Psychosomatic Study of Angina Pectoris HITOSHI ISHIKAWA, M.D., INEKO TAWARA, M.D., HIROKO OHTSUKA, R.N., MACHIKO TAKEYAMA, R.N., and TACHIO KOBAYASHI, M.D. • In the medical history, the first exact description of the clinical symptoms, of angina pectoris was made by Heberden. At that time he already mentioned that the anginal attack was induced by emotional stress. Since then, the relationship between the anginal attack and emotion have been studied by many researchers with clinical description and experimental study using animals or humans. And few doubt the fact that anginal attack is induced by emotion. In our country, many reports were presented concerning the relationship between emotion and anginal attack or ST-T change in the ECG by Kanehisa 14 , Ikemi 1c" Hinohara 1 \ Kobayashii. and Ishikawa l8 • Our present study was done in an attempt to analyze the mechanism of emotional angina (angina induced by emotion) in statistical and experimental study. MATERIAL AND METHOD Subjects: Forty-four cases of myocardial infarction, 44 cases of angina pectoris, 12 cases of coronary sclerosis. A total of 100 cases having anginal pain. To these patients, a questionnaire study on anginal pain, Cornell Medical Index (CMI) and Yatabe-Guilford personality test were administered. Twenty-four cases out of these were selected for the following procedure: Using going-up-and-down-stairs exercise as the physical loading and life history taking as the emotional loading, continuous ECG was recorded by telemetering method and blood pressure was measured repeatedly. Urinary catecholamine excretion level before and after the loading (by Lund's modified method), as well as measurements of levels of blood POe, PCO e, pH, base excess (Astrup method), lactic acid and pyruvic acid concentration (enzyme method, UV test) were all done. From Fourth Depa,'tment of Internal Medicine, The Faculty of Medicine, The University of Tokyo.
390
RESULTS 1. Questionnaire study A questionnaire was given to 100 subjects with anginal pain from the clinic and hospitalized patients of our hospital. It was found that anginal attacks occurred with the following causes: 39 by physical stress, 3 by coldness, 4S by both physical and emotional stress and 13 during rest. Approximately one half of the total number developed anginal pain because of both physical and emotional stress. The results of the Cornell Medical Index questionnaire and the Yatabe-Guilford personality test of the two groups, namely the subjects who developed anginal pain by physical and emotional stress and those who developed anginal pain by physical stress alone were compared. Some neurotic tendencies were observed in the Cornell Medical Index results of the former group; however, no specific differences in the personality pattern were found in the Yatabe-Guilford personality test.
II. Experimental study An experimental study of anginal attack induced by emotional stress was attempted. The methods used were: 1) Hypnotic suggestion; 2) Stress interview; 3) Intake of life history including incidence of illness. The findings of the three methods were compared. Under hypnosis, suggestions concerning anginal attack were made and continuous recording of the electrocardiogram by the telemetering method was employed. As is shown in Fig. 1, one subject among four studied showed increase in heart rate through suggestion, however, there was no change in electrocardiogram. Stress interview was performed on 7 subjects and the changes in ECG were observed by the same telemetering method. The content of the interview included conversation on sudden death caused by anginal attack, informing the patient of the ECG change ocVolume XII
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curring during the interview and other stressful topics. As in shown in Fig. 2, only one subject showed an increase in heart rate and ST-T change in the ECG. No anginal attack occurred. An interview to take the patient's life history as usually performed in clinical practice was done while observing the changes in the ECG. Among 4 subjects studied, 3 showed an increase in heart rate, change in ECG and developed an anginal attack when a specific topic was discussed. As an experimental method, in comparison to the hypnotic suggestion or stress interview, the taking of the patient's life history proved to be more effective in producing emotional
stress meaningful to the individual which in turn induced anginal pain. This fact indicates the apparent difference of emotional stress for each individual. It is interesting to note that the past social incidence influences the present emotional status of the patient most strongly in developing an anginal attack. In studying the reproducibility of emotionally induced angina, the same stress condition was repeated in 3 cases. As is shown in Fig. 3, in one case, even after one year, the same ECG change appeared. However, in the other two, the reaction became weaker by the repetition of interview. (According to our study, the upright of the T is considered bad, as same as, the upright of ST.)
