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Type A behavior: A frequently misdiagnosed and rarely treated medical disorder
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Type A behavior: A frequently misdiagnosed and rarely treated medical disorder Meyer Friedman, M.D. San Francisco, Calif.
Ever since 1959 when I and Rosenman ~ first described the overt components of type A behavior and called attention to its possible relationship to the premature onset of clinical coronary heart disease (CHD), I have continued to attempt to discover as much as I could about the nature of this behavior. Thus, I and various colleagues 2-7 discovered in the 1960s and early 1970s that type A behavior could elevate the serum Cholesterol, triglyceride, norepinephrine, adrenocorticotropic hormone (ACTH), and testosterone levels, perhaps accounting for possible damage to blood vessels. Most of these biochemical and hormonal findings have been confirmed, s-9 As these laboratory studies were being done, Rosenman and I in 1960 and 1961 initiated the Western Collaborative Group Study ~° to determine whether type A behavior possessed predictive power for the incidence of clinical CHD. Results n showed that the behavior was a contributing factor. These findings subsequently were confirmed by the Framingham investigators 12 and other epidemiologic groups. In 1977 and 1978, several of us 13 attempted to modify type A behavior in postinfarction subjects. Although this study was planned to run for 5 years, a special committee from the National Heart, Lung, and Blood Institute, after perusing the data, concluded that the study should be discontinued because they believed it was obvious, even at the end of 3 years, that the data demonstrated that type A behavior could be modified and the cardiac recurrence rate dramatically lowered in the experimental group given type A counseling."' ~5 A subsequent study 18 that involved for the first time healthy officers at the Army War College,
From the Meyer Friedman Institute, Mt. Zion Hospital and Medical Center. Received for publication Oct. 22, 1987; accepted Dec. 1, 1987. Reprint requests: Meyer Friedman institute, Mt. Zion Hospital and Medical Center, San Francisco, CA 94120.
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Carlisle, Pa., demonstrated that modification of type A behavior also could be achieved in normal middle-aged individuals. As my associates and I were conducting these studies, several groups of epidemiologists reported 17'18 that they were not able to find any relationship whatsoever between type A behavior and the future incidence of either first or recurrent myocardial infarctions. Also, several other investigatorsl~. 2o reported that of the two overt components (impatience and hostility) that comprised type A behavior, only hostility appeared to them to be "toxic." I shall now discuss these recent studies. First, I believe that we were responsible to some degree for the recent confusing results because in our first publication I describing type A behavior we designated it as an emotional complex rather than what it really is, namely, a medical disorder. A second mistake we made at the outset was to describe our examination as an interview. The third error was the failure of the editor of the Journal of the American Medical Association in 1964 to allow us to describe in the article we submitted 1° precisely how we diagnosed type A behavior. He insisted (to save some printing costs) that this description be printed in an appendix that would not be published when the article first appeared but in reprints: As a result, probably few investigators had the opportunity to read the warning that we printed in italics in that appendix. Certainly it cannot be stressed too greatly that the correct diagnosis of a subject depends far more upon his motor and emotional qualities (i.e., his physical signs and symptoms) accompanying his response to specific questions than the actual content of his answers. To minimize or to misunderstand this last differential is to fail in the correct behavioral assessment of a subject. Unfortunately, this warning went completely unheeded by the biostatisticians, biometricians, epidemiologists, and academic psychologists who, not
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recognizing that type A behavior was a medical disorder and not being familiar with or possessing expertise in clinical diagnostic methodology, attempted to accomplish the detection of type A behavior by requesting their subjects to respond to a stereotyped series of questions presented to them either in the form of a questionnaire or similar questions presented to them by nonprofessional, skimpily trained persons. Unfortunately, most epidemiologists, biometricians, and perhaps the majority of academic psychologists have had little or no clinical experience with coronary patients. If they had such experience, they would recognize that although almost every patient with CHD exhibits type A behavior, 13by no means are all of them either aware of or consciously willing to admit their possession of impatience and/or free-floating hostility. These investigators, intent on obtaining data that appeared to permit objective analysis, were not cognizant of the subjective provenance of the data they obtained. Perhaps the saddest example of what can happen when sophisticated statistics are coupled with clinical obtuseness was the results obtained by Shekelle et slY in the MRFIT study and Case et al. TM in the Multicenter Post Infarction Research Group study. TM Shekelle et al.~7 at the outset only administered to the approximate 12,000 MRFIT enrollees a questionnaire that contained nothing designed to detect the possible presence of free-floating hostility, one of the two components of type A behavior.* Seeking apparently to correct this egregious error in design, these same investigators decided to assemble a series of questions derived from those I constructed over 27 years ago for our interviewers in the WCGS. ~° Except as Scherwitz23 correctly pointed out, they arbitrarily, without truly testing the coronary validity of their questions, employed ad hoc, poorly chosen, inadequately trained, nonprofessional clerks to present the questions to 3110 of their MRFIT subjects. Shekelle et al. 17 repeatedly called attention to what they believed was the pristine loveliness of their design, pointing out how well trained their interviewers were and that Dr. Rosenman served to select and teach the interviewers and also arbitrate differences when they arose. All this sounds good on paper, but actually the training of most of the MRFIT interviewers was done by two nonprofessional women who had worked for me *I cannot understand why, despite our repeatedly emphasizing since 1969~' and thereafter L3"~5.22that free-floating hostility is one of the two overt components of type A behavior, various investigators continue to separate hostility from type A behavior. How can one take one half of a disorder and t r e a t it as unrelated to the disorder of which it is a major component?
