- Email: [email protected]
Invited review psychological interventions in cardiovascular disease
/ourno/ oJPsychosomolrc Prmted in Great Britain.
Rexmch,
Vol. 29, No. 5. PP. 44-456,
0022-3999/E $3.00+ .W ‘-’ 1985 Pergamon Press Ltd.
1985.
INVITED REVIEW PSYCHOLOGICAL INTERVENTIONS CARDIOVASCULAR DISEASE DEREK
W.
IN
JOHNSTON
(Received 21 February 1985) Abstract-The literature on the behavioural treatment of primary hypertension, reduction of Type A behaviour, and psychological interventions during acute coronary care and rehabilitation after a myocardial infarction are selectively reviewed. There is growing evidence that relaxation and stress management can lower blood pressure by useful amounts in mild primary hypertension although the mechanisms underlying these reductions are unclear. Type A behaviour has been reduced in patients following a myocardial infarction and this led to reduced morbidity. Other interventions following myocardial infarction, both when the patient is in hospital and after discharge have produced at best only modest benefits and are, therefore, not widely applicable. Future research in rehabilitation should be directed at reducing the disabilities of patients with clearly identifiable problems that stem from their response to cardiovascular disease. INTRODUCTION MOST OF the standard risk factors for cardiovascular disease have a substantial behavioural component, e.g. blood lipids may in part relate to diet, stress has been implicated in the aetiology and maintenance of primary hypertension and smoking and Type A, or coronary prone, behaviour are exclusively behavioural risk factors. Furtherore, cardiovascular disease is not only the product of behaviour but it also powerfully affects behaviour since both acute and chronic distress and disability can result from such disease, perhaps most obviously following a myocardial infarction (MI). It is not possible in this review to cover all the relevant psychological interventions and I shall concentrate on those interventions that deal primarily with stress as a possible cause of cardiovascular disorders and distress as a likely consequence. I shall not therefore cover attempts to alter smoking behaviour nor shall I review the literature on psychological interventions designed to help patients cope with the symptoms of coronary heart disease such as angina or arrhythmias. These may well be stress related but there has been little advance in the psychological management of such conditions since the preliminary studies reported some time ago [l]. This review will cover the behavioural treatment of primary hypertension, the reduction of Type A behaviour, psychological interventions in acute coronary care and the role of both psychological interventions and exercise in rehabilitation after myocardial infarction. PRIMARY
HYPERTENSION
Two main approaches to the behavioural reduction of blood hypertension have been studied; cardiovascular biofeedback stress management. The effects of biofeedback have been appointing. Laboratory studies of normal volunteers suggest biofeedback is no more likely to reduce blood pressure than Address for correspondence: D. W. Johnston, Oxford
Department
OX3 7JX. U.K. 447
of Psychiatry,
pressure in primary and relaxation and almost entirely disthat cardiovascular a variety of much Warneford
Hospital,
448
DEREK
W.
JOHNSTON
simpler procedures that do not involve feedback [2-51 and studies of hypertensive patients have obtained similar results [7, 81. Two clinical studies have been slightly more positive. Glasgow et al. [9] claim that a very simple form of blood pressure feeback used at home was, when combined with relaxation training, more effective than either relaxation or biofeedback alone. However, the superiority of the combination of relaxation and biofeedback was not marked and was only obtained on a few of a multitude of blood pressure measures. Goldstein et al. [lo] using more conventional laboratory blood pressure feedback showed that such feedback was slightly more effective than relaxation or self-monitoring in lowering pressure in the laboratory, although not outside it. However, relaxation which as we shall see below is normally found to be a moderately effective treatment for mild hypertension, was strikingly ineffective in this study and it would therefore be quite unsound to conclude that there is a strong case for advocating biofeedback in the treatment of mild primary hypertension. Biofeedback is based on the assumption that the skill of controlling a visceral response can be acquired in the same way as a more conventional motor response; this view has been under increasing challenge [ll, 121 and it is probably more realistic to knowledge that stress is likely to be involved in blood pressure elevation and that treatment should therefore be directed at reducing that stress. A number of investigations of relaxation training and stress management have shown reliable reductions in pressure [ 13-221 although some contrary findings have been reported [6, lo]. In general the effective studies have examined patients with higher blood pressure than the ineffective, and have incorporated home practice in relaxation and instruction in the use of relaxation to cope with day-to-day stressors. One can, therefore, conclude that relaxation training can lower the blood pressure of patients who fall towards the top end of the mildly hypertensive range, i.e. with diastolic pressures of at or near 100 mmHg and after such treatment such patients will have pressures that are at or near the normotensive range. These effects persist for at least 15 months after the end of treatment [13, 14, 18, 231 and these reductions have been confirmed using semi-automatic ambulatory blood pressure recording in the work setting [18, 231. As yet there are no studies demonstrating unequivocal changes in health or reduction of coronary heart disease following relaxation and stress management although a study by Little et al. [24] showed that hypertensive women receiving relaxation training are less likely to be admitted to hospital during their pregnancy and Pate1 et al. [25] has recently reported a reduction in the incidence of coronary heart disease in the four years following relaxation training. Since relaxation and stress management lower blood pressure it is obviously important to establish the mechanism or mechanisms underlying this effect. One of the most important issues with any apparently effective psychological technique is to establish specificity since complex and plausible psychological treatments may well operate primarily through non-specific or placebo processes. The evidence suggests that the effects of relaxation on blood pressure are not primary non-specific since controlled investigations show that relaxation leads to a greater reduction in pressure than does simply attending the clinic and sitting quietly there [3], receiving various forms of supportive psychotherapy [15-171 and we have recently shown that an elaborate, plausible and acceptable form of mild exercise did not lead to reliable reductions in pressure, whereas relaxation did [26]. Therefore, it appears very
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unlikely that the effects of relaxation and stress management are simply due to the non-specific effects of procedures such as taking an interest in the patient or offering a plausible treatment. The most straightforward explanation of the effect of relaxation is that it operates to lower blood pressure directly and patients who regularly and assiduously practice the technique will show beneficial reductions in pressure. If relaxation operates in this way then presumably the effects would be seen most clearly immediately after the patient had been relaxing. However, both studies of both healthy, normotensive volunteers [27-291 and hypertensives [26, 30, 311 have failed to show consistent reductions in pressure immediately after relaxation. Other evidence that there is not a simple direct effect of relaxation on blood pressure is provided by the very variable correlations that are typically found between the amount of relaxation practice carried out during treatment and the actual reductions in pressure obtained [21, 22, 26, 321. It would be naive to assume that there is a simple relationship between amount of relaxation and blood pressure reductions; however, these results, taken with the difficulties in demonstrating a direct effect of relaxation, suggest that relaxation does not operate primarily by lowering blood pressure directly. The above studies are entirely concerned with resting blood pressure and it can be argued that relaxation may show its effect when the subject is under some kind of stress. At least four studies of hypertensive patients have examined the effects of relaxation on cardiovascular reactivity provoked by laboratory stressors ranging from mental arithmetic to dynamic exercise. Only one has shown a positive effect with relaxation reducing the pressor response to both the cold pressor test and dynamic exercise [33]. Two others [lo, 261 have failed to show any effect of relaxation on reactivity to a variety of laboratory stressors and one [34] actually showed anxiety management training to be associated with increased reactivity to some stressors. The final mechanism to be considered is possible neurogenic and hormonal changes associated with relaxation. Most investigators assume that primary hypertension is, at least in part, related to increased activity in the sympathetic nervous system or heightened sensitivity to SNS input and there have, therefore, been a number of attempts to determine the effects of relaxation on the sympathetic nervous system. The results have been very variable. Plasma dopa-beta-hydroxylase was reduced in only one of two studies [17, 351. Cottier et al. [36] found significant reductions in plasma adrenaline in comparison with a placebo control group but two other studies [26, 371 failed to find any effect of relaxation on various measures of urinary catecholamines. Four studies have failed to find reductions in plasma renin activity [lo, 36-381 although Pate1 [14] did find reductions in both plasma renin and aldosterone immediately after a course of relaxation training. The effects were no longer detectable six months later although blood pressure remained at its reduced level. McGrady et al. [37] also obtained reductions in plasma aldosterone. The answer to the puzzling diversity of the studies may lie in the heterogeneity of the patients studied who have ranged in average age from their late 20’s [35] to their late 50’s [17] and were variously medicated and unmedicated [17, 14, 361. When such heterogeneity is taken in conjunction with the widely held view that hypertension is unlikely to have a similar basis in all patients or at all stages in the condition [39-41] it is hardly surprising that confusion reigns. Future studies of neuro-
