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Individualized Stress Management for Primary Hypertension
A Randomized Trial
Wolfgang Linden, PhD;
Joseph W. Lenz, PhD;
Andrea H. Con, MA
Arch Intern Med. 2001;161:1071-1080.
ABSTRACT
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Objective To test the efficacy of individualized stress management for primary
hypertension in a randomized clinical trial with the use of ambulatory blood
pressure (BP) measures.
Methods Men and women aged 28 to 75 years with mean ambulatory BP greater than140/90
mm Hg received 10 hours of individualized stress management by means of semistandardized
treatment components. They were randomly assigned to immediate treatment (n
= 27) or a wait list control group (n = 33). Participants on the wait list
were subsequently offered treatment. Six-month follow-up data were available
from 36 of the 45 participants who completed treatment. Measures were 24-hour
ambulatory BP, lipid levels, weight, and psychological measures.
Results Blood pressure was significantly reduced in the immediate treatment
group and did not change in control subjects (-6.1 vs +0.9 mm Hg for
systolic and –4.3 vs +0.0 mm Hg for diastolic pressure). When the wait
list control group was later treated, BP was similarly reduced by –7.8
and –5.2 mm Hg, and for the combined sample, total change at follow-up
was –10.8 and –8.5 mm Hg. Level of BP at the beginning of treatment
was correlated with BP change (r = 0.45 [P<.001] and 0.51 [P<.001], respectively),
and amount of systolic BP change was positively correlated with reduction
in psychological stress (r = 0.34) and change in
anger coping styles (r = 0.35-0.41).
Conclusions Individualized stress management is associated with ambulatory BP reduction.
The effects were replicated and further improved by follow-up. Reductions
in psychological stress and improved anger coping appear to mediate the reductions
in BP change.
INTRODUCTION
PSYCHOLOGICAL treatments for hypertension (consisting of relaxation,
biofeedback, and/or stress management) have at best received mixed support
from expert panels, which concluded that they are not very promising given
inconclusive findings.1-3
The current study was designed to integrate such cautious conclusions of consensus
conferences with a more optimistic view that arises from meta-analytic reviews.
We posit that the discrepancy between consensus group recommendations and
conclusions from meta-analytic reviews is due to conceptual, measurement,
and trial protocol differences that have been shown to affect blood pressure
(BP) outcomes but were not appropriately dealt with in most study protocols.
EFFECTS OF DIFFERENT TRIAL PROTOCOLS ON OBSERVED OUTCOME
Psychological stress is widely considered to contribute to the development
of primary hypertension. The epidemiologic evidence of a link between stress
and high BP is very convincing,4 yet the biopsychosocial
pathway that would explain how stress can lead to disease is less clear.5-6 Consistent with these findings on stress-hypertension
linkage, psychological treatments are designed to reduce stress by targeting
deficient cognitive and behavioral stress-coping strategies and by reducing
sympathetic arousal. Most reviewers report some clinical benefits associated
with behavioral interventions to reduce arousal, and numerous reviews of this
literature7-10
suggest variable pretreatment to posttreatment effect sizes that range from d = 0.40 to d = 1.4.
Observed outcomes vary substantially as a function of study design.
Jacob et al9 identified 75 controlled clinical
trials of relaxation therapies for hypertension and noted that treatments
starting with high initial BP also produced greater reductions (r = 0.75 for systolic BP [SBP] and r = 0.64
for diastolic BP [DBP]). Differential pretreatment levels had not been considered
in the recommendations of the consensus groups1-3
or previous reviews and may have led to an underestimation of the efficacy
of psychosocial treatments.
Linden and Chambers10 conducted a meta-analysis
of hypertension treatment outcomes including comparisons of nondrug treatments
with pharmacologic agents. Ninety controlled trials of psychosocially based
treatments were identified and were broken down into single-component and
multicomponent relaxation therapy, and individualized, cognitive-behavioral
therapies. Of the nondrug approaches, weight reduction–physical exercise
and individualized, cognitive-behavioral psychological therapy were particularly
effective and did not differ from drug treatments in observed raw effect sizes
for SBP reductions. Drug therapies were initiated at higher initial levels
of BP than nondrug therapies, with average pressures of 154.1 vs 145.4 mm
Hg SBP and 101.5 vs 94.3 mm Hg DBP for drug and nondrug treatments, respectively.
