(Hypertension. 1996;27:1059-1064.)
© 1996 American Heart Association, Inc.
Articles |
Anticipatory Blood Pressure Response to Exercise Predicts Future High Blood Pressure in Middle-aged Men
From the Human Population Laboratory, Western Consortium for Public Health (S.A.E., D.E.G.); the Human Population Laboratory, California Department of Health Services (G.A.K.), Berkeley, Calif; and the Research Institute of Public Health and Department of Community Health and General Practice, University of Kuopio (Finland) (J.T.S.).
 |
Abstract |
|---|
 Top Abstract IntroductionMethodsResultsDiscussionReferences |
|---|
Abstract Increases in blood pressure during the period of emotional arousal attendant to impending exertion are well documented, yet the etiologic significance of these elevations is unknown. Research suggests that exaggerated cardiovascular responses to psychological stress may be importantly related to hypertension. We examined blood pressure reactivity in anticipation of an exercise stress test in relation to future hypertension in the Kuopio Ischemic Heart Disease Risk Factor Study, a population-based study of middle-aged men from Eastern Finland. Subjects were 508 unmedicated men with resting blood pressure less than 165/95 mm Hg who completed a bicycle ergometer stress test at baseline and whose hypertensive status was assessed at 4 years of follow-up. Systolic and diastolic reactivity were calculated as the difference between blood pressure measured after seated rest on the bicycle ergometer before initiation of exercise and mean seated resting blood pressure measured 1 week earlier. Logistic regression models adjusted for age and resting blood pressure revealed a graded association between quartiles of reactivity and risk of subsequent hypertension (
165/95 mm Hg), with men showing systolic
responses greater than or equal to 30 mm Hg or diastolic
responses greater than 15 mm Hg at nearly four times the risk of
becoming hypertensive (odds ratios, 3.80 [95% confidence interval,
1.90 to 7.63] and 3.65 [95% confidence interval, 1.86 to 7.17],
respectively) relative to the least-reactive groups
(systolic response, <10 mm Hg; diastolic
response, <5 mm Hg). Adjustments for traditional risk factors for
hypertension did not alter these associations. Results demonstrate the
clinical significance of the pressor response in anticipation of
exercise and support the hypothesis that cardiovascular
reactivity to psychological challenge plays a role in the etiology of
hypertension.
Key Words: cardiovascular system • hypertension • exercise • blood pressure • risk factors
|
Introduction |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Exaggerated BP responses during both dynamic and isometric exercise are associated with increased risk of future hypertension.1 2 3 4 Surprisingly, BP increases in anticipation of exercise, which are well documented,5 have not been examined in relation to hypertension risk. The period preceding exercise can be characterized as a period of emotional, behavioral, and physiological arousal attendant to an impending challenge. Thus, BP elevations in anticipation of exercise reflect cardiovascular adjustments in response to psychological and behavioral stresses, a phenomenon described as cardiovascular reactivity.6
Several lines of evidence suggest that behaviorally induced cardiovascular reactivity may be causally related to and/or a risk marker for hypertension.7 8 Research with spontaneously hypertensive rats has found that the prehypertensive state is accompanied by exaggerated nervous system reactivity that contributes to the progression of the hypertension,9 10 a process that is accelerated by exposure to long-term stress.11 Among humans, men at greatest risk for hypertension, determined by high normal resting BP and/or a parental history of hypertension, also show the most exaggerated BP responses during casual stethoscopic readings (a "white coat" effect)12 13 and during standard laboratory challenges.14 15 16 17 Also, borderline hypertensive individuals (SBP=140 to 164 mm Hg and/or DBP=90 to 94 mm Hg) show exaggerated heart rate and/or BP responses to various stressors relative to normotensive individuals.18 19 20 21
Nonetheless, support for the reactivity hypothesis is limited at present, largely because of a lack of adequate and appropriate prospective studies8 22 and/or the use of selected or convenience samples (eg, male medical students or military officers23 24 25 26 ). Some early studies, which relied solely on the cold pressor test, found that "hyperreactors" to the cold pressor test were more likely to develop hypertension over time.25 27 28 29 Others, however, have failed to identify such an association.23 24 26 It also has been shown that exaggerated BP responses to tasks requiring a more active behavioral component than that required by the cold pressor test (eg, serial subtraction task, unsignaled reaction time task, isometric handgrip) are associated with higher, albeit still normotensive, BP levels 6 to 15 years later.13 30 Thus, it remains to be seen whether exaggerated BP responses to a psychologically challenging stressor predict future hypertension.