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at the Brunn Institute, Mount Zion Hospital & Medical Center, San Francisco. One of these two persons was never employed as an examiner, and the second I found unable to function credibly as an examiner. Dr. Scherwitz, in studying why the MRFIT interviews failed to predict CHD in the 3110 subjects, compared the behavior of the MRFIT interviewers with that of the WCGS examiners who I had trained in 1960 and 1961 and who did find type A behavior predictive of increased incidence of clinical CHD. He discovered that the WCGS examiners, unlike the MRFIT interviewers, were first clinically oriented to recognize type A behavior as it presented itself in patients with CHD. They thus knew what to look for in a clinical sense. He also found that the WCGS examiners, unlike the majority of MRFIT interviewers, evinced real interest in their interviewees, interrupted far less frequently, and asked questions that were not stereotyped or necessarily forescheduled but were tailored to the interviewees' circumstances. Frequently the MRFIT interviewers were abrupt and interrupted interviewees to ask them the next question from their list before the interviewees had time to answer the question first presented to them. The MRFIT interviewers also appeared aggressive or presented the questions in a singsong, totally disinterested manner. In short, the examiners trained for the WCGS conducted themselves as truly caring persons who were intent not to check off a list of questions but to diagnose the presence or absence of a medical disorder. The MRFIT interviewers were instructed to act, and most did act, as "human questionnaires." After reading the findings and preliminary conclusions of Scherwitz,23it is easy to understand why the five or six ad hoc lay interviewers proved unable to provide a predictive relationship between type A behavior and incidence of future infarctions. I believe I can understand too, why Rosenman24 is reported to have said that the interviewing in the MRFIT study was sadly deficient. He also added that he did not select the interviewers and that he refused to train some of them because they were so incompetent. Of course, if the situation were as bad as Dr. Rosenman now describes it, I do not understand why he continued to participate in the study. Dr. Rosenman is not correct in believing that subjects with true type A behavior refrained from enrolling in the MRFIT study. I say this because it has been our experience that individuals who possess an elevated serum cholesterol level almost always exhibit type A behavior; likewise, persons who smoke excessively or have hypertension also almost
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always exhibit type A behavior. Because all MRFIT subjects have at least two of these three putative coronary risk factors, I believe that well over 90 % of them had type A behavior. Indeed one of the Chicago interviewers diagnosed 98 % of the MRFIT subjects she questioned as subjects with type A behavior,23 and one of the San Francisco interviewers also had to b e "reinstructed" by one of the epidemiologists because she too initially adjudged all the MRFIT subjects she questioned as exhibiting type A behavior. I believe that if the epidemiologists in charge of the program had first acquainted themselves with and had received instruction concerning the clinical subtleties of type A behavior and its extraordinarily close relationship to hypertension, hypercholesterolemia, and excessive cigarette smoking, they would have known from the start that the labeling of such a large fraction of their heavily smoking, hypercholesterolemic, and hypertensive subjects as type B signaled some grievous error in their diagnostic procedure, but this was not done. In view of this clinical naivet~, I believe it is understandable why Dr. Scherwitz, after carefully studying the mechanical, abrasive behavior of most of the MRFIT interviewers, concluded that "because there is substantial circumstantial evidence indicating that measurement errors occurred, the MRFIT type A findings should be interpreted with extreme caution." The Wall Street Journal, much less diplomatic than Dr. Scherwitz, labeled the MRFIT project (costing the taxpayers $110 million) "a debacle." If we have been correct in our own observations concerning halving the coronary recurrence rate in postinfarction subjects given type A behavioral counseling, the widely disseminated negative findings of the MRFIT study have delayed the introduction of a procedure that could have prolonged the lives of hundreds of thousands of patients with CHD; this was not just a debacle, it was and is an avoidable tragedy of huge proportions. There is a second epidemiologic study conducted clinically even more erroneously than the MRFIT study, which I shall describe now. In November 1983, at the annual meeting of the American Heart Association and 16 months later in the New England Journal of Medicine, Case et al.ls reported the results of their 1- to 3-year follow-up of 866 patients who, while still hospitalized (in nine different hospitals located in New York, Rochester, N.Y., St. Louis, and Tucson) and suffering from an acute myocardial infarction, were given the Jenkins' questionnaire25to be filled out by the nurses caring for them. Their results suggested to Case et al.18 that postinfarction subjects who registered a high score
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on the Jenkins' questionnaire later had no greater mortality from CHD than postinfarction subjects who registered a low score on the same questionnaire, and consequently they were classified as type B. These conclusions not only were widely disseminated by all components of the media but Dr. Case also prepared a cassette describing his views, which was packaged attractively in an advertising brochure (announcing in bold type that the "myth of type A" was exposed) and was distributed widely by a pharmaceutical company intent on selling its particular cardiac drug. Now I should like to point out some of the facts of which most writers (particularly free-lance journalists) who referred to this study apparently were not aware. Fact 1. Fully a year before Case et al. 18published their 1985 article, I sent at Case's request, seven references to articles that we had written in the 1970s in which we had warned that the Jenkins' questionnaire contained nothing designed to detect the presence of hostility, one of the two basic overt components of type A behavior. Fact 2. Again, approximately a year before the article, is I had pointed out repeatedly to Dr. Case that we had been describing type A behavior as consisting of both impatience and free-floating hostility. Nevertheless, in the article, Case et al. 18 arbitrarily assumed that hostility and type A behavior were separate entities. Certainly if a physician refers to a disorder that we first described, it seems to me that this same physician should accept our description of the disorder's components and not arbitrarily isolate one of these two components and assume that it is a disorder separate from that of which it is a component. Fact 3. The 1985 articleis also was published despite my journey 11 months earlier to Dr. Case's hospital, where I demonstrated to him and his associates that in employing clinical diagnostic procedures, they could detect the presence of severe type A behavior in the postinfarction patients (one of whom was a cardiologist) whom they had presented to me as postinfarction patients with type B behavior. Indeed the hostility of one of these patients became so severe that the examination had to be discontinued abruptly. Fact 4. Even if a questionnaire could be depended on to detect the presence of a medical disorder, the presentation of a series of questions concerned with excess competitive drive, aggressiveness, and impatience to a patient while he is still struggling for his life (and possibly still in shock and pain, suffering
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from a life-threatening arrhythmia, receiving intravenous therapy, and above all,is extremely anxious) and the expectation of a correct response is something that even an amateur psychologist would know is clinical folly, as Halperin and Littman ~ and Abbott et al.27 pointed out in their criticisms of this same study. N o amount of sophisticated statistical maneuvers of data received under such dreadful clinical circumstances can obscure or make up for the fundamental error of erroneous clinical design. Yet this was precisely what was done by Case et al.18 when they ordered coronary care nurses to distribute the Jenkins' questionnaire to patients stillsuffering from an acute myocardial infarction. Fact 5. It was only when the Jenkins' questionnaires were collected from the nine hospitals, after they had been distributed i to 3 years earlierto their acutely illpatients, that Case et al.TM discovered that 40 % of the expected 866 questionnaires could not be found. A n unexplained loss of 4 0 % of the initial cohort of experimental subjects of course renders the results of any epidemiologic study questionable. The authors accordingly explained that "retrospective contact with nurses who had enrolled patients in the study indicated that the predominant reason for non-participation was a lack of fluency in the English language." H o w m a n y nurses from each of the nine hospitals were questioned? H o w m a n y of the nurses giving the questionnaires i to 3 years earlier were still available for such questioning? Precisely what questions were asked of these nurses? W h a t responses were received? The investigators did not say. Moreover, it is not accurate to describe individuals who were enrolled as "nonparticipants" solely because 1 to 3 years later no response from them to a questionnaire could be found. Again, no amount of statisticalsophistication can obscure this example of clinicalsloppiness. I a m emphasizing this last shoddiness of experimental procedure for several reasons. First, because the authors insisted in the discussion of their 1985 publication 18 that their 866 postinfarction population was a representative American population. If this were so, then what the authors were suggesting is that 40 % of all American postinfarction patients are illiterate,as they intimate their cohort was. This, of course, is sheer demographic nonsense, as all American cardiologists will recognize. Certainly in our Recurrent Coronary Prevention Project, in enrolling 1065 participants from the San Francisco Bay area (containing as m a n y or more nonwhite minorities as some of the cities from which Case et al.~8 obtained their patients), we were not able to find a single person who could not complete the
