Relaxation and stress management in the treatment of essential hypertension

Journal of Psychosomatic Research, Vol. 30, No. 4, pp. 437-450, 1986. Printed in Great Britain.

0022-3999/86 $3.00+ .00 Pergamon Journals Ltd.

RELAXATION AND STRESS MANAGEMENT IN THE TREATMENT OF ESSENTIAL HYPERTENSION M. J.

IRVINE,D. W. JOHNSTON,D. A. JENNER and G. V. MARIE

(Received 20 August 1985; accepted in revised f o r m 12 December 1985) Abstract--Thirty-two male and female hypertensives, 34 to 65 yr of age, systolic blood pressure (SBP) less than 200 mmHg and diastolic blood pressure (DBP) between 90 and 109 mmHg, were randomly allocated to receive either relaxation and stress management (experimental condition) or mild physical exercise (control condition). Half the participants were taking antihypertensive drugs, which were constant for six months prior to the study and controlled during the study. Outcome measures included various measures of blood pressure in the clinic and at home, cardiovascular responsiveness, moods and 24-hr urinary adrenaline and noradrenaline. The study schedule consisted of 3-months baseline, 10 weeks treatment and 3-months follow-up. Relaxation was superior to the control procedure in reducing blood pressure as assessed by nurses blind to the participants' treatment at post-treatment for DBP and at follow-up for DBP and SBP.

INTRODUCTION

TREATMENT recommendations for uncomplicated mild hypertension are controversial, particularly as the potential side effects of the antihypertensive medications are not negligible [ 1, 2]. The U.S. Joint National Committee on Detection, Evaluation and Treatment of High Blood Pressure recommends nondrug therapies, including relaxation therapy, as the initial treatment for all individuals with uncomplicated mild hypertension [3]. In a recent review [4], we suggest that there is compelling findings from a substantial number of studies suggesting that relaxation and stress management programmes can lower blood pressure by clinically significant amounts. The most impressive and systematic research on relaxation therapy has been provided by Patel and colleagues in the U.K. [5, 6] and Agras and Taylor and colleagues in the U.S.A. [7-10]. Many questions on the use of these techniques have yet to be examined, the most important of which are the extent to which the effect is specific to relaxation, the generalization of the treatment effects and the psychological and physiological mechanisms that underlie these effects. Relaxation has been compared with no treatment [6], regular blood pressure measurement and attendance at the health clinic [ 5, 11 ] and supportive psychotherapy [8, 10]. In all cases relaxation was more powerful than the control procedures. This is encouraging but it can be argued that these procedures did not control for all possible powerful non-specific aspects of treatment particularly a treatment as complex as Patel's. An adequate control group should be similar to the experimental treatment in a wide range of characteristics including induction of similar expectations of treatment gain in the participants, the involvement of equally elaborate and plausible procedures and the presence of as much structure and between-session homework and measurement. It is highly unlikely that clinic attendance or psychotherapy are equal to stress management in these respects and therefore far from ideal controls. Address for correspondence: M. J. Irvine, Psychiatry Research Dept,, College Wing, Toronto General Hospital, 200 Elizabeth Street, Toronto, Ontario, Canada M5G 2C4. 437

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M . J . IRVINE et al.

The primary aim of this study is therefore to compare the effectiveness of a relaxation and stress management treatment modelled very closely on that used by Patel, with a control procedure which attempts to match the most significant nonspecific features of that package and to assess the adequacy of this match by assessing participants' expectations. The generalization of treatment effects is particularly important in the behavioural treatment of hypertension. If relaxation is to be a viable treatment for hypertension, the effect of the intervention has to be present during times other than when the individual is engaged in relaxation practice. Southam et al. [9] have recently shown that blood pressure measured semiautomatically at frequent intervals during a working day is reduced by relaxation training. In the present study we measured generalizability by obtaining records of the participants' self-recorded blood pressure at home and by examining cardiovascular reactivity to laboratory stress tasks. Both methods have been used in the past with some success [12, 13]. As a preliminary attempt to examine the mechanisms underlying relaxation, psychological factors were assessed by various measures of moods and physiological factors were assessed by measures of 24-hr urinary excretion of catecholamines. Finally the effects of relaxation on both medicated and unmedicated hypertensive participants were examined. METHOD

Experimental design The design was a two-way factorial experiment with treatment group (relaxation vs control) and drug status (medicated vs unmedicated) as the two between subject factors. The study schedule consisted of a three-month baseline, a ten-week treatment period, and a three-month follow-up period.