The present study examined the relationship between cardiovascular reactivity to a psychological stressor, ie, BP elevations in anticipation of a bicycle ergometer stress test, and subsequent high BP in a randomly selected, population-based sample of middle-aged men. This report is from the Kuopio Ischemic Heart Disease Risk Factor Study (KIHD), designed in part to examine associations between promising but unestablished behavioral and psychosocial risk factors and cardiovascular diseases and other outcomes.31 Available data on health habits, family illness history, and various anthropometric and demographic measures enabled us to examine potential confounding influences of other risk factors for hypertension.
|
Methods |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Study Population
The KIHD study is an ongoing, population-based study designed to investigate previously unestablished risk factors for carotid atherosclerosis, ischemic heart disease, mortality, and other outcomes among middle-aged men from the Kuopio region in Eastern Finland, an area of high coronary morbidity and mortality.32 A total of 2682 participants (82.9% of those eligible), aged 42, 48, 54, or 60 years, were enrolled in the study between March 1984 and December 1989. Follow-up examinations were conducted between March 1991 and December 1993 on those men who had undergone ultrasound examination of the right and left carotid arteries at baseline. A total of 1229 were eligible for the follow-up study; of these, 52 had died, were unable to participate because they were suffering severe illness or had migrated away from the region, and 139 could not be contacted or refused to participate. Thus, the follow-up study included 1038 participants or 88.2% of those eligible and able to participate. Average time to follow-up was 4.1 years (range, 2.3 to 5.2 years).
For the present analyses, subjects were excluded if they
had missing BP data at baseline or follow-up (n=10), were
hypertensive (according to World Health Organization criteria, ie, BP
165/95 mm Hg or on antihypertensive medications) (n=345), did not
participate in the bicycle ergometer test (n=97), or had missing data
on the covariates at baseline (n=78). Thus, the results reported herein
are based on 508 initially normotensive men who performed the exercise
tolerance test at baseline and had complete information on covariates
at baseline and hypertension status at follow-up. Subject
characteristics are shown in Table 1
. A comparison of
the 175 KIHD participants with missing data on the bicycle ergometer
test and/or baseline covariates with the 508 subjects with complete
data revealed no significant differences in baseline resting BP or body
mass index (both P>.18).
|
Baseline and Follow-up Examinations
Examinations were carried out over 2 days, 1 week apart, at both
baseline and follow-up and consisted of a wide variety of
biochemical, physiological, anthropometric, and
psychosocial measures. In addition, a linear-slope maximal exercise
tolerance test on an upright bicycle ergometer was administered at the
baseline exam. Medical history and medication use were checked during a
medical examination at both baseline and follow-up.
BP Measurement and Reactivity Assessment
The BP data used in the present analyses were
obtained on two occasions by a trained observer using a random-zero
muddler sphygmomanometer (Hawksley). The BP measurement protocol on the
first examination day was as follows: 15 minutes of supine rest with BP
measured at minutes 5, 10, and 15; standing rest with one BP reading
taken after 1 minute; and 10 minutes of seated rest with BP measured at
minutes 5 and 10. For the present analyses, the averages of
the two seated SBP and DBP measurements were considered resting SBP and
DBP, respectively. A second measure of sitting BP was obtained on the
second examination day 1 week later after the subject had been seated
on the bicycle ergometer for 5 minutes but before the exercise test
protocol was begun. Measurements on both examination days occurred in
the mornings. Anticipatory SBP and DBP responses (SBP
, DBP) were
calculated as the difference between the seated BP reading obtained
before exercise and the mean seated resting BP obtained on the first
examination day.
These SBP and DBP responses in anticipation of exercise constituted our measures of cardiovascular reactivity. Prior studies of reactivity have not used a preexercise period as a stressor; however, participants were encouraged to perform at their best level and knew that the results of the test would be an indicator of their cardiovascular health status. In an area with known high rates of cardiovascular morbidity and mortality,32 this impending knowledge could be particularly stress inducing. Furthermore, any increase in BP that occurred during this anticipatory period was in excess of metabolic demand because physical work had not yet begun and thus could be attributed to the person's psychological response to the demand characteristics of the setting. Research has shown that this anticipation response is characterized by an interplay of neural, hormonal, and mechanical factors that ready the cardiovascular system for the impending exertion, is cerebral in origin, and is most likely to occur in situations with a high degree of emotional involvement.5
Hypertensive Status at Follow-up
The BP measurement protocol at follow-up was identical to
that of the baseline protocol, with resting SBP and DBP calculated as
the averages of two seated measurements obtained at minutes 5 and 10 of
a 10-minute seated rest. A subject was considered to be hypertensive at
the 4-year follow-up exam if his resting SBP was greater than or
equal to 165 mm Hg or his resting DBP was greater than or equal to 95
mm Hg or if he was currently taking antihypertensive medications. A
total of 116 men (22.8%) met these criteria.