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forms we asked them to fill out. If, however, we only began to collect and examine our forms 3 years later, we might have lost some. Then if we asked some nurse or technician why the forms were lost, they conceivably might have told us that it was because many of our subjects were illiterate. Even if such had taken place, we would have had enough common sense not to publish such guesses as scientific data. We also would have been ashamed to do so. Second, the coronary mortality suffered by those 350 "non-participants" of the study by Case et ai.,ls whose questionnaires could not be found was twice that of the "participants" whose questionnaires could be found. Thus, failure to find a questionnaire supposedly given I to 3 years earlier to patients who were suffering from an acute infarction appeared to be as forbidding a risk factor as a low ejection fraction or frequent ventricular premature contractions. This finding serves as a signal warning of what can occur in a study when clinical common sense gives way to statistical preoccupation! In short, employing a tool that was found useless a decade earlier for the diagnosis of type A behavior, being unable to retrieve the same diagnostic tool from 40% of their participants 1 to 3 years later, concluding (depending on the unchecked memory of perhaps several nurses) that this 40% of their patients could not read or write English, and finally, ignoring the fact that hostility is one of the two major components of type A behavior, Case et al.18 published this article that can only impede and not advance our knowledge of the role of the central nervous system in the pathogenesis of clinical CHD. Certainly their publication furnishes no luster either to the medical school that supported it or the journal that published this study. It would not be fair to criticize the M R F I T study or that of Case et al.18 and fail to mention that I believe that we also made a serious error in failing to detect in 1960 and 1961 the presence of type A behavior in participants of the WCGS 1° who possessed this behavior and later developed clinical CHD. One of the chief reasons for this failure was our inability then to differentiate hostility from what we considered excessive aggression. It was not until 19692~ that we discovered that besides impatience, hostility also was an overt component of type A behavior, and in 197422 we described methods of modifying this particular component. As a consequence, many hostile subjects in 1960 and 1961 were incorrectly diagnosed as individuals with type B behavior. Also, at that earlier period we had not yet discovered a number of physical signs that indicate the presence of type A behavior in over 95% of
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patients with CHD. 18In short, I believe that in 1960 and 1961 if we had the diagnostic armamentarium we now possess, we would have labeled as type A ~lmost every WCGS participant who subsequently died from clinical CHD during the next decade.* Despite the relatively rudimentary diagnostic procedure employed in the WCGS in 1960 and 1961,l° the incidence of clinical CHD in participants who were diagnosed as having type A behavior was significantly greater than that found in participants who had been labeled type B when they were reexamined 8~/2 years later. 11Moreover, despite the above described deficiencies in our earlier attempts to diagnose types A and B behavior, even when the WCGS participants were surveyed by Ragland** et al.~ 22 years later (chiefly by postcard or telephone) and when they all were over 60 years of age (many over 75 years of age), nevertheless the coronary mortality of those subjects diagnosed 22 years earlier as exhibiting type A behavior was 26 % greater than participants diagnosed as type B. This study, however, has many deficiencies, not least of which was the failure of the authors to have any kind of clinical contact with the participants. Accordingly, all their data are those obtained 22 years after their subjects were diagnosed. What changes and in which subjects behavioral changes occurred during the hiatus of at least 14 years of no clinical contact cannot even be guessed at in this study. It also is extremely puzzling to me how after a lapse of 22 years the authors were able to trace, with the exception of approximately 30 subjects, 99 % of the 3154 initially enrolled participants. This is particularly puzzling when it was reported 4½ years after this same study that 45 subjects could not be found, and after 8~/2 years approximately 228 of the 3154 participants could not be traced. 11 Certainly in the RCPP we made every effort to keep track of our 862 subjects; nevertheless, in just 4~/2 years we were unable to trace 82 subjects. Given these discrepancies, I remain mystified by this reported follow-up achievement of Ragland et ai.2s During the past decade several investigators, 19'2° while recognizing that hostility had earlier been described as one of the two components of type A *I say this because, as already stated, we detected in the RCPP ~3 the presence of type A behavior in over 95% of the 966 successively admitted postinfarction subjects. **Ragland and another statistician recently reported 3~that in their 14-year postcard follow-up of 257 coronary patientS, patients classified as type B 28 years ago died more frequently than those classified as type A. These authors, however, did not mention that a number of these same coronary patients received type A behavioral counseling for 4~/2 years following their first infarction in the Recurrent Coronary Prevention Project. Although there were a number of other serious flaws in this study, this avoidable omission alone invalidates the results of their study.
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behavior, nevertheless believe it alone is the "toxic factor." Here again, reliance on questionnaires rather than direct examination of patients with CHD had been employed. Williams et al.,19 for example, leaned heavily on the later coronary mortality of medical students who scored positively many years earlier on the Cook-Medley Hostility questionnaire. However, McCramie et al. ~ studied the later coronary morbidity and mortality of medical students who took the same questionnaire before and again after entering medical school and found no evidence whatsoever to indicate that the hostility observed in their subjects was followed decades later by increased incidence of coronary morbidity or mortality. Does this report of McCramie et al. 29 mean that Williams et al. lg and Dembroski et al. 2° were wrong in believing that hostility (one of the two major components of type A behavior) has relevance to the pathogenesis of clinical CHD? Not at all. What it does mean, however, is that the use of any type of questionnaire to diagnose or detect a medical disorder is essentially fallible. For example, I asked 22 of our ambulatory, symptomless coronary patients to respond to the Cook-Medley questionnaire. Although all 22 participants exhibited two or more neurologic signs indicative of the presence of hostility, only 10 scored as hostile persons on the questionnaire. I believe that the hostility component of type A behavior is "toxic" and agree with Dembroski et al. ~° that if subjects seethe rather than vent their anger, they may be more likely to have sustained higher levels of norepinephrine, ACTH, testosterone, and excess wasting of growth hormone.3°Despite, however, close questioning of hundreds of patients with CHD, neither they nor I am willing to absolve impatience, the other major component of type A behavior, from "toxic" responsibility. Let clinicians and researchers recognize that even if only hostility had relevance to clinical CHD, nothing intensifies hostility more certainly than impatience. It also is important to bear in mind that according to the Oxford English Dictionary, irritability and irascibility are given as synonyms of impatience. These two states are varieties of hostility. Certainly if my colleagues do not recognize this last truth, I doubt if they have had much clinical contact with coronary patients. However, I am more than a little surprised at how few investigators who write articles about type A behavior ever actually treat patients with CHD. I end this editorial by pointing out that the true "'toxic" factor in type A behavior is the inadequate security and self-esteem that initiates and fuels the
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CARDIAC COUNSELING (Sectioe !) TYPE A/CARDIAC COUNSELING (Section 2)
8.07.OCUMULATIVE ANNUALiZED RECURRENCE RATE (PERCENT)
6.05.04.03.0~
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e
9 I~' is is El 2 ' 4 u 30 ~3 ~ . .ONT.S or OaSERVAT*ON
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Fig. 1. This graph illustrates the cumulative, annualized recurrence rate in postinfarction patients who (1) received group cardiac counseling (upper curve) and (2) received group cardiac and type A behavioral counseling (lower curve). Note that the 95 % confidence limits of the respective recurrence rates no longer intersect at the end of 36 months. After the first year, significantly fewer (p <:0.05) cardiac deaths occurred in the group given type A counseling in addition to cardiac counseling. (From Friedman M. AM HEARTJ 1986;112:659.)