After adjustment for differences in initial pressure levels, the effects for
nondrug therapies increased, and the effect size of individualized psychological
therapy matched the effect sizes of drug treatments for SBP and DBP reduction.
These findings suggest that the more comprehensive nondrug therapies can be
effective especially when differences in pretreatment BP levels are accounted
for.
MEASUREMENT CONSIDERATIONS
The choice of BP measurement protocols also influences the observed
treatment effects. Significant decisions are where to sample (physician office
vs ambulatory), who measures (physician, nurse, or patient), how many samples
to take, and at what intervals. Studies with longer baselines resulted in
smaller treatment effects, suggesting that high initial BP readings falsely
boost observed treatment effects. Part of what appears to be a treatment effect
is in fact habituation to measurement.11 Probably
the most promising avenue for avoiding the reliability and validity problems
of office measures is via the use of ambulatory BP devices to obtain 24-hour
BP averages. Ambulatory BP monitoring (ABPM) is the approach recommended by
the National High Blood Pressure Education Program12
because ambulatory BPs have (1) much improved test-retest stability given
the increased number of measures and wider sampling and (2) a greater potential
for differentiating patients with true hypertension from measurement-reactive
patients, also known as "white-coat" responders.13-14
Because white-coat responders do not habituate to measurement, they cannot
be detected in the office despite repeated office measures. Furthermore, ABPM
is more clinically meaningful in that 24-hour averaged ambulatory BPs are
better long-term predictors of the development of hypertension than resting
measures in the laboratory,15-16
and they also relate more closely to target-organ damage than do laboratory
measures.17-18 Disadvantages of
ABPM are higher equipment cost and a more cumbersome protocol that requires
high motivation of the patient.
RATIONALE FOR THE CURRENT PROPOSAL
As shown above, variations in study design and measurement protocol
affect outcomes. Features that likely inflate the magnitude of observed BP
reductions are office measures and short baselines.9, 11
The magnitude of expectable change is low with low entrance BPs, and it is
falsely reduced when the design does not permit exclusion of white-coat responders.
In terms of technique-specific outcome, the adoption of a standardized rather
than an individualized approach is associated with smaller reductions in BP.9-10
OBJECTIVES AND HYPOTHESES
This study attempted to remedy past criticisms of hypertension trials
by (1) including ABPM to test the generalizability of effects in the natural
environment, (2) giving patients the apparently most potent intervention (ie,
individualized psychological therapy based on a cognitive-behavioral stress
management conceptualization), (3) including patients with sufficiently high
initial BPs that improvement is biologically more likely, (4) testing for
generalizability by including measures of multiple cardiovascular risk factors
(ie, weight, exercise habits, lipid profiling, anger, and hostility),19-22 (5)
including follow-up measures, and (6) replicating a type of intervention that
clinicians actually use in daily practice.
PATIENTS AND METHODS
PROCEDURE
Patients were recruited via newspaper advertisements and screened on
the telephone for inclusion criteria other than ABPM. They were asked to come
to the clinic to give informed consent and undergo office BPs, ABPM, and the
other measures. Patients who met the criteria for elevated ambulatory BP were
sent to the commercial laboratory adjacent to the university for a blood sample
(ie, lipid profiling).
Eligible patients were then randomly assigned to a delayed or an immediate
treatment condition. All patients were treated for 10 weekly 1-hour sessions
and then reassessed with ABPM and all other measures approximately 3 months
later. The same test package was repeated at 6-month follow-up. Subjects assigned
to delayed treatment were asked to come to the clinic for monthly checkups
to ensure that their BP had not undergone significant increases that might
require immediate treatment. If resting BPs had increased by more than 10%,
we recommended a physician visit. Medication treatment status was monitored
to determine whether patients continued to meet the inclusion criterion.
