Blood Pressure Reactions To Acute Mental Stress and Future Blood Pressure Status

Pre-print.
Cite as Blood Pressure Reactions to Acute Mental Stress and Future Blood Pressure Status: Data From the 12-Year FollowUp of the West of Scotland Study Carroll, D., Phillips, A., Der, G., Hunt, K. & Benzeval, M. 1 Nov 2011 In : Psychosomatic
Medicine. 73, 9, p. 737-742
Blood pressure reactions to acute mental stress and future blood pressure status: Data
from the 12-year follow-up in the West of Scotland Study
Running head: Stress reactivity and future blood pressure
Douglas Carroll, PhDa, Anna C. Phillips, PhDa, Geoff Der, PhDb, Kate Hunt, PhDb, and
Michaela Benzeval, MScb
School of Sport and Exercise Sciences, University of Birmingham, Birmingham,
England
b
MRC/CSO Social and Public Health Unit, University of Glasgow, Glasgow, Scotland
Words:3961
Tables:2
Figures:1
Address correspondence to: Douglas Carroll, PhD, School of Sport and Exercise
Sciences, University of Birmingham, Birmingham B15 2TT, England. E-mail
carrolld@bham.ac.uk
1
Pre-print. Cite as Blood Pressure Reactions to Acute Mental Stress and Future Blood Pressure Status: Data From the 12-Year FollowUp of the West of Scotland Study Carroll, D., Phillips, A., Der, G., Hunt, K. & Benzeval, M. 1 Nov 2011 In : Psychosomatic
Medicine. 73, 9, p. 737-742
Blood pressure reactions to acute mental stress and future blood pressure: Data from the
12-year follow-up in the West of Scotland Study
Douglas Carroll, Anna C. Phillips, Geoff Der, Kate Hunt, and Michaela Benzeval
Medicine. 73, 9, p. 737-742
Abstract
Objective: The reactivity hypothesis was tested using data from a 12 year follow-up of
blood pressure. It was examined whether blood pressure reactions to acute mental stress
predicted future blood pressure resting levels, as well as the temporal drift in resting
blood pressure, and whether the prediction was affected by sex, age, and socioeconomic
status. Methods: Resting blood pressure was recorded at an initial baseline and in
response to a mental stress task. Twelve years later resting blood pressure was again
assessed. Data were available for 1196 participants, comprising, at the time of stress
testing, 437 24-year olds, 503 44-year olds, and 254 63-year olds, 645 women and 551
men, and 531 were from manual socioeconomic households and 661 non-manual
socioeconomic households. Results: In multivariate linear regression models, adjusting
for a number of potential confounders, systolic blood pressure reactivity positively
predicted future resting systolic blood pressure, as well as the upward drift in systolic
blood pressure over the 12 years, = .10, p < .001 in both cases. The effect sizes were
smaller than those reported from an earlier 5-year follow-up. The analogous associations
for diastolic blood pressure reactivity were not statistically significant. In multivariate
logistic regression, high systolic blood pressure reactivity was associated with an
increased risk of being hypertensive 12 years later, OR = 1.03, 95%CI 1.01 1.04, p < .
001. Conclusions: The present findings that greater reactivity is associated with higher
future resting blood pressure, more upward drift in resting blood pressure, and future =
hypertension provide support for the reactivity hypothesis.
Medicine. 73, 9, p. 737-742
Key words: Systolic blood pressure; diastolic blood pressure; reactivity; acute mental
stress; hypertension; prospective study.
DBP = diastolic blood pressure; PASAT = paced auditory serial addition test; SBP =
systolic blood pressure
Medicine. 73, 9, p. 737-742
INTRODUCTION
The reactivity hypothesis has proved to be both extremely influential and
exceptionally durable (1, 2); at its simplest, it posits that large magnitude cardiovascular
reactions to acute psychological stress play a role in the development of cardiovascular
pathology in general and high blood pressure in particular (3-5). It is certainly the case
that the cardiovascular adjustments observed during acute psychological stress differ
from those that occur during physical exertion in that the latter are closely coupled with
the metabolic demands of motor behaviour whereas the former are apparently uncoupled
from the energy demands of behaviour and might be properly regarded as metabolically
exaggerated (6). Thus, it is easy to see why, in contrast to the biologically appropriate and
health enhancing adjustments during physical activity, large magnitude cardiovascular
reactions to psychological stress might be considered pathophysiological.
Although the original reactivity hypothesis is not without its critics (7), direct evidence
in support comes from a number of large scale cross-sectional and prospective
observational studies that attest to positive associations between the magnitude of
cardiovascular reactions to acute psychological stress tasks and future blood pressure
status (8-18), markers of systemic atherosclerosis (19-22), and left ventricular mass
and/or hypertrophy of the heart (23-25). The effect sizes are generally small but the
evidence is certainly consistent with the main tenets of the reactivity hypothesis (26).
Previously, we reported prospective analyses of data from the West of Scotland Study
(8). Blood pressure was measured at rest and in response to an acute mental stress task;
resting blood pressure was assessed five years later. Greater systolic blood pressure
stress reactivity was associated with 5-year follow-up resting systolic blood pressure and
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also with the upward drift in resting systolic blood pressure over time. The magnitude of
the prediction appeared to vary with sex and socioeconomic position. In the present
study, we report the outcome of analyses of data from a subsequent follow-up assessment
of blood pressure within the West of Scotland Study, 12 years on from the stress testing
session. This affords further opportunity to test the reactivity hypothesis with a more
protracted follow-up than the majority of other previous studies using mental stress tasks.
It is difficult to discern from previous studies the effect of duration of follow-up on the
prognostic significance of reactivity for future blood pressure status. Although studies
have varied in follow-up duration, they also vary in many other ways, such as the nature
and provocativeness of the stress task and the population studied. This makes it
problematic to attribute variations in the magnitude of the association been reactivity and
cardiovascular outcomes to variations in length of follow-up. However, one study,
Whitehall II, has separately reported on a 5-year (9) and 10-year follow-up (10). Systolic
blood pressure reactions to mental stress afforded the same magnitude of independent
prediction of systolic blood pressure levels at both follow-ups. It has been contended that
the most consistent and robust associations between reactivity and future blood pressure
status emerge from studies with younger samples and that a preponderance of older
participants in some prospective studies is responsible for the modest effects seen (27).
The present study, because of the three narrow age cohorts recruited, is perhaps uniquely
placed to consider age variations in the predictive power of reactivity on cardiovascular
outcomes. Finally, the current analysis also examines the reactivity hypothesis in the
context of a dataset that allows adjustment for a range of potential confounding variables.
Medicine. 73, 9, p. 737-742
MATERIALS AND METHODS

