Psychophysiology, •• (2012), ••–••. Wiley Periodicals, Inc. Printed in the USA.

Copyright © 2012 Society for Psychophysiological Research

DOI: 10.1111/j.1469-8986.2012.01463.x

Increased blood pressure reactions to acute mental stress are

associated with 16-year cardiovascular disease mortality

DOUGLAS CARROLL,a ANNIE T. GINTY,a GEOFF DER,b KATE HUNT,b MICHAELA BENZEVAL,b and
ANNA C. PHILLIPSa
a
School of Sport and Exercise Sciences, University of Birmingham, Birmingham, England
b
Medical Research Council/Chief Scientist Office (MRC/CSO) Social and Public Health Sciences Unit, University of Glasgow, Glasgow, Scotland

Abstract
Exaggerated cardiovascular reactions to acute psychological stress may be involved in the etiology of cardiovascular
pathology. The present analysis examined the association between the magnitude of systolic and diastolic blood pressure
reactions to stress and cardiovascular disease mortality. Participants were 431 (229 women) from the West of Scotland
Twenty-07 Study, aged 63 years at the time of stress testing, where blood pressure was measured during resting baseline
and mental arithmetic stress. Participants’ vital status was tracked for the next 16 years, during which time 38 had died
of cardiovascular disease. Both systolic and diastolic blood pressure reactions were positively associated with cardio-
vascular disease mortality. This association could reflect the long-term erosive effects of exaggerated reactivity on the
vasculature as well as its short-term capacity to trigger acute cardiovascular events.
Descriptors: Cardiovascular disease mortality, Systolic blood pressure, Diastolic blood pressure, Cardiovascular
reactivity, Acute stress

The reactivity hypothesis posits that large magnitude cardiovascu- to predict what cardiovascular activity should have been during
lar reactions to acute psychological stress play a role in the devel- stress given contemporary levels of oxygen consumption. The
opment of cardiovascular pathology (Light, 1981; Manuck, recorded levels of stress-related cardiovascular activity were well
Kasprowicz, & Muldoon, 1990; Obrist, 1981). The hypothesis has in excess of what was predicted (Balanos et al., 2010; Carroll,
proved to be both influential and durable (Turner, 1994; Wright & Phillips, & Balanos, 2009). Thus, it is easy to see why, in contrast
Gendolla, 2011). It is certainly the case that the cardiovascular to the biologically appropriate and health-enhancing adjustments
adjustments observed during acute psychological stress differ from during physical activity, large magnitude cardiovascular reactions
those that occur during physical exertion in that the latter are to psychological stress might be considered pathophysiological.
closely coupled with the metabolic demands of motor behavior, More direct evidence in support of the reactivity hypothesis
whereas the former are apparently uncoupled from the energy comes from a number of large-scale cross-sectional and prospec-
demands of behavior and might be properly regarded as meta- tive observational studies that attest to positive associations
bolically exaggerated. For example, in two recent studies in our between the magnitude of cardiovascular reactions to acute psy-
laboratory, we measured cardiovascular activity and oxygen con- chological stress tasks and future blood pressure status and hyper-
sumption during acute stress exposure and graded submaximal tension (Carroll, Phillips, Der, Hunt, & Benzeval, 2011; Carroll,
cycling. The individual oxygen consumption–cardiovascular activ- Ring, Hunt, Ford, & Macintyre, 2003; Carroll, Smith, Sheffield,
ity regression equations calculated for graded exercise allowed us Shipley, & Marmot, 1995; Carroll et al., 2001; Markovitz, Raczyn-
ski, Wallace, Chettur, & Chesney, 1998; Matthews, Woodall, &
Allen, 1993; Newman, McGarvey, & Steele, 1999), markers of
The West of Scotland Twenty-07 Study is funded by the UK Medical systemic atherosclerosis (Barnett, Spence, Manuck, & Jennings,
Research Council (53462), and the data were originally collected by the 1997; Everson et al., 1997; Lynch, Everson, Kaplan, Salonen, &
MRC Social and Public Health Sciences Unit. Further information about Salonen, 1998; Matthews et al., 1998), and left ventricular mass
the data can be found at http://2007study.sphsu.mrc.ac.uk/. We are grateful
to all of the participants in the study, and to the survey staff and research and/or hypertrophy of the heart (Georgiades, Lemne, de Faire,
nurses who carried it out. The data are employed here with the permission Lindvall, & Fredrikson, 1997; Kapuku et al., 1999; Murdison et al.,
of the Twenty-07 Steering Group (Project No. EC201003). GD (5TK30), 1998). The effect sizes are generally small but the evidence is
KH (5TK50), and MB (5TK10) are funded by the Medical Research certainly consistent with the main tenets of the reactivity hypoth-
Council.
Address correspondence to: Anna C. Phillips, Ph.D., School of Sport
esis. A recent meta-analysis of 36 studies confirms this conclusion;
and Exercise Sciences, University of Birmingham, Edgbaston, Birmingham the authors report an aggregate r = .091, p < .001, which connotes
B15 2TT, England, UK. E-mail: a.c.phillips@bham.ac.uk a small but highly significant effect (Chida & Steptoe, 2010).
bs_bs_banner