Initially eligible were 168 participants. After completing the consent
phase, the first 24-hour BP monitoring, and the questionnaires, 11 patients
decided that they did not want to continue with the study because of the discomfort
and the inconvenience associated with ambulatory monitoring. Ninety-seven
of the remaining 157 patients were excluded because their 24-hour BP mean
was below 140 mm Hg SBP or 90 mm Hg DBP. This left 60 patients for random
assignment into the 2 treatment conditions (n = 27 in the immediate treatment
group and n = 33 in the wait list control group). Four patients in the treatment
condition did not complete treatment and provided no posttreatment data. Of
the wait-listed patients, 4 had changed their drug regimen and had to be excluded
from the analyses, while 3 refused to participate in the posttest. This left
a sample of 49 for the pretreatment-posttreatment vs control comparison (23
in the immediate treatment group and 26 in the wait list control group). One
participant in the immediate treatment condition provided pertinent BP data
but refused to complete the questionnaires, thus reducing the sample size
for the questionnaire comparisons to 22. Five patients in the immediate treatment
condition refused to return for follow-up, thus leaving 18 participants at
follow-up.
Completion of the second 24-hour ABPM in the wait list control group
showed that only 22 still had ABPM levels greater than 140/90 mm Hg. All 22
were offered treatment; they all accepted and completed treatment. Four of
these 22 delayed treatment completers refused to return for a follow-up test.
Altogether, 45 patients received treatment and 36 patients also completed
the follow-up. The overall protocol and the number of patients available at
each step is outlined in Figure 1.
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Flow chart of patients available at each stage of the protocol. BP
indicates blood pressure.
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INTERVENTION
A unique feature of this study was that patients did not receive a fully
standardized intervention. To guarantee a high level of quality and maximal
treatment benefit, (1) the interventions were delivered by 3 PhD-level psychotherapists
(including J.W.L.) with specific training in cognitive-behavioral intervention
for psychosomatic patients, (2) the therapists used a set of techniques and
a theoretical orientation that was supported as efficacious in the psychotherapy
literature at large,22-23 (3)
each therapist first conducted a thorough assessment of psychological risk
factors for cardiovascular disease present in a given patient, and (4) treatment
relied as much as possible on manual-type descriptions of interventions. The
most frequently offered standardized therapy components were Autogenic Training,24-25 thermal biofeedback,26
cognitive therapy,27 anxiety management,28 and type A hostile behavior reduction.29
This individualized approach has been used for about 10 years in our clinic,
and we have a good track record with successful case studies. Therapists were
instructed to record which problems were targeted with which interventions.
Analysis of the patient records showed that, on average, each patient received
3.8 interventions. Most often used were treatment of anger or hostility (39/45),
Autogenic Training (37/45), and discussion of relationship or existential
issues (29/45); less often used were biofeedback (20/45) and cognitive therapy
for anxiety (18/45) or depression (10/45).
Patients were hypertensive with 24-hour mean ambulatory BP of or exceeding
140 mm Hg SBP and 90 mm Hg DBP. Both drug-free and drug-treated patients were
included, given that a medicated patient who met criteria effectively had
uncontrolled hypertension (this is consistent with expert panel recommendations1). Patients taking medication were asked to maintain
their dosage at a stable level throughout the study. This, however, did not
preclude medication changes when the patient and his or her physician saw
an urgent need for change, and appropriate qualifying statements were included
with the consent form. Exclusion criteria were type 1 diabetes mellitus, hypertension
of known organic origin, and congestive heart failure. There was no upper
age limit for eligibility.