Data Analyses
The relation between SBP and hypertensive status was assessed
with a series of age-adjusted logistic regression models with the
anticipatory responses modeled both continuously and categorically.
(Categories of anticipatory BP responses were created on the basis of
natural breaks in the distribution of scores for SBP and DBP.
These categories formed approximate quartiles as follows. SBP: <10
mm Hg, 25.6%; 10 to 19 mm Hg, 24.2%; 20 to 29 mm Hg, 26.2%; 30
mm Hg, 24.0%. DBP; <5 mm Hg, 25.9%; 5 to 9 mm Hg, 27.9%; 10
to 15 mm Hg: 22.2%; >15 mm Hg: 24.0%.) Subsequent age-adjusted
models examined potential confounding by smoking, alcohol consumption,
physical activity, body mass index, and positive maternal and paternal
histories of hypertension. A parallel series of logistic regression
models examined the association between DBP and risk of high BP.
Seven subjects with missing DBP readings before exercise were excluded
from the models of DBP. Consistent with prior
research,33 we found that resting SBP and resting DBP at
baseline significantly predicted high BP at follow-up in the full
KIHD study sample (OR=1.07 [95% CI, 1.06 to 1.08] and 1.16 [95%
CI, 1.14 to 1.19] for an increase of 1 mm Hg in SBP and DBP,
respectively). Consequently, all SBP models were also adjusted for
baseline resting SBP, and all DBP models were adjusted for baseline
resting DBP. All statistical analyses were conducted with
LOGISTIC and GLM procedures from SAS,34 version 6.09,
installed on a Sun Sparcstation 20.
|
Results |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
Mean (±SD) SBP
was +20.2 (±14.2) mm Hg and mean (±SD)
DBP was +9.8 (±7.7) mm Hg. Both SBP and DBP responses were
positively associated with age (both P<.0001).
In a logistic regression model, with SBP entered as a continuous
variable, SBP significantly predicted subsequent high BP after
adjusting for age and resting SBP (OR=1.03 [95% CI, 1.01 to 1.05]).
Similarly, DBP modeled continuously significantly predicted high BP
at follow-up, after adjusting for age and resting DBP (OR=1.07
[95% CI, 1.03 to 1.10]).
A logistic regression model that included SBP in approximate
quartiles (<10 mm Hg; 10 to 19 mm Hg; 20 to 29 mm Hg; 30 mm Hg)
revealed a dose-response relationship, with the most-reactive
group at nearly four times the risk of having high BP at follow-up
relative to the least-reactive group, after adjusting for age and
resting SBP (OR=3.80 [95% CI, 1.90 to 7.63]) (see the
Figure). Men in the second and third quartiles of SBP
also were at significantly increased risk of high BP compared with the
nonreactors (OR=2.07 [95% CI, 1.04 to 4.11] and 2.78 [95% CI, 1.41
to 5.48], respectively). Subsequent adjustments for baseline smoking,
physical activity, alcohol consumption, body mass index, and maternal
and paternal histories of hypertension did not importantly affect these
associations (see Table 2).
|
|
A similar pattern of findings was seen with DBP modeled in
approximate quartiles (<5 mm Hg; 5 to 9 mm Hg; 10 to 15 mm Hg; >15
mm Hg), with both the third and fourth quartiles of reactors at
significantly increased risk of subsequent high BP relative to the
nonreactors (OR=2.24 [95% CI, 1.11 to 4.51] and 3.65 [95% CI, 1.86
to 7.17], respectively) after adjusting for age and resting DBP (see
the Figure
). Controlling for baseline smoking, physical activity,
alcohol consumption, body mass index, and parental hypertension did not
effectively alter these relationships (see Table 2).
Although our sample of 508 did not include any men with established
hypertension (BP 165/95 mm Hg) or taking antihypertensive
medications at baseline, 25% did have a baseline resting BP in the
borderline hypertensive range (SBP of 140 to 164 mm Hg and/or DBP of
90 to 94 mm Hg) and 34% reported a history of cerebrovascular stroke
or coronary heart disease, including angina or previous
myocardial infarction; were taking medication for cardiac
insufficiency; or experienced ischemic episodes during the
exercise test. Thus, to determine whether our measure of anticipatory
BP reactivity would predict subsequent hypertensive status among
initially disease-free men, we repeated the logistic regression
models excluding the 266 men (52%) who showed borderline hypertensive
pressures at rest and/or who showed evidence of coronary heart
disease or cerebrovascular stroke. Although the number of men with high
BP at follow-up was small in this remaining very healthy group of
subjects (37 of 242 men), we did find a graded association between
quartiles of anticipatory BP at baseline and risk of high BP at
follow-up. Indeed, healthy men who showed SBP greater than or
equal to 30 mm Hg or DBP greater than 15 mm Hg were at more than
five times the risk of showing hypertensive pressures at follow-up
relative to the least-reactive men, after adjusting for age and
resting BP (OR=5.21 [95% CI, 1.50 to 18.2] and 5.90 [95% CI, 1.58
to 22.0] for SBP and DBP, respectively). These associations were
maintained in models that also adjusted for the other known risk
factors for hypertension (Table 3).