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391
PSYCHOSOMATICS again. At that time, his heart rate was stable, but the same ECG change was observed. However, the physical reaction as a whole became less intense as the interview was repeated. This patient was introspective and had a hypochondriac attitude toward illness. Moreover he was not content with the compensation settlement for the accident. During the interview, when the issue was mentioned, he openly expressed hostility toward the one who had injured him. His attacks seemed to be a secondary gain. Case 2. This 63-year-Old male's father died when the patient was 3 years old. After his mother's remarriage, he was brought up by his aunt. At the age of 32, he was involved in an accident while working in factory and had a leg amputation. This patient was hospitalized for 2 months with the diagnosis of angina pectoris and during his stay in hospital, we performed 5 interviews with the same procedure. Each time, at the mention of the accident, the patient became excited and an increase in heart rate with ECG change were simultaneously observed. Following that, an anginal attack was induced. His character in general was self-controlling but he had occasional outbursts of temper.
III. Case Reports Case 1. This 55-year-old male was involved in a traffic accident 6 months prior to admission and since then he began to complain of a slight tightening sensation in the left side of his chest, left shoulder and left arm. Although he himself saw these symptoms as the sequelae of the traffic accident, he was diagnosed as a myocardial infarction and was admitted to our hospital. His hospital course showed progressive improvement. So after 2 months his doctor told him that he could leave the hospital. Following that his attacks returned with frequency and his discharge was postponed. As his attacks decreased again in frequency, he was told that he might leave the hospital. Again, his symptoms returned. All in all, he stayed in the hospital for 10 months. During his hospital stay, we performed 3 experimental interviews. During the first and the third interview, the patient revealed an increase in heart rate, ST-T change in the ECG and developed an anginal attack at the mention of the traffic accident. Taking medicine (Propranolol) in the second interview, he showed no marked change in heart rate and had no anginal attack. One year after discharge, he was examined
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ANGINA PECTORIS-ISHIKAWA ET AL.
'Through the repeated interview, he obtained insight as to the relationship between his emotional states and anginal attacks and has begun to control his emotions. The physical reaction itself decreased in severity as the interview was repeated, at the 6th interview performed one year later, he showed no physical change.
As shown in both cases, patients initially revealed such reactions as increase in heart rate, elevation of blood pressure, change in ECG and development of an anginal attack in close association with emotional changes. However, as the interview was repeated, these
reactions became less intense. In the first case, the patient maintained his hypochondriacal attitude toward illness. He was anxious about the increase in heart rate during the interview, which resulted in a vicious circle psychosomatically. He continued to reveal the same reaction to the stress produced by interview and his frequent attacks developed each time. On the contrary, the second case acquired the proper insight into the psychosomatic relationships. The heart rate became stable and the number of attacks lessened.
Change in Heart Rote and E.C.G. duri"9 Interview concerning Life History Co.. H.M.
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had a leg amputation. There was a great amount of bleeding." Figure 5 November-December 1971
393
PSYCHOSOMATICS
position, acid-base balance, pyruvic acid, lactic and urine catecholamine excretion were measured before and after both stresses were given. In comparing the number of anginal attacks induced by both stresses, 9 developed an anginal attack by physical stress and 7 showed ECG changes alone. By emotional stress, 3 developed an anginal attack and 6 showed changes in the ECG alone. The percentage of attacks induced by physical stress were greater. As is shown in Fig. 6, with physical stress, there was increase in heart rate;
IV. Physiological study In order to analyze the developmental mechanism of an emotionally induced anginal attack, a physiological study was attempted of those who developed angina by physical stress and those who developed angina by emotional stress. Twenty-four subjects with coronary heart disease were studied. Physical stress was given by having the subject climb up and down stairs; for emotional stress, an interview on the patient's life history was performed. The heart rate, blood pressure, blood gas com-
Physiological Change during Emotional and Physical Stress HR
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Change in Heart Rate under Emotional Stress • Effort Angina o Emotional Angina
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394
Volume
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ANGINA PECTORIS-ISHIKAWA ET AL.