Measures included 24-hour ABPM, office resting BP, a lipids profile,
psychological scales (daily stress, trait anger, preferred anger coping style,
hostility, anxiety, and depression), weight, and exercise habits. Psychological
scales included a 1-to-9 Likert scale asking patients to rate the average
stress level on the day of ABPM, the Cook-Medley Hostility Inventory,30 the Beck Depression Inventory,31
the State-Trait Anxiety Inventory,32 the State-Trait
Anger Scale,33 the Interpersonal Support Evaluation
List social support scale,34 the Balanced Inventory
of Desirable Responding,35 and the Behavioral
Anger Response Questionnaire.36 These scales
were chosen because of their satisfactory psychometric properties and the
availability of norms. Subjects were also asked how many alcoholic beverages
per week they consumed and how much time per week they spent exercising (defined
as "exercising to the point of sweating"). For clarification of the notion
of "1 alcoholic beverage," type and quantity of beverages were defined.
The Cook-Medley Hostility Inventory is derived from the Minnesota Multiphasic
Personality Inventory, has 50 self-descriptive items, and refers to feelings
of distrust toward others (high scores refer to elevated hostility). The State-Trait
Anxiety Inventory contains 20 items scored on a 1 to 4 scale. The Beck Depression
Inventory is a 21-item self-report tool with responses scored from 1 to 3.
The State-Trait Anger Scale (20 items) taps the overall level of anger or
predisposition to react angrily. The Interpersonal Support Evaluation List
is a 36-item questionnaire assessing emotional, instrumental, and self-esteem
support that people perceive as available from others. The Balanced Inventory
of Desirable Responding has 2 subscales (20 items each) that tap impression
management (a tendency to present oneself in a positive light) and self-deception
(a more unconscious chronic habit of underestimating stress and personal flaws).
The Behavioral Anger Response Questionnaire is a newly developed and extensively
validated tool with 37 items and a 6-factor structure; each factor forms a
subscale. The subscales describe different preferred styles of responding
to anger provocation: aggressive responding, assertion, social support seeking,
diffusion, avoidance, and rumination.
Weight was determined via a standard clinic scale (balance model), at
the same time of day, with light clothing. Blood pressure and heart rate activity
in the natural environment were monitored (Spacelabs Model 90207 monitors;
Spacelabs, Redmond, Wash). The ABPM monitors (weighing 700 g) were fitted
in the morning to the subject, pretested (ie, readings were compared with
those of Dinamap [Critikon Corp, Tampa, Fla] laboratory monitors), and returned
at the same time on the next day for analysis. Validation work suggests that
the Spacelabs 90207 monitor is a reliable and accurate device.37
Office resting BP measurements were taken after a 5-minute rest period
without human interaction as recommended by Linden et al,38
in a comfortably seated position, with the arm fully supported, by means of
an automated monitor (Dinamap 845). Five measures were taken and averaged
to maximize reliability.
Lipid profiles (providing levels of cholesterol, low- and high-density
lipoproteins, ratio of low-density to high-density lipoproteins, and triglycerides)
were obtained by sending patients to a commercial laboratory adjacent to campus
where a nurse oversaw standardized sampling and storage of the blood samples.
The assays followed standard laboratory procedures. These blood samples were
initially taken after the ABPM but before therapy was begun.
RESULTS
BASELINE CHARACTERISTICS
Means and SDs for demographic and lifestyle factors for the immediate
treatment and the wait list control groups at the time of randomization are
given in Table 1. Group differences
were tested via  2 tests for categorical variables and via
2-tailed t tests for interval-scaled variables.
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Table 1. Subject Characteristics
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As Table 1 indicates, there
were no meaningful differences between these groups at the point of random
assignment. On the whole, this was a sample with fairly healthy lifestyles,
ie, few smokers, modest reported alcohol intake, and a typically moderate
physical exercise habit.
BP AND LIPID CHANGE FOR IMMEDIATE TREATMENT VS WAIT LIST CONTROL GROUPS
Office resting BP, ambulatory means (broken down into 24-hour mean and
daytime [8 AM to 7 PM] vs nighttime [7 PM to 8 AM]), and lipid levels at baseline
as well as treatment-induced changes from pretreatment to posttreatment and
pretreatment to follow-up are given in Table 2. Heart rate data were also available but, consistent with
other treatment study results, there was no significant variability over time
in any condition, so that detailed reporting appeared redundant.