Participants Male and female hypertensive individuals who were between 34 and 65 yr of age and who had diastolic blood pressure (DBP) between 90 and 109 m m H g (phase V) at three recent visits to their general practitioner were invited to participate in the study by their general practitioner who sent them a letter detailing the nature of the study. A diastolic blood pressure within this range represents mildly raised blood pressure in accordance with the blood pressure criteria for mild hypertension employed by the Medical Research Council Working Party on the study of drug treatment for mild hypertension in the United Kingdom [ 14]. Individuals who were interested returned a stamped addressed card acknowledging their interest and were contacted by the first author (J. I.) who met with each person individually to explain the nature of the study in more detail. Individuals were excluded if there were: (1) physical changes secondary to raised blood pressure, that is, opthalamic, renal or cardiac indications for drug treatment; (2) previous myocardial infarction or stroke; (3) angina pectoris or intermittent claudication; (4) some other concurrent serious medical disorder; (5) pregnancy; (6) currently suffering from a significant psychiatric disorder as defined by present use of antidepressant or antipsychotic medications or psychiatric diagnosis reported in the participant's medical record; and (7) female taking contraceptive pill. Individuals who were taking antihypertensive medication had to be on a fixed drug regimen and dosage for at least six months prior to referral and this remained controlled throughout the study period. Suitable participants had their blood pressure measured, while seated, by the clinic nurse on two separate occasions, using a random-zero sphygmomanometer (London School of Hygiene sphygmomanometer). Individuals were asked to participate in the study if their DBP, as measured by the clinic nurse, averaged between 90 and 109 m m H g and their systolic blood pressure (SBP) averaged less than 200 mmHg. One-hundred and forty-eight participants were approached by their general practitioner, 62 were interested, of these the blood pressure of 22 fell below criteria, in one it was too high and one had medical complications. The remaining 38 participants entered the study and signed a consent form detailing the measurement procedures and informing them that they would receive one of two behavioural treatments. The study was approved by the Central Oxfordshire Health Authority Ethics Committee. Six participants dropped out of the study during the baseline period (before either they or the therapist was aware of the treatment allocation). Details of the remaining 32 are shown in Table I.

Procedure Participants were randomly allocated within sex and drug status (medicated vs unmedicated) to the relaxation treatment or the placebo treatment. Except for the therapist and the participants, all other people

Relaxation therapy for hypertension

439

TABLE I.--GROuPS' CHARACTERISTICS

Group

Sex

Age (yr)

Drugs (no. subjects)

Relaxation, drug

5 female 3 male

Mean=50 SD = 6.9

2 Aprinox; 2 Navidrex K; 2 Navidrex K & Tenormin; 1 Navidrex K & Inderal; 1 Catapres

Relaxation, no drug Control, drug

3 5 4 4

female male female male

Mean = 42 SD=9.8 Mean = 49 SD = 8.4

Control, no drug

3 female 5 male

Mean = 50 SD = 7.4

1 1 2 I

Moduretic; Aprinox Navidrex K; Slow Trasicor & Moduretic; 2 Inderal & Navidrex K; 1 Aldomet & Inderal

SD= standard deviation.

involved with the study were kept 'blind' to the participants' treatment group. During baseline neither the participants nor the therapist knew the participants' group allocation. Participants were seen for treatment in their usual Health Centre. Treatments Relaxation and stress management. The relaxation treatment was based closely on the relaxation and stress management programme of Patel [ 5 ] and was developed after close consultation with Dr C. Patel. It involved ten one hour weekly treatment sessions during which participants met individually with the therapist. In the first two sessions educational information concerning stress and its effect on the cardiovascular system were discussed, followed by 8 sessions when the participants received training in relaxation and the use of skin resistance biofeedback and the application of stress management techniques in every day life. Full details can be found in Irvine [15]. The first author (J. I.) conducted all therapy sessions. Placebo control treatment. The placebo control treatment was mild physical exercises which were specifically designed to be too mild to improve cariovascular fitness. The general information about blood pressure and hypertension given to the relaxation participants was given to the control participants. Also given was a specific rationale for the therapeutic value of exercise for hypertension. Briefly, they were told that exercise could lower peripheral resistance through the dilation of the arterioles and therapy reduce blood pressure. While performing the exercises, participants were given skin resistance biofeedback and the rationale given for biofeedback was that an increase in the tone from the biofeedback unit indicated an increase in alertness and arousal as a result of the enhanced blood circulation. They were told that increased alertness indicated more active brain function, while increased arousal indicated improved blood circulation throughout the body. The exercises consisted of mobility and flexibility exercises typical of 'warm-up' exercises. Participants met individually with the therapist (J. I.) for ten 1 hr weekly sessions. Full details about the programme can be obtained in Irvine [15]. Measures Clinic blood pressure. At referral, pretreatment, post-treatment and follow-up, blood pressurewas taken by the nurse on two occasions and two readings were taken at each occasion. These readings were averaged. Therapist's measures. Blood pressure measurements by the therapist were taken at referral, ten weeks into the baseline, at each treatment appointment and at the end of follow-up. Two readings were taken at each appointment, using a simple aneroid sphygmomanometer (Lumisphyg Deluxe Aneroid Sphygmomanometer) and were averaged. The aneroid sphygmomanometer was routinely calibrated at