1
2 D. Carroll et al.

No study to date, however, has examined the association Answers were given orally and the correctness of the answers
between cardiovascular stress reactions and cardiovascular disease recorded as a measure of performance. The first sequence of 30
(CVD) mortality. Data from the West of Scotland Twenty-07 Study numbers was presented at a rate of one every 4 s, and the second at
affords just such an analyses; the eldest of the three age cohorts was one every 2 s. In all, the task lasted 3 min. Only those who regis-
circa 63 years old at the time of stress testing, and their mortality tered a score on the PASAT were included in the analyses. Of a
status has been tracked for the subsequent 16 years. On the basis of possible score of 60, the mean (SD) score was 40.86 (9.03).
the reactivity hypothesis, we anticipated a positive association Systolic blood pressure (SBP) and diastolic blood pressure
between the magnitude of blood pressure reactions to acute stress (DBP) were recorded using a brachial cuff and a semiautomatic
and subsequent risk of CVD death. sphygmomanometer (model 705CP, Omron, Weymouth, UK). This
blood pressure measuring device is recommended by the European
Society of Hypertension (O’Brien, Waeber, Parati, Staessen, &
Method Myers, 2001). After questionnaire completion (taking at least an
hour), there was a formal 5-min period of relaxed sitting, at the end
Participants of which a resting baseline reading was taken. Task instructions
were then given and participants allowed a brief practice to ensure
Data analyses focused on the eldest of the three discrete age cohorts
they understood the requirements of the PASAT. Two further blood
that comprise the West of Scotland Twenty-07 Study (Benzeval
pressure readings were then taken, the first initiated 20 s into the
et al., 2009). Participants were all from the Glasgow area and have
task (during the slower sequence of numbers) and the second ini-
been surveyed periodically since 1988. They were virtually all
tiated 110 s later (during the faster sequence of numbers). The two
Caucasian, commensurate with the area’s demographics. The West
task readings were averaged and the resting baseline value sub-
of Scotland Study’s principal aim was to investigate the processes
tracted, to yield reactivity measures for SBP and DBP.
that generate and maintain socio inequalities in health (Macintyre,
Vital status was then continuously monitored. The end point of
1987). Participants were chosen randomly with probability propor-
monitoring for the present analyses was November 7, 2011, that is,
tional to the overall population of the same age within selected
16 years after the cardiovascular stress testing exposure. The study
postal code areas based on a stratified sample of postal codes
participants were flagged using the UK’s National Health Service
(Ecob, 1987). The present analysis is based on the third wave of
Central Registry, which provided notification of death as well as
data collection, and the effective sample size was 431 (229
cause of death. Mortality due to CVD was classified using the
women). At the time of cardiovascular stress testing in 1995/96,
International Classification of Diseases (ICD) (World Health
participants were all around 63 years old: mean (SD) age was 63.57
Organisation, 1992) codes: ICD-9: 390–434, 436–448, and ICD-
(0.61). The study was approved by the appropriate ethics commit-
10: I00–I78, which comprised acute rheumatic fever; chronic rheu-
tees, conducted in accordance with the Declaration of Helsinki, and
matic heart diseases; hypertensive diseases; ischemic heart
all participants provided informed consent.
diseases; pulmonary heart disease and diseases of pulmonary cir-
culation; other forms of heart disease; cerebrovascular diseases;
Procedure and diseases of arteries, arterioles, and capillaries.

