increased risk of ABI and all strokes. Prehypertension was
not associated with ABI or all strokes in men or women when
the analysis was performed separately by gender.
Prehypertension and Risk of MI and CAD
A total of 11 802 person observations with a mean follow-up
period of 9.7⫾1.5 years were categorized as hypertensive
(n⫽6292), prehypertensive (n⫽4253), and normotensive
(n⫽1257). The observed events rate for MI was 138 (3.2%)
and 647 (10.3%) for prehypertensive and hypertensive person
observations, respectively. After adjusting for potential confounders, prehypertension was significantly associated with
an increased risk for MI (RR, 3.5; 95% CI, 1.6 to 7.5). The
risk of CAD was higher among persons with prehypertension
(RR, 1.7; 95% CI, 1.2 to 2.4) compared with normotensive
persons (Table 2). Hypertension was associated with an
increased risk of MI and CAD. When the analysis was
performed separately by gender, prehypertension was associated with MI (RR, 4.2; 95% CI, 1.6 to 12) and CAD (RR, 3.4;
95% CI, 2.0 to 5.6) in men but not in women.
PAR and High-Risk Strata for Prehypertension
The PAR associated with prehypertension was estimated to
be 47% (95% CI, 18% to 70%) for MI and 20% (95% CI, 7%
to 34%) for CADs. Among the 4219 prehypertensive person
observations, the predictors of CADs were as follows: age 45
to 64 years (RR, 2.9; 95%, CI 2.0 to 4.3) and age ⱖ65 years
(RR, 4.4; 95% CI, 2.6 to 7.5), men (RR, 2.5; 95% CI, 1.9 to
4.3), diabetes mellitus (RR, 2.1; 95% CI, 1.2 to 3.6), and
hypercholesterolemia (RR, 1.5; 95% CI, 1.1 to 2.1). Other
variables, including body mass index and cigarette smoking,
were not associated with an increased risk for MI. We
analyzed the effect of systolic and diastolic BP in participants
with prehypertension. We found a relationship between
higher systolic BP and increased risk of MI (RR, 1.02; 95%
CI, 1.01 to 1.04) and ABI (RR, 1.05; 95% CI, 1.02 to 1.08).
There was no relationship observed between higher diastolic
BP and risk of MI or ABI.
Discussion
Salient Findings of the Study
We observed that persons classified as prehypertensive were
more likely to develop hypertension over the 50-year
follow-up period compared with those with normal BP.
Therefore, we used the technique of pooled repeated measures to account for the variations in BP status over time. Our
study demonstrates that prehypertension is associated with a
higher risk of MI and CAD but not ischemic or all strokes. As
expected, the risk of MI and CAD associated with prehypertension was lower than the risk observed with hypertension.
We did not observe a relationship between prehypertension
and risk of ABI. We observed a relationship between systolic
BP and ABI in prehypertensive participants, consistent with
previous studies,10,11 but not with diastolic BP. It is possible
that the relationship between prehypertension and ABI is not
observed because of the use of diastolic BP in defining this
category. Because we included participant data up to elderly
ages, it is possible that the contribution of hypertension to the
risk of stroke diminished in the elderly cohort, as suggested in
1862
Stroke
September 2005
previous studies.12,13 Another potential explanation is the
presence of insulin resistance among persons with borderline
to mild hypertension. A study conducted in Japan evaluated
the incidence of stroke and MI during a 7-year follow-up in
584 men with borderline to mild hypertension.14 A greater
risk for MI but not stroke was observed and attributed to
insulin resistance.
Mild Elevation of BP and Cardiovascular Diseases
Downloaded from http://stroke.ahajournals.org/ by guest on May 5, 2017
Previous reports have suggested that mild BP elevations are
associated with an increased thickness of the carotid intima
and media,15 altered cardiac morphological features,16 and
diastolic ventricular dysfunction.17 Vasan et al18 classified
6859 participants in the Framingham Heart Study who were
initially free of hypertension and cardiovascular disease into
optimal (systolic BP ⬍120 mm Hg and diastolic BP
⬍80 mm Hg), normal (systolic BP of 120 to 129 mm Hg or
diastolic BP of 80 to 84 mm Hg), or high-normal (systolic BP
of 130 to 139 mm Hg or diastolic BP of 85 to 89 mm Hg). An
increased risk for death resulting from cardiovascular diseases, recognized MI, stroke, or congestive heart failure was
observed among persons with high-normal BP compared with
optimal BP. Lewington et al19 reported on 1 million adults
with no previous vascular disease evaluated in 61 prospective
observational studies of BP and mortality. During 12.7
million person years at risk, there was a direct association
observed with vascular (and overall) mortality with elevated
BP, even with BP ⬎115/75 mm Hg.
