CIinical Science and Molecular Medicine (1975) 48, 171s-174s. Yoga and biofeedback in the management of ‘stress’ in hypertensive patients C. PATEL Croydon, Surrey Summary 1. Psychophysical relaxation exercises based on yogic principles and reinforced by biofeedback instruments were used for behaviour modification in sixteen hypertensive subjects. 2. Preliminary studies indicated that their pressor response to emotional and physical stimuli became less exaggerated and less protracted compared with controls. Key words: behaviour therapy, biofeedback, emotional stress, environmental stress, hypertension, operant conditioning, pressor response, psychophysiological exercises, Yoga. Introduction Physical and emotional stimuli are effective in modifying blood pressure in man. Pressor responses to various stimuli are exaggerated and protracted in hypertensive patients (Brod, Fencl, Heji & Jirka, 1959; Brod, 1960, 1963, 1970; Shapiro, 1961; Sokolow, Werdegar, Perloff, Cowan & Brenenstuhl, 1970; Amery, Julius, Whitlock & Conway, 1967; Sannerstedt, 1966; Wolf, Pfeiffer, Riply, Winter & Wolf, 1948). The true pressure load on the left ventricle and vessel walls is neither the resting pressure nor the occasional peak of pressure in response to a mental or emotional stress but the integrated average pressure over longer periods. Anti-hypertensivedrugs taken in adequate amounts lower the resting pressures but there is no evidence that they prevent the pressure rises associated with intermittent excitatory discharges provoked by events in daily life. As Smirk (1967) has pointed out, the physiologically induced peaks of increased pressure in response to emotions are added to a high base-line pressure and the two together carry the final height of the pressure to degrees which contribute to the hypertensive cardiovascular disease. As the subjects get older, various organs begin to deteriorate under the onslaught of the transient pressure elevations. Intensive emotional disturbances are known to precede complications like the malignant phase of hypertension (Reiser, Rosenman & Ferris, 195 I ) , congestive heart failure (Chambers & Reiser, 1953), or myocardial infarction (Russek, 1967). Cardiovascular complications may be precipitated by emotional tension (Reiser rt a/., 1951; Chambers & Reiser, 1953). The advantages of any therapy that could reduce the magnitude or duration of these pressure rises are obvious. Significant reduction in blood pressure from relaxation exercises, with or without biofeedback, have been reported previously (Datey, Deshmukh, Dalvi & Vinekar, 1969; Patel, 1973; Patel & Datey, 1974a, b; Shapiro, Tursky & Schwartz, 1971 ; Benson, Rosner & Marzetta, 1974; Elder & Rinz, 1973; Deabler, Fidel, Dillenkoffer & Elder, 1973). Although no long-term follow-up results have yet been published one group has been followed up for 1 year now with very satisfactory maintenance of reduction of blood pressure (unpublished work). This communication presents the results of a preliminary investigation to see if the regular practice of such an exercise could alter the pressor response to ‘stress’. Patients Thirty-two patients, twenty-one females and eleven males, between the ages of 34 and 75 years (average age 5 8 5 ) , with essential hypertension of known duration from 6 months to 13 years (average = 5.7 years) were randomly divided into a treatment group Correspondence: Dr Chandra Patel, 1 I Upfield, Croydon, Surrey. 171s C . Patel 172s and a control group. Fourteen patients in the treatment group and fifteen in the control group were receiving anti-hypertensive drugs. Methods The patients were given two ‘stress’ tests: an exercise test’ and a ‘cold pressor test’ at the beginning, and repeated after 6 weeks. Base-line blood pressure was first obtained after a 20 rnin rest in the supine position. The exercise test consisted of climbing a 9 inch step twenty-five times. I n the cold pressor test, the patient was alerted 60s in advance about the test to be performed; the left hand was then immersed in water at 4°C for 80 s. Blood pressure was taken during the alert, at the end of each test and every 5 min until it returned to the original value or up to a maximum of 40 min. All the measurements were taken by a trained nurse using a mercury sphygmomanometer. The maximum rise in systolic and diastolic pressures as well as the time taken for ‘recovery’ in each case were recorded. Differences in the above measurement obtained during the repetition of the tests were compared within the groups as well as between the groups by Student’s t-test. In the 6 weeks’ between-tests period, all patients attended the clinic twice weekly. The patients in the treatment group were given 30 min of training in relaxation and meditation based on yogic principles. This training was reinforced, with biofeedback instruments giving auditory signals relating to galvanic skin resistance, electromyographic activity and alpha waves in the electroencephalograph. TABLE 1. Changes in blood pressure (B.P.) and recorery times for the exercise test and cold pressor test in treated and untreated groiips of patients For details of tests and treatment see the Methods section. Pre. = first