Testing sessions were conducted by trained nurses in a quiet Data Analyses

room in the participants’ homes. Demographic and other infor-
mation was obtained by questionnaire. Household socioeconomic Differences between those who had and had not died from CVD on
status (SES) was characterized as manual or nonmanual from the the various covariates were compared using c2 (categorical data)
occupation (or final occupation, if retired) of the head of house- and analysis of variance (ANOVA) (continuous data). Average SBP
hold, using the Registrar General’s classification system (OPCS, and DBP levels during the stress tests were compared to baseline
1980). From questions on smoking behavior, participants were values using repeated measures ANOVA. SBP and DBP stress
classified as never, ex, or current smokers. Long-standing chronic reactivity were then computed as the average task value minus the
illness status was determined by the question, “Do you have any baseline. For the ANOVAs, partial h2 is reported as a measure of
long-standing illness, disability, or infirmity? By long-standing, I effect size. Cox’s proportional hazard models were used to analyze
mean anything that has troubled you over a period of time or that the CVD mortality data. First, we examined the association
is likely to affect you over a period of time.” From a raft of between blood pressure stress reactivity and CVD mortality in
questions on physical activity, a summary measure of whether or unadjusted models. Second, we tested models that adjusted for age,
not participants met the then-recommended guidelines of five sex, SES, smoking, BMI, physical activity, long-standing chronic
moderate or three strenuous bouts of activity per week was illness, baseline blood pressure, and antihypertensive medication.
derived. Height and weight were measured and body mass index Finally, analogous analyses were undertaken for all-cause
(BMI) computed. mortality.
The acute stress task was the paced auditory serial arithmetic
test (PASAT), which has been shown in numerous studies to reli- Results
ably perturb the cardiovascular system (Ring, Burns, & Carroll,
2002; Winzer et al., 1999), and to demonstrate good test-retest Thirty-eight participants had died from CVD during the 16 years
reliability (Willemsen et al., 1998). The nurses were all trained in subsequent to stress testing. The key characteristics of those who
administering the PASAT by the same trainer and followed a had and had not died of CVD are summarized in Table 1. Current
written protocol. The test comprised a series of single digit smokers, those from manual socioeconomic households, those who
numbers presented by audiotape. Participants were required to add were physically inactive, and those with long-standing illness were
sequential number pairs, while at the same time retaining the more likely to have died of CVD. Men were more likely than
second of the pair in memory to add to the next number presented. women to have died of CVD, but this effect did not meet the
Stress reactivity and cardiovascular disease mortality 3