Participants
Data were collected as part of the West of Scotland Twenty-07 Study. Participants
were all from Glasgow and surrounding areas in Scotland and have been followed up at
intervals since the initial baseline survey in 1987 (28). Full details of the sampling
methodology and the structure of the sample is provided elsewhere (29). The analyses
here are of data from the third follow-up (referred to as baseline hereafter), at which
participants underwent standard cardiovascular stress testing, and from the fifth and final
follow-up, during which resting blood pressure was measured. A characteristic feature of
the sample is that it comprises three distinct age cohorts, the rationale for which is again
provided elsewhere (30). The mean (SD) lag between baseline and the follow-up was
12.4 (0.40) years. The effective sample size for the present analyses, i.e., those who had
complete cardiovascular data at both time points was 1196 (73% of those for whom
reactivity data were available at baseline). The reasons for non-participation at follow-up
were: refusal to participate 38%; died/incapacitated 33%; moved house/not
contactable 29%. At baseline the mean (SD) age was 41.1 (0.43) years and there were
437 (37%) 24-year olds, 503 (42%) 44-year olds, and 254 (21%) 63-year olds. There
were 645 (55%) women and 551 (45%) men, and 531 (45%) were from manual
occupational households and 661 (55%) non-manual occupational households. Ninetyeight (8%) reported taking antihypertensive medication at baseline and the mean (SD)
body mass index of the sample at the time was 25.6 (4.11) kg/m2.
Apparatus and Procedure