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least monthly. During treatment blood pressure was measured before and after relaxation/exercise practise but only the before practise readings were used in the analysis of the results. Participants" b l o o d pressure measures. Throughout the eight and one half months study, participants selfrecorded blood pressure daily, in the morning and evening. Participants were warned to avoid taking the blood pressure reading within half an hour following a meal, a cup of tea or coffee, or smoking a cigarette. An aneroid s p h y g m o m a n o m e t e r and stethoscope were used. These were regularly checked for accuracy by calibrating them against a mercury sphygmomanometer. This was done routinely at the start of baseline, at the start of treatment and at the end of treatment. Self-measurement of blood pressure was easily learned and subsequent checks on the participants' performance were satisfactory (i.e. therapist and participant did not disagree by more than 4 m m H g at the blood pressure measurement training session). Cardiovascular reactivity measures. Cardiovascular reactivity in response to performing mental arithmetic, a reaction-time task and isometric exercise was assessed in the psychophysiological laboratory. The cardiovascular measures were inter-beat-interval and ECG R-wave to radial pulse interval (RPI). RPI is inversely related to SBP [16]. As the measures did not reveal any consistent differences between treatment conditions they will not be described in detail. Full details can be obtained in lrvine [15]. Urinary catecholamines. At the end of baseline and at post-treatment, participants gave a 24-hr urine sample which was analyzed for adrenaline and noradrenaline. Adrenaline and noradrenaline appear to be released in response to cognitive and emotional demands and have been implicated in the 'stress' response [17]. Subsamples of 30 ml from each urine sample were taken and stored at -20 C. They were analyzed when complete pretreatment and post-treatment samples had been collected from all 32 participants. Urinary adrenaline and noradrenaline were analyzed by the high performance liquid chromatograph technique (HPLC) with electrochemical detection [ 18]. The assay technique used for plasma was adapted by Jenner for urine.

Self-report measures.

(1) The McNair and Lorr Profile of Moods States (POMS) 1191. The POMS was completed daily for five week days prior to treatment and for five week days following treatment. The adjectives measure five m o o d states: tension, fatigue, vigour, depression and anger. (2) Participants' records of relaxation/exercise practice. During treatment and follow-up, participants recorded the time, length and success Irated on a 0 (not successful) to 3 (extremely successful) scale] of each relaxation/exercise practice. (3) Treatment expectancy and participants' evaluations of treatment. Treatment expectancy was measured after the first week of treatment so that participants had some experience with the technique but could not know the outcome. The questionnaire contained five questions which asked the participants to rate how worried they were about their hypertension and to estimate the amount (mmHg) they expected their blood pressure to change. There were also questions which asked the participants to estimate their expectations regarding the improvements to their general health and well-being. The treatment evaluation questionnaire was given at the end of treatment. There were 26 questions asking the participant to evaluate various aspects of the treatment programme. Examples of some of the questions are: (1) Did the programme help your blood pressure? (2) Were the number of training sessions: too many; too few; about right? (3) How important was taking breaks from your daily activities to practise the programme? (4) How important was the biofeedback? (5) How does the p r o g r a m m e compare with your initial expectations? Responses consisted of three or four choices, one of which had to be circled. (4) Medication compliance. Participants' daily records of medication use indicated no treatment group differences and good compliance.

RESULTS Analysis of variance showed that the groups were similar with respect to age, weight, SBP and DBP as measured

by the clinic nurse at referral, and as Table I demonstrates,

medication (i.e. use of diuretics or beta-blockers) was similar in the drug groups. The participants average body weight, measured at referral and at post-treatment, did not change groups.

over the study and there was no difference

between

the treatment

441

Relaxation therapy for hypertension TABLE II.--CLINIC NURSES' BLOOD PRESSURE DATA Group

Referral mean (SD) (SBP m m Hg DPB m m Hg)

Pretreatment mean (SD) (SBP m m Hg DPB m m Hg)

Post-treatment m e a n (SD) (SBP m m Hg DPB m m Hg)

Follow-up mean (SD) (SBP m m Hg DPB m m Hg)

Relaxation, drug Relaxation, no drug Control, drug Control, no drug

146.7 95.5 146.8 98.0 141.6 97.2 151.5 100.1

136.0 92.6 144.8 94.2 127.4 84.2 148.1 93.5

135.1 88.2 138.2 89.0 128.6 85.5 149.4 98.0

129.6 85.8 138.1 91.2 130.9 89.2 149.6 93.8

(7.5) (5.9) (11.6) (3.8) (10.8) (4.5) (8.2) (6.8)

(13.7) (9.3) (4.8) (5.6) (12.6) (5.8) (13.2) (8.4)

(11.4) (9.4) (8.3) (6.4) (12.5) (9.3) (11.6) (4.9)

(12.0) (9.8) (8.4) (6.4) (15.5) (12.7) (16.1) (12.3)

SD= standard deviation, SBP = systolic blood pressure, DBP = distolic pressure.