Table 1. Characteristics of Those Who Had and Had Not Died of

Cardiovascular Disease

Did not die of

Died of CVD CVD
(N = 38) (N = 393)
M (SD) M (SD) p
Age 63.51 (0.62) 63.58 (0.64) .49
Body mass index 25.35 (4.46) 26.39 (4.28) .16
N (%) N (%)
Sex Male 23 (61) 179 (46) .08
Female 15 (39) 214 (54)
Socioeconomic Manual 29 (76) 207 (53) .006
status Nonmanual 9 (24) 183 (46)
Smoking Never 5 (13) 150 (38) .005
Ex 14 (37) 126 (32)
Current 19 (50) 117 (30)
Met activity Yes 3 (8) 110 (28) .01 Figure 1. CVD mortality survival curves for participants in the top quartile
criterion No 33 (92) 281 (72) of SBP reactors versus the rest of the sample.
Long-standing Yes 10 (26) 37 (9) .001
illness No 28 (74) 356 (91)

of SBP and DBP stress reactivity with the rest of the sample.
Finally, SBP and DBP reactivity were not significantly associated
with all-cause mortality risk in either unadjusted, HR = 0.999, 95%
conventional criterion of statistical significance. The stress task
CI 0.987–1.011, p = .87 and HR = 1.012, 95% CI 0.995–1.029,
perturbed both SBP, F(1,430) = 261.94, p < .001, h2 = .379, and
p = .16, respectively, or fully adjusted models, HR = 1.002, 95% CI
DBP, F(1,430) = 338.03, p < .001, h2 = .440; the summary statis-
0.989–1.016, p = .74 and HR = 1.016, 95% CI 0.996–1.037,
tics are presented in Table 2.
p = .12, respectively.
Unadjusted hazard models revealed positive, but nonsignificant,
associations between SBP stress reactivity, heart rate (HR) = 1.019,
95% CI 0.995–1.044, p = .12, and DBP stress reactivity, Discussion
HR = 1.029, 95% CI 0.994–1.066, p = .10, and CVD mortality.
However, in models that adjusted for age, sex, SES, smoking, BMI, In multivariate Cox’s proportional hazard models, adjusting for
physical activity, long-standing chronic illness, baseline blood age, sex, SES, smoking, BMI, physical activity, long-standing
pressure, and antihypertensive medication, these positive associa- chronic illness, and resting blood pressure, exaggerated SBP and
tions were statistically significant for both SBP reactivity, DBP reactions to an acute psychological stress task were associated
HR = 1.032, 95% CI 1.003–1.062, p = .03, and DBP reactivity, with an increase in the risk of CVD, but not all-cause, mortality
HR = 1.049, 95% CI 1.003–1.096, p = .04. The main variables over the subsequent 16 years. This finding extends previous obser-
whose absence appeared to suppress the association between blood vations linking cardiovascular stress reactivity to future blood pres-
pressure reactivity and CVD mortality were long-standing illness, sure status (Carroll et al., 1995, 2001, 2003; Markovitz et al., 1998;
SES, and physical activity. In models that adjusted only for these Matthews et al., 1993; Newman et al., 1999), markers of systemic
three variables, the strength of the association between reactivity atherosclerosis (Barnett et al., 1997; Everson et al., 1997; Lynch
and CVD mortality was of the same order as that evident in the
fully adjusted models: HR = 1.030, 95% CI 1.004–1.057, p = .03,
and HR = 1.044, 95% CI 1.005–1.086, p = .03, for SBP and DBP
reactivity, respectively. In the fully adjusted models, then, for every
one standard deviation increase in SBP and DBP stress reactivity
there was a 3% and 5% increase, respectively, in the likelihood of
having died of CVD during the 16 years of monitoring. The rel-
evant survival curves based on these adjusted models are displayed
in Figures 1 and 2, for SBP and DBP stress reactivity, respectively.
These compare rather than contrast participants in the top quartiles

Table 2. Systolic and Diastolic Blood Pressure Levels at Baseline

and During the Stress Task

Baseline Stress task

M (SD) M (SD) p
Systolic blood pressure 144.35 (21.67) 156.68 (22.80) <.001
Diastolic blood pressure 83.83 (11.17) 90.79 (13.23) <.001 Figure 2. CVD mortality survival curves for participants in the top quartile
of DBP reactors versus the rest of the sample.
4 D. Carroll et al.