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Testing sessions were conducted by trained nurses in a quiet room in the participants
homes. Demographic and medication status at baseline was obtained by questionnaire.
Household socioeconomic status was characterize as manual and non-manual from the
occupational status of the head of household, using the Registrar General classification
system (30). Participants were asked whether they were taking any blood pressure
lowering medication and their medicine repositories checked for confirmation. Height
and weight was measured and body mass index computed. The acute stress task was the
paced auditory serial arithmetic test (PASAT), which has been shown in numerous studies
to reliably perturb the cardiovascular system (31, 32), and to demonstrate good test-retest
reliability (33). The nurses were all trained in administering the PASAT by the same
trainer and followed a written protocol. The test comprised a series of single digit
numbers presented by audiotape. Participants were instructed by the nurse to add
sequential number pairs, while at the same time retaining the second of the pair in
memory to add to the next number presented. Answers were given orally and the number
of correct answers was recorded by the nurse, who remained in the room, as a measure of
performance. The first sequence of 30 numbers was presented at a rate of one every 4
seconds, and the second at one every 2 seconds. The task lasted 3 minutes. Only those
who registered a score on the PASAT were included in the analyses. Of a possible score
of 60, the mean (SD) score was 44.6 (9.09).
Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were recorded using
a brachial cuff and a semi-automatic sphymomanometer (model 705CP, Omron,
Weymouth, UK). This blood pressure measuring device is recommended by the
European Society of Hypertension (34). After questionnaire completion (taking at least
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Medicine. 73, 9, p. 737-742
an hour), there was a formal 5-minute period of relaxed sitting, at the end of which a
resting baseline reading was taken. Task instructions were then given and participants
allowed a brief practice to ensure they understood the requirements of the PASAT. Two
further blood pressure readings were then taken, the first initiated 20 seconds into the task
(during the slower sequence of numbers) and the second initiated 110 seconds later
(during the faster sequence of numbers). The two task readings were averaged and the
resting baseline value subtracted, to yield reactivity measures for SBP and DBP.
At the follow-up, 12 years later, resting blood pressure was again recorded using the
Omron in the participants homes by nurses. As before, blood pressure measurement
followed the same lengthy questionnaire protocol and 5 minutes of relaxed sitting. Three
measurements were taken approximately 1 minute apart; the second two measurements,
one from the right arm and one from the left, were averaged as the measure of resting
blood pressure. The following criteria were used to define hypertension at the 12 year
follow-up: being on antihypertensive medication, or resting systolic blood pressure
140mmHg, or resting diastolic blood pressure 90mmHg.
Statistical Analyses
Repeated measures ANOVA was used to confirm that the PASAT significantly
increased SBP and DBP and to examine the drift in resting blood pressure between
baseline assessment and final follow-up 12 years later. 2 was adopted as a measure of
effect size. The association between SBP and DBP reactivity at baseline and resting SBP
and DBP at the fifth and final follow-up were examined by correlation and then by
multiple linear regression using the following additional covariates: age cohort, sex,
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PASAT performance, socioeconomic status at baseline, resting blood pressure at baseline,