Clinic blood pressure Table I! shows the nurses' blood pressure data averaged within groups at referral, pretreatment, post-treatment and follow-up. Blood pressure changes during the baseline, i.e. from referral to pretreatment, were tested with repeated measures analysis of variance. Analysis of covariance, with pretreatment BP as a covariate, was used to test the treatment group differences in post-treatment and follow-up blood pressures. Analysis of covariance was employed to test the effects of treatment since it reduces the bias caused by differences between groups that exist before the treatments are administered, t-tests were used to examine change in blood pressure following treatment. During the 3-month baseline DBP decreased, F (1, 28)= 31.38, p <0.0001, and the decrease interacted with the participants' random allocation to treatment group, F (1, 28)=7.18, p <0.01. A Tukey HSD test [20] revealed that the decrease was greater in the participants who had been allocated to the control treatment. DBP measured at pretreatment was similar in the two treatment groups, however, medicated participants had lower DBP, F(1, 28) = 4.26, p < 0.05. SBP also decreased during baseline, F, (1, 28)= 9.55, p < 0.01. The decrease was similar among groups although there was a tendency for the medicated participants to exhibit a greater decrease and SBP at pretreatment was lower in the medicated participants F (1, 28)= 11.27, p <0.01. Since BP measurement is reactive, that is, the novelty or anxiety about having blood pressure measured can temporarily elevate the participant's BP, the decrease in BP with repeated measurements over time may reflect an habituation effect. Alternatively, the decrease in BP over the baseline period may be explained by regression to the mean. Analysis of covariance revealed a treatment group difference on DBP, F (1, 27)= 7.06, p < 0.05, following treatment. A dependent t-test showed that DBP decreased significantly only in the relaxation group, t (15) = 4.48, p < 0.001. The results were replicated at follow-up, F (1, 27)=4.28, p < 0 . 0 5 . SBP following treatment was similar in both treatment groups and did not differ significantly from pretreatment. However, by follow-up there was a treatment group difference, F (1, 27)=4.13, p <0.05. SBP decreased in only the relaxation group, t (15)=2.98, p <0.01. The effects of treatment were not reliably different in medicated or unmedicated

442

M.J. IRVINEet

al.

participants. Therefore, the clinic nurses' BP results indicate that there was a relaxation t r e a t m e n t effect on D B P at p o s t - t r e a t m e n t a n d f o l l o w - u p a n d on S B P at f o l l o w - u p irrespective o f w h e t h e r or not the p a r t i c i p a n t s were also t a k i n g a n t i h y p e r t e n s i v e medication. F i g u r e 1 d i s p l a y s the t h e r a p i s t ' s r e a d i n g o f p a r t i c i p a n t s ' b l o o d pressure a v e r a g e d within groups at the nine t r e a t m e n t sessions c o m m e n c i n g with week 2 o f the t r e a t m e n t p e r i o d . T h e d a t a over the baseline p e r i o d are n o t p r e s e n t e d , b a s i c a l l y the b l o o d pressure change during baseline was the same as that sustained by the nurses' readings. 160

150 ~o. ",.o-"

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140

130 E E

i k

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41

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= 120

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=

= R e l a x a t i o n , drug

o---~ Re l a x a t i o n , no drug

.~ --,. C o n t r o l ,

drug

o---o C o n t r o l ,

no drug

100 ck 90

80

70 I

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1

2

3

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Weeks FIG. l . - - B l o o d pressure measured by therapist across nine weeks o f treatment.

T h e results were tested with r e p e a t e d m e a s u r e s , analyses o f v a r i a n c e with tests o f linear a n d q u a d r a t i c t r e n d s [ 21 ]. B o t h D B P , F (8,224) = 4.71, p < 0.0001, a n d SBP, F ( 8 , 2 2 4 ) = 2.01, p < 0.05, decreased across the t r e a t m e n t weeks, in a highly significant linear t r e n d , F ( 1 , 2 8 ) = 17.42, p < 0.001 for D B P a n d F ( 1 , 28) = 10.55, p < 0 . 0 1 for S B P . H o w e v e r , there were no significant m a i n effects for t r e a t m e n t g r o u p suggesting t h a t BP d e c r e a s e d similarly in b o t h the r e l a x a t i o n t r e a t m e n t g r o u p a n d the c o n t r o l g r o u p . Since the m e d i c a t e d subjects were on this m e a s u r e n o r m o t e n s i v e p r i o r to

Relaxation therapy for hypertension

443

treatment and it is known that the effects of treatment is heavily dependent on the initial level [22] the results were re-analyzed for the unmedicated participants only. A trend analysis showed a linear trend downward in DBP, F (1, 14)= 25.34, p < 0.001, and a significant interaction in the linear trend with treatment group, F (1, 14)=9.13, p <0.01. The decrease across treatment weeks was steeper in the unmedicated relaxation subjects. Although in the same direction the effect was not significant on SBP trend. Therefore, separating the drug and no drug participants in the analysis of the therapist's BP results across treatment weeks indicated a superior relaxation treatment effect on DBP with the drug-free participants. Analysis of covariance was used to test the treatment effect on the therapist's measures of blood pressure at follow-up. The blood pressure measured at the beginning of week 1 of the treatment period was used as the covariate. The groups' blood pressures in week 1 of the treatment period (pretreatment value) and at the end of follow-up are shown in Table III. TABLE III.--SYSTOLIC BLOOD PRESSURE (SBP) AND DIASTOLICBLOODPRESSURE (DBP) MEASUREDBY THE THERAPIST AT PRETREATMENT AND FOLLOW-UP Pretreatment mean (SD) (mm Hg)

Group

Relaxation, drug Relaxation, no drug Control, drug Control, no drug

SBP DBP SBP DBP SBP DBP SBP DBP

138.5 88.6 139.6 89.8 131.1 84.0 152.9 94.0

(8.1) (11.8) (5.3) (6.4) (13.4) (6.1) (11.7) (8.1)

Follow-up mean (so) (ram Hg) 132.5 82.2 137.4 79.4 128.9 79.0 152.6 93.9

(8.4) (8.4) (11.4) (5.1) (14.3) (9.0) (19.0) (12.8)

SD = standard deviation.