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genie mechanisms should therefore concentrate on homogeneous groups of patients, preferably selected because of a known abnormality in the parameter felt to underlie the effects of relaxation, e.g. if it is hoped to demonstrate that relaxation reduces measures of sympathetic activity then patients should be selected who have clearly detectable elevated catecholamines. Very closely related to the question of mechanism is the important issue of which patients benefit from relaxation and stress management. It is very unlikely all patients can benefit from this form of treatment since it is improbable that hypertension is invariably related to the factors that might be thought to be changed by relaxation. In an influential early review Jacob et al. [42] showed that initial level of blood pressure was a powerful determinant of the reductions obtained by relaxation training, patients with the higher pressures doing better. More recent research has confirmed this view [14, 461. Cottier et al. [36] have shown that patients with heightened sympathetic tone, indicated by higher initial heart rate and plasma noradrenaline, benefit more from training. In a rather pessimistic discussion of these results Cottier et al. suggest that relaxation should only be offered in young, anxious patients with a high sympathetic tone. This conclusion is unreasonable since it ignores the very positive outcomes that have been obtained in studies of patients that do not approximate to these criteria [13, 141. We are not yet in a position to decide who will benefit from relaxation. In part this is bec,ause we do not know how the treatment works in primary hypertension. As I have indicated above a number of studies have failed to confirm that relaxation operates directly to lower blood pressure or blood pressure reactivty or to reduce activity in the sympathetic nervous system. While it must be anticipated that future, better studies will clarify these questions, it is also essential that we widen the range of variables examined. It is surprising that very few studies have examined the behavioural outcome of this behavioural technique and to date we know very little about how the behaviour and cognitions of hypertensives are affected by relaxation and stress management. A few studies have shown moderate reductions in anxiety that do not relate to reduction in pressure [15, 441 although others have failed to find such reductions [26, 361. This is hardly surprising since hypertensives are not characterised by undue levels of distress and it is therefore unlikely that reduction in psychological distress underlie the effectiveness of relaxation in the majority of patients. Future studies should examine the effects of relaxation and stress management on the ability of the patient to cope with day-to-day stressors and also examine more wide-ranging changes in patients’ attitudes and life-style stemming from relaxation and stress management. TYPE A BEHAVIOUR
Type A or coronary prone behaviour is a behaviour pattern characterised by intense competitiveness, sense of being under extreme time pressure and easily provoked hostility. It is now recognised as an independent risk factor for coronary heart disease [45]. While there have been a number of interesting preliminary attempts to alter Type A behaviour in non-clinical groups [46] there is only one substantial clinical study of Type A modification yet available, the Recurrent Coronary Prevention Project (RCPP) [47, 481. This large scale study examined the effects of an extensive behavioural change programme on the reinfarction rate of approximately
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six hundred patients who had suffered at least one MI and three hundred controls. Patients were randomly allocated to either a group behaviour modification programme that occupied 24 sessions spread over three years, or 20 sessions of careful cardiological management. The experimental treatment essentially consisted of virtually all the techniques now in use in cognitive behaviour therapy, to firstly, enable patients to identify Type A behaviour and its role in their lives and then to generate a treatment programme that would enable them to change that behaviour. Among the techniques used were progressive muscular relaxation, self-monitoring, self-reinforcement, cognitive restructuring and behavioural contracting. These were designed to enable the patients to alter their environment, their behaviour and their cognitions in a way that decreased the likelihood of all aspects of Type A behaviour. Type A behaviour, as measured both by the structured interview (the most valid measure of Type A available) and various questionnaires, was reduced by approximately one standard deviation at the end of the three years in the experimental group and by a significantly smaller amount in the controls. In the total sample of patients 43.8% of the experimental group and 25.2% of the control group reduced their Type A behaviour: 17.6% of the experimental and 3.7% of the controls did so substantially. After three years only 7.2% of the experimental group had suffered a reinfarction or sudden cardiac death compared to 13.2% of the controls. This highly reliable difference was largely the result of the reduction in patients suffering nonfatal reinfarction which accounted for 4.1% of the experimental group and 10.6% of the controls. The possible mediating role of Type A behaviour in this reduction was examined by comparing the reinfarction rate in the second and third year separately in those patients who had or had not shown reliable reductions in Type A behaviour at the end of the first year. One point seven per cent of the patients whose Type A behaviour had changed suffered a further cardiac event compared to 8.6% of those who did not; persuasive evidence that changing Type A behaviour changes the risk of coronary heart disease. This interpretation is further strengthened by the authors failure to find any difference between the experimental and control group at the end of the three years in the number who were hypertensive, the mean level of serum cholesterol, or the numbers receiving either anti-hypertensive or antiarrhythmic medication. The scale and impressive outcome of this study make it particularly important that its limitations are recognised. It may not be possible to generalise from this highly selected sample of post MI patients to other post MI patients or to other healthy individuals. One can readily see that patients who have responded to advertisements to take part in a behavioural intervention, as these patients had, might well respond better than a random selection of post MI patients and furthermore the experience of one or more MI’s might well motivate patients to change their behaviour in a way that would be hard to achieve in healthy people who believe themselves to be profiting from their Type A behaviour. The other major problem is the lack of an adequate exploration in this study of the placebo or non-specific factors involved in such a complex, extensive form of treatment. Particularly in this selected group of patients the behavioural treatment might well be more plausible and attractive than even the most enthusiastic cardiological care and it is therefore unclear which, if any, of the specific component in the cognitive behavioural package actually produced the changes in Type A behaviour and the reduction in the reinfarction
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rate. This splendid study makes the exploration of these issues of pressing importance. It is to be hoped that future studies will also take the opportunity to use clinical interventions of this kind to determine the underlying physiological events that link Type A behaviour to coronary heart disease. ACUTE CORONARY CARE
Immediately after a myocardial infarction the patient’s survival is obviously the main concern. Nevertheless two valuable, if curiously uninfluential, studies of the effects of psychological intervention during the patient’s stay in the Coronary Care Unit have been reported. Gruen [49] compared supportive psychotherapy designed to enable patients to develop his or her own coping resources with routine care. Patients receiving such counselling spent less time both in the CCU and in the hospital in general and during their stay in the CCU had fewer supraventricular arrhythmias. Treated patients were less depressed but no less anxious during their stay in hospital and four months later the patients who had received psychotherapy were judged both by themselves and by their physicians to be less anxious and to have resumed more day to day activities. Cromwell and his colleagues have described a very ambitious study of different forms of patient management in the CCU [50, 511. Over 150 patients received either a high level of information about their heart attack and the nature of coronary heart disease, or very little, they were placed in either a very lively hospital environment or a dull one and finally they either participated actively in their treatment or had a passive role. Patients who received a great deal of information about their heart condition and were either placed in a stimulating environment or played an active role in their treatment were moved from the C.C.U. earlier and left the hospital after a shorter period than did patients who received similar information about their heart disease and were placed in a dull environment in which they played a passive role. Discharge from hospital is a very complex outcome measure and must depend on, among other things, the patient’s actual physical recovery, the staff’s perception of that recovery and the patient’s desire to leave the hospital, but even allowing for that one has some sympathy with the author’s conclusion that high information may be beneficial if the patients can either distract themselves from it or use it as part of their efforts to control their environment. It is unhelpful when patients are simply left to lie and worry. REHABILITATION