taking blood pressure medication at baseline, and body mass index at baseline. The
covariates were always entered at step 1 and reactivity at step 2. Initial focus for the
regression analyses was the whole sample. Where significant overall associations
emerged, these were followed by subgroup analyses; analogous regression models were
tested separately for women and men, manual and non-manual socioeconomic group, and
the three age cohorts. Following on from our previous analyses (8), similar analyses
were performed on resting blood pressure drift over the 12 years between assessments
(i.e., resting blood pressure at the fifth follow-up minus resting blood pressure at
baseline). From the linear regression analyses, we report , the standardized regression
coefficient. Finally, the association between SBP and DBP reactivity and hypertension
was examined using logistic regression, first testing unadjusted models and then testing
models adjusting for the variables listed above.
RESULTS
The summary data for the 1647 participants who successfully underwent stress testing at
baseline are presented in Table 1. Those (N = 1196) who were available at 12-year
follow-up did not differ from those (N = 451) who were not available in either SBP
reactivity (p = .72) or DBP reactivity (p = .53); this was also the case for comparisons
involving specific reasons for dropping out.
[Insert Table 1 about here]
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Blood pressure reactions to acute stress

Table 1 presents the means and SD for the key blood pressure variables. The increases
in SBP and DBP to the stress task were statistically significant, F(1, 1195) = 1197.76, p
< .001, 2 = .501, and F(1, 1195) = 753.28, p < .001, 2 = .387. The mean (SD) upward
drift in resting SBP over 12 years was 4.10 (22.68) mmHg; this increase was statistically
significant, F(1, 1195) = 39.23, p < .001, 2 = .032. The drift for DBP, 0.84 (13.79)
mmHg was much more modest but still statistically significant, F(1, 1195) = 4.47, p = .
04, 2 = .004.
[Insert Table 2 about here]
Reactivity and resting blood pressure 12 years later

SBP reactivity was positively correlated with resting SBP 12 years later, r (1194) = .
08, p = .004; there was no such correlation between DBP reactivity and subsequent
resting DBP, p = .24. We then tested a hierarchical linear regression model with resting
SBP at the fifth, i.e., 12-year, follow-up as the dependent variable with the following
covariates, age cohort, sex, PASAT performance, socioeconomic status at baseline,
resting blood pressure at baseline, taking blood pressure medication at baseline, and body
mass index at baseline, entered at step one and SBP reactivity at step 2. In this model,
SBP reactivity emerged as a significant predictor of resting SBP at the 12-year follow-up,
= .10, p < .001, R2 = .010: the greater the SBP reactivity, then, the higher the
subsequent resting SBP. The other significant predictors of 12-year resting SBP in this
model were: higher initial resting SBP, = .30, p < .001; being in the older age cohort,
= .21, p < .001; having a larger body mass index, = .08, p = .003; being male, = .13, p
11
Medicine. 73, 9, p. 737-742
< .001; coming for a manual social class background, = .08, p = .001. The complete
model explained 27% of the variance in 12-year resting SBP. In the analogous model for
DBP, DBP reactivity was not a statistically significant predictor of 12-year resting DBP,
= .05, p = .06, R2 = .003. Finally, since it has been argued that aerobic fitness and/or
physical activity may be a serious confounder in studies such as this (35), we tested a
final model which in addition to the covariates above we also adjusted for leisure
physical activity, determined as whether participants engaged in five moderate or three
strenuous bouts of exercise per week. SBP reactivity continued to predict resting SBP 12
years later, = .08, p = .004, R2 = .006.
Effects of sex, age, and socioeconomic position on the prediction of 12-year followup SBP
Similar multiple linear regression analyses were undertaken separately for men and
women, the three age cohorts, and the two socioeconomic position groups. SBP
reactivity was positively associated with subsequent resting SBP for both men, = .10, p
= .01, R2 = .010, and women, = .12, p = .002, R2 = .011, and for manual, = .11, p
= .004, R2 = .011, and non-manual, = .10, p = .007, R2 = .009, social class groups.
SBP reactivity significantly predicted 12-year resting SBP levels in the youngest cohort,
= .14, p = .001, R2 = .017, the middle cohort, = .09, p = .04, R2 = .008, but not the
oldest cohort, = .12, p = .06, R2 = .013. There was no significant interaction effect on
cohort SBP reactivity on follow-up resting SBP.
Reactivity and the 12-year upward drift in blood pressure