|
Given that exaggerated BP responses during exercise have previously
been shown to predict hypertension,1 2 3 4 we also examined
the association between BP achieved during exercise and hypertensive
status at follow-up. Consistent with prior
research,3 35 36 37 an exaggerated exercise BP response was
defined as SBP greater than or equal to 230 mm Hg and/or DBP greater
than or equal to 110 mm Hg at any point during the exercise protocol.
(The bicycle ergometer test lasted for a maximum of 14 minutes, and BP
was measured every 2 minutes beginning with minute 2.) Data on BP
during exercise were available for 497 subjects; of these, 154 (31%)
met the criteria for exaggerated SBP and/or DBP during exercise. An
age-adjusted logistic regression model showed that subjects with an
exaggerated exercise response were three times more likely to have high
BP at follow-up than subjects with a normal exercise response
(OR=3.10 [95% CI, 2.01 to 4.78]). Given this finding, we then
repeated the logistic regression analyses of SBP and DBP
and included a dichotomous variable for exaggerated exercise BP as
a covariate as well as all other risk factors. The graded associations
were still apparent, with those in the highest quartiles of SBP
and/or DBP before exercise at more than three times the risk of
having hypertensive BP levels at follow-up relative to the
nonreactors (OR=3.38 [95% CI, 1.59 to 7.16] and 3.17 [95% CI, 1.53
to 6.59] for SBP and DBP, respectively). In the SBP model,
exaggerated exercise BP was a statistically significant covariate
(OR=1.87, P=.01); however, in the DBP model, it was not
(OR=1.34, P=.27).
|
Discussion |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
To the best of our knowledge, this is the first study to show an association between cardiovascular reactivity to a psychological challenge and incident hypertension or high BP in an unselected population. The fact that increasingly larger BP responses during the exercise anticipation phase were related to increasingly greater risk of hypertensive pressures in a very healthy subsample suggests that cardiovascular reactivity per se has negative consequences even in the absence of clinical disease. This observation has implications for the early detection and treatment of individuals at risk for hypertension.
Our data also demonstrate the clinical significance of the pressor response during the anticipation phase of exercise. This response is a recognized phenomenon5 38 39 ; however, it generally has not been a focus of interest, unlike the response to exercise, in part because higher pressure levels are achieved after the initiation of exercise.40 Priming of the cardiovascular system is beneficial in preparing for exercise, which may serve to increase performance.5 Our data also indicate that exaggerated BP responses during the anticipation phase of an exercise stress test, responses indicative of psychologically mediated sympathetic arousal, are a precursor of pressor dysregulation.
Moreover, we found that the risk of high BP at follow-up associated
with SBP and DBP was not substantially diminished after
exaggerated exercise BP responses were taken into account. These
findings lend additional support to the reactivity hypothesis; that is,
our data demonstrate that it is the sympathetic activation attendant to
emotional arousal but in excess of metabolic requirements
that has adverse effects on the vascular system. Such reactivity may be
enhancing the hypertensive process or may be an expression of a basic
tendency toward hypertension.
Sympathetic activation during the anticipation phase of exercise is manifested as an increase in cardiac output with no compensatory decrease in vascular resistance.5 Folkow41 has shown that the heart and blood vessels undergo structural adaptations in response to the pressure overload that accompanies chronic elevations in BP. These structural adaptations serve to maintain higher pressure levels and may contribute to a structurally induced hyperreactivity.42 Thus, it is biologically plausible that repeated sympathetic activation in the absence of metabolic need that leads to BP elevations beyond the normotensive range, as may occur in emotionally arousing situations, could then lead to sustained pressor increases. If the activation observed in anticipation of exercise in the present study is indicative of heightened sympathetic activation experienced by these men in response to other emotionally arousing stimuli, it is perhaps not surprising then that the risk of having high BP at follow-up increased as reactivity levels increased.