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Table 2. Physical Health Indicators: Pretreatment and Change From Pretreatment
to Posttreatment and Pretreatment to Follow-up Values*
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The treatment response was analyzed via residualized change score analysis,
which is a type of covariance analysis that individually adjusts for any potential
confound of differences in baselines that may affect subsequent degree of
change. Residualized change scores are derived by calculating the predicted
change score as a function of the correlation between baseline and subsequent
change scores. Residualized change scores are superior to covariance analyses
because they have no requirement of parallel regression slopes and it is not
necessary to have high intercorrelations of baselines values with change scores.39-40 Multivariate analyses were rejected
because the cardiovascular and lipid variables are different classes of biologic
end points, and also because the daytime and nighttime ABPM means were a function
of the 24-hour means; inclusion in the same multivariate analysis would have
introduced an overly liberal bias toward finding statistical significance.
A different analysis strategy was used for posttreatment to follow-up comparisons
because the wait list group had now been treated and there was no longer a
2-group design; simple F tests for repeated measures were conducted instead.
Residualized change score analyses showed significantly greater 24-hour
ABPM change in the treated group relative to controls (SBP, F1,47
= 6.02, P = .02; DBP, F1,47 = 7.5, P = .009). Further analyses of daytime BP changes also
demonstrated treatment benefits for SBP (F1,47 = 4.3, P = .04) and DBP (F1,47 = 4.2, P
= .04) reductions. The same was true for nighttime BPs, with F1,47
= 4.3, P = .04 for SBP and F1,47 = 5.6, P = .02 for DBP. The office BP readings in the treated
group changed about as much as did the ABPM readings, but, because the control
group showed BP declines parallel to that of the treated group, there was
no significant effect of treatment vs control (F1,47 = 0.81, P = .37 for SBP; F1,47 = 1.17, P = .28 for DBP). There was no change in any of the lipid variables
or in body weight (all F values were <1).
In the slightly smaller sample (n = 18) available for follow-up, there
was a further reduction in 24-hour DBP (F1,16 = 9.51, P = .007) and a trend toward lower SBP (F1,16 = 2.9, P = .10). No further changes were observed in office BPs.
Given that changes in the pretreatment to posttreatment phase are equally
apparent in day and night readings, no further analysis on this feature was
executed for the follow-up data. To determine the generalizability of the
follow-up changes, the amount of BP change for those not completing follow-up
was compared with the full sample data. As Table 2 shows, the full sample showed reductions of –6.1 and
–4.3 mm Hg from posttreatment to follow-up, and the corresponding numbers
for the noncompleters were –3.5 and –3.1 mm Hg, suggesting that
they were not a particularly distinct subgroup. There was no change in body
weight or any of the lipid variables during follow-up.
PSYCHOLOGICAL CHANGES DURING TREATMENT AND FOLLOW-UP
Pretreatment values and changes in psychological variables are displayed
in Table 3. With the use of a
traditional cutoff of P<.05, none of the psychological
variables changed significantly more in the treated group than in the control
group. Trends toward treatment-related changes were apparent in daily stress
(F1,47 = 3.03, P = .09) and avoidance
as an anger coping style (F1,47 = 2.91, P
= .09), suggesting that treated patients reported slightly less stress and
more use of avoidance. Analyses of the posttreatment to follow-up changes
(with the use of simple F tests for repeated measures) for dependent measures
showed no significant additional changes on any psychological variable.
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Table 3. Psychological Variables: Pretreatment and Change From Pretreatment
to Posttreatment and Pretreatment to Follow-up Values*
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CHANGES IN THE DELAYED TREATMENT GROUP ONCE TREATED
Given the study protocol, there was no control condition for the evaluation
of the wait list control group once it had become the delayed treatment condition.
However, there was no change in the ambulatory BP of the wait list control
group during the main treatment phase (Table 2). Therefore, simple repeated-measures F tests were used
to determine treatment-related changes. Also, because some patients receiving
treatment in phase 2 did not complete the follow-up (n = 5), the analyses
of the posttreatment to follow-up changes (and pretreatment to follow-up changes)
needed to be conducted separately with a correspondingly smaller sample size.