et al., 1998; Matthews et al., 1998), and left ventricular mass and/or The present study is not without limitations. First, the sample
hypertrophy of the heart (Georgiades et al., 1997; Kapuku et al., size is modest and there were only 38 CVD deaths. However, the
1999; Murdison et al., 1998). It also offers unique support to the study had sufficient power to detect significant associations between
reactivity hypothesis which contends that, over the life course, stress reactivity and CVD mortality. Second, the effects sizes are
exaggerated cardiovascular reactions to acute stress exposures play small. However, they are of the same order as or larger than those we
a role in the development of cardiovascular pathology. That the reported previously from this study for cardiovascular reactivity and
associations are evident in multivariate analyses but are not statis- the upward drift of blood pressure over time and hypertension
tically significant in univariate analyses might be regarded as (Carroll et al., 2003, 2011). Further, although in advance of replica-
curious. However, given that so many other factors contribute to tion it would be premature to speculate on the health implications of
CVD mortality (in our analyses, smoking, physical inactivity, long- our findings, it is perhaps worth pointing out that at an individual
standing illness, and low SES were all highly predictive), we would level the risk of dying from CVD associated with high blood
contend the univariate model is suboptimal and that only multivari- pressure reactivity was greater than that associated with high BMI in
ate models afford a proper test of our original hypothesis. Indeed, the present study. Third, the present sample was relatively older than
in models entering, in addition to reactivity, only physical activity, those in the majority of the prospective studies of stress reactivity,
SES, and illness, both SBP and DBP reactivity were as strongly and this may limit generalization. However, two previous studies of
predictive of CVD mortality as they were in our fully adjusted reactivity and cardiovascular outcomes stress tested samples that
models. were in their mid to late 50s (Lynch et al., 1998; Matthews et al.,
It is unclear what the mechanisms are that link exaggerated 1998). Further, it is almost inevitable in a study of CVD mortality
blood pressure stress reactivity to future CVD mortality. There that the sample will be older at entry; otherwise, there would be
are at least two possible routes. First, evidence indicates (see insufficient events to analyze in a realistic time frame. Fourth,
above) that exaggerated pressor responses across the life course observational studies, even prospective ones, cannot definitively
are associated prospectively with the preconditions for CVD mor- determine causality. There is always the issue of confounding by
tality: hypertension and atherosclerosis. Whereas we were able to some unmeasured or poorly measured variable (Christenfeld, Sloan,
adjust for resting blood pressure and antihypertensive medication Carroll, & Greenland, 2004). However, we did adjust statistically for
in the present study, we have no data on concurrent arterial ste- many potential confounders. Finally, the reliance on self-report for
nosis. Second, acute stress exposure has been implicated in trig- important health-related measures such as smoking and long-
gering acute CVD events (Tofler et al., 1990). Earthquakes, standing illness might also be regarded as a weakness. However, the
missile attacks, and even key sporting events have all been linked concordance in reported smoking status between adjacent surveys in
to increased hospital admissions for and/or mortality from CVD this study exceeded 90%, and self-reported smoking behavior cor-
(Bergovec et al., 1992; Carroll, Ebrahim, Tilling, Macleod, & relates strongly with cotinine and other biochemical measures of
Smith, 2002; Leor & Kloner, 1996; Meisel et al., 1991; Tri- smoking (Woodward, Moohan, & Tunstall-Pedoe, 1999). In addi-
chopoulos, Katsouyanni, Zavitsanos, Tzonou, & Dalla-Vorgia, tion, the methodology used to ascertain long-standing illness has
1983; Witte, Bots, Hoes, & Grobbee, 2000). Laboratory stress shown little bias in reporting (Macintyre, 1987).
exposures that increase blood pressure also increase hematocrit In conclusion, individuals who show large magnitude SBP and
and blood viscosity, and reduce coagulation time (de Boer et al., DBP reactions to acute psychological stress are at increased risk of
2007) creating what might be regarded as a prothrombic state. subsequently dying from CVD. This finding adds support to the
Indeed, the evidence suggests that such rheological changes are hypothesis that exaggerated stress reactivity plays a role in cardio-
mediated by the arterial pressure stress response (de Boer et al., vascular pathology, through its long-term erosive effects on the
2007). Accordingly, exaggerated blood pressure stress reactivity vasculature and/or by serving as a short-term prothrombic trigger
may be accompanied by greater prothrombic changes. for acute cardiovascular events.