emergence of impatience and hostility. It is this emotional malady, often deeply anchored, that was the target we dealt with in the RCPP. I believe also that it was our ability to enhance the security and/or self-esteem of so many of our participants that was responsible for the halving of the coronary recurrence rate of the type A counseled postinfarction participants in the RCPP. 1~ Although these latter results were published in 1984, not a single reference to the probable causal role of insecurity and/or inadequate self-esteem (in the pathogenesis of type A behavior) appeared in the July 1987 Circulation monograph, sl reporting the proceedings of the special conference (jointly sponsored by the American Heart Association and the National Heart, Lung, and Blood Institute) dealing with behavioral medicine and cardiovascular disease. I believe this omission in the 227-page monograph, which otherwise contained 39 reports (including those of 15 "task force" committees), is rather tragic. Again let me warn, as we unsuccessfully attempted to do in 1959 when we introduced the type A concept, that it will not be easy for just any psychiatrist, psychologist, or cardiologist to replicate the results that we obtained in the R C P P ~3-15or at the U.S. Army War College. ]6 Successful reduction in type A behavior depends in great part on certain qualities of the group counselor. He or she does not need to be a psychiatrist, psychologist, or
cardiologist.* However, he or she should possess integrity, ability to care for others, a minimum of certain type A characteristics himseff or herself, and a capacity to convince others concerning adoption of new belief systems and new ways of doing things. The group counselor also must possess good judgment, ability to laugh at himself or herself, and a basic knowledge of the humanities. Obviously such counselors are not easy to find, but we found them for the RCPP, the War College studies, and for our ongoing group counseling program in the San Francisco Bay area. I believe that eventually a group of counselors will be found whose results in reducing the intensity of type A behavior and the recurrence rate of coronary accidents will exceed those obtained in the RCPP. 1315Ideally, such competent counselors can be found and should be subsidized as soon as possible because hundreds of tholx~ands of Americans are dying prematurely from CHD who could be saved (Fig. 1). I might add that when such qualified counselors are found and if the design of the study is planned by physicians possessing clinical acumen, the R C P P results can be replicated at a cost of one-fiftieth that of the ill-designed, ill-fated M R F I T study. Finally, it is wise to keep in mind that diagnostic *One of the most successful modifiers of type A behavior is Col. Frederick Drews, Director of the Army Physical Fitness Research Institute at the Army War College, Carlisle, Pa.
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discoveries, whether they had to do with the detection of such disparate diseases as Addison's, Alzheimer's, or more recently, acquired immunodeficiency syndrome were anecdotal not epidemiologic or statistical accomplishments. I do not believe this mode of discovery is or soon will become obsolete. REFERENCES
1. Friedman M, Rosenman RH. Association of specific overt behavior pattern with blood and cardiovascular findings. JAMA 1959;76:1286. 2. Friedman M, Byers SO, Rosenman RH, Elevitch FR. Coronary prone individuals (type A behavior pattern): some biochemical characteristics. JAMA 1970;212:1030. 3. Friedman M, Byers SO, Rosenman RH. Serum lipids and conjunctival circulation after fat ingestion in men exhibiting Type A behavior pattern. Circulation 1964;29:874. 4. Friedman M, St. George S, Byers SO, Rosenman RH. Excretion of catecholamines 17-ketosteroids, 17-hydroxy-corticolds and 5-hydroxy-indole in men exhibiting a particular behavior pattern (A), associated with high incidence of clinical coronary heart disease. J Clin Invest 1960;39:758. 5. Friedman M, Byers SO, Dimnont J, Rosenman RH. Plasma cateCholaInine response of coronary-prone subjects (.Type A) to a special challenge. Metabolism 1975;25:205. 6. Friedman M, Byers SO, Rosenman RH. Plasma ACTH and cortisol concentration of coronary prone subjects. Proc Soc Exp Biol Med 1972;140:681. 7. Zumoff B, Rosenfeld RS, Friedman M, Byers SO, Rosenman RH, Hellman L. Elevated daytime urinary excretion of testosterone glucuromide in men with the Type A behavior pattern. Psychosom Med 1984;40:223. 8. Grundy SM, Griffin AC. Effects of periodic medical stress on serum cholesterol levels. Circulation 1959;19:490. 9. Williams RB, Lane JD, Kuhn CM, Meosh W, White AD, Shanberg SM. Type A behavior and elevated physiological and neuroendocrine responses to cognitive tasks. Science 1982;218:483. 10. Rosenman RH, Friedman M, Straus R, et al. A predictive study of coronary heart disease. The Western Collaborative Group Study. JAMA 1964;189:15. 11. Rosenman RH, Brand RJ, Jenkins CD, Friedman M, Straus R, Wurm M. Coronary heart disease in the Western Collaborative Group Study: final follow-up experience of 81/2 years. JAMA 1975;233:872. 12. Haynes SG, Feinleib M, Levine S, Scotch N, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study. III. Eight year incidence of coronary heart disease. Am J Epidemiol 1980;111:37. 13. Friedman M, Thoresan CE, Gill JJ, et al: Feasibility of altering Type A behavior pattern after myocardial ;nfarction. Recurrent Coronary Prevention Project study: methods, baseline results and preliminary findings. Circulation 1982; 66:83. 14. Friedman M, Thoresen CE, Gill JJ, et al. Alteration of Type
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A behavior and reduction in cardiac recurrences in post myocardial infarction patients. AM HEARTJ 1984;108:237. 15. Friedman M, Thoresen CE, Gill JJ, et al. Alteration of Type A behavior and its effect on cardiac recurrences in post myocardial infarction patients: summary results of the Recurrent Coronary Prevention Project. AM HEARTJ 1986; 112:653. 16. Gill JJ, Price VA, Friedman M, et al. Reduction of Type A behavior in healthy middle-aged American military officers. AM HEARTJ 1985;!10:503. 17. Shekelle R, Hully SB, Neaton J, et al. The MRFIT behavior pattern study. II. Type A behavior and incidence of coronary heart disease. Am J Epidemiol 1985;122:555. 18. Case RH, Hiller SS, Case NB, Moss AJ, Multicenter Post Infarction Research Group. Type A behavior and survival after acute myocardial infarction. N Engl J Med 1985; 312:737. 19. Williams RB, Barefoot JC, Shekelle RB. The health consequences of hostility. In: Chesney MA, Rosenman RH, eds. Anger, hostility and behavioral medicine. New York: McGraw-Hill, 1985:173. 20. Dembroski TM, MacDougall JM, Williams RB, Harley TL, Blumenthal JA. Components of Type A, hostility and anger in; relationship to angiographic findings. Psychosom Med 1985;47:219. 21. Friedman M. The pathogenesis of coronary artery disease. New York: McGraw-Hill, 1969. 22. Friedman M, Rosenman RH. Type A behavior and your heart. New York: Alfred A. Knopf, 1974. 23. Scherwitz L. Interviewer stylistics and Type A predictiveness for CHD incidence: clues for an engagement hypothesis. Presented to Kansas Series in Clinical Psychology, May 10-11, 1986, Lawrence, Kansas. 24. Rosenman RH. As quoted in Psychology Today. "Type A on trial." 1987;Feb:46. 25. Jenkins CD, Rosenman RH, Zyzonski SJ. Prediction of clinical coronary heart disease by a test for the coronary prone behavior pattern. N Engl J Med 1974;290:1271. 26. Halperin PJ, Littman AB. Letter to the Editor. N Engl J Med 1985;310:431. 27. Abbott AV, Peters BK, Vogel ME. Letter to the Editor. N Engl J Med 1985;310:431. 28. Ragland DR, Brand RJ, Rosenman RH, Newmann R. Coronary heart disease mortality in the Western Collaborative Group Study: follow-up experience of 22 years. A m J Epidemiol (In press). 29. McCramie EW, Watkins LO, Brandsma JM, Sisson BD. Hostility, coronary heart disease (CHD) incidence and total mortality: lack of association in a 25-year follow-up study of 478 physicians. J Behav M e d 1986;9(2):119. 30. Friedman M, Byers SO, Rosenman RH, Newmann R. Coronary prone individuals (Type A behavior pattern). Growth hormone responses. J A M A 1971;217:929. 31. Conference on behavioral medicine and cardiovascular disease [Monograph 6]. Circulation 1987;76: 32. Ragland DR, Brand RJ. Type A behavior and mortailityfrom coronary heart disease. N Engl J Med 1988;318:65.