tcst; Post. = test repeated after 6 weeks. N.S. = Not significant. Systolic B.P. Max. rise (mmHg) -_ Exercise test Treatment group ( n = 16) Pre. Post. Diff. P Control group ( n = 16) Pre. Post Diff. P Treatment vs. control group difference Cold pressor test Treatment group ( n = 16) t = P = Pre. Post. Diff. P Control group ( n = 16) Treatment vs. control group difference 18.43 8.75 9.68 9.25 4.12 5.13 13.12 6.25 6.87 <0.005 <0.05 < 0.05 29.62 26.87 2.75 N.S. 18.13 17.20 0.93 N.S. 3.8 1 7.3 I 3.50 N.S. 5.62 13.62 8.00 N.S. 0.9725 = P = 2.6216 2.6493 3.9868 N.S. < 0.02 < 0.02 <0.001 19.31 10.75 8.56 < 0.025 18.12 5.62 12.50 7.3 I 2.19 5.12 < 0.005 < 0.005 12.8 I 4.69 8.12 < 0.025 14.37 17.50 -3.12 N.S. 6.06 14.56 - 8.5 N.S. 4.68 13.75 - 9.07 N.S. N.S. t Recovery time (rnin) 27.43 18.8 I 8.62 <0.025 - 11.50 P Max. rise (mmHg) - 22.31 33.81 Pre. Post. Diff. Recovery time (rnin) Diastolic B.P. 3.2581 io.01 3.41 65 < 0.01 4.8049 < 0~001 3.572 < 0.01 Yoga and stress in hypertension (For details of principle and procedures see Kamiya, Barber, Dicava, Miller, Shapiro & Stoya, 1971; Shapiro, Barber, Dicara, Kamiya, Miller & Stoyva, 1973.) Patients were asked to practise relaxation and meditation at home twice daily for 20 min. They were also asked to make frequent checks of their tension and quick relaxation several times a day. Red traffic lights, ringing telephones and other personal situations served as signals to perform quick relaxation lasting 30 s to 3 min. Results During the alert preceding the cold pressor test the blood pressure rose in most patients. The changes were of small magnitude and were not statistically analysed. Other results are given in Table 1. In the treatment group there was a significant reduction in the ‘pressure rises’ as well as in recovery time (P<O.O5). Mere repetition of the tests did not influence these indications of ‘stress’, as is shown by the results in the control group; some measurements increased. When the differences between the groups were compared by unpaired t-tests, all measurements except the systolic pressure rise after exercise showed significant improvement in the treated group (P < 0.02). Discussion The mean response to ‘stress’ became less exaggerated and less protracted in the group whose behaviour was modified as a result of training in the psychophysical exercise. Assuming that systolic elevation primarily indicates increase in cardiac output and that during exercise most of the increase would be in proportion to the metabolic demand, one could not expect a great deal of reduction in the systolic rise due to relaxation training except for the rise that could possibly be due to emotional aspects of the exercise (Wolf, Carbon, Shepard & Wolf, 1955). However, the mechanism of systolic elevation probably differs in different age groups and it is impossible to make any simple deduction (Amery et al., 1967). Two to three patients in the treatment group during pre-treatment tests and two to three patients in the control group during pre- as well as post-control tests failed to recover or reach the original level of blood pressure in the designated 173s time. However, when the tests were repeated after the relaxation training, every patient recovered. There are several deficiencies in the data. It is known that circulatory readjustment starts as soon as the event is over. A continuous automatic measurement of blood pressure during and after the test would be more suitable. Since the measurements are intermittent, the calculated recovery time is only approximate. Most of the patients were on anti-hypertensive drugs, which might have altered the response. However, since we are concerned with the change in response rather than the actual response, the data are in this respect still valid. It is difficult to know what situations will produce ‘stress’ response in our highly complex environment, in which psychological and socio-economic patterns are changing at an accelerated pace. Continuous understanding of the relationship of environmental ‘stress’ to cardiovascular pathology and effective ways of coping with ‘stress’ could lead us to new preventive and therapeutic approaches. Results of this preliminary investigation clearly justify further research, Acknowledgments This study was supported by a Research Grant from the South West Thames Regional Health Authority. I thank Professor K. Datey, Emeritus Professor of Cardiology, K.E.M. Hospital, Bombay, for his advice on the design of the experiment. I also thank Professor T. Pilkington of St George’s Hospital for his helpful suggestions and advice in writing this paper. References AMERY, A., JULIUS,S., WHITLOCK, L.S.& CONWAY, J. (1967) Influence of hypertension on haemodynamic response to exercise. Circulation, 36, 231-237. B. (1974) Decreased BENSON, H., ROSNER, B.A. & MARZETTA, blood pressures in pharmacologically treated hypertensive patients who regularly elicited the relaxation response. Loncet, i, 289-291. BROD, J. (1960) Essential hypertension. Haemodynamic observations with bearing on its pathogenesis. Lanret, ii, 773-778. BROD, J. (1963) Haemodynamic basis of acute pressor reactions and hypertension. 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