References

Balanos, G. M., Phillips, A. C., Frenneaux, M. P., McIntrye, D., Lykidis, C., Carroll, D., Phillips, A. C., Der, G., Hunt, K., & Benzeval, M. (2011). Blood
Griffin, H. S., & Carroll, D. (2010). Metabolically exaggerated cardiac pressure reactions to acute mental stress and future blood pressure
reactions to acute psychological stress: The effects of resting blood status: Data from the 12-year follow-up of the West of Scotland
pressure status and possible underlying mechanisms. Biological Psy- Study. Psychosomatic Medicine, 73, 737–742. doi: 10.1097/PSY.
chology, 85, 104–111. doi: 10.1016/j.biopsycho.2010.06.001 0b013e3182359808
Barnett, P. A., Spence, J. D., Manuck, S. B., & Jennings, J. R. (1997). Carroll, D., Ring, C., Hunt, K., Ford, G., & Macintyre, S. (2003). Blood
Psychological stress and the progression of carotid artery disease. pressure reactions to stress and the prediction of future blood pressure:
Journal of Hypertension, 15, 49–55. doi: 10.1097/00004872- Effects of sex, age, and socioeconomic position. Psychosomatic Medi-
199715010-00004 cine, 65, 1058–1064. doi: 10.1097/01.PSY.0000097330.58739.26
Benzeval, M., Der, G., Ellaway, A., Hunt, K., Sweeting, H., West, P., & Carroll, D., Smith, G. D., Sheffield, D., Shipley, M. J., & Marmot, M. G.
MacIntyre, S. (2009). Cohort profile: West of Scotland Twenty-07 (1995). Pressor reactions to psychological stress and prediction of future
Study: Health in the community. International Journal of Epidemiol- blood pressure: Data from the Whitehall II Study. British Medical
ogy, 38, 1215–1223. doi: 10.1093/ije/dyn213 Journal, 310, 771–776. doi: 10.1136/bmj.310.6982.771
Bergovec, M., Mihatov, S., Prpic, H., Rogan, S., Batarelo, V., & Sjerobab- Carroll, D., Smith, G. D., Shipley, M. J., Steptoe, A., Brunner, E. J., &
ski, V. (1992). Acute myocardial infarction among civilians in Zagreb Marmot, M. G. (2001). Blood pressure reactions to acute psychological
city area. Lancet, 339, 303. doi: 10.1016/0140-6736(92)91370-N stress and future blood pressure status: A 10-year follow-up of men in
Carroll, D., Ebrahim, S., Tilling, K., Macleod, J., & Smith, G. D. (2002). the Whitehall II Study. Psychosomatic Medicine, 63, 737–743. doi:
Admissions for myocardial infarction and World Cup football: Database 0033-3174/01/6305-0737
survey. British Medical Journal, 325, 1439–1442. Chida, Y., & Steptoe, A. (2010). Greater cardiovascular responses to labo-
Carroll, D., Phillips, A. C., & Balanos, G. M. (2009). Metabolically exag- ratory mental stress are associated with poor subsequent cardiovascular
gerated cardiac reactions to acute psychological stress revisited. Psy- risk status: A meta-analysis of prospective evidence. Hypertension, 55,
chophysiology, 46, 270–275. doi: 10.1111/j.1469-8986.2008.00762.x 1026–1032. doi: 10.1161/HYPERTENSIONAHA.109.146621
Stress reactivity and cardiovascular disease mortality 5