with emotional stress, the rise in blood pressure was significant. As for the blood composition, through physical stress, there was increase in POt, decrease in PCO t , decrease in blood pH, decrease in base excess and increase in lactic acid. These effects were not noted with emotional stress. The urine catecholamine excretion was not effected. It was found that there was a definite difference in the physiological mechanism between physical stress and emotional stress; nevertheless, there was no qualitative difference in the physiological pattern of the group developing an anginal attack or ECG change from the group who showed no change. A quantitative difference was observed in those developing an attack or change in ECG. In order to find the physical and psychological condition in which anginal attacks occur, the characteristics of the 11 subjects who develooed angina by physical stress (effort angina) and 5 subjects who developed angina by physical and emotional stress (emotional angina) were compared. There was no significant difference in ~ex, age and cardiovascular findings. In comparing heart rate and blood pressure prior to the stress, in the group of emotional angina, even before the stress was given, there was a faster heart rate and elevation in minimum blood pressure with no difference in maximum blood pressure in comparison with the group of effort angina. The increase in heart rate and rise in maximum and minimum blood pressure were significant in the group of emotional angina. From abovementioned facts, it is speculated that in the subjects reactive to emotional stress, the stress is already acting on the subjects even before the interview, which is indicated by the heart rate and blood pressure. In studying the psychological difference of the 2 groups through the findings from the Cornell Medical Index and Yatabe-Guilford personality test, it was found that in both groups, in the Cornell Medical Index, the score on cardiovascular complaints (column c) and the score on aggressiveness, column o of the emotional complaints were high. There were no differences in the groups. However, when an accident or problem in the famNovember-December 1971
ily or work were discussed, anxiety toward an anginal attack was brought out, consisting of an emotional reaction with hostility or anxiety coupled with a change in heart rate and blood pressure, followed by a change in ECG. DISCUSSION
Coronary insufficiency is the condition in which Ot supply through the coronary artery does not meet the O 2 demand of the myocardium. Consequently, the myocardium is in a state of hypoxia. Coronary insufficiency can be caused by either an over-demand of Ot or an abnormal decrease of supply. Increased demand occurs under such condition as exercise or emotional stress. Both increase the work load of the myocardium. Decrease in Ot supply can be caused by decreased coronary blood flow due to coronary stenosis or spasm, and lowered Ot blood saturation. If we focus upon emotion, increased demand arises from increased heart rate due to emotional changes, increased myocardial work load due to elevated blood pressure or increased myocardial 0" demand due to the direct influence of such agents as catecholamines on the myocardium. A decreased supply arises from coronary sp2sm through the autonomic nervous system secondary to emotional changes, leading to transient coronary stenosis and subsequent decrease in coronary blood flow. Recently, by dint of coronary arteriography, the !'resence of transient spasm of coronary artery has been demonstrated. Therefore it is generally accepted, based on firmer facts that in the mechanism of coronary insufficiency by emotional changes, increased demand plays a more important role. Raab" et al asserted that in the increased myocardial O 2 demand by emotional chang-e, catecholamines and corticosteroids are working as mediators. Raab 10 and Krzywanek observed an increase in heart rate and elevation of blood pressure under sensory and mental stress in healthv subjects. And these findings were more marked among the emotionally unstable. NestelP' found that, compared with the control group, the coronary patient is likely to show a higher degree of such reaction as 395
PSYCHOSOMATICS
increase in heart rate increase in urinary excretion of catecholamines and VMA excretion by emotional stress. Robinson 5 insists that the increased myocardial O 2 demand resulting from an increased heart rate and elevated blood pressure must be the prime factor in the etiological mechanisms of an anginal attack induced by exercise and emotional stress. The results of our study coincided with his findings. Yet by comparing exercise loading with emotional loading, it was observed that the former is more likely to induce an increase in heart rate and the latter an elevation of blood pressure. From these facts, we assume that the different stress have different loading effects on the myocardium. As to the personality traits of coronary patients, Dunbar12 described them as follows' self-controlled, persevering, over-endeavour~ plan successful, capacity of steady application toward this goal. However, generally speaking, researchers today are critical of the idea that patients of a certain disease have characteristic personality traits. Rosenman 13 proposed the idea of ''behavior pattern." And as a behavior pattern of coronary patients, he proposed behavior pattern A, that is, aggressive, ambitious, impulsive. competitive and energetic in personality and in behavior, very strong, speedy, rapid-speaking, restless and short tempered. Physically, hypercholesteremia and hypertension are commonly found. This behavior pattern interacts with the external environment and the behavior of pattern A happens to correspond well to the urban life of civilized western society. And this may explain the high incidence of coronary disease amonS?; those who live in a civilIi zed urban society. The aim of our study was not to study personality traits of coronary patients but to know whether those who developed angina pectoris through emotional stress have special traits both physically and psychologically compared with the other types of angina. As already mentioned, we did not find any particular deviation in personality traits. As for 396
physical traits, they often showed large fluctuation in heart rate and blood pressure. CONCLUSION
1) Some anginal attacks are induced by emotional stress; however the majority are also induced by physical stress and only few by emotional stress alone. 2) As a method for experimental emotional stress, the interview method including the patient's life history and past illnesses proved to be most effective in inducing anginal attacks. 3) The increase in heart rate is significant after physical stress along with hyperventilation and lactic acidosis. With emotional stress, the rise in blood pressure is significant. The physiological mechanism differs in both stress conditions. 4) As a physical characteristic of subjects reacting to emotional stress, the heart rate and blood pressure are unstable and easily tend to became elevated. As a result, it is speculated that the myocardial energy expenditure increases producing changes in the electrocardiogram and is then followed by an anginal attack. As a psychological characteristic, emotional reactions such as anxiety and hostility toward the source of trauma, disease and problems in human relationship were significant. Acknowledgment: The authors wish to thank Professor Ikemi of Kyushu University for his guidance and advice in carrying out this study.