The biological and psychological pretreatment characteristics as well
as treatment- and follow-up–related changes are displayed in Table 4.
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Table 4. Physical Health and Psychological Indicators for the Delayed-Treatment
Group: Pretreatment and Change From Pretreatment to Posttreatment and Pretreatment
to Follow-up Values*
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Statistical analyses showed that SBP and DBP dropped significantly as
a function of treatment (F1,20 = 9.71, P
= .005, and F1,20 = 13.7, P<.001, respectively)
and improved further from the end of treatment to follow-up (F1,16
= 17.8, P<.001, and F1,16 = 22.4, P<.001). There also were improvements on some of the
psychological end points. Social support increased (F1,20 = 4.74, P = .04) and use of diffusion in angering situations increased
(F1,20 = 6.68, P = .02). Some other effects
approached traditional levels of significance: depression was reduced (F1,20 = 4.96, P = .05), as was trait anger (F1,20 = 4.11, P = .06). Small increases in use
of diffusion and assertion as preferred anger coping styles were also noted
(F1,20 = 4.02, P = .06, and F1,20 = 3.08, P = .10, respectively).
Given that ABPM levels of patients in the wait list group had not changed
from the pretreatment to posttreatment measures in phase 1 (see Table 2 for detail), the effectiveness of treatment for phase 1
vs phase 2 could easily and meaningfully be compared by computing effect sizes
for change. The effect size for SBP changes from pretreatment to posttreatment
was d = 0.60, and d = 0.91
for the pretreatment to follow-up comparison; the corresponding scores in
phase 2 were d = 0.68 and d
= 1.00. For DBP, the scores were d = 0.59 for pretreatment
to posttreatment and d = 1.24 for pretreatment to
follow-up. The corresponding figures in phase 2 were d
= 0.80 and d = 1.13. These effect sizes suggest that
the overall treatment effect was very similar irrespective of whether patients
were in the immediate or the delayed treatment conditions.
DROPOUTS DURING FOLLOW-UP
Of interest was how many patients completed treatment but not follow-up
and how these patients may have differed from the others. For reasons of parsimony
and maximal statistical power, these questions were analyzed on the combined
samples (ie, those treated immediately together with those receiving delayed
treatment). Of 36 patients completing follow-up, 12 reported changes in their
antihypertensive drug regimen during this time; 2 decreased their dosages,
3 replaced one type of medication with another, and 7 either increased the
dosage or added another drug to their regimen. The 7 patients with increased
medication intake represent a potential threat to the interpretability of
follow-up data because the medication changes represent a confounding treatment.
For this reason, the average amount of BP change during follow-up was compared
for the full sample of 36 completers with a reduced sample of 29 after removal
of those in whom potential treatment confounds were present. The average BP
change during follow-up was -3.9 mm Hg and –3.9 mm Hg (SBP and
DBP, respectively). When the sample was reduced to 29 by removing those with
medication increases, the average change was –3.0 and –3.4, respectively.
These differences were not considered a serious threat to the interpretability
of the DBP results from the full sample of 36, whereas they do suggest a slightly
weakened effect for SBP.
INDIVIDUAL VARIATION IN TREATMENT OUTCOME
Although treatment was associated with significant mean group changes
in ABPM, reporting of group means can hide considerable variability in treatment
responses. If not all patients benefit alike, then it is important to learn
who can benefit so that valuable resources are not wasted on hypertensive
patients who are not responsive to psychological intervention.41
With the use of a cutoff of a 5–mm Hg reduction in ABPM values (from
pretreatment to posttreatment), only 55% of treated patients were above this
cutoff for SBP change and only 50% were above the cutoff for DBP change, suggesting
that only about half the treated patients showed clinically meaningful changes.