Preexercise BP was based on just one BP reading during the
anticipation phase. The consistency and strength of the
observed associations as well as significant positive correlations
between anticipatory BP and SBP and DBP during exercise
(r=.30 and r=.65, P<.001) suggest
that the single reading obtained during anticipation was a valid
indicator of BP during that phase. It is likely that the associations
observed here would have been even stronger if the random
interindividual variability could have been attenuated by averaging
over several BP readings. Thus, additional BP measurements during this
phase would have been desirable and are recommended in order to address
the stability of BP during exercise anticipation.
The majority of men in our study whose resting BP at follow-up was
greater than or equal to 165/95 mm Hg were not taking antihypertensive
medication at the time of their follow-up examination. Hypertensive
status in our study was determined by an average of two readings over a
10-minute seated rest on one occasion. Current recommendations are that
hypertension be diagnosed only after high BP readings are obtained
during at least two clinic visits43 ; therefore, we cannot
properly say that these men were diagnosed hypertensive individuals.
However, a comparison of the resting SBP and DBP measured at
follow-up with a 6-day average of resting SBP and DBP measured at
home (via a portable, oscillometric BP monitor), which was available
for 93% of our subjects, indicates that the average BP obtained during
the follow-up exam was a good indicator of average daily BP among
our participants (r
.7, P<.0001). Thus, it is
likely that many of the men in our study with resting BP greater than
or equal to 165/95 mm Hg at the follow-up examination would meet
the criteria for diagnosed hypertension.
Our findings may not be generalizable to younger, nonwhite populations
or to women; however, available data are suggestive. Matthews et
al30 found that DBP in response to standardized
psychomotor challenges was associated with higher, albeit still
normotensive, resting BP 6.5 years later among white middle-aged
women and men and among their teenaged sons. Also, Kasagi and
colleagues29 showed a higher incidence of hypertension
among Japanese men and women who were systolic hyperreactors (a
systolic increase of 15 mm Hg or more) to the cold pressor
test, relative to normal reactors, but only among those 40 years old or
older at baseline. Even though the ethnic and demographic homogeneity
of our study population serves to reduce confounding effects and to
increase statistical power, it will be important for future studies to
test the reactivity hypothesis on more demographically varied
samples.
In summary, our results support the hypothesis that cardiovascular reactivity to psychological or emotional stimuli is important in the etiology of hypertension. Moreover, our findings indicate that the risk associated with reactivity is independent of traditional risk factors for hypertension. Future research will have to determine the degree to which reactivity is specific to an individual or group or to situations as well as examine the relation between reactivity and hypertension in minority and female populations. Given the health costs of hypertension and the importance of early detection of the disorder, it appears that the sympathetic activation that accompanies emotional arousal and is manifest as exaggerated BP reactivity is a significant risk factor that has clinical relevance as an indicator of a prehypertensive state.
|
Selected Abbreviations and Acronyms |
|---|
|
|
Acknowledgments |
|---|
This work was supported by grant HL-44199 from the National Heart, Lung, and Blood Institute and by grants from the Academy of Finland and the Finnish Ministry of Education. The authors thank Dr Bill Lovallo, Veterans Affairs Medical Center and University of Oklahoma Health Sciences Center, Oklahoma City, for his thoughtful comments on an earlier draft of this article.
|
Footnotes |
|---|
Reprint requests to Susan A. Everson, PhD, MPH, Human Population Laboratory, Western Consortium for Public Health, 2151 Berkeley Way, Annex 2, Suite 300, Berkeley, CA 94704-1011. E-mail hyper1@cmsa.berkeley.edu.
Received December 5, 1995; first decision January 8, 1996; accepted January 31, 1996.
|
References |
|---|
|
TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Chaney RH, Eyman RK. Blood pressure at rest and during maximal dynamic and isometric exercise as predictors of systemic hypertension. Am J Cardiol. 1988;62:1058-1061. [Medline] [Order article via Infotrieve]
2. Dlin RA, Hanne N, Silverberg DS, Bar-Or O. Follow-up of normotensive men with exaggerated blood pressure response to exercise. Am Heart J. 1983;106:316-320. [Medline] [Order article via Infotrieve]
3. Jackson AS, Squires WG, Grimes G, Beard EF. Prediction of future resting hypertension from exercise blood pressure. J Cardiac Rehab. 1983;3:263-268.
4. Wilson NV, Meyer BM. Early prediction of hypertension using exercise blood pressure. Prev Med. 1981;10:62-68. [Medline] [Order article via Infotrieve]
5. Smith EE, Guyton AC, Manning RD, White RJ. Integrated mechanisms of cardiovascular response and control during exercise in the normal human. Prog Cardiovasc Dis. 1976;18:421-443. [Medline] [Order article via Infotrieve]
6. Sherwood A, Turner JR. A conceptual and methodologic overview of cardiovascular reactivity research. In: Turner JR, Sherwood A, Light KC, eds. Individual Differences in Cardiovascular Response to Stress. New York, NY: Plenum Press; 1992:3-32.