AFTER MYOCARDIAL
INFARCTION
Myocardial Infarction is a risk factor for a further MI and psychosocial distress and disability. Rehabilitation can attempt to reduce either or both of these risks and programmes aimed at one may well effect the other. Psychological programmes are, at least superficially, very diverse, ranging from counselling from nurses to extensive group psychotherapy [52-541. However, it is likely that a variety of counselling and psychotherapeutic methods share common features, such as attempts to reduce current anxiety, deal with compliance with the medical regime, provide information on the nature of heart disease and encourage patients to undertake an appropriate level of activity. An apparently quite different approach is represented by the various exercise based rehabilitation programmes which at least initially were offered because of the potentially beneficial effects of exercise on the cardiovascular system,
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but are now believed to have powerful adjunctive psychological effects and may be used for that reason. Naismith et al. [52] have shown that psychological counselling from a nurse counsellor had little effect, apart from increased social independence six months after MI, but patients scoring high on Neuroticism, as measured by the EPI, were more likely to have a good outcome if they received counselling. This suggests that not all patients need special counselling, but those who are either prone to anxiety or are unusually anxious and troubled as a result of their MI may benefit. Mayou et al. [55] also compared counselling and routine care and found that three months after MI there was no evidence of counselling having a beneficial effect on psychosocial adjustment. The patients appeared to make a rather satisfactory recovery whatever treatment they received and this may again suggest that only a sub-set of patients are likely to benefit from counselling. The view that counselling should not be offered routinely to all patients, but only those displaying some kind of unusual distress or disability was pursued by Stern [56], who studied patients with either very low work capacity as assessed by an exercise test, and/or undue anxiety and depression six weeks after an MI. Patients received either standard care or group counselling. The effects were modest. Patients receiving counselling were less depressed and more sociable and friendly than untreated patients shortly after treatment, but these differences had largely disappeared one year later. There is little reason to believe that exercise programmes reduce morbidity or mortality, but the psychological benefits remain of interest. Mayou [28] compared exercise with standard care in patients immediately following an MI. Patients expressed considerable enthusiasm for the exercise programme but the way in which it was helpful was not detectable on standard exercise testing, measures of activity in daily life or psychological adjustment. The most comprehensive study of exercise has been the National Exercise and Heart Disease Project, described in various papers by Shaw, Stern and others [56-581. This study involved two stages: In the first, over 600 men who had suffered an MI during the previous three years underwent a brief exercise programme and were then assigned randomly to a three year programme or simply left to their own devices. In common with other exercise programmes there was no convincing reduction in mortality or morbidity, nor did psychological state, measured on a variety of questionnaires, differentiate those who were allocated to a continuing exercise regime or left alone. Work capacity on treadmill testing was moderately improved in exercising subjects, although the difference had disappeared by the end of the study. In a later study in which patients who had not made a satisfactory recovery from their infarct were assigned either to a 36 session exercise programme or routine care, it was again shown that there was no consistent psychological benefit [59]. Comparisons of exercise and counselling have shown little difference between them although counselling may produce marginally greater psychological change [55,59]. The effects of psychological interventions in patients who have had a myocardial infarction are, at best, modest and there seems little reason to offer such help routinely. Since it is almost certainly very difficult to identify, at an early stage, those patients who will require assistance it may be best to delay a decision until the patient’s distress and disability seems undue compared to his or her peers, who have adjusted satisfactorily to their MI. Perhaps three months after the infarct would be an appropriate time to assess the patient for psychological help. The most appro-
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priate form of psychological intervention is unclear at present and presumably depends on the patients problems, which should be clearly identified so that specific and rationally derived therapies can be applied. Since the majority of patients make a satisfactory long-term adjustment after an MI, there may seem little reason for psychological intervention during the period while the patient is still in the C.C.U. However, little research has been done on this issue and future research should attempt to determine if either patients are suffering significant distress that can be usefully reduced or if mortality or morbidity is reduced during this dangerous period. The tentative results of Gruen [49] suggesting that counselling might have an effect on arrythmias and the growing literature on the effects of stress on arrthymias [60] both suggest this possibility is well worth investigation. OVERVIEW
The most exciting developments in psychological interventions in cardiovascular disease are in the reduction of risk factors. The two main areas of such research are at peculiarly different stages. It is now clear that behavioural methods can reduce blood pressure and that the effect is specific. Future studies should be directed at identifying those patients to whom the treatment can be best applied, the mechanisms through which treatments operate and also large-scale studies are necessary to show that the reductions in pressure are matched by appropriate reductions in risk. The research in Type A modification has shown that risk can be reduced by procedures that change Type A behaviour and future research should be directed at exploring the specificity of these changes and also the mechanisms whereby Type A reduction is translated into risk reduction. Specificity should also be an essential issue in future studies of psychological interventions in rehabilitation, although it may be advisable to concentrate initially qn the selection of the most appropriate patients in which it can be demonstrated that interventions have effects that are commensurate with effort involved. Acknowledgement-The author preparation of this paper.
was in receipt
of grants
from the Medical
Research
Council
during
the
REFERENCES
1. JOHNSTON DW. The behavioural treatment of the symptoms of ischemic heart disease. In Behaviourol Treatment of Disease (Edited by SURWIT R, WILLIAMS R, STEPTOE A, BIESNER R), pp. 115-127. New York; Plenum, 1982. 2. STEPTOE A. Blood pressure control: a comparison of feedback and instructions using pulse transit time feedback. Psychophysioll976; 13: 528-536. 3. STEPTOE A. The regulation of blood pressure reactions to taxing conditions using pulse transit time feedback and relaxation. Psychophysiol1978; 15: 429-438. 4. SURWIT RS, HAGER JL, FELDMAN T. The role of feedback in voluntary control of blood pressure in instructed subjects. JApplBehavAnall977; 10:625-631. 5. LUTZ DJ, HOLMES DS. Instructions to change blood pressure and diastolic blood pressure feedback: their effects on diastolic blood pressure, systolic blood pressure and anxiety. J Psychosom Res
1981; 25:479-485. 6. SURWIT TS, SHAPIRO D, GOOD MI. Comparison biofeedback
and meditation
in the treatment
of cardiovascular biofeedback, neuromuscular of borderline essential hypertension. J Cons C/in
Psycho1 1978; 46: 252-263. 7.
FRANKEL BL, PATEL DJ, HORWITZ D, FRIEDWALD MT, GAARDNER KP. Treatment with biofeedback and relaxation techniques. Psychosom Med 1978; 40: 276-293.
of hypertension
Interventions
in cardiovascular
455
disease
8. BLANCHARD ER, MILLER ST, ABEL CC, HAYNES MR, WICKER R. Evaluation treatment of essential hypertension JApplBehav Anal 1979; 12: 99-l 10.
9.
of biofeedback
in the
GLAXXJW MS, GAARDNER KR, ENGEL BT, Behavioural treatment of high blood pressure: II Acute and sustained effects of relaxation and systolic blood pressure biofeedback. Psychosom Med 1982;
44: 155-171. 10. GOLDSTEIN lB, SHAPIRO D, THANAOPAVARAN C. Comparison of drug and behavioural treatments of essential hypertension. Hlth Psycholl982; 1: 7-26. 11. JOHNSTON DW, LETHEM J. The production of specific decreases in interbeat interval and the motor skill analogy. Psychophysioll981; 18: 288-300. 12. JOHNSTON DW. Biofeedback, relaxation and related procedures in the treatment of psychophysiological disorders. In Health Care and Human Behaviour (Edited by STEPTOE A, MATHEWS A), pp. 267-300. London: Academic Press, 1984. 13. PATEL C, NORTH WRS. Randomised controlled trial of yoga and biofeedback in the management of hypertension. Lancet 1975; II: 93-95. 14. PATEL C, MARMOT MG, TERRY DJ. Controlled trial of biofeedback-aided behavioural methods in reducing mild hypertension. Br Med J 1981; 282: 2005-2008. 15. BALI LR. Long- term effect of relaxation on blood pressure and anxiety levels in essential hypertensive males: A controlled study. Psychosom Med 1979; 41: 637-646. 16. TAYLOR CB, FARQUHAR JW, NELSON E, AGRAS WS. Relaxation therapy and high blood pressure.
Arch Gen Psychiat 1977; 34: 339-342. 17. 18. 19. 20. 21. 22.