There was a significant main effect for treatment group on DBP, F (1, 27) = 6.21, p < 0 . 0 5 , and a significant interaction between treatment and drug status, F (1, 27) = 5.36, p <0.05. Fisher's Protected LSD test [23] showed that both relaxation groups had lower DBP than the unmedicated control participants but did not differ f r o m the medicated control participants. It is noticeable that the latter participants had the lowest blood pressures prior to treatment. SBP at follow-up did not differ between groups and was not different from pretreatment. Therefore, the follow-up results confirmed a superior relaxation treatment effect on DBP with the drug-free participants. The low pretreatment blood pressure in the control, drug participants may have limited the power to detect treatment group differences with the drug participants.

Participants" self-measurements of blood pressure Tables IV and V show the groups' SBP and DBP for pretreatment (mean of the daily blood pressures in the month prior to treatment), post-treatment (mean of the daily blood pressures in the month following treatment) and follow-up (mean of the daily blood pressures in the third follow-up month) for morning and evening respectively. Not shown are the baseline blood pressures recorded in the morning

444

M . J . IRVlNE et al. TABLE IV.--PARTICIPANTS'

S E L F - M E A S U R E M E N T S OF BLOOD P R E S S U R E AT

PRETREATMENT, POST-TREATMENT AND FOLLOW-UP: MORNING

Group

Relaxation, drug Relaxation, no drug Control, drug Control, no drug

Pretreatment mean (SD) (mm Hg) SBP DBP SBP DBP SBP DBP SBP DBP

131.7 83.6 132.1 84.8 133.6 84.7 144.6 92.0

(10.0) (6.3) (8.9) (6.1) (18.6) (7.2) (12.3) (4.2)

Post-treatment mean (SD) (mm Hg) 125.6 78.6 131.0 81.8 129.9 81.6 142.8 87.3

(8.3) (7.4) (6.8) (5.6) (19.6) (8.6) (12.6) (5.4)

Follow-up mean (SD) (mm Hg) 125.0 78.0 131.3 82.1 130.7 79.8 140.2 86.9

(8.1) (6.4) (5.6) (5.7) (23.8) (9.4) (15.4) (7.8)

SD = standard deviation, SBP = systolic blood pressure, DBP = diastolic blood pressure. t-tests revealed that DBP (p < 0.001) decreased significantly at posttreatment and follow-up. SBP (t9 < 0.01) decreased significantly at posttreatment and follow-up.

TABLE V.--PARTICIPANTS'

S E L F - M E A S U R E M E N T S OF BLOOD P R E S S U R E AT

PRETREATMENT, POST-TREATMENT AND FOLLOW-UP: EVENING

Group

Relaxation, drug Relaxation, no drug Control, drug Control, no drug

Pretreatment mean (SD) (mm Hg) SBP DBP SBP DBP SBP DBP SBP DBP

131.9 82.2 134.1 85.8 134.3 85.3 147.5 92.8

(9.2) (9.9) (10.2) (5.2) (15.5) (6.1) (12.9) (5.3)

Post-treatment mean (SD) (mm Hg) 127.0 79.2 130.4 81.1 131.5 81.4 144.2 88.5

(7.6) (9.3) (6.5) (6.7) (19.1) (7.6) (12.6) (5.4)

Follow-up mean (so) (mm Hg) 126.4 81.2 132.3 82.5 134.4 81.7 140.2 87.2

(6.5) (5.3) (7.3) (6.9) (23.2) (8.1) (11.6) (6.9)

SD = standard deviation, SBP = systolic blood pressure, DBP = diastolic blood pressure. t-tests revealed that DBP decreased significantly at post-treatment (19 <0.01) and follow-up (17 <0.0001). SBP decreased significantly at post-treatment (p <0.01) and follow-up (p <0.01).

and evening for the three months prior to treatment. Blood pressure had largely stabilised at the end of this period. Analysis of covariance was used to test the post-treatment and follow-up results, using the pretreatment blood pressure as the covariate. Blood pressure decreased significantly from pretreatment to post-treatment and the decreases were maintained at follow-up, however, there were no treatment group differences.