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SBP reactivity was positively correlated with the upward drift in SBP resting levels
during the 12 years since baseline, r (1194) = .22, p < .001; DBP reactivity was positively
correlated with upward drift in resting DBP, r (1194) = .23, p <.001. The same
multivariate regression models as those above were then tested. SBP reactivity continued
to predict SBP upward drift, = .10, p < .001, R2 = .009. However, for DBP reactivity,
the prediction of DBP upward drift was no longer statistically significant, = .05, p = .
06, R2 = .003. In a final model, which in addition to the covariates above also adjusted
for leisure physical activity, SBP reactivity continued to predict SBP drift, = .08, p = .
02, R2 = .005. Again, it is important to note here that leisure physical activity data were
only available for the two older cohorts.
Effects of sex, age, and socioeconomic position on the prediction of SBP upward
drift
As with absolute 12-year follow-up SBP levels, the multivariate regression models
were tested separately for men and women, the three age cohorts, and the two
socioeconomic position groups. The outcomes were virtually identical to those reported
above for absolute level. SBP reactivity predicted subsequent resting SBP for both men,
= .09, p = .01, R2 = .008, and women, = .11, p = .002, R2 = .011, and for manual,
= .11, p = .004, R2 = .011, and non-manual, = .10, p = .007, R2 = .008, socioeconomic
status groups. As before, SBP reactivity was a stronger predictor of SBP upward drift in
the youngest cohort, = .14, p = .001, R2 = .018, than in the middle, = .09, p = .04,
R2 = .007, and older, = .11, p = .06, R2 = .010, cohorts. Again, however, there was no
significant interaction effect of cohort SBP reactivity on SBP upward drift.
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Reactivity and hypertension