BRAUER A, HORLICK LF, NELSON B, FARQUHAR JU, AGRAS WS. Relaxation therapy for essential hypertension: a Veterans Administration out-patients study. JBehav Med 1979; 2: 21-29. SOUTHAM MA, AGRAS WS, TAYLOR CB, KRAEMER HC. Relaxation training: Blood pressure during the working day. Arch Gen Psychiat 1982; 39: 715-717. CROWTHER JH. Stress management training and relaxation imagery in the treatment of essential hypertension. JBehavMed 1983; 6: 169-187. SEER P, RAEBURN JM. Meditation training and essential hypertension: a methodological study. J Behav Med 1980; 3: 59-73. GOLDSTEIN IB, SHAPIRO D, THANOPAVARAN C. Home relaxation techniques for essential hypertension. Psychosom Med 1984; 46: 399-414. CHARLESWORTH EA, WILLIAMS BJ, BAER PE. Stress management at the worksite for hypertension: compliance, cost-benefit, health care and hypertension-related variables. Psychosom Med 1984;
46: 387-397. 23. 24. 25.
AGRAS WS, SOUTHAM MA, TAYLOR BC. Long-term persistence of relaxation-induced blood pressure lowering during the working day. J Cons C/in Psycho1 1983; 51: 792-794. LITTLE BE, HAYWORTH J, BENSON P, HALL F, BEARD RW, DEWHURST J, PRIEST RG. Treatment of hypertension in pregnancy by relaxation and biofeedback. Lancet 1984; 1: 865-867. PATEL C, MC, DJ, M, B, M. of in coronary four follow BrMed 1985; 1103-l
26.
J, of
27.
DW, hypertension. A, A.
Self-regull982; TASTO
HUEBNER
CR, the
30.
DW. of JE,
Behav 31.
32.
GV.
and
for control
cardiovascular
The
of
relaxation
Ther
14:
management
the
to
tasks.
149-166. Behav
29.
D,
self-control the interval pulse time. DL, effects muscle
Ther
stress response
Med on
blood
the
pressure
exercise
of
feedback
46: of
hyper-
13:
P, L, R, H. pressure, rate resniratorv to single of a replication.-JPsychosom Res 1978; 22: 493-501 .I JACOB RG, BEADEL DC, SHAPIRO AP. The relaxation word of the day: a simnle techniaue to measure
adherence to relaxation. JBehav Assess 1984; 6: 159-165. PATEL C. Yoga and biofeedback in the management of ‘stress’ in hypertensive patients. Clin Sci MolecMed 1975; 28: Suppl; 171-174. 34. JORGENSEN RS, HOUSTON BK, ZURAWSKI RM. Anxiety management training in the treatment of essential hypertension. Behav Res Therap 1981; 19: 467-474. 35. STONE RA, DELEO J. Psychotherapeutic control of hypertension. NEng JMed 1976; 294: 80-84. 36. COTTIER C, SHAPIRO K, JULIUS S. Treatment of mild hypertension with progressive muscle relaxation: predictive value of indexes of sympathetic tone. Arch Intern Med 1984; 144: 1954-1958. 37. MCGRADY AV, YONKER R, TAN SY, FINE TH, WOERNER M. The effect of biofeedback-assisted relaxation on blood pressure and selected biochemical parameters with essential hypertension. Biofeed Self-reg 198 1; 6: 343-354.
33.
DEREK W. JOHNSTON
456 38.
POLLACK AA, WEBER MA, CASE DB, LARAGH JH. Limitations of transcendental meditation in the treatment of essential hypertension. Lancet 1977; 1: 71-72. 39. GOLDSTEIN DS. Plasma catecholamines and essential hypertension: An analystical review. Hypertension 1983; 5: 86-99. 40. ESLER M, JULIUS S, ZWEIFLER A, RANDALL 0, HARBURG E, GARDINER H, DEQUATTRO V. Mild highrenin essential hypertension. Neurogenic human hypertension. NewEng JA4ed 1973; 269: 405-411. 41. JULIUS S, ESLER M. Autonomic nervous cardiovascular regulation in borderline hypertension.
A J Cardioll975; 36: 685-696. 42.
JACOB RG, KRAMER HG, AGRAS WS. Relaxation
therapy in the treatment of hypertension.
Arch Gen
Psychiat 1977; 34: 1417-1427. 43. 44.
PETERS RK, BENSON H, PETERS JM. Daily relaxation breaks in a working population: II Effects on blood pressure. Am JPublic Health 1977; 67: 954-959. WADDEN TA. Predicting treatment response to relaxation therapy for essential hypertension. J Nerv
Ment Dis 1983;171:683-689. 45. The Review Panel on Coronary-Prone
Behaviour and Coronary Heart Disease, Coronary-prone behaviour and coronary heart disease: A criticarreview. Circulation 1981; 63: 1199-1215. 46. JOHNSTON DW. Behavioural treatment in the reduction of coronary risk factors: Type A behaviour and blood pressure. Br J C/in Psycho1 1982; 21: 281-294. 47. FRIEDMAN M, THORESEN CE, GILL CE, ULMER D, THOMPSON L, POWELL L, PRICE V, ELEK SR, RABIN DD, BREALL WS, PIAGET G, DIXON T, BOURG E, LEVY RA, TASTO DL. Feasibility of altering Type A behaviour patterns after myocardial infarction. Recurrent coronary prevention project study: Methods, baseline results and preliminary findings. Circulation 1982; 66: 83-92. 48. FRIEDMAN M, THORENSEN CE, GILL JJ, POWELL LH, ULMER D, THOMPSON L, PRICE V, RABIN DD, BREALL WS, DIXON T, LEVY R, BOURG E. Alteration of Type A behaviour and reduction in cardiac recurrences in post-myocardial infarction patients. Am Heart J 1984; 108: 237-248. 49. GRUEN W. Effects of brief psychotherapy during the hospitalization period on the recovery process in heart attacks. JConsult Clin Psycho1 1975; 43: 223-232. 50. CROMWELL RL, BUTTERFIELDEC, BRAYFIELD FM, CURRY JJ. Acute myocardial infarction: reaction and recovery. Mosby; St. Louis, 1977. 51. CROMWELL RL, LEVENKRON JC. Psychological care of acute coronary patients. In Health Cure and Human Behaviour (Edited by STEPTOE A, MATHEWS A), pp. 209-229. Academic Press; London, 1984. 52. NAISMITH LD, ROBINSON JF, SHAW GB, MACINTYRE MMJ. Psychosocial rehabilitation after infarction. BrMed J 1979; 1: 439-442. 53. IBRAHIM MA, FELDMAN JG, SULLTZ HA, STAIMAN MC, YOUNG LJ, DEAN D. Management after myocardial infarction: a controlled trial of the effects of group psychotherapy. Int J Psychiut Med 1974; 5: 253-268. 54. RAHE RH, WARD H, HAYNES V. Brief group therapy in myocardial infarction: three to four year follow up of a controlled trial. Psychosom Med 1979; 41: 229-241. 55. MAYOU R, MACMAHON D, SLEIGHT P, FLORENCIO MJ. Early rehabilitation after myocardial infarction. Lancer 1981; 11: 1399-1401. 56. SHAW L. Effects of a prescribed, supervised exercise program on mortality and cardiovascular morbidity in myocardial infarction subjects. Am JCurdioll981; 48: 39-46. 57. STERN MJ, CLEARY P. National exercise and heart disease project. Psychosocial changes observed during a low-level exercise program. Arch Intern Med 1981;141: 1463-1467. 58. STERN MJ, CLEARY P. The national exercise and heart disease project. Long-term psychosocial outcome. Arch Intern Med 1982; 142: 1093-1097. 59. STERN MJ, GORMAN PA, KASLOW L. The group counselling versus exercise therapy study: a controlled intervention with post myocardial infarction subjects. Arch Intern Med 1983; 143: 1719-1725. 60. LOWN B, VERRIER RL, RABINOWITZ SH. Neural and psychologic mechanisms and the problem of sudden cardiac death. Am J Cardioll977; 39: 890-902.