REFERENCES 1. White, P.D.: Heart Disease. MacMillan Co.,
New York, 1951. 2. Schimert, G. : Die
Coronarerkrankungen. Handbuch der Inneren Medizin. (Bergmann)
Band 9, Teil 3, Springer-Verlag, Berlin, 1961. 3. Dreyfuss, F.: Role of emotional stress preceding coronary occlusion. Am. J. Cardiol., 3: 590, 1959. 4. Sprague, H.B.: Emotional factors in coronary heart disease. Circulation, 23: 648, 1961. 5. Robinson, RE.: Relation of heart rate and systolic blood pressure to the onset of the pain in angina pectoris. Circulation, 35: 1073, 1967. 6. Friedberg: Disease of the heart. Saunders Co., Philadelphia, 1956. 7. Wolf, S.: Cardiovascular reactions to symbolic stimuli. Circulation, 11: 287, 1958. Volume XII
ANGINA PECTORIS-ISHIKAWA ET AL. 8. Minc, S.: Emotions and ischemic heart disease. Am. Heart J., 73: 713,1967. 9. Raab, W.: Prevention of ischemic heart disease. C.C. Thomas. Springfield, 1966. 10. Raab, W.: Emotional and sensory stress factors in myocardial pathology. Am. Heart J., 72: 538, 1966.
173: 1320, 1960. 14. Kanehisa, T.: Emotion and electrocardiogram change. Saishinigaku, 18: 1961, 1963 (in
Japanese). 15. Ikemi, U.: Neurosis and PSD. Gendainaikagaku taikei, 5, Nakayama Publisher, 1960 (in
Japanese).
11. Nestel, P. J.: Catecholamine secretion and
16. Hinohara S. and Shinoda, T.: Emotional fac-
sympathetic nervous responses to emotion in men with and without angina pectoris. Am.
tors in angina pectoris. Sei8hinshintaiigaku, 3: 257,1963 (in Japanese). 17. Kobayashi, T.: Stress and coronary heart disease. Saishinigaklt 18: 113, 1963 (in Japanese). 18. Ishikawa, H.: Psychosomatic study on angina pectoris. Second International Congress for PSM and Hypnosis. Abstracts of papers p.
Heart J., 73: 227,1967. 12. Dunbar. F.: Emotions and bodily change. Columbia Univ. Press, New York, 1954. 13. Rosenman, R. H.: Overt behavior pattern in
coronary disease; detection of overt behavior pattern A in patient with coronary disease by a new psychophysiological procedure. JAMA,
49, 1967.
The American Society 0/ Psychoanalytic Physicians announces its policy of admitting all physicians to its varied categories of membership. Psychoanalytic psychodynamics are considered by the Society to be vital in understanding human behavior and relationships. In these troubled times, it is especially imperative that physicians become thoroughly acquainted with psychodynamics to improve their skills in relating to patients. The Society provides an open forum 'n psychoanalytic medicine and plans ultimately to establish a training program for all interested physicians. Your inquiry is invited. GEORGE J. TRAIN, M.D. Past President and Editor of Newsletter 371 Parkside Avenue Brooklyn, N.Y. 11226
November-December 1971