Furthermore, to identify the characteristics of those who benefited
from treatment and those who did not, we computed correlations for pretreatment
variables with BP change from pretreatment to follow-up, and for BP change
as a function of change in psychological end points. Only the treated sample
for whom follow-up data were available was used for these analyses (n = 36).
Given the exploratory nature of these tests, only some of the key findings
are reported here.
Patients reporting infrequent use of aggression and assertion as preferred
anger coping styles at baseline showed significantly greater SBP change due
to treatment (correlations with DBP change showed a similar pattern but failed
to meet a P<.05 criterion). Also, low levels of
self-deception at pretreatment predicted greater SBP change (r = 0.33). Number of antihypertensive drugs was not a predictor of
either SBP or DBP change. Interestingly, high levels of triglycerides at pretreatment
could be statistically linked to greater 24-hour SBP. Overall, however, few
baseline indices (demographic, biological, or psychological) predicted differential
treatment responses.
Initial BP level was strongly predictive of subsequent change; SBP level
at pretreatment (24-hour average) correlated with SBP change at posttreatment
and follow-up (r = 0.45 [P<.001]
and r = 0.51 [P<.001],
respectively). The DBP level at pretreatment correlated with DBP change at
posttreatment and follow-up (r = 0.18 [P = .23] and r = 0.58 [P<.001], respectively). When SBP improved, so did DBP (r = 0.91 for pretreatment to posttreatment and r = 0.90 for pretreatment to follow-up changes, respectively).
Finally, the interrelationships of change in psychological variables
with change in 24-hour ABPM were studied to determine whether effective change
of targeted psychological end points also accounted for change in ambulatory
BP. There were some but overall few significant correlations. Patients who
reported more frequent use of support seeking and avoidance after treatment
and less use of aggression also showed greater systolic BP reductions (r = 0.41, P = .01; r = 0.35, P = .04; and r = -0.38, P = .02, respectively). Judging
by the direction of correlations, DBP was similarly affected by the same psychological
change variables, but none of these correlations was significant. Greater
use of assertion as an anger coping style showed a trend toward an association
with lower DBP (r = 0.30, P
= .08). Given the small sample sizes and the exploratory nature of these tests,
results should be interpreted with caution.
COMMENT
The goal of this study was to test whether a psychological intervention
(individualized stress management) can be an efficacious treatment for primary
hypertension. The findings confirm that 10 hours of such treatment, costing
approximately US $800 per patient to deliver, can lead to significant and
clinically meaningful reductions in both systolic and diastolic 24-hour mean
BP in at least a subgroup of patients. In contrast, the untreated wait list
control group showed no change in ambulatory BP means during the 3 months
of observation. The positive treatment results were equally apparent in daytime
and nighttime ambulatory readings. Furthermore, when the group initially placed
on the wait list was treated later, the same positive treatment response was
replicated. This was most apparent when BP changes were translated into effect
sizes: they were almost identical for pretreatment to posttreatment changes
and for the posttreatment to follow-up changes. In addition, treatment effects
improved further during the 6 months of follow-up. These latter findings should
be interpreted with caution, as 20% of participants were not available for
the follow-up. Nevertheless, this does not appear to create a critical systematic
bias because the noncompleters had been approximately as successful with treatment
initially than those completing all measures. Whether treatment gains apparent
at 6-month follow-up translate into even longer, stable benefits remains to
be determined.
We posit that a powerful effect must have been present, because the
study not only found a positive result with a relatively small sample but
also succeeded in replicating the finding with another small sample. This
observed replication of an effect supports the strength of the findings.
Interestingly, there was no corresponding treatment effect in office
BPs because both controls and treated patients showed similar-sized, albeit
small, reductions in BP from pretreatment to posttreatment. Hence, the use
of ambulatory BP in this study produced results that are clearly different
from office BP results. Given the growing literature on the superior criterion
validity of ABPM, it was reassuring to see that our intervention showed the
treatment benefits most clearly on ABPM. It appears that habituation to measurement
is a serious threat to office readings and that it is likely to account for
the differential results between office readings and ABPM.