Rexmch,
Vol. 29, No. 5. PP. 44-456,
0022-3999/E $3.00+ .W ‘-’ 1985 Pergamon Press Ltd.
1985.
INVITED REVIEW PSYCHOLOGICAL INTERVENTIONS CARDIOVASCULAR DISEASE DEREK
W.
IN
JOHNSTON
(Received 21 February 1985) Abstract-The literature on the behavioural treatment of primary hypertension, reduction of Type A behaviour, and psychological interventions during acute coronary care and rehabilitation after a myocardial infarction are selectively reviewed. There is growing evidence that relaxation and stress management can lower blood pressure by useful amounts in mild primary hypertension although the mechanisms underlying these reductions are unclear. Type A behaviour has been reduced in patients following a myocardial infarction and this led to reduced morbidity. Other interventions following myocardial infarction, both when the patient is in hospital and after discharge have produced at best only modest benefits and are, therefore, not widely applicable. Future research in rehabilitation should be directed at reducing the disabilities of patients with clearly identifiable problems that stem from their response to cardiovascular disease. INTRODUCTION MOST OF the standard risk factors for cardiovascular disease have a substantial behavioural component, e.g. blood lipids may in part relate to diet, stress has been implicated in the aetiology and maintenance of primary hypertension and smoking and Type A, or coronary prone, behaviour are exclusively behavioural risk factors. Furtherore, cardiovascular disease is not only the product of behaviour but it also powerfully affects behaviour since both acute and chronic distress and disability can result from such disease, perhaps most obviously following a myocardial infarction (MI). It is not possible in this review to cover all the relevant psychological interventions and I shall concentrate on those interventions that deal primarily with stress as a possible cause of cardiovascular disorders and distress as a likely consequence. I shall not therefore cover attempts to alter smoking behaviour nor shall I review the literature on psychological interventions designed to help patients cope with the symptoms of coronary heart disease such as angina or arrhythmias. These may well be stress related but there has been little advance in the psychological management of such conditions since the preliminary studies reported some time ago [l]. This review will cover the behavioural treatment of primary hypertension, the reduction of Type A behaviour, psychological interventions in acute coronary care and the role of both psychological interventions and exercise in rehabilitation after myocardial infarction. PRIMARY
HYPERTENSION
Two main approaches to the behavioural reduction of blood hypertension have been studied; cardiovascular biofeedback stress management. The effects of biofeedback have been appointing. Laboratory studies of normal volunteers suggest biofeedback is no more likely to reduce blood pressure than Address for correspondence: D. W. Johnston, Oxford
Department
OX3 7JX. U.K. 447
of Psychiatry,
pressure in primary and relaxation and almost entirely disthat cardiovascular a variety of much Warneford
Hospital,
448
DEREK
W.
JOHNSTON
simpler procedures that do not involve feedback [2-51 and studies of hypertensive patients have obtained similar results [7, 81. Two clinical studies have been slightly more positive. Glasgow et al. [9] claim that a very simple form of blood pressure feeback used at home was, when combined with relaxation training, more effective than either relaxation or biofeedback alone. However, the superiority of the combination of relaxation and biofeedback was not marked and was only obtained on a few of a multitude of blood pressure measures. Goldstein et al. [lo] using more conventional laboratory blood pressure feedback showed that such feedback was slightly more effective than relaxation or self-monitoring in lowering pressure in the laboratory, although not outside it. However, relaxation which as we shall see below is normally found to be a moderately effective treatment for mild hypertension, was strikingly ineffective in this study and it would therefore be quite unsound to conclude that there is a strong case for advocating biofeedback in the treatment of mild primary hypertension. Biofeedback is based on the assumption that the skill of controlling a visceral response can be acquired in the same way as a more conventional motor response; this view has been under increasing challenge [ll, 121 and it is probably more realistic to knowledge that stress is likely to be involved in blood pressure elevation and that treatment should therefore be directed at reducing that stress. A number of investigations of relaxation training and stress management have shown reliable reductions in pressure [ 13-221 although some contrary findings have been reported [6, lo]. In general the effective studies have examined patients with higher blood pressure than the ineffective, and have incorporated home practice in relaxation and instruction in the use of relaxation to cope with day-to-day stressors. One can, therefore, conclude that relaxation training can lower the blood pressure of patients who fall towards the top end of the mildly hypertensive range, i.e. with diastolic pressures of at or near 100 mmHg and after such treatment such patients will have pressures that are at or near the normotensive range. These effects persist for at least 15 months after the end of treatment [13, 14, 18, 231 and these reductions have been confirmed using semi-automatic ambulatory blood pressure recording in the work setting [18, 231. As yet there are no studies demonstrating unequivocal changes in health or reduction of coronary heart disease following relaxation and stress management although a study by Little et al. [24] showed that hypertensive women receiving relaxation training are less likely to be admitted to hospital during their pregnancy and Pate1 et al. [25] has recently reported a reduction in the incidence of coronary heart disease in the four years following relaxation training. Since relaxation and stress management lower blood pressure it is obviously important to establish the mechanism or mechanisms underlying this effect. One of the most important issues with any apparently effective psychological technique is to establish specificity since complex and plausible psychological treatments may well operate primarily through non-specific or placebo processes. The evidence suggests that the effects of relaxation on blood pressure are not primary non-specific since controlled investigations show that relaxation leads to a greater reduction in pressure than does simply attending the clinic and sitting quietly there [3], receiving various forms of supportive psychotherapy [15-171 and we have recently shown that an elaborate, plausible and acceptable form of mild exercise did not lead to reliable reductions in pressure, whereas relaxation did [26]. Therefore, it appears very
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unlikely that the effects of relaxation and stress management are simply due to the non-specific effects of procedures such as taking an interest in the patient or offering a plausible treatment. The most straightforward explanation of the effect of relaxation is that it operates to lower blood pressure directly and patients who regularly and assiduously practice the technique will show beneficial reductions in pressure. If relaxation operates in this way then presumably the effects would be seen most clearly immediately after the patient had been relaxing. However, both studies of both healthy, normotensive volunteers [27-291 and hypertensives [26, 30, 311 have failed to show consistent reductions in pressure immediately after relaxation. Other evidence that there is not a simple direct effect of relaxation on blood pressure is provided by the very variable correlations that are typically found between the amount of relaxation practice carried out during treatment and the actual reductions in pressure obtained [21, 22, 26, 321. It would be naive to assume that there is a simple relationship between amount of relaxation and blood pressure reductions; however, these results, taken with the difficulties in demonstrating a direct effect of relaxation, suggest that relaxation does not operate primarily by lowering blood pressure directly. The above studies are entirely concerned with resting blood pressure and it can be argued that relaxation may show its effect when the subject is under some kind of stress. At least four studies of hypertensive patients have examined the effects of relaxation on cardiovascular reactivity provoked by laboratory stressors ranging from mental arithmetic to dynamic exercise. Only one has shown a positive effect with relaxation reducing the pressor response to both the cold pressor test and dynamic exercise [33]. Two others [lo, 261 have failed to show any effect of relaxation on reactivity to a variety of laboratory stressors and one [34] actually showed anxiety management training to be associated with increased reactivity to some stressors. The final mechanism to be considered is possible neurogenic and hormonal changes associated with relaxation. Most investigators assume that primary hypertension is, at least in part, related to increased activity in the sympathetic nervous system or heightened sensitivity to SNS input and there have, therefore, been a number of attempts to determine the effects of relaxation on the sympathetic nervous system. The results have been very variable. Plasma dopa-beta-hydroxylase was reduced in only one of two studies [17, 351. Cottier et al. [36] found significant reductions in plasma adrenaline in comparison with a placebo control group but two other studies [26, 371 failed to find any effect of relaxation on various measures of urinary catecholamines. Four studies have failed to find reductions in plasma renin activity [lo, 36-381 although Pate1 [14] did find reductions in both plasma renin and aldosterone immediately after a course of relaxation training. The effects were no longer detectable six months later although blood pressure remained at its reduced level. McGrady et al. [37] also obtained reductions in plasma aldosterone. The answer to the puzzling diversity of the studies may lie in the heterogeneity of the patients studied who have ranged in average age from their late 20’s [35] to their late 50’s [17] and were variously medicated and unmedicated [17, 14, 361. When such heterogeneity is taken in conjunction with the widely held view that hypertension is unlikely to have a similar basis in all patients or at all stages in the condition [39-41] it is hardly surprising that confusion reigns. Future studies of neuro-