Christenfeld, N. J., Sloan, R. P., Carroll, D., & Greenland, S. (2004). Risk myocardial infarction and sudden death in Israeli civilians. Lancet, 338,
factors, confounding, and the illusion of statistical control. Psychoso- 660–661. doi: 10.1016/0140-6736(91)91234-L
matic Medicine, 66, 868–875. Murdison, K. A., Treiber, F. A., Mensah, G., Davis, H., Thompson, W., &
de Boer, D., Ring, C., Wood, M., Ford, C., Jessney, N., McIntyre, D., & Strong, W. B. (1998). Prediction of left ventricular mass in youth with
Carroll, D. (2007). Time course and mechanisms of mental stress- family histories of essential hypertension. American Journal of Medical
induced changes and their recovery: Hematocrit, colloid osmotic pres- Sciences, 315, 118–123. doi: 10.1097/00000441-199802000-00008
sure, whole blood viscosity, coagulation times, and hemodynamic Newman, J. D., McGarvey, S. T., & Steele, M. S. (1999). Longitudinal
activity. Psychophysiology, 44, 639–649. doi: 10.1111/j.1469- association of cardiovascular reactivity and blood pressure in Samoan
8986.2007.00536 adolescents. Psychosomatic Medicine, 61, 243–249.
Ecob, R. (1987). The sampling scheme, frame and procedures for the cohort O’Brien, E., Waeber, B., Parati, G., Staessen, J., & Myers, M. G. (2001).
studies (Working Paper No. 6). Glasgow, Scotland: MRC Medical Soci- Blood pressure measuring devices: Recommendations of the European
ology Unit. Society of Hypertension. British Medical Journal, 322, 531–536. doi:
Everson, S. A., Lynch, J. W., Chesney, M. A., Kaplan, G. A., Goldberg, 10.1136/bmj.322.7285.531
D. E., Shade, S. B., . . . Salonen, J. T. (1997). Interaction of workplace Obrist, P. (1981). Cardiovascular psychophysiology: A perspective. New
demands and cardiovascular reactivity in progression of carotid athero- York, NY: Plenum Press.
sclerosis: Population based study. British Medical Journal, 314, 553– OPCS (Office of Population Censuses and Surveys). (1980). Classifica-
558. doi: 10.1136/bmj.314.7080.553 tion of occupations, 1980. London, England: HMSO. Retrieved from
Georgiades, A., Lemne, C., de Faire, U., Lindvall, K., & Fredrikson, M. http://www.camsis.stir.ac.uk/Data/Britain91.html#Occupational_
(1997). Stress-induced blood pressure measurements predict left ven- Classification.
tricular mass over three years among borderline hypertensive men. Ring, C., Burns, V. E., & Carroll, D. (2002). Shifting hemodynamics of
European Journal of Clinical Investigation, 27, 733–739. doi: 10.1046/ blood pressure control during prolonged mental stress. Psychophysiol-
j.1365-2362.19971800729.x ogy, 39, 585–590. doi: 10.1111/1469-8986.3950585
Kapuku, G. K., Treiber, F. A., Davis, H. C., Harshfield, G. A., Cook, B. B., Tofler, G. H., Stone, P. H., Maclure, M., Edelman, E., Davis, V. G., Rob-
& Mensah, G. A. (1999). Hemodynamic function at rest, during acute ertson, T., . . . Muller, J. E. (1990). Analysis of possible triggers of acute
stress, and in the field: Predictors of cardiac structure and function 2 myocardial infarction (the MILIS study). American Journal of Cardi-
years later in youth. Hypertension, 34, 1026–1031. ology, 66, 22–27. doi: 10.1016/0002-9149(90)90729-K
Leor, J., & Kloner, R. A. (1996). The Northridge earthquake as a trigger for Trichopoulos, D., Katsouyanni, K., Zavitsanos, X., Tzonou, A., & Dalla-