Five hundred and seventy-five (48%) participants met the criteria for hypertension at
the 12-year follow-up. In an unadjusted model, SBP reactivity positively predicted risk
for hypertension, OR = 1.01, 95%CI 1.00 1.02, p < .03. In the model adjusting for the
same covariates that we adjusted for in linear regression above, SBP reactivity continued
to predict the 12-year risk for hypertension, OR = 1.03, 95%CI 1.01 1.04, p < .001; if
anything the association between SBP reactivity and future hypertension was stronger in
the multivariate model. As illustration, we plot per cent of participants with hypertension
for tertiles of SBP reactivity in Figure 1. Tertiles were formed from the raw, unadjusted,
SBP reactivity values. DBP reactivity did not significantly predict hypertension.
We also examined new incident hypertension by removing participants who were
hypertensive at baseline. In this analysis, antihypertensive medication status at baseline
was no longer used as a covariate. In this new fully adjusted model, SBP reactivity
continued to predict hypertension 12 years later, OR = 1.03, 95%CI 1.01 1.04, p = .001.
Analogously, we also examined the association between SBP reactivity and later onset
hypertension by removing participants who were hypertension at the earlier 5-year follow
up. Again, SBP reactivity predicted hypertension at 12 years, OR = 1.03, 95%CI 1.01
1.04, p <.001 Finally, as sensitivity analyses, we re-run the original fully adjusted model
defining hypertension solely in terms of the blood pressure criteria in one case and solely
in terms of self-reported antihypertensive medication in the other case. Thirty eight per
cent of participants were categorized as hypertensive using the former criterion and 22%
using the latter criterion. In both instances, SBP reactivity predicted future hypertension,
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OR = 1.02, 95%CI 1.00 1.03, p = .007 and OR = 1.02, 95%CI 1.01 1.04, p = .003,
respectively.
[Insert Figure 1 about here]
DISCUSSION
There was a positive bivariate relationship between the magnitude of SBP reactions to
a mental stress exposure and resting SBP 12 years later. This association was still evident
following adjustment for a range of potential confounding variables, such as age, sex,
socioeconomic status, body mass index, performance score on the stress task, and resting
blood pressure at the earlier time point. No analogous association emerged for DBP from
bivariate and multivariate analyses. As such, our findings closely replicate those we
reported previously from the 5-year follow-up (8). In addition, SBP reactivity was also
positively associated in both bivariate and multivariate analyses with the upward drift in
resting SBP over the 12 years between follow-ups. Although there was a bivariate
relationship between DBP reactivity and the 12-year change in resting DBP, the
association was no longer significant after adjustment for covariates in multivariate
analysis. With the exception of this last result, our findings replicate those reported from
the 5-year follow-up (8). Overall, though, the observed effect sizes were small with SBP
reactivity accounting for only 1% of the variance in resting SBP 12 years later and in SBP
upward drift, as compared to 2% and over 3% respectively in the 5-year follow-up.
Nevertheless, the present effect sizes are exactly in line with the aggregate effect size in a
recent meta-analysis of reactivity and cardiovascular disease outcomes (26). Further, in
the present multivariate regressions we adjusted for substantially more covariates than in
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the 5-year follow-up analyses. However, in models that adjusted only for age, body mass
index, and initial resting blood pressure, the outcomes were very much the same as those
reported above with SBP reactivity accounting for just over 1% of the variance in 12-year
resting SBP and SBP upward drift. Thus, it would appear that the associations between
reactivity and the blood pressure outcomes are simply weaker at the more distal followup. Not only did SBP reactivity predict future resting SBP and the 12-year upward drift
in SBP, it also predicted future hypertension status. Those with higher SBP reactivity
were more likely to meet the criteria for hypertension 12 years later; no analogous
association was evident for DBP reactivity.
The subgroup analyses indicated effects of much the same order for men and women
and participants from manual and non-manual socioeconomic groups. It has been argued
that the most consistent and robust associations between reactivity and future blood
pressure status emerge from studies with younger samples and that a preponderance of
older participants in some prospective studies may be responsible for the modest effects
seen (27). As indicated, the present study, by virtue of the three narrow age cohorts
recruited, was perhaps uniquely placed to examine age variations in the predictive power
of reactivity on future blood pressure status. However, the age cohort SBP reactivity
interaction effects on the SBP outcomes were not statistically significant, indicating that
age did not moderate the association between SBP reactivity and future blood pressure
status.
It is worth noting that the upward drift in resting blood pressure over the 12 years of
the study was noticeably modest. As we speculated previously, this could reflect the
possibility that participants with higher initial resting blood pressures could be receiving
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antihypertensive medication by the later follow-up, and as a consequence would have