450
DEREK W. JOHNSTON
genie mechanisms should therefore concentrate on homogeneous groups of patients, preferably selected because of a known abnormality in the parameter felt to underlie the effects of relaxation, e.g. if it is hoped to demonstrate that relaxation reduces measures of sympathetic activity then patients should be selected who have clearly detectable elevated catecholamines. Very closely related to the question of mechanism is the important issue of which patients benefit from relaxation and stress management. It is very unlikely all patients can benefit from this form of treatment since it is improbable that hypertension is invariably related to the factors that might be thought to be changed by relaxation. In an influential early review Jacob et al. [42] showed that initial level of blood pressure was a powerful determinant of the reductions obtained by relaxation training, patients with the higher pressures doing better. More recent research has confirmed this view [14, 461. Cottier et al. [36] have shown that patients with heightened sympathetic tone, indicated by higher initial heart rate and plasma noradrenaline, benefit more from training. In a rather pessimistic discussion of these results Cottier et al. suggest that relaxation should only be offered in young, anxious patients with a high sympathetic tone. This conclusion is unreasonable since it ignores the very positive outcomes that have been obtained in studies of patients that do not approximate to these criteria [13, 141. We are not yet in a position to decide who will benefit from relaxation. In part this is bec,ause we do not know how the treatment works in primary hypertension. As I have indicated above a number of studies have failed to confirm that relaxation operates directly to lower blood pressure or blood pressure reactivty or to reduce activity in the sympathetic nervous system. While it must be anticipated that future, better studies will clarify these questions, it is also essential that we widen the range of variables examined. It is surprising that very few studies have examined the behavioural outcome of this behavioural technique and to date we know very little about how the behaviour and cognitions of hypertensives are affected by relaxation and stress management. A few studies have shown moderate reductions in anxiety that do not relate to reduction in pressure [15, 441 although others have failed to find such reductions [26, 361. This is hardly surprising since hypertensives are not characterised by undue levels of distress and it is therefore unlikely that reduction in psychological distress underlie the effectiveness of relaxation in the majority of patients. Future studies should examine the effects of relaxation and stress management on the ability of the patient to cope with day-to-day stressors and also examine more wide-ranging changes in patients’ attitudes and life-style stemming from relaxation and stress management. TYPE A BEHAVIOUR
Type A or coronary prone behaviour is a behaviour pattern characterised by intense competitiveness, sense of being under extreme time pressure and easily provoked hostility. It is now recognised as an independent risk factor for coronary heart disease [45]. While there have been a number of interesting preliminary attempts to alter Type A behaviour in non-clinical groups [46] there is only one substantial clinical study of Type A modification yet available, the Recurrent Coronary Prevention Project (RCPP) [47, 481. This large scale study examined the effects of an extensive behavioural change programme on the reinfarction rate of approximately
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six hundred patients who had suffered at least one MI and three hundred controls. Patients were randomly allocated to either a group behaviour modification programme that occupied 24 sessions spread over three years, or 20 sessions of careful cardiological management. The experimental treatment essentially consisted of virtually all the techniques now in use in cognitive behaviour therapy, to firstly, enable patients to identify Type A behaviour and its role in their lives and then to generate a treatment programme that would enable them to change that behaviour. Among the techniques used were progressive muscular relaxation, self-monitoring, self-reinforcement, cognitive restructuring and behavioural contracting. These were designed to enable the patients to alter their environment, their behaviour and their cognitions in a way that decreased the likelihood of all aspects of Type A behaviour. Type A behaviour, as measured both by the structured interview (the most valid measure of Type A available) and various questionnaires, was reduced by approximately one standard deviation at the end of the three years in the experimental group and by a significantly smaller amount in the controls. In the total sample of patients 43.8% of the experimental group and 25.2% of the control group reduced their Type A behaviour: 17.6% of the experimental and 3.7% of the controls did so substantially. After three years only 7.2% of the experimental group had suffered a reinfarction or sudden cardiac death compared to 13.2% of the controls. This highly reliable difference was largely the result of the reduction in patients suffering nonfatal reinfarction which accounted for 4.1% of the experimental group and 10.6% of the controls. The possible mediating role of Type A behaviour in this reduction was examined by comparing the reinfarction rate in the second and third year separately in those patients who had or had not shown reliable reductions in Type A behaviour at the end of the first year. One point seven per cent of the patients whose Type A behaviour had changed suffered a further cardiac event compared to 8.6% of those who did not; persuasive evidence that changing Type A behaviour changes the risk of coronary heart disease. This interpretation is further strengthened by the authors failure to find any difference between the experimental and control group at the end of the three years in the number who were hypertensive, the mean level of serum cholesterol, or the numbers receiving either anti-hypertensive or antiarrhythmic medication. The scale and impressive outcome of this study make it particularly important that its limitations are recognised. It may not be possible to generalise from this highly selected sample of post MI patients to other post MI patients or to other healthy individuals. One can readily see that patients who have responded to advertisements to take part in a behavioural intervention, as these patients had, might well respond better than a random selection of post MI patients and furthermore the experience of one or more MI’s might well motivate patients to change their behaviour in a way that would be hard to achieve in healthy people who believe themselves to be profiting from their Type A behaviour. The other major problem is the lack of an adequate exploration in this study of the placebo or non-specific factors involved in such a complex, extensive form of treatment. Particularly in this selected group of patients the behavioural treatment might well be more plausible and attractive than even the most enthusiastic cardiological care and it is therefore unclear which, if any, of the specific component in the cognitive behavioural package actually produced the changes in Type A behaviour and the reduction in the reinfarction
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DEREKW. JOHNSTON
rate. This splendid study makes the exploration of these issues of pressing importance. It is to be hoped that future studies will also take the opportunity to use clinical interventions of this kind to determine the underlying physiological events that link Type A behaviour to coronary heart disease. ACUTE CORONARY CARE
Immediately after a myocardial infarction the patient’s survival is obviously the main concern. Nevertheless two valuable, if curiously uninfluential, studies of the effects of psychological intervention during the patient’s stay in the Coronary Care Unit have been reported. Gruen [49] compared supportive psychotherapy designed to enable patients to develop his or her own coping resources with routine care. Patients receiving such counselling spent less time both in the CCU and in the hospital in general and during their stay in the CCU had fewer supraventricular arrhythmias. Treated patients were less depressed but no less anxious during their stay in hospital and four months later the patients who had received psychotherapy were judged both by themselves and by their physicians to be less anxious and to have resumed more day to day activities. Cromwell and his colleagues have described a very ambitious study of different forms of patient management in the CCU [50, 511. Over 150 patients received either a high level of information about their heart attack and the nature of coronary heart disease, or very little, they were placed in either a very lively hospital environment or a dull one and finally they either participated actively in their treatment or had a passive role. Patients who received a great deal of information about their heart condition and were either placed in a stimulating environment or played an active role in their treatment were moved from the C.C.U. earlier and left the hospital after a shorter period than did patients who received similar information about their heart disease and were placed in a dull environment in which they played a passive role. Discharge from hospital is a very complex outcome measure and must depend on, among other things, the patient’s actual physical recovery, the staff’s perception of that recovery and the patient’s desire to leave the hospital, but even allowing for that one has some sympathy with the author’s conclusion that high information may be beneficial if the patients can either distract themselves from it or use it as part of their efforts to control their environment. It is unhelpful when patients are simply left to lie and worry. REHABILITATION