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Type A behavior: A frequently misdiagnosed and rarely treated medical disorder Meyer Friedman, M.D. San Francisco, Calif.
Ever since 1959 when I and Rosenman ~ first described the overt components of type A behavior and called attention to its possible relationship to the premature onset of clinical coronary heart disease (CHD), I have continued to attempt to discover as much as I could about the nature of this behavior. Thus, I and various colleagues 2-7 discovered in the 1960s and early 1970s that type A behavior could elevate the serum Cholesterol, triglyceride, norepinephrine, adrenocorticotropic hormone (ACTH), and testosterone levels, perhaps accounting for possible damage to blood vessels. Most of these biochemical and hormonal findings have been confirmed, s-9 As these laboratory studies were being done, Rosenman and I in 1960 and 1961 initiated the Western Collaborative Group Study ~° to determine whether type A behavior possessed predictive power for the incidence of clinical CHD. Results n showed that the behavior was a contributing factor. These findings subsequently were confirmed by the Framingham investigators 12 and other epidemiologic groups. In 1977 and 1978, several of us 13 attempted to modify type A behavior in postinfarction subjects. Although this study was planned to run for 5 years, a special committee from the National Heart, Lung, and Blood Institute, after perusing the data, concluded that the study should be discontinued because they believed it was obvious, even at the end of 3 years, that the data demonstrated that type A behavior could be modified and the cardiac recurrence rate dramatically lowered in the experimental group given type A counseling."' ~5 A subsequent study 18 that involved for the first time healthy officers at the Army War College,
From the Meyer Friedman Institute, Mt. Zion Hospital and Medical Center. Received for publication Oct. 22, 1987; accepted Dec. 1, 1987. Reprint requests: Meyer Friedman institute, Mt. Zion Hospital and Medical Center, San Francisco, CA 94120.
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Carlisle, Pa., demonstrated that modification of type A behavior also could be achieved in normal middle-aged individuals. As my associates and I were conducting these studies, several groups of epidemiologists reported 17'18 that they were not able to find any relationship whatsoever between type A behavior and the future incidence of either first or recurrent myocardial infarctions. Also, several other investigatorsl~. 2o reported that of the two overt components (impatience and hostility) that comprised type A behavior, only hostility appeared to them to be "toxic." I shall now discuss these recent studies. First, I believe that we were responsible to some degree for the recent confusing results because in our first publication I describing type A behavior we designated it as an emotional complex rather than what it really is, namely, a medical disorder. A second mistake we made at the outset was to describe our examination as an interview. The third error was the failure of the editor of the Journal of the American Medical Association in 1964 to allow us to describe in the article we submitted 1° precisely how we diagnosed type A behavior. He insisted (to save some printing costs) that this description be printed in an appendix that would not be published when the article first appeared but in reprints: As a result, probably few investigators had the opportunity to read the warning that we printed in italics in that appendix. Certainly it cannot be stressed too greatly that the correct diagnosis of a subject depends far more upon his motor and emotional qualities (i.e., his physical signs and symptoms) accompanying his response to specific questions than the actual content of his answers. To minimize or to misunderstand this last differential is to fail in the correct behavioral assessment of a subject. Unfortunately, this warning went completely unheeded by the biostatisticians, biometricians, epidemiologists, and academic psychologists who, not
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recognizing that type A behavior was a medical disorder and not being familiar with or possessing expertise in clinical diagnostic methodology, attempted to accomplish the detection of type A behavior by requesting their subjects to respond to a stereotyped series of questions presented to them either in the form of a questionnaire or similar questions presented to them by nonprofessional, skimpily trained persons. Unfortunately, most epidemiologists, biometricians, and perhaps the majority of academic psychologists have had little or no clinical experience with coronary patients. If they had such experience, they would recognize that although almost every patient with CHD exhibits type A behavior, 13by no means are all of them either aware of or consciously willing to admit their possession of impatience and/or free-floating hostility. These investigators, intent on obtaining data that appeared to permit objective analysis, were not cognizant of the subjective provenance of the data they obtained. Perhaps the saddest example of what can happen when sophisticated statistics are coupled with clinical obtuseness was the results obtained by Shekelle et slY in the MRFIT study and Case et al. TM in the Multicenter Post Infarction Research Group study. TM Shekelle et al.~7 at the outset only administered to the approximate 12,000 MRFIT enrollees a questionnaire that contained nothing designed to detect the possible presence of free-floating hostility, one of the two components of type A behavior.* Seeking apparently to correct this egregious error in design, these same investigators decided to assemble a series of questions derived from those I constructed over 27 years ago for our interviewers in the WCGS. ~° Except as Scherwitz23 correctly pointed out, they arbitrarily, without truly testing the coronary validity of their questions, employed ad hoc, poorly chosen, inadequately trained, nonprofessional clerks to present the questions to 3110 of their MRFIT subjects. Shekelle et al. 17 repeatedly called attention to what they believed was the pristine loveliness of their design, pointing out how well trained their interviewers were and that Dr. Rosenman served to select and teach the interviewers and also arbitrate differences when they arose. All this sounds good on paper, but actually the training of most of the MRFIT interviewers was done by two nonprofessional women who had worked for me *I cannot understand why, despite our repeatedly emphasizing since 1969~' and thereafter L3"~5.22that free-floating hostility is one of the two overt components of type A behavior, various investigators continue to separate hostility from type A behavior. How can one take one half of a disorder and t r e a t it as unrelated to the disorder of which it is a major component?