acute myocardial infarction. American Journal of Cardiology, 77, Vorgia, P. (1983). Psychological stress and fatal heart attack: The Athens
1230–1232. (1981) earthquake natural experiment. Lancet, 1, 441–444. doi:
Light, K. C. (1981). Cardiovascular responses to effortful active coping: 10.1016/S0140-6736(83)91439-3
Implications for the role of stress in hypertension development. Psycho- Turner, J. R. (1994). Cardiovascular reactivity and stress. New York, NY:
physiology, 18, 216–225. Plenum Press.
Lynch, J. W., Everson, S. A., Kaplan, G. A., Salonen, R., & Salonen, J. T. Willemsen, G., Ring, C., Carroll, D., Evans, P., Clow, A., & Hucklebridge,
(1998). Does low socioeconomic status potentiate the effects of height- F. (1998). Secretory immunoglobulin A and cardiovascular reactions to
ened cardiovascular responses to stress on the progression of carotid mental arithmetic and cold pressor. Psychophysiology, 35, 252–259.
atherosclerosis? American Journal of Public Health, 88, 389–394. doi: doi: 10.1111/1469-8986.3530252
10.2105/AGPH.88.3.389 Winzer, A., Ring, C., Carroll, D., Willemsen, G., Drayson, M., & Kendall,
Macintyre, S. (1987). West of Scotland Twenty-07: Health in the commu- M. (1999). Secretory immunoglobulin A and cardiovascular reactions to
nity. The survey’s background and rationale (Working Paper No. 7). mental arithmetic, cold pressor, and exercise: Effects of beta-adrenergic
Glasgow, Scotland: MRC Medical Sociology Unit. blockade. Psychophysiology, 36, 591–601. doi: 10.1111/1469-
Manuck, S. B., Kasprowicz, A. L., & Muldoon, M. F. (1990). Behaviourally 8986.3650591
evoked cardiovascular reactivity and hypertension: Conceptual issues Witte, D. R., Bots, M. L., Hoes, A. W., & Grobbee, D. E. (2000). Cardio-
and potential associations. Annals of Behavioral Medicine, 12, 17–29. vascular mortality in Dutch men during 1996 European football cham-
Markovitz, J. H., Raczynski, J. M., Wallace, D., Chettur, V., & Chesney, pionship: Longitudinal population study. British Medical Journal, 321,
M. A. (1998). Cardiovascular reactivity to video game predicts subse- 1552–1554. doi: 10.1136/bmj.321.7276.1552
quent blood pressure increases in young men: The CARDIA study. Woodward, M., Moohan, M., & Tunstall-Pedoe, H. (1999). Self-reported
Psychosomatic Medicine, 60, 186–191. smoking, cigarette yields and inhalation biochemistry related to the
Matthews, K. A., Owens, J. F., Kuller, L. H., Sutton-Tyrrell, K., Lassila, H. incidence of coronary heart disease: Results from the Scottish Heart
C., & Wolfson, S. K. (1998). Stress-induced pulse pressure change Health Study. Journal of Epidemiology and Biostatistics, 4, 285–295.
predicts women’s carotid atherosclerosis. Stroke, 29, 1525–1530. doi: World Health Organisation, 1992. International statistical classification of
10.1161/01.STR.29.8.1525 diseases and related health problems. Geneva, Switzerland: WHO.
Matthews, K. A., Woodall, K. L., & Allen, M. T. (1993). Cardiovascular Wright, R. A., & Gendolla, G. H. E. (Eds.). (2011). How motivation affects
reactivity to stress predicts future blood pressure status. Hypertension, cardiovascular response: Mechanisms and applications. Washington,
22, 479–485. DC: APA Press.
Meisel, S. R., Kutz, I., Dayan, K. I., Pauzner, H., Chetboun, I., Arbel, Y., &
David, D. (1991). Effect of Iraqi missile war on incidence of acute (Received June 8, 2012; Accepted July 19, 2012)