7. Krantz DS, Manuck SB. Acute psychophysiologic reactivity and risk of cardiovascular disease: a review and methodologic critique. Psychol Bull. 1984;96:435-464. [Medline] [Order article via Infotrieve]
8. Lovallo WR, Wilson MF. The role of cardiovascular reactivity in hypertension risk. In: Turner JR, Sherwood A, Light KC, eds. Individual Differences in Cardiovascular Response to Stress. New York, NY: Plenum Press; 1992:165-186.
9.
Smith PG, Poston CW, Mills E. Ontogeny of
neural and non-neural contributions to arterial blood
pressure in spontaneously hypertensive rats.
Hypertension. 1984;6:54-60.
10. Yao H, Matsumoto M, Hirano M, Kuroki T, Tsutsumi T, Uchimera H, Nakamura K, Nakahara T, Masatoshi F. Involvement of brain stem noradrenergic neurons in the development of hypertension in spontaneously hypertensive rats. Neurochem Res. 1989;14:75-79. [Medline] [Order article via Infotrieve]
11. Yamori Y, Matsumoto M, Yamabe H, Okamoto K. Augmentation of spontaneous hypertension by chronic stress in rats. Jpn Circ J. 1969;33:399-409. [Medline] [Order article via Infotrieve]
12. Bernardy NC, Everson SA, al'Absi M, Schott H, Lovallo WR. Risk for hypertension predicts the `white coat' effect in young men. Psychologische Beitrage. 1995;37:26-31.
13.
Light KC, Dolan CA, Davis MR, Sherwood A.
Cardiovascular responses to an active coping challenge
as predictors of blood pressure patterns 10 to 15 years later.
Psychosom Med. 1992;54:217-230.
14. al'Absi M, Everson SA, Lovallo WR. Exaggerated cardiovascular responses to mental stress in men with high-normal resting systolic pressure and parental history of hypertension. Int J Psychophysiol. 1995;20:155-160. [Medline] [Order article via Infotrieve]
15. Ditto B. Parental history of essential hypertension, active coping, and cardiovascular reactivity. Psychophysiology. 1986;23:62-70. [Medline] [Order article via Infotrieve]
16. Hastrup JL, Light KC, Obrist PA. Parental hypertension and cardiovascular response to stress in healthy young adults. Psychophysiology. 1982;19:615-622. [Medline] [Order article via Infotrieve]
17.
Jorgensen RS, Houston BK. Family history of
hypertension, personality patterns, and cardiovascular
reactivity to stress. Psychosom Med. 1986;48:102-117.
18. Drummond PD. Cardiovascular reactivity in mild hypertension. J Psychosom Res. 1983;27:291-297. [Medline] [Order article via Infotrieve]
19. Drummond PD. Cardiovascular reactivity in borderline hypertensives during behavioral and orthostatic stress. Psychophysiology. 1985;22:621-628. [Medline] [Order article via Infotrieve]
20. Eliasson K, Hjemdahl P, Kahan T. Circulatory and sympatho-adrenal responses to stress in borderline and established hypertension. J Hypertens. 1983;1:131-139. [Medline] [Order article via Infotrieve]
21.
Steptoe A, Melville D, Ross A. Behavioral
response demands, cardiovascular reactivity, and
essential hypertension. Psychosom Med. 1984;46:33-48.
22. Fredrikson M, Matthews KA. Cardiovascular responses to behavioral stress and hypertension: a meta-analytic review. Ann Behav Med. 1990;12:30-39.
23. Eich RH, Jacobsen EC. Vascular reactivity in medical students followed for 10 yr. J Chronic Dis. 1967;20:583-592. [Medline] [Order article via Infotrieve]
24. Harlan WR Jr, Osborne RK, Graybiel A. Prognostic value of the cold pressor test and the basal blood pressure. Am J Cardiol. 1964;13:832-837.
25.
Menkes MS, Matthews KA, Krantz DS, Lundberg U, Mead LA,
Qaqish B, Liang K-Y, Thomas CB, Pearson TA.
Cardiovascular reactivity to the cold pressor test as a
predictor of hypertension. Hypertension. 1989;14:524-530.
26. Armstrong HG, Rafferty JA. Cold pressor test follow-up study for seven years on 166 officers. Am Heart J. 1950;39:484-490.
27. Barnett PH, Hines KA, Schirger A, Gage RP. Blood pressure and vascular reactivity to the cold pressor test. JAMA. 1963;183:845-848.