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at the Brunn Institute, Mount Zion Hospital & Medical Center, San Francisco. One of these two persons was never employed as an examiner, and the second I found unable to function credibly as an examiner. Dr. Scherwitz, in studying why the MRFIT interviews failed to predict CHD in the 3110 subjects, compared the behavior of the MRFIT interviewers with that of the WCGS examiners who I had trained in 1960 and 1961 and who did find type A behavior predictive of increased incidence of clinical CHD. He discovered that the WCGS examiners, unlike the MRFIT interviewers, were first clinically oriented to recognize type A behavior as it presented itself in patients with CHD. They thus knew what to look for in a clinical sense. He also found that the WCGS examiners, unlike the majority of MRFIT interviewers, evinced real interest in their interviewees, interrupted far less frequently, and asked questions that were not stereotyped or necessarily forescheduled but were tailored to the interviewees' circumstances. Frequently the MRFIT interviewers were abrupt and interrupted interviewees to ask them the next question from their list before the interviewees had time to answer the question first presented to them. The MRFIT interviewers also appeared aggressive or presented the questions in a singsong, totally disinterested manner. In short, the examiners trained for the WCGS conducted themselves as truly caring persons who were intent not to check off a list of questions but to diagnose the presence or absence of a medical disorder. The MRFIT interviewers were instructed to act, and most did act, as "human questionnaires." After reading the findings and preliminary conclusions of Scherwitz,23it is easy to understand why the five or six ad hoc lay interviewers proved unable to provide a predictive relationship between type A behavior and incidence of future infarctions. I believe I can understand too, why Rosenman24 is reported to have said that the interviewing in the MRFIT study was sadly deficient. He also added that he did not select the interviewers and that he refused to train some of them because they were so incompetent. Of course, if the situation were as bad as Dr. Rosenman now describes it, I do not understand why he continued to participate in the study. Dr. Rosenman is not correct in believing that subjects with true type A behavior refrained from enrolling in the MRFIT study. I say this because it has been our experience that individuals who possess an elevated serum cholesterol level almost always exhibit type A behavior; likewise, persons who smoke excessively or have hypertension also almost
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always exhibit type A behavior. Because all MRFIT subjects have at least two of these three putative coronary risk factors, I believe that well over 90 % of them had type A behavior. Indeed one of the Chicago interviewers diagnosed 98 % of the MRFIT subjects she questioned as subjects with type A behavior,23 and one of the San Francisco interviewers also had to b e "reinstructed" by one of the epidemiologists because she too initially adjudged all the MRFIT subjects she questioned as exhibiting type A behavior. I believe that if the epidemiologists in charge of the program had first acquainted themselves with and had received instruction concerning the clinical subtleties of type A behavior and its extraordinarily close relationship to hypertension, hypercholesterolemia, and excessive cigarette smoking, they would have known from the start that the labeling of such a large fraction of their heavily smoking, hypercholesterolemic, and hypertensive subjects as type B signaled some grievous error in their diagnostic procedure, but this was not done. In view of this clinical naivet~, I believe it is understandable why Dr. Scherwitz, after carefully studying the mechanical, abrasive behavior of most of the MRFIT interviewers, concluded that "because there is substantial circumstantial evidence indicating that measurement errors occurred, the MRFIT type A findings should be interpreted with extreme caution." The Wall Street Journal, much less diplomatic than Dr. Scherwitz, labeled the MRFIT project (costing the taxpayers $110 million) "a debacle." If we have been correct in our own observations concerning halving the coronary recurrence rate in postinfarction subjects given type A behavioral counseling, the widely disseminated negative findings of the MRFIT study have delayed the introduction of a procedure that could have prolonged the lives of hundreds of thousands of patients with CHD; this was not just a debacle, it was and is an avoidable tragedy of huge proportions. There is a second epidemiologic study conducted clinically even more erroneously than the MRFIT study, which I shall describe now. In November 1983, at the annual meeting of the American Heart Association and 16 months later in the New England Journal of Medicine, Case et al.ls reported the results of their 1- to 3-year follow-up of 866 patients who, while still hospitalized (in nine different hospitals located in New York, Rochester, N.Y., St. Louis, and Tucson) and suffering from an acute myocardial infarction, were given the Jenkins' questionnaire25to be filled out by the nurses caring for them. Their results suggested to Case et al.18 that postinfarction subjects who registered a high score
April 1988 American Heart Journal
on the Jenkins' questionnaire later had no greater mortality from CHD than postinfarction subjects who registered a low score on the same questionnaire, and consequently they were classified as type B. These conclusions not only were widely disseminated by all components of the media but Dr. Case also prepared a cassette describing his views, which was packaged attractively in an advertising brochure (announcing in bold type that the "myth of type A" was exposed) and was distributed widely by a pharmaceutical company intent on selling its particular cardiac drug. Now I should like to point out some of the facts of which most writers (particularly free-lance journalists) who referred to this study apparently were not aware. Fact 1. Fully a year before Case et al. 18published their 1985 article, I sent at Case's request, seven references to articles that we had written in the 1970s in which we had warned that the Jenkins' questionnaire contained nothing designed to detect the presence of hostility, one of the two basic overt components of type A behavior. Fact 2. Again, approximately a year before the article, is I had pointed out repeatedly to Dr. Case that we had been describing type A behavior as consisting of both impatience and free-floating hostility. Nevertheless, in the article, Case et al. 18 arbitrarily assumed that hostility and type A behavior were separate entities. Certainly if a physician refers to a disorder that we first described, it seems to me that this same physician should accept our description of the disorder's components and not arbitrarily isolate one of these two components and assume that it is a disorder separate from that of which it is a component. Fact 3. The 1985 articleis also was published despite my journey 11 months earlier to Dr. Case's hospital, where I demonstrated to him and his associates that in employing clinical diagnostic procedures, they could detect the presence of severe type A behavior in the postinfarction patients (one of whom was a cardiologist) whom they had presented to me as postinfarction patients with type B behavior. Indeed the hostility of one of these patients became so severe that the examination had to be discontinued abruptly. Fact 4. Even if a questionnaire could be depended on to detect the presence of a medical disorder, the presentation of a series of questions concerned with excess competitive drive, aggressiveness, and impatience to a patient while he is still struggling for his life (and possibly still in shock and pain, suffering