Biochemical data The groups' mean urinary excretion of noradrenaline and adrenaline at pretreatment and post-treatment are presented in Table VI. Because some participants failed to collect complete 24-hr samples, the group sizes were: medicated relaxation=6; unmedicated relaxation = 7; medicated control = 6; unmedicated control = 6. Analysis

Relaxation therapy for hypertension TABLE

VI.--URINARY

NORADRENALINE

AND

ADRENALINE

445 AT

PRETREAT-

MENT AND POST-TREATMENT

Group

Noradrenaline /~g/24-hr PrePostmean (SD) mean (sD)

Relaxation, drug Relaxation, no drug Control, drug Control, no drug

42.3

(13.2) 4 3 . 5

(10.9)

8.0

(4.6)

7.9

(4.3)

54.7

(25.6) 5 2 . 6

(36.0) 14.0

(5.9)

12.1

(3.8)

44.3

(26.4) 3 9 . 7

(10.1)

9.8

(6.0)

9.3

(5.2)

38.1

(8.3)

(14.1)

6.9

(0.7)

6.5

(3.4)

36.4

Adrenaline #g/24-hr PrePostmean (SD) mean (SD)

SD standard deviation, p.g= micrograms. =

o f c o v a r i a n c e revealed that there were no t r e a t m e n t g r o u p differences with either m e a s u r e a n d t-tests showed t h a t c o n c e n t r a t i o n s were u n c h a n g e d f r o m p r e t r e a t m e n t .

Self-report data (1) Mood scales. T h e M c N a i r a n d L o r r P r o f i l e o f M o o d s State [19] was c o m p l e t e d for five consecutive days p r i o r to t r e a t m e n t a n d five consecutive days after t r e a t m e n t . T h e m e a n s for each m o o d state for p r e t r e a t m e n t a n d for p o s t - t r e a t m e n t were c a l c u l a t e d a n d the t r e a t m e n t effect was tested by analysis o f c o v a r i a n c e . A second set o f analyses was carried out for the m a x i m u m m o o d score for each o f the m o o d states in the five days and again tested b y analysis o f covariance. The analyses revealed no t r e a t m e n t g r o u p differences a n d there was little i n d i c a t i o n t h a t the m e a s u r e s d i f f e r e d b e t w e e n pre- a n d p o s t - t r e a t m e n t . It was striking that p r e t r e a t m e n t scores were very low, i n d i c a t i n g little e m o t i o n a l distress, a n d this m a y have restricted the scope for change. (2). Participants" records o f practice. A n a l y s i s o f the m e a n n u m b e r a n d d u r a t i o n o f practice sessions per week showed t h a t p a r t i c i p a n t s c o m p l i e d with instructions to a c o n s i d e r a b l e extent, at least d u r i n g the t r e a t m e n t p e r i o d . C o n t r o l p a r t i c i p a n t s p r a c t i c e d m o r e f r e q u e n t l y in the m o r n i n g t h a n d i d r e l a x a t i o n p a r t i c i p a n t s (6 vs 4, F ( 1 , 2 8 ) = 8.76, p < 0.01) a n d b o t h g r o u p s increased the frequency over sessions f r o m an average o f 4 in week 1 to 5 in the final week o f t r e a t m e n t ( F (6, 1 6 8 ) = 2 . 7 4 , p < 0.05). P r a c t i c e f r e q u e n c y in the evening was the same in b o t h g r o u p s at 5 a n d increasing f r o m 4 to 5 over the course o f t r e a t m e n t (F(6, 168) = 3.69, p < 0.01). During the follow-up practice frequency decreased until at the end o f three m o n t h s it averaged 4 in the m o r n i n g a n d 3 in the evening. A n a l y s i s o f the length o f time spent at each practice d u r i n g t r e a t m e n t i n d i c a t e d t h a t in the m o r n i n g the average length o f time was 9 min. T h e r e was a significant i n t e r a c t i o n between t r e a t m e n t g r o u p a n d weeks, F (6, 1 6 8 ) = 4 . 5 8 , p < 0 . 0 0 1 . N o t surprisingly, the c o n t r o l g r o u p s increased the length o f each practice session across t r e a t m e n t f r o m 5 to 9 min, since they were b o t h a d d i n g new exercises a n d increasing the repetitions o f each exercise, while the r e l a x a t i o n g r o u p s r e m a i n e d the s a m e across weeks at 11.9 min. The analysis o f the evening d a t a d u r i n g t r e a t m e n t i n d i c a t e d a m a i n effect for t r e a t m e n t g r o u p , F ( 1 , 28) = 20.28, p < 0.0001. The relaxation groups spent on average