The success of this study is in some contrast to previous reports1, 3 and therefore warrants careful interpretation.
Initially, it had been posited that this study might turn out promising results
because of 3 design characteristics. First, it was argued that nondrug intervention
trials typically start off with relatively low initial BP levels and that
large subsequent reductions in BPs would be unlikely because of floor effects.
This study confirmed that high initial levels of BP were also strongly predictive
of degree of change (r = 0.51 and 0.58). Given that
24-hour ambulatory means are typically 5 to 10 points lower than office means1 and that our sample had ambulatory means of 153/97
mm Hg at pretreatment, this study had the potential to lead to substantial
reductions in BP. The second promising feature was that of ABPMs being used
as entry criteria, thus eliminating subjects with white-coat hypertension
from inclusion. About half of all potential participants in this study had
been told by their physicians in the recent past that their office BPs were
greater than 140/90 mm Hg, but they failed to meet the ABPM entry criterion
for this study. Because the incidence of white-coat hypertension is typically
reported to be around 20% to 30%, there is strong reason to believe that subjects
with white-coat hypertension were in fact excluded. The third argument was
that individually tailored interventions would be more potent than standardized
ones. The current protocol did not have a standardized treatment control group,
and no direct test of standardized vs individualized treatment was possible.
Nevertheless, the observed effect sizes conform closely to those reported
previously,10 where it had been demonstrated
that individualized treatment was superior to standardized treatments.
Neither lipid levels nor body weight changed in either group, suggesting
that no generalization of BP change to these other biological end points had
occurred. The same observation also implies that the observed treatment benefit
for BP was not likely to be caused by any dramatic changes in eating or exercise
behavior that could have confounded the psychological treatment benefits.
We did not systematically assess potential confounding of BP changes caused
by changes in salt intake; this could have an effect on outcomes, but it does
not appear very likely because salt reduction (even when it is systematically
implemented) tends to produce only small BP reductions.17
The psychological measures served primarily to explore the pathway of
psychological characteristics leading to higher stress levels, which in turn
were presumed to contribute to BP elevations. On the whole, the psychological
changes were small, although all the signs point in the right direction. In
the delayed treatment group, psychological changes were stronger and this
may be partly because of the absence of a control group. The pattern of changes,
however, was the same and most consistent for social support, perceived stress,
and anger coping styles. Interestingly, stress reduction– and anger
coping–related changes were also the ones that correlated with amount
of BP change. Given the exploratory nature of these analyses and the potential
for experiment-wise error, these results should be interpreted with caution.
Nevertheless, it appears that changes in anger coping habits and stress reduction
are the most promising targets for attempts to reduce BP. This observation
is not entirely surprising given the long and fruitful history of studies
linking stress and anger to hypertension.42-44
The overall results were promising, but the variability in treatment
outcome needs to be highlighted, because only half of all treated patients
showed major improvements if a criterion of –5 mm Hg is used as a definition
of success. Analyses of baseline characteristics as predictors of outcome
showed that age, sex, and medication status were not significant predictors
of BP reduction, but high SBP and DBP levels at pretreatment were. It was
reassuring to see that age was not an impairment of treatment success. Of
the psychological characteristics, only self-deception appears to predict
lesser treatment benefits. It is therefore premature to make distinct recommendations
about which patients should be offered the psychological intervention. At
this time, we recommend considering patients for psychological treatment who
report a great deal of subjective stress and/or find psychological interventions
inherently appealing. The current sample consisted of relatively educated
patients who were psychologically minded and willing to be active players
in their health care. Other patients may prefer to control hypertension exclusively
with medication or other lifestyle changes.
In terms of research, the logical next step would be to directly compare
the individualized treatment offered herein with the best available standardized
treatment, using ABPM and a relatively high BP entry criterion. In addition,
we need to continue researching the link of psychological factors and BP change
over time so as to strengthen the currently tenuous models of a pathway from
emotion and behavior to hypertension and cardiovascular disease in general.
In this regard, stress and anger coping styles appear to be a particularly
promising area of research.
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