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from a life-threatening arrhythmia, receiving intravenous therapy, and above all,is extremely anxious) and the expectation of a correct response is something that even an amateur psychologist would know is clinical folly, as Halperin and Littman ~ and Abbott et al.27 pointed out in their criticisms of this same study. N o amount of sophisticated statistical maneuvers of data received under such dreadful clinical circumstances can obscure or make up for the fundamental error of erroneous clinical design. Yet this was precisely what was done by Case et al.18 when they ordered coronary care nurses to distribute the Jenkins' questionnaire to patients stillsuffering from an acute myocardial infarction. Fact 5. It was only when the Jenkins' questionnaires were collected from the nine hospitals, after they had been distributed i to 3 years earlierto their acutely illpatients, that Case et al.TM discovered that 40 % of the expected 866 questionnaires could not be found. A n unexplained loss of 4 0 % of the initial cohort of experimental subjects of course renders the results of any epidemiologic study questionable. The authors accordingly explained that "retrospective contact with nurses who had enrolled patients in the study indicated that the predominant reason for non-participation was a lack of fluency in the English language." H o w m a n y nurses from each of the nine hospitals were questioned? H o w m a n y of the nurses giving the questionnaires i to 3 years earlier were still available for such questioning? Precisely what questions were asked of these nurses? W h a t responses were received? The investigators did not say. Moreover, it is not accurate to describe individuals who were enrolled as "nonparticipants" solely because 1 to 3 years later no response from them to a questionnaire could be found. Again, no amount of statisticalsophistication can obscure this example of clinicalsloppiness. I a m emphasizing this last shoddiness of experimental procedure for several reasons. First, because the authors insisted in the discussion of their 1985 publication 18 that their 866 postinfarction population was a representative American population. If this were so, then what the authors were suggesting is that 40 % of all American postinfarction patients are illiterate,as they intimate their cohort was. This, of course, is sheer demographic nonsense, as all American cardiologists will recognize. Certainly in our Recurrent Coronary Prevention Project, in enrolling 1065 participants from the San Francisco Bay area (containing as m a n y or more nonwhite minorities as some of the cities from which Case et al.~8 obtained their patients), we were not able to find a single person who could not complete the
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forms we asked them to fill out. If, however, we only began to collect and examine our forms 3 years later, we might have lost some. Then if we asked some nurse or technician why the forms were lost, they conceivably might have told us that it was because many of our subjects were illiterate. Even if such had taken place, we would have had enough common sense not to publish such guesses as scientific data. We also would have been ashamed to do so. Second, the coronary mortality suffered by those 350 "non-participants" of the study by Case et ai.,ls whose questionnaires could not be found was twice that of the "participants" whose questionnaires could be found. Thus, failure to find a questionnaire supposedly given I to 3 years earlier to patients who were suffering from an acute infarction appeared to be as forbidding a risk factor as a low ejection fraction or frequent ventricular premature contractions. This finding serves as a signal warning of what can occur in a study when clinical common sense gives way to statistical preoccupation! In short, employing a tool that was found useless a decade earlier for the diagnosis of type A behavior, being unable to retrieve the same diagnostic tool from 40% of their participants 1 to 3 years later, concluding (depending on the unchecked memory of perhaps several nurses) that this 40% of their patients could not read or write English, and finally, ignoring the fact that hostility is one of the two major components of type A behavior, Case et al.18 published this article that can only impede and not advance our knowledge of the role of the central nervous system in the pathogenesis of clinical CHD. Certainly their publication furnishes no luster either to the medical school that supported it or the journal that published this study. It would not be fair to criticize the M R F I T study or that of Case et al.18 and fail to mention that I believe that we also made a serious error in failing to detect in 1960 and 1961 the presence of type A behavior in participants of the WCGS 1° who possessed this behavior and later developed clinical CHD. One of the chief reasons for this failure was our inability then to differentiate hostility from what we considered excessive aggression. It was not until 19692~ that we discovered that besides impatience, hostility also was an overt component of type A behavior, and in 197422 we described methods of modifying this particular component. As a consequence, many hostile subjects in 1960 and 1961 were incorrectly diagnosed as individuals with type B behavior. Also, at that earlier period we had not yet discovered a number of physical signs that indicate the presence of type A behavior in over 95% of
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patients with CHD. 18In short, I believe that in 1960 and 1961 if we had the diagnostic armamentarium we now possess, we would have labeled as type A ~lmost every WCGS participant who subsequently died from clinical CHD during the next decade.* Despite the relatively rudimentary diagnostic procedure employed in the WCGS in 1960 and 1961,l° the incidence of clinical CHD in participants who were diagnosed as having type A behavior was significantly greater than that found in participants who had been labeled type B when they were reexamined 8~/2 years later. 11Moreover, despite the above described deficiencies in our earlier attempts to diagnose types A and B behavior, even when the WCGS participants were surveyed by Ragland** et al.~ 22 years later (chiefly by postcard or telephone) and when they all were over 60 years of age (many over 75 years of age), nevertheless the coronary mortality of those subjects diagnosed 22 years earlier as exhibiting type A behavior was 26 % greater than participants diagnosed as type B. This study, however, has many deficiencies, not least of which was the failure of the authors to have any kind of clinical contact with the participants. Accordingly, all their data are those obtained 22 years after their subjects were diagnosed. What changes and in which subjects behavioral changes occurred during the hiatus of at least 14 years of no clinical contact cannot even be guessed at in this study. It also is extremely puzzling to me how after a lapse of 22 years the authors were able to trace, with the exception of approximately 30 subjects, 99 % of the 3154 initially enrolled participants. This is particularly puzzling when it was reported 4½ years after this same study that 45 subjects could not be found, and after 8~/2 years approximately 228 of the 3154 participants could not be traced. 11 Certainly in the RCPP we made every effort to keep track of our 862 subjects; nevertheless, in just 4~/2 years we were unable to trace 82 subjects. Given these discrepancies, I remain mystified by this reported follow-up achievement of Ragland et ai.2s During the past decade several investigators, 19'2° while recognizing that hostility had earlier been described as one of the two components of type A *I say this because, as already stated, we detected in the RCPP ~3 the presence of type A behavior in over 95% of the 966 successively admitted postinfarction subjects. **Ragland and another statistician recently reported 3~that in their 14-year postcard follow-up of 257 coronary patientS, patients classified as type B 28 years ago died more frequently than those classified as type A. These authors, however, did not mention that a number of these same coronary patients received type A behavioral counseling for 4~/2 years following their first infarction in the Recurrent Coronary Prevention Project. Although there were a number of other serious flaws in this study, this avoidable omission alone invalidates the results of their study.