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14 min at each evening practice whereas the control groups spent on average 8 min. However, as with the morning data, there was a significant interaction in the linear trend with treatment group, F(1, 28) = 4.85, p < 0.05, again due to the control groups increasing the time spent at each practice as new exercises were added and repetitions were increased across treatment weeks. By follow-up, neither average length of morning practice nor average length of evening practice differed between the treatment groups. Participants' ratings of success at practice did not differ between the treatment groups either in the morning or evening during treatment or in the morning and evening during follow-up. (3) T r e a t m e n t expectancy and treatment evaluation measures. (i) Treatment Expectancy Questionnaire. The Kruskal-Wallis one-way analysis of variance was used to compare groups on the five questions in this questionnaire. The results showed that the groups were similar in their responses to each question. (ii) Treatment Evaluation Questionnaire. The Kruskal-Wallis one-way analysis of variance was used to compare groups on the 26 questions in this questionnaire. The groups were found to be similar on all but one of the questions. For example, there was no difference between groups on the question: 'Did the (relaxation/exercise) programme help your blood pressure?', most answered that it helped 'moderately'. To the question: 'Do you believe the (relaxation/exercise) programme will help other people who have high blood pressure?', most answered it would by 'quite a bit'. However, one question discriminated among groups. This question was: ' H o w does the (relaxation/exercise) programme compare with what you initially expected from it?' Fourteen of the relaxation participants answered that the treatment was 'better than I expected' whereas 10 of the control participants answered that the treatment was 'about what I expected'. DISCUSSION

The main outcome of this study is reasonably clear-cut. On blind assessment of the participants' blood pressure in their general practitioners' surgery, participants treated with relaxation and stress management showed a greater reduction in pressure than participants treated with the control procedure. This was true for diastolic pressure immediately after the course of treatment and for both diastolic and systolic pressure three months later. This is, as far as we know, the first test of Patel's treatment package against a complex control procedure. However, blood pressure reductions associated with relaxation were only superior to the control procedure for recordings made at the Health Centres; participants' own records of blood pressure did not show any particular advantage for relaxation training and neither treatment was associated with any reduction in cardiovascular reactivity in the laboratory. It is important to determine if these negative results are due to the inadequacies of this treatment or of our assessment of it. Before considering these issues, however, the adequacy of the control treatment must be assessed. It had been our aim to produce a treatment that matched relaxation and stress management very closely. From our perspective we did this since both treatments involved attending the general practice surgery, learning the skill there, practising that skill at home and attempting to use it through the day, in addition to health education etc. However, equally important is whether the treatments were similar from the participants's perspective. This was assessed by participants' responses to

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expectancy questionnaires, both prior to and following treatment, and indirectly by assessing the time spent practising the techniques. Prior to actually receiving treatment there was no difference between the participants in their expectations of therapeutic gain; they had high expectations of both treatments. Rather surprisingly, following treatment this was still the case with the exception that participants who had received relaxation and stress management regarded it as rather better than expected, the control treatment was as expected. Since this was one significant finding in a large number of statistical comparisons, it may be a chance effect. However, the result is impressively consistent and we are inclined to believe it. Even if this difference is accepted, at the end of treatment participants in both conditions are generally content with the treatments they have received. Practice records also confirm that both treatments maintained participant interest and motivation to a similar extent. The total duration of time spent in practice was similar in both treatments; the control participants practising more frequently but for slightly shorter periods of time than the relaxation participants. We would therefore argue that the control procedure used in this study does successfully match many of the features of relaxation and stress management and induces a similar expectation and commitment in participants and consequently our results can be taken as indicating that relaxation and stress management is the active ingredient in this treatment approach. The failure to find differences in participants' own records of blood pressure and cardiovascular reactivity is potentially serious since at the worst it could indicate that participants only learn to produce rather temporary decreases in pressure when it is being measured in the Health Centre. Before accepting this conclusion it is worth remembering that blood pressure recorded at home was on average lower than that recorded in the surgery making it very difficult to detect therapeutic change which is known to relate to the initial level of pressure [22]. Glasgow et al. [ 12] also used home blood pressure measurements and failed to find reliable effects of behavioural treatments on morning and evening pressures. They did, however, find marginal therapeutic affects on blood pressure measured during the afternoon, when it was initially somewhat higher. These differences could simply reflect some form of floor effect and be entirely dependent of the pressure or, more interestingly, they reflect the factors that elevate pressure in the afternoon or in the clinic (which indeed typically was in the afternoon). A plausible hypothesis is that participants are busy or more aroused in the afternoon or when having their blood pressure measured by a health professional than prior to breakfast or their evening meal. This would suggest that relaxation and stress management are operating as when one might hope, that is, they reduce the pressor response to various forms of stressors and they will therefore not reflect a therapeutic effect when such stressors are lacking, or at least not affecting blood pressure. If our explanation of the failure to find effects on home blood pressure reading is related to the low level of stress at the times of measurement then this makes our failure to find therapeutic effects in the laboratory reactivity testing puzzling. Our findings are not unique. Patel has reported that relaxation and stress management reduce the pressor response to the cold pressor test and dynamic exercise [ 13 ], but a number of studies using rather different stressors and different forms of behavioural treatment have failed to find reductions in reactivity [24-27 ]. The reasons for these failures are unclear. The tests used in this study did produce cardiovascular effects