Population-Attributable Risk
The public health impact of a risk factor depends not only on
the magnitude of the RR but also on the prevalence of the risk
factor in the population.9,20 Because PAR takes into account
the strength of the association and the prevalence of the
exposure, the effect of eliminating various risk factors can be
compared.20 The PAR associated with prehypertension was
47% and 20% for MI and CAD, respectively. That implies
that 47% of the MI in the population could be reduced by
treatment of prehypertension. However, if the risk factors are
clustered within individuals, PAR is an overestimate of the
effect of a risk factor. Because cardiovascular risk factors do
cluster within individuals, PAR may overestimate the effect
of a single risk factor such as prehypertension.
Risk Factors for Cardiovascular Disease in
Prehypertensive Patients
We observed that the risk of CAD with prehypertension was
higher among persons aged 45 to 64 years and ⱖ65 years.
Men had twice the risk compared with women. Investigators
have suggested a higher threshold before initiating antihypertensive therapy for women because of the lower prevalence of
cardiovascular events in middle-aged women compared with
men.21 The adverse cardiovascular consequences of prehypertension were increased in the presence of diabetes mellitus
and hypercholesterolemia. Recent studies have suggested a
higher risk of cardiovascular events with mildly elevated
diastolic BP among diabetics compared with nondiabetics
with similar BP levels.22 The reason for increased suscepti-
bility to cardiovascular events at relatively lower BPs among
diabetics is not completely understood.
Issues Related to Data Interpretation
The prospective community-based large sample and the
comprehensive longitudinal surveillance for cardiovascular
events are strengths of the present study. The use of BP
measurements as outpatient as opposed to ambulatory monitoring may inaccurately classify some patients as prehypertensive.23 We used an average of 3 measurements to provide
a more accurate categorization of BP status. Because the
study included data from ⬇5 decades of observation, we
adjusted for the change in BP status over time by reclassifying the hypertension status in all patients every 10 years. The
fact that our sample was predominantly white persons limits
the generalizability of our findings. Additionally, some of the
factors such as subfractions of cholesterol, sleep status, and
physical activity were not adjusted in the model because
pertinent data were not collected.
Conclusions
Our study suggests that prehypertension is a risk factor for MI
and CAD. The PAR is high enough to evaluate the efficacy of
antihypertensive treatment for prehypertensive patients in
clinical trials, particularly in selected patients.
References
1. Chobanian AV, Bakris GL, Black HR, Cushman WC, Green LA, Izzo JL
Jr, Jones DW, Materson BJ, Oparil S, Wight JT Jr, Roccella EJ; National
Heart, Lung, and Blood Institute Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure; National
High Blood Pressure Education Program Coordinating Committee. The
Seventh Report of the Joint National Committee on Prevention,
Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7
report. J Am Med Assoc. 2003;289:2560 –2572.
2. Joint National Committee on Prevention Detection, Evaluation, and
Treatment of High Blood Pressure. The sixth report of the Joint National
Committee on Prevention, Detection, Evaluation, and Treatment of High
Blood Pressure. Arch Intern Med. 1997;157:2413–2446.
3. Dawber TR, Meadors GF, Moore FE. Epidemiologic approaches to heart
disease: the Framingham Study. Am J Public Health. 1951;41:279 –286.
4. Kannel WB, Wolf PA, Garrison RJ, eds. Section 34: Some Risk Factors
Related to the Annual Incidence of Cardiovascular Disease and Death in
Pooled Repeated Biennial Measurements: Framingham Heart Study,
30-Year Follow-Up. Bethesda, Md: US Department of Health and Human
Services; 1987.
5. Wolf PA, D’Agostino RB. Epidemiology of stroke. In: Barnett HJM,
Mohr JP, Stein BM, Yatsu F, eds. Stroke: Pathophysiology, Diagnosis,
and Management. 3rd ed. New York: Churchill Livingstone; 1998:6 –7.
6. Brand FN, Larson M, Friedman LM, Kannel WB, Castelli WP. Epidemiologic assessment of angina before and after myocardial infarction: the
Framingham Study. Am Heart J. 1996;132:174 –178.
7. Wilson PW, D’Agostino RB, Sullivan L, Parise H, Kannel WB. Overweight and obesity as determinants of cardiovascular risk: the Framingham experience. Arch Intern Med. 2002;162:1867–1872.
8. Cupples LA, D’Agostino RB, Anderson K, Kannel WB. Comparison of
baseline and repeated measure covariate techniques in the Framingham
Heart Study. Stat Med. 1988;7:205–222.
9. Hennekens CH, Buring JE. Epidemiology in Medicine. 1st ed. Boston:
Little, Brown, and Co; 1987.
10. Qureshi AI, Suri MFK, Mohammad Y, Guterman LR, Hopkins LN.
Isolated and borderline isolated systolic hypertension relative to
long-term risk and type of stroke: a 20-year follow-up of the National
Health and Nutrition Survey. Stroke. 2002;33:2781–2788.