registered smaller upward drifts in blood pressure (7). Compared to 8% at baseline, when
stress testing was undertaken, 21% reported taking antihypertensive medication at the
fifth and final follow-up and when these participants were removed larger mean upward
drifts were observed, mean = 7.12 (SD = 20.04) mmHg and mean = 3.20 (SD = 12.10)
mmHg for SBP and DBP drift respectively. Further, with these participants removed, the
associations between SBP reactivity and the SBP outcomes in the multivariate analyses
were somewhat stronger, = .14, p < .001, R2 = .017 and = .15, p < .001, R2 = .020
for 12-year resting SBP and SBP upward drift respectively. This would suggest that
antihypertensive medication is not only masking upward blood pressure drift over time, it
is also somewhat attenuating the association between reactivity and future blood pressure
status. In addition, given that participants in the youngest cohort were less likely to be
taking antihypertensive medication, 3% as opposed to 22% and 52% in the middle and
oldest cohort respectively, this attenuation effect of medication on the link between
reactivity and future blood pressure could account for why we tended to see the strongest
association in the youngest cohort.
This study is not without its limitations. First, there was high variability in resting
blood pressure, upward blood pressure drift, and reactivity. However, given the
standardized procedures for measuring blood pressure, this is unlikely to reflect
measurement error. In addition, other epidemiological studies of the same magnitude,
such as Caerphilly (36) and Whitehall II (9, 10), reports similar SDs for blood pressure.
Second, determining causality from even prospective observational studies is fraught
with pitfalls (37). However, in the present analyses we adjusted for a broad range of
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potential confounders, more than most previous studies (26). Nevertheless, residual
confounding as a consequence of poorly measured or unmeasured variables cannot be
wholly discounted. In addition, prospective observational analyses cannot distinguish
with certainty between prodromal markers of disease and factors that play a causal
pathophysiological role. Third, 451 (27%) of the participants who were stress tested at
baseline were unavailable for assessment 12 years later. For 137, this was because they
had died or were incapacitated in the interim. However, SBP reactivity did not differ
between those who remained in the study and those who did not: 11.5 and 11.3 mmHg,
respectively. Fourth, the baseline and task durations in the present study were relatively
short, and the number of blood pressure readings were small in comparison to other
studies. However, it is likely that, given these limitations, the effect sizes observed in this
study underestimate the true predictive value of reactivity.
In conclusion, greater SBP reactions to acute psychological stress were associated
with resting SBP 12 years later, more upward drift in SBP levels over time, and a greater
likelihood of suffering from hypertension at the 12-year follow-up. These associations
withstood adjustment for a range of covariates. Although the effect sizes for SBP
reactivity were weaker than those found at a 5-year follow-up in this study (8), they were
the same order of magnitude as those observed for body mass index. The analogous
associations for DBP reactivity were not statistically significant in multivariate analyses.
There was some indication that antihypertensive medication tended to attenuate the
relationship between SBP reactivity and the SBP outcomes. Overall, our findings lend
support to the original reactivity hypothesis.
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Acknowledgements
The West of Scotland Twenty-07 Study is funded by the UK Medical Research Council
and the data were originally collected by the MRC Social and Public Health Sciences
Unit. We are grateful to all of the participants in the Study, and to the survey staff and
research nurses who carried it out. The data are employed here with the permission of the
Twenty-07 Steering Group (Project No. EC201003). GD, KH, and MP are funded by the
Medical Research Council.
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Table 1: Socio-demographics of the sample at baseline (N = 1647)
Variable
Age
Sex (male)
Non-manual occupation group
BMI
Current smokers
Current drinker
Physical activity
PASAT performance score
Mean / N
42.2
757
870
25.7
593
1497
300
43.8
SD / %
15.45
46
53
4.26
36
91
18
9.20
23
Medicine. 73, 9, p. 737-742
Table 2. Mean (SD) of the key blood pressure variables (N = 1196)
Variable
SBP (mmHg)
DBP (mmHg)
Initial resting blood pressure
128.23 (20.26)
78.76 (11.71)
Reactivity
11.54 (11.54)
6.87 (8.65)
Final resting blood pressure at 12 years
132.34 (22.35)
79.60 (13.79)
24
Medicine. 73, 9, p. 737-742
Figure 1. Percentage meeting the criteria for hypertension by tertiles of SBP reactivity
25
Medicine. 73, 9, p. 737-742
26

Blood Pressure Reactions To Acute Mental Stress and Future Blood Pressure Status

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Blood Pressure Reactions To Acute Mental Stress and Future Blood Pressure Status

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Running head: Stress reactivity and future blood pressure

School of Sport and Exercise Sciences, University of Birmingham, Birmingham,

MATERIALS AND METHODS

Apparatus and Procedure

PASAT performance, socioeconomic status at baseline, resting blood pressure at baseline,

[Insert Table 1 about here]

Blood pressure reactions to acute stress

Reactivity and resting blood pressure 12 years later

Reactivity and the 12-year upward drift in blood pressure

Reactivity and hypertension

antihypertensive medication by the later follow-up, and as a consequence would have

Table 1: Socio-demographics of the sample at baseline (N = 1647)

Table 2. Mean (SD) of the key blood pressure variables (N = 1196)

Initial resting blood pressure

Final resting blood pressure at 12 years

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