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that were reliable both before and after treatment but whether or not laboratory stress testing is an accurate analogue to reactivity in real life is not known. Furthermore, participants in this study were not instructed to attempt to lower their blood pressure during the tasks. The reasons for not so instructing participants are obvious. Relaxation and stress management were taught as skills the participant should attempt to use in stressful situations and part of the assessment of these skills is the preparedness of participants to use them when appropriate. In addition, it is not clear what instructions would be appropriate for the control participants who did not receive training that was directed at lowering blood pressure in the short term. Unfortunately it could be argued that participants might not choose to use relaxation and stress management during artificial laboratory stressors produced by us when we did not tell them to do so. In future research it might well be profitable to find out if participants attempted to lower their pressure during laboratory testing and also to systematically vary the instructions to participants during such testing. In addition, techniques for assessing reactivity during real life stressors are urgently required. Before leaving the blood pressure results, the reduction of blood pressure during the three month baseline is worthy of comment. It has been shown that blood pressure drops over time, possibly because of habituation to measurement or regression to the mean, and such drops are typically confounded with the effects of treatment, although the provision of various control groups allows an estimate of the effects. We attempted to separate out the effects of the drop during baseline from treatment effects by using a prolonged baseline with frequent self-determinations of pressure and we appear to have been at least partially successful. For example, blood pressure as assessed by the nurses did drop over the baseline period by an average of 8/7 m m H g and then dropped further in participants receiving the behavioural treatment but not in the controls. The latter finding suggests that pressure had stabilized by the end of the three months. When the drop during the baseline is added to the drop achieved over the treatment period, then the total reduction of pressure in this study is of a comparable order to that reported by others. There was also a tendency for some variation in the drop over the baseline period in the different treatment conditions. These effects presumably reflect chance variation and did not compromise the treatment outcome since these effects did not reliably differ between treatment conditions. However, there was a tendency for the medicated participants to have lower blood pressures at the end of baseline compared with drug-free participants. This tendency may have compromised comparisons of treatment effects between medicated and unmedicated participants. Nevertheless, it could not have biased the primary comparison of the treatment effect since the lower level of blood pressure in the medicated participants did not reliably interact with the treatment conditions. The findings from the biochemical analysis were entirely negative. The literature on the effects of behavioural treatment on these measures is inconsistent. For example, Brauer et al. [8] failed to replicate Stone and DeLeo's [28] finding that plasma dopamine-beta hydroxylase (a norepinephrine metabolite) decreased after relaxation therapy. Patel et al. [6] found a decrease in plasma renin whereas Goldstein et al. [26] found an increase in recumbent plasma renin following relaxation treatment. McGrady et al. [29] found no change in plasma renin or urinary catecholamines, however, like Patel el al. [6] they found a decrease in plasma aldosterone. McGrady et al. [29] also found decreases in urinary cortisol following relaxation treatment.

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Studies with n o r m o t e n s i v e s have also p r o d u c e d a m b i g u o u s findings [24, 30, 31]. This m a y reflect the h e t e r o g e n e i t y o f m e c h a n i s m s u n d e r l y i n g essential h y p e r t e n s i o n , or the difficulties in carrying o u t relevant m e a s u r e m e n t or indeed o u r i g n o r a n c e o f h o r m o n a l effects o f r e l a x a t i o n training either in hypertensives or n o r m a l s . In the present study 24-hr urinary samples were taken and it can be argued that either urinary or p l a s m a samples t a k e n o v e r s h o r t e r time periods w h e n the p a r t i c i p a n t s m i g h t be in m o r e a r o u s i n g situations c o u l d well be m o r e sensitive. U n f o r t u n a t e l y we did not h a v e the resources to carry o u t m o r e detailed analysis. It is t h e r e f o r e p r o b a b l y safest to c o n c l u d e f r o m this study a n d indeed f r o m the literature in general that the physiological m e c h a n i s m s underlying the effects o f relaxation an d stress m a n a g e m e n t are u n k n o w n at present. T h e psychological mechanisms are similarly elusive. W e were u n a b l e to show any systematic t r e a t m e n t - r e l a t e d changes in m o o d in this study. This is very plausibly e x p l a i n e d as the result o f the low level o f m o o d d i s t u r b a n c e in this g r o u p o f participants. In f u t u r e research it is essential that m e a s u r e s used are m o r e sensitive to n o r m a l v a r i a t i o n s in m o o d . In s u m m a r y , the m a i n findings are that the effectiveness o f one o f the most powerful o f the b e h a v i o u r a l t r e a t m e n t s , P a t e l ' s r e l a x a t i o n and stress m a n a g e m e n t package, was replicated in this study on the m e a s u r e o f b l o o d pressure used m o s t widely in p r e v i o u s studies a n d f u r t h e r m o r e o u r c o m p a r i s o n o f this t r e a t m e n t with a c o m p l e x c o n t r o l suggested strongly that these positive t h e r a p e u t i c effects are the direct and specific effect o f r e l a x a t i o n and stress m a n a g e m e n t . Acknowledgements--We would like to thank Dr. Chandra Patel for her generous help in enabling us to

replicate her treatment programme. We would like to thank Ciba Laboratories, Wimblehurst Road, Horsham, West Sussex, U.K., for the loan of the film, 'Stress, Personality and Cardiovascular Disease'. This research was supported in part by a grant from the Medical Research Council to D. W. Johnston.

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