AFTER MYOCARDIAL
INFARCTION
Myocardial Infarction is a risk factor for a further MI and psychosocial distress and disability. Rehabilitation can attempt to reduce either or both of these risks and programmes aimed at one may well effect the other. Psychological programmes are, at least superficially, very diverse, ranging from counselling from nurses to extensive group psychotherapy [52-541. However, it is likely that a variety of counselling and psychotherapeutic methods share common features, such as attempts to reduce current anxiety, deal with compliance with the medical regime, provide information on the nature of heart disease and encourage patients to undertake an appropriate level of activity. An apparently quite different approach is represented by the various exercise based rehabilitation programmes which at least initially were offered because of the potentially beneficial effects of exercise on the cardiovascular system,
Interventions
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but are now believed to have powerful adjunctive psychological effects and may be used for that reason. Naismith et al. [52] have shown that psychological counselling from a nurse counsellor had little effect, apart from increased social independence six months after MI, but patients scoring high on Neuroticism, as measured by the EPI, were more likely to have a good outcome if they received counselling. This suggests that not all patients need special counselling, but those who are either prone to anxiety or are unusually anxious and troubled as a result of their MI may benefit. Mayou et al. [55] also compared counselling and routine care and found that three months after MI there was no evidence of counselling having a beneficial effect on psychosocial adjustment. The patients appeared to make a rather satisfactory recovery whatever treatment they received and this may again suggest that only a sub-set of patients are likely to benefit from counselling. The view that counselling should not be offered routinely to all patients, but only those displaying some kind of unusual distress or disability was pursued by Stern [56], who studied patients with either very low work capacity as assessed by an exercise test, and/or undue anxiety and depression six weeks after an MI. Patients received either standard care or group counselling. The effects were modest. Patients receiving counselling were less depressed and more sociable and friendly than untreated patients shortly after treatment, but these differences had largely disappeared one year later. There is little reason to believe that exercise programmes reduce morbidity or mortality, but the psychological benefits remain of interest. Mayou [28] compared exercise with standard care in patients immediately following an MI. Patients expressed considerable enthusiasm for the exercise programme but the way in which it was helpful was not detectable on standard exercise testing, measures of activity in daily life or psychological adjustment. The most comprehensive study of exercise has been the National Exercise and Heart Disease Project, described in various papers by Shaw, Stern and others [56-581. This study involved two stages: In the first, over 600 men who had suffered an MI during the previous three years underwent a brief exercise programme and were then assigned randomly to a three year programme or simply left to their own devices. In common with other exercise programmes there was no convincing reduction in mortality or morbidity, nor did psychological state, measured on a variety of questionnaires, differentiate those who were allocated to a continuing exercise regime or left alone. Work capacity on treadmill testing was moderately improved in exercising subjects, although the difference had disappeared by the end of the study. In a later study in which patients who had not made a satisfactory recovery from their infarct were assigned either to a 36 session exercise programme or routine care, it was again shown that there was no consistent psychological benefit [59]. Comparisons of exercise and counselling have shown little difference between them although counselling may produce marginally greater psychological change [55,59]. The effects of psychological interventions in patients who have had a myocardial infarction are, at best, modest and there seems little reason to offer such help routinely. Since it is almost certainly very difficult to identify, at an early stage, those patients who will require assistance it may be best to delay a decision until the patient’s distress and disability seems undue compared to his or her peers, who have adjusted satisfactorily to their MI. Perhaps three months after the infarct would be an appropriate time to assess the patient for psychological help. The most appro-
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priate form of psychological intervention is unclear at present and presumably depends on the patients problems, which should be clearly identified so that specific and rationally derived therapies can be applied. Since the majority of patients make a satisfactory long-term adjustment after an MI, there may seem little reason for psychological intervention during the period while the patient is still in the C.C.U. However, little research has been done on this issue and future research should attempt to determine if either patients are suffering significant distress that can be usefully reduced or if mortality or morbidity is reduced during this dangerous period. The tentative results of Gruen [49] suggesting that counselling might have an effect on arrythmias and the growing literature on the effects of stress on arrthymias [60] both suggest this possibility is well worth investigation. OVERVIEW
The most exciting developments in psychological interventions in cardiovascular disease are in the reduction of risk factors. The two main areas of such research are at peculiarly different stages. It is now clear that behavioural methods can reduce blood pressure and that the effect is specific. Future studies should be directed at identifying those patients to whom the treatment can be best applied, the mechanisms through which treatments operate and also large-scale studies are necessary to show that the reductions in pressure are matched by appropriate reductions in risk. The research in Type A modification has shown that risk can be reduced by procedures that change Type A behaviour and future research should be directed at exploring the specificity of these changes and also the mechanisms whereby Type A reduction is translated into risk reduction. Specificity should also be an essential issue in future studies of psychological interventions in rehabilitation, although it may be advisable to concentrate initially qn the selection of the most appropriate patients in which it can be demonstrated that interventions have effects that are commensurate with effort involved. Acknowledgement-The author preparation of this paper.
was in receipt
of grants
from the Medical
Research
Council
during
the
REFERENCES
1. JOHNSTON DW. The behavioural treatment of the symptoms of ischemic heart disease. In Behaviourol Treatment of Disease (Edited by SURWIT R, WILLIAMS R, STEPTOE A, BIESNER R), pp. 115-127. New York; Plenum, 1982. 2. STEPTOE A. Blood pressure control: a comparison of feedback and instructions using pulse transit time feedback. Psychophysioll976; 13: 528-536. 3. STEPTOE A. The regulation of blood pressure reactions to taxing conditions using pulse transit time feedback and relaxation. Psychophysiol1978; 15: 429-438. 4. SURWIT RS, HAGER JL, FELDMAN T. The role of feedback in voluntary control of blood pressure in instructed subjects. JApplBehavAnall977; 10:625-631. 5. LUTZ DJ, HOLMES DS. Instructions to change blood pressure and diastolic blood pressure feedback: their effects on diastolic blood pressure, systolic blood pressure and anxiety. J Psychosom Res
1981; 25:479-485. 6. SURWIT TS, SHAPIRO D, GOOD MI. Comparison biofeedback
and meditation
in the treatment
of cardiovascular biofeedback, neuromuscular of borderline essential hypertension. J Cons C/in
Psycho1 1978; 46: 252-263. 7.
FRANKEL BL, PATEL DJ, HORWITZ D, FRIEDWALD MT, GAARDNER KP. Treatment with biofeedback and relaxation techniques. Psychosom Med 1978; 40: 276-293.
of hypertension
Interventions
in cardiovascular
455
disease
8. BLANCHARD ER, MILLER ST, ABEL CC, HAYNES MR, WICKER R. Evaluation treatment of essential hypertension JApplBehav Anal 1979; 12: 99-l 10.
9.
of biofeedback
in the
GLAXXJW MS, GAARDNER KR, ENGEL BT, Behavioural treatment of high blood pressure: II Acute and sustained effects of relaxation and systolic blood pressure biofeedback. Psychosom Med 1982;
44: 155-171. 10. GOLDSTEIN lB, SHAPIRO D, THANAOPAVARAN C. Comparison of drug and behavioural treatments of essential hypertension. Hlth Psycholl982; 1: 7-26. 11. JOHNSTON DW, LETHEM J. The production of specific decreases in interbeat interval and the motor skill analogy. Psychophysioll981; 18: 288-300. 12. JOHNSTON DW. Biofeedback, relaxation and related procedures in the treatment of psychophysiological disorders. In Health Care and Human Behaviour (Edited by STEPTOE A, MATHEWS A), pp. 267-300. London: Academic Press, 1984. 13. PATEL C, NORTH WRS. Randomised controlled trial of yoga and biofeedback in the management of hypertension. Lancet 1975; II: 93-95. 14. PATEL C, MARMOT MG, TERRY DJ. Controlled trial of biofeedback-aided behavioural methods in reducing mild hypertension. Br Med J 1981; 282: 2005-2008. 15. BALI LR. Long- term effect of relaxation on blood pressure and anxiety levels in essential hypertensive males: A controlled study. Psychosom Med 1979; 41: 637-646. 16. TAYLOR CB, FARQUHAR JW, NELSON E, AGRAS WS. Relaxation therapy and high blood pressure.
Arch Gen Psychiat 1977; 34: 339-342. 17. 18. 19. 20. 21. 22.