11. O’Donnell CJ, Ridker PM, Glynn RJ, Berger K, Ajani U, Manson JE,
Hennekens CH. Hypertension and borderline isolated systolic hypertension increase the risks of cardiovascular disease and mortality in male
physicians. Circulation. 1997;95:1132–1137.
Qureshi et al
12. Trenkwalder P, Hendricks P, Schoniger R. Rossberg J, Lydtin H, Hense
HW. Hypertension as a risk factor for cardiovascular morbidity and
mortality in an elderly German population: the prospective STEPHY II
study Starnberg Study on Epidemiology of Parkinsonism and Hypertension in the Elderly. Eur Heart J. 1999;20:1752–1756.
13. Casiglia E, Mazza A, Tikhonoff V, Pavei G, Privato G, Schenal N, Pesina
AC. Weak effect of hypertension and other classic risk factors in the
elderly who have already paid their toll. J Hum Hypertens. 2002;16:
21–31.
14. Takishita S, Abe I, Kobayashi K, Takata Y, Eto T, Fukiyama K, Kojima
K. Insulin and cardiovascular diseases in Japanese work-site population
with borderline to mild hypertension. Hypertens Res. 1996;19:S13–S18.
15. Lonati L, Cuspidi C, Sampieri L, Boselli L, Bocciolone M, Leonetti G,
Zanchetti A. Ultrasonographic evaluation of cardiac and vascular changes
in young borderline hypertensives. Cardiology. 1993;83:298 –303.
16. Escudero E, De Lena S, Graff-Iversen S, Almiron M, Cingolani HE. Left
ventricular diastolic function in young men with high normal blood
pressure. Can J Cardiol. 1996;12:959 –964.
17. Kimura Y, Tomiyama H, Nishikawa E, Watanabe G, Shiojima K,
Nakayama T, Yoshida H, Kuwata S, Kinouchi T, Doba N. Characteristics
of cardiovascular morphology and function in the high-normal subset of
Prehypertension and Cardiovascular Diseases
18.
19.
20.
21.
22.
23.
1863
hypertension defined by JNC-VI recommendations. Hypertens Res. 1999;
22:291–295.
Vasan RS, Larson MG, Leip EP, Evans JC, O’Donnell CJ, Kannel WB,
Levy D. Impact of high-normal blood pressure on the risk of cardiovascular disease. N Eng J Med. 2001;345:1291–1297.
Lewington S, Clarke R, Qizilbash N, Peto R, Collins R. Prospective
Studies Collaboration. Age-specific relevance of usual blood pressure to
vascular mortality: a meta-analysis of individual data for one million
adults in 61 prospective studies. Lancet. 2002;360:1903–1913.
Macera CA, Powell KE. Population-attributable risk: implications of
physical activity dose. Med Sci Sports Exercise. 2001;33:S635–S639.
Suarez C How should we treat hypertensive women with cardiac and
renal impairment? Am J Hypertens. 1997;10:242S–246S.
Snow V. Weiss KB. Mottur-Pilson C. Clinical Efficacy Assessment
Subcommittee of the American College of Physicians. The evidence base
for tight blood pressure control in the management of type 2 diabetes
mellitus. Ann Intern Med. 2003;138:587–592.
Staessen JA, Asmar R, De Buyzere M, Imai Y, Parati G, Shimada K,
Stergiou G, Redon J, Verdecchia P; Participants of the 2001 Consensus
Conference on Ambulatory Blood Pressure Monitoring. Task Force II:
blood pressure measurement and cardiovascular outcome. Blood Press
Monit. 2001;6:355–370.
Downloaded from http://stroke.ahajournals.org/ by guest on May 5, 2017
Is Prehypertension a Risk Factor for Cardiovascular Diseases?
Adnan I. Qureshi, M. Fareed K. Suri, Jawad F. Kirmani, Afshin A. Divani and Yousef
Mohammad
Downloaded from http://stroke.ahajournals.org/ by guest on May 5, 2017
Stroke. 2005;36:1859-1863; originally published online August 4, 2005;
doi: 10.1161/01.STR.0000177495.45580.f1
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright © 2005 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628
The online version of this article, along with updated information and services, is located on the
World Wide Web at:
http://stroke.ahajournals.org/content/36/9/1859
Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published
in Stroke can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office.
Once the online version of the published article for which permission is being requested is located, click
Request Permissions in the middle column of the Web page under Services. Further information about this
process is available in the Permissions and Rights Question and Answer document.
Reprints: Information about reprints can be found online at:
http://www.lww.com/reprints
Subscriptions: Information about subscribing to Stroke is online at:
http://stroke.ahajournals.org//subscriptions/