28.
Wood DL, Sheps SG, Elveback LR, Schirger A. Cold
pressor test as a predictor of hypertension.
Hypertension. 1984;6:301-306.
29.
Kasagi F, Akahoshi M, Katsutaro S. Relation
between cold pressor test and development of hypertension based on
28-year follow-up. Hypertension. 1995;25:71-76.
30.
Matthews KA, Woodall KL, Allen MT.
Cardiovascular reactivity to stress predicts future
blood pressure status. Hypertension. 1993;22:479-485.
31. Salonen JT. Is there a continuing need for longitudinal epidemiologic research? The Kuopio Ischemic Heart Disease Risk Factor Study. Ann Clin Res. 1988;20:46-50. [Medline] [Order article via Infotrieve]
32. Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Cambridge, Mass: Harvard University Press; 1980.
33. Kannel WB. Hypertension and the risk of cardiovascular disease. In: Laragh JH, Brenner BM, eds. Hypertension: Pathophysiology, Diagnosis, and Management. New York, NY: Raven Press Publishers; 1990:101-117.
34. SAS Users' Guide: Statistics. Cary, NC: SAS Institute; 1990.
35. Irving JB, Bruce RA, DeRouen TA. Variations in and significance of systolic pressure during maximal exercise (treadmill) testing. Am J Cardiol. 1977;39:841-848. [Medline] [Order article via Infotrieve]
36. Sannerstedt R. Exercise in the patient with arterial hypertension. Practical Cardiol. 1981;7:89-100.
37.
Wolthuis RA, Froelicher VF, Fisher J, Triebwasser
JH. The response of healthy men to treadmill exercise.
Circulation. 1977;55:153-157.
38.
Bevegard BS, Shepherd JT. Regulation of the
circulation during exercise in man. Physiol Rev. 1967;47:178-232.
39.
Rushmer RF, Smith DA. Cardiac control.
Physiol Rev. 1959;39:41-68.
40. Sagawa K, Kumada M, Schramm LP. Nervous control of the circulation. In: Guyton AC, Jones CE, eds. Cardiovascular Physiology. London, UK: Butterworth; 1974:197-232.
41. Folkow B. `Structural factor' in primary and secondary hypertension. Hypertension. 1990;16:89-101.
42.
Folkow B. Physiological
aspects of primary hypertension. Physiol Rev. 1982;62:347-504.
43.
Joint National Committee on the Detection, Evaluation
and Treatment of High Blood Pressure. The fifth report of the Joint
National Committee on Detection, Evaluation, and Treatment of High
Blood Pressure (JNC V). Arch Intern Med. 1993;153:154-183.
This article has been cited by other articles:
 |
|
 |
|
  S Kurl, M Ala-Kopsala, H Ruskoaho, T Makikallio, K Nyyssonen, O Vuolteenaho, J Sivenius, J T Salonen, and J A Laukkanen Plasma N-terminal fragments of natriuretic peptides predict the risk of stroke and atrial fibrillation in men Heart, July 1, 2009; 95(13): 1067 - 1071. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Laukkanen, S. Kurl, M. Ala-Kopsala, O. Vuolteenaho, H. Ruskoaho, K. Nyyssonen, and J. T. Salonen Plasma N-terminal fragments of natriuretic propeptides predict the risk of cardiovascular events and mortality in middle-aged men Eur. Heart J., May 2, 2006; 27(10): 1230 - 1237. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Laukkanen, S. Kurl, J. Eranen, M. Huttunen, and J. T. Salonen Left Atrium Size and the Risk of Cardiovascular Death in Middle-aged Men Arch Intern Med, August 8, 2005; 165(15): 1788 - 1793. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. A. Laukkanen, S. Kurl, R. Salonen, T. A. Lakka, R. Rauramaa, and J. T. Salonen Systolic Blood Pressure During Recovery From Exercise and the Risk of Acute Myocardial Infarction in Middle-Aged Men Hypertension, December 1, 2004; 44(6): 820 - 825. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. A. Matthews, C. R. Katholi, H. McCreath, M. A. Whooley, D. R. Williams, S. Zhu, and J. H. Markovitz Blood Pressure Reactivity to Psychological Stress Predicts Hypertension in the CARDIA Study Circulation, July 6, 2004; 110(1): 74 - 78. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. E. Ming, G. K. Adler, R. C. Kessler, L. F. Fogg, K. A. Matthews, J. A. Herd, and R. M. Rose Cardiovascular Reactivity to Work Stress Predicts Subsequent Onset of Hypertension: The Air Traffic Controller Health Change Study Psychosom Med, July 1, 2004; 66(4): 459 - 465. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Carroll, C. Ring, K. Hunt, G. Ford, and S. Macintyre Blood Pressure Reactions to Stress and the Prediction of Future Blood Pressure: Effects of Sex, Age, and Socioeconomic Position Psychosom Med, November 1, 2003; 65(6): 1058 - 1064. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. M. McCaffery, M. Bleil, M. F. Pogue-Geile, R. E. Ferrell, and S. B. Manuck Allelic Variation in the Serotonin Transporter Gene-Linked Polymorphic Region (5-HTTLPR) and Cardiovascular Reactivity in Young Adult Male and Female Twins of European-American Descent Psychosom Med, September 1, 2003; 65(5): 721 - 728. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. A. Matthews, K. Salomon, S. S. Brady, and M. T. Allen Cardiovascular Reactivity to Stress Predicts Future Blood Pressure in Adolescence Psychosom Med, May 1, 2003; 65(3): 410 - 415. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. W. Kamarck and W. R. Lovallo Cardiovascular Reactivity to Psychological Challenge: Conceptual and Measurement Considerations Psychosom Med, January 1, 2003; 65(1): 9 - 21. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. R. Schwartz, W. Gerin, K. W. Davidson, T. G. Pickering, J. F. Brosschot, J. F. Thayer, N. Christenfeld, and W. Linden Toward a Causal Model of Cardiovascular Responses to Stress and the Development of Cardiovascular Disease Psychosom Med, January 1, 2003; 65(1): 22 - 35. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
W. R. Lovallo and W. Gerin Psychophysiological Reactivity: Mechanisms and Pathways to Cardiovascular Disease Psychosom Med, January 1, 2003; 65(1): 36 - 45. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. A. Treiber, T. Kamarck, N. Schneiderman, D. Sheffield, G. Kapuku, and T. Taylor Cardiovascular Reactivity and Development of Preclinical and Clinical Disease States Psychosom Med, January 1, 2003; 65(1): 46 - 62. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Carroll, G. D. Smith, M. J. Shipley, A. Steptoe, E. J. Brunner, and M. G. Marmot Blood Pressure Reactions to Acute Psychological Stress and Future Blood Pressure Status: A 10-Year Follow-Up of Men in the Whitehall II Study Psychosom Med, September 1, 2001; 63(5): 737 - 743. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Andre-Petersson, G. Engstrom, B. Hagberg, L. Janzon, G. Steen, D. A. Lane, D. Carroll, and G. Y.H. Lip Adaptive Behavior in Stressful Situations and Stroke Incidence in Hypertensive Men: Results From Prospective Cohort Study "Men Born in 1914" in Malmo, Sweden Editorial Comment: Results From Prospective Cohort Study "Men Born in 1914" in Malmo, Sweden Stroke, August 1, 2001; 32(8): 1712 - 1720. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Everson, J. W. Lynch, G. A. Kaplan, T. A. Lakka, J. Sivenius, J. T. Salonen, and K. A. Matthews Stress-Induced Blood Pressure Reactivity and Incident Stroke in Middle-Aged Men Editorial Comment : Something Old and Something New Stroke, June 1, 2001; 32(6): 1263 - 1270. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. W. Kamarck, J. Eranen, J. R. Jennings, S. B. Manuck, S. A. Everson, G. A. Kaplan, and J. T. Salonen Anticipatory Blood Pressure Responses to Exercise Are Associated With Left Ventricular Mass in Finnish Men : Kuopio Ischemic Heart Disease Risk Factor Study Circulation, September 19, 2000; 102(12): 1394 - 1399. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. A. Everson, G. A. Kaplan, D. E. Goldberg, and J. T. Salonen Hypertension Incidence Is Predicted by High Levels of Hopelessness in Finnish Men Hypertension, February 1, 2000; 35(2): 561 - 567. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D. Lane, D. Carroll, and G.Y.H. Lip Psychology in coronary care QJM, August 1, 1999; 92(8): 425 - 431. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. C. Light, S. S. Girdler, A. Sherwood, E. E. Bragdon, K. A. Brownley, S. G. West, and A. L. Hinderliter High Stress Responsivity Predicts Later Blood Pressure Only in Combination With Positive Family History and High Life Stress Hypertension, June 1, 1999; 33(6): 1458 - 1464. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Rozanski, J. A. Blumenthal, and J. Kaplan Impact of Psychological Factors on the Pathogenesis of Cardiovascular Disease and Implications for Therapy Circulation, April 27, 1999; 99(16): 2192 - 2217. [Abstract] [Full Text] [PDF]
|
|
| |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||