BRAUER A, HORLICK LF, NELSON B, FARQUHAR JU, AGRAS WS. Relaxation therapy for essential hypertension: a Veterans Administration out-patients study. JBehav Med 1979; 2: 21-29. SOUTHAM MA, AGRAS WS, TAYLOR CB, KRAEMER HC. Relaxation training: Blood pressure during the working day. Arch Gen Psychiat 1982; 39: 715-717. CROWTHER JH. Stress management training and relaxation imagery in the treatment of essential hypertension. JBehavMed 1983; 6: 169-187. SEER P, RAEBURN JM. Meditation training and essential hypertension: a methodological study. J Behav Med 1980; 3: 59-73. GOLDSTEIN IB, SHAPIRO D, THANOPAVARAN C. Home relaxation techniques for essential hypertension. Psychosom Med 1984; 46: 399-414. CHARLESWORTH EA, WILLIAMS BJ, BAER PE. Stress management at the worksite for hypertension: compliance, cost-benefit, health care and hypertension-related variables. Psychosom Med 1984;
46: 387-397. 23. 24. 25.
AGRAS WS, SOUTHAM MA, TAYLOR BC. Long-term persistence of relaxation-induced blood pressure lowering during the working day. J Cons C/in Psycho1 1983; 51: 792-794. LITTLE BE, HAYWORTH J, BENSON P, HALL F, BEARD RW, DEWHURST J, PRIEST RG. Treatment of hypertension in pregnancy by relaxation and biofeedback. Lancet 1984; 1: 865-867. PATEL C, MC, DJ, M, B, M. of in coronary four follow BrMed 1985; 1103-l
26.
J, of
27.
DW, hypertension. A, A.
Self-regull982; TASTO
HUEBNER
CR, the
30.
DW. of JE,
Behav 31.
32.
GV.
and
for control
cardiovascular
The
of
relaxation
Ther
14:
management
the
to
tasks.
149-166. Behav
29.
D,
self-control the interval pulse time. DL, effects muscle
Ther
stress response
Med on
blood
the
pressure
exercise
of
feedback
46: of
hyper-
13:
P, L, R, H. pressure, rate resniratorv to single of a replication.-JPsychosom Res 1978; 22: 493-501 .I JACOB RG, BEADEL DC, SHAPIRO AP. The relaxation word of the day: a simnle techniaue to measure
adherence to relaxation. JBehav Assess 1984; 6: 159-165. PATEL C. Yoga and biofeedback in the management of ‘stress’ in hypertensive patients. Clin Sci MolecMed 1975; 28: Suppl; 171-174. 34. JORGENSEN RS, HOUSTON BK, ZURAWSKI RM. Anxiety management training in the treatment of essential hypertension. Behav Res Therap 1981; 19: 467-474. 35. STONE RA, DELEO J. Psychotherapeutic control of hypertension. NEng JMed 1976; 294: 80-84. 36. COTTIER C, SHAPIRO K, JULIUS S. Treatment of mild hypertension with progressive muscle relaxation: predictive value of indexes of sympathetic tone. Arch Intern Med 1984; 144: 1954-1958. 37. MCGRADY AV, YONKER R, TAN SY, FINE TH, WOERNER M. The effect of biofeedback-assisted relaxation on blood pressure and selected biochemical parameters with essential hypertension. Biofeed Self-reg 198 1; 6: 343-354.
33.
DEREK W. JOHNSTON
456 38.
POLLACK AA, WEBER MA, CASE DB, LARAGH JH. Limitations of transcendental meditation in the treatment of essential hypertension. Lancet 1977; 1: 71-72. 39. GOLDSTEIN DS. Plasma catecholamines and essential hypertension: An analystical review. Hypertension 1983; 5: 86-99. 40. ESLER M, JULIUS S, ZWEIFLER A, RANDALL 0, HARBURG E, GARDINER H, DEQUATTRO V. Mild highrenin essential hypertension. Neurogenic human hypertension. NewEng JA4ed 1973; 269: 405-411. 41. JULIUS S, ESLER M. Autonomic nervous cardiovascular regulation in borderline hypertension.
A J Cardioll975; 36: 685-696. 42.
JACOB RG, KRAMER HG, AGRAS WS. Relaxation
therapy in the treatment of hypertension.
Arch Gen
Psychiat 1977; 34: 1417-1427. 43. 44.
PETERS RK, BENSON H, PETERS JM. Daily relaxation breaks in a working population: II Effects on blood pressure. Am JPublic Health 1977; 67: 954-959. WADDEN TA. Predicting treatment response to relaxation therapy for essential hypertension. J Nerv
Ment Dis 1983;171:683-689. 45. The Review Panel on Coronary-Prone
Behaviour and Coronary Heart Disease, Coronary-prone behaviour and coronary heart disease: A criticarreview. Circulation 1981; 63: 1199-1215. 46. JOHNSTON DW. Behavioural treatment in the reduction of coronary risk factors: Type A behaviour and blood pressure. Br J C/in Psycho1 1982; 21: 281-294. 47. FRIEDMAN M, THORESEN CE, GILL CE, ULMER D, THOMPSON L, POWELL L, PRICE V, ELEK SR, RABIN DD, BREALL WS, PIAGET G, DIXON T, BOURG E, LEVY RA, TASTO DL. Feasibility of altering Type A behaviour patterns after myocardial infarction. Recurrent coronary prevention project study: Methods, baseline results and preliminary findings. Circulation 1982; 66: 83-92. 48. FRIEDMAN M, THORENSEN CE, GILL JJ, POWELL LH, ULMER D, THOMPSON L, PRICE V, RABIN DD, BREALL WS, DIXON T, LEVY R, BOURG E. Alteration of Type A behaviour and reduction in cardiac recurrences in post-myocardial infarction patients. Am Heart J 1984; 108: 237-248. 49. GRUEN W. Effects of brief psychotherapy during the hospitalization period on the recovery process in heart attacks. JConsult Clin Psycho1 1975; 43: 223-232. 50. CROMWELL RL, BUTTERFIELDEC, BRAYFIELD FM, CURRY JJ. Acute myocardial infarction: reaction and recovery. Mosby; St. Louis, 1977. 51. CROMWELL RL, LEVENKRON JC. Psychological care of acute coronary patients. In Health Cure and Human Behaviour (Edited by STEPTOE A, MATHEWS A), pp. 209-229. Academic Press; London, 1984. 52. NAISMITH LD, ROBINSON JF, SHAW GB, MACINTYRE MMJ. Psychosocial rehabilitation after infarction. BrMed J 1979; 1: 439-442. 53. IBRAHIM MA, FELDMAN JG, SULLTZ HA, STAIMAN MC, YOUNG LJ, DEAN D. Management after myocardial infarction: a controlled trial of the effects of group psychotherapy. Int J Psychiut Med 1974; 5: 253-268. 54. RAHE RH, WARD H, HAYNES V. Brief group therapy in myocardial infarction: three to four year follow up of a controlled trial. Psychosom Med 1979; 41: 229-241. 55. MAYOU R, MACMAHON D, SLEIGHT P, FLORENCIO MJ. Early rehabilitation after myocardial infarction. Lancer 1981; 11: 1399-1401. 56. SHAW L. Effects of a prescribed, supervised exercise program on mortality and cardiovascular morbidity in myocardial infarction subjects. Am JCurdioll981; 48: 39-46. 57. STERN MJ, CLEARY P. National exercise and heart disease project. Psychosocial changes observed during a low-level exercise program. Arch Intern Med 1981;141: 1463-1467. 58. STERN MJ, CLEARY P. The national exercise and heart disease project. Long-term psychosocial outcome. Arch Intern Med 1982; 142: 1093-1097. 59. STERN MJ, GORMAN PA, KASLOW L. The group counselling versus exercise therapy study: a controlled intervention with post myocardial infarction subjects. Arch Intern Med 1983; 143: 1719-1725. 60. LOWN B, VERRIER RL, RABINOWITZ SH. Neural and psychologic mechanisms and the problem of sudden cardiac death. Am J Cardioll977; 39: 890-902.