April 1988 American Heart Journal
behavior, nevertheless believe it alone is the "toxic factor." Here again, reliance on questionnaires rather than direct examination of patients with CHD had been employed. Williams et al.,19 for example, leaned heavily on the later coronary mortality of medical students who scored positively many years earlier on the Cook-Medley Hostility questionnaire. However, McCramie et al. ~ studied the later coronary morbidity and mortality of medical students who took the same questionnaire before and again after entering medical school and found no evidence whatsoever to indicate that the hostility observed in their subjects was followed decades later by increased incidence of coronary morbidity or mortality. Does this report of McCramie et al. 29 mean that Williams et al. lg and Dembroski et al. 2° were wrong in believing that hostility (one of the two major components of type A behavior) has relevance to the pathogenesis of clinical CHD? Not at all. What it does mean, however, is that the use of any type of questionnaire to diagnose or detect a medical disorder is essentially fallible. For example, I asked 22 of our ambulatory, symptomless coronary patients to respond to the Cook-Medley questionnaire. Although all 22 participants exhibited two or more neurologic signs indicative of the presence of hostility, only 10 scored as hostile persons on the questionnaire. I believe that the hostility component of type A behavior is "toxic" and agree with Dembroski et al. ~° that if subjects seethe rather than vent their anger, they may be more likely to have sustained higher levels of norepinephrine, ACTH, testosterone, and excess wasting of growth hormone.3°Despite, however, close questioning of hundreds of patients with CHD, neither they nor I am willing to absolve impatience, the other major component of type A behavior, from "toxic" responsibility. Let clinicians and researchers recognize that even if only hostility had relevance to clinical CHD, nothing intensifies hostility more certainly than impatience. It also is important to bear in mind that according to the Oxford English Dictionary, irritability and irascibility are given as synonyms of impatience. These two states are varieties of hostility. Certainly if my colleagues do not recognize this last truth, I doubt if they have had much clinical contact with coronary patients. However, I am more than a little surprised at how few investigators who write articles about type A behavior ever actually treat patients with CHD. I end this editorial by pointing out that the true "'toxic" factor in type A behavior is the inadequate security and self-esteem that initiates and fuels the
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Type A behavior and coronar) disease
Number4
I
....
i0.0 ~9.0-
935
CARDIAC COUNSELING (Sectioe !) TYPE A/CARDIAC COUNSELING (Section 2)
8.07.OCUMULATIVE ANNUALiZED RECURRENCE RATE (PERCENT)
6.05.04.03.0~
2.0. 1.00.0 0
3
e
9 I~' is is El 2 ' 4 u 30 ~3 ~ . .ONT.S or OaSERVAT*ON
42 45 4'8 s,
Fig. 1. This graph illustrates the cumulative, annualized recurrence rate in postinfarction patients who (1) received group cardiac counseling (upper curve) and (2) received group cardiac and type A behavioral counseling (lower curve). Note that the 95 % confidence limits of the respective recurrence rates no longer intersect at the end of 36 months. After the first year, significantly fewer (p <:0.05) cardiac deaths occurred in the group given type A counseling in addition to cardiac counseling. (From Friedman M. AM HEARTJ 1986;112:659.)
emergence of impatience and hostility. It is this emotional malady, often deeply anchored, that was the target we dealt with in the RCPP. I believe also that it was our ability to enhance the security and/or self-esteem of so many of our participants that was responsible for the halving of the coronary recurrence rate of the type A counseled postinfarction participants in the RCPP. 1~ Although these latter results were published in 1984, not a single reference to the probable causal role of insecurity and/or inadequate self-esteem (in the pathogenesis of type A behavior) appeared in the July 1987 Circulation monograph, sl reporting the proceedings of the special conference (jointly sponsored by the American Heart Association and the National Heart, Lung, and Blood Institute) dealing with behavioral medicine and cardiovascular disease. I believe this omission in the 227-page monograph, which otherwise contained 39 reports (including those of 15 "task force" committees), is rather tragic. Again let me warn, as we unsuccessfully attempted to do in 1959 when we introduced the type A concept, that it will not be easy for just any psychiatrist, psychologist, or cardiologist to replicate the results that we obtained in the R C P P ~3-15or at the U.S. Army War College. ]6 Successful reduction in type A behavior depends in great part on certain qualities of the group counselor. He or she does not need to be a psychiatrist, psychologist, or
cardiologist.* However, he or she should possess integrity, ability to care for others, a minimum of certain type A characteristics himseff or herself, and a capacity to convince others concerning adoption of new belief systems and new ways of doing things. The group counselor also must possess good judgment, ability to laugh at himself or herself, and a basic knowledge of the humanities. Obviously such counselors are not easy to find, but we found them for the RCPP, the War College studies, and for our ongoing group counseling program in the San Francisco Bay area. I believe that eventually a group of counselors will be found whose results in reducing the intensity of type A behavior and the recurrence rate of coronary accidents will exceed those obtained in the RCPP. 1315Ideally, such competent counselors can be found and should be subsidized as soon as possible because hundreds of tholx~ands of Americans are dying prematurely from CHD who could be saved (Fig. 1). I might add that when such qualified counselors are found and if the design of the study is planned by physicians possessing clinical acumen, the R C P P results can be replicated at a cost of one-fiftieth that of the ill-designed, ill-fated M R F I T study. Finally, it is wise to keep in mind that diagnostic *One of the most successful modifiers of type A behavior is Col. Frederick Drews, Director of the Army Physical Fitness Research Institute at the Army War College, Carlisle, Pa.
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discoveries, whether they had to do with the detection of such disparate diseases as Addison's, Alzheimer's, or more recently, acquired immunodeficiency syndrome were anecdotal not epidemiologic or statistical accomplishments. I do not believe this mode of discovery is or soon will become obsolete. REFERENCES
1. Friedman M, Rosenman RH. Association of specific overt behavior pattern with blood and cardiovascular findings. JAMA 1959;76:1286. 2. Friedman M, Byers SO, Rosenman RH, Elevitch FR. Coronary prone individuals (type A behavior pattern): some biochemical characteristics. JAMA 1970;212:1030. 3. Friedman M, Byers SO, Rosenman RH. Serum lipids and conjunctival circulation after fat ingestion in men exhibiting Type A behavior pattern. Circulation 1964;29:874. 4. Friedman M, St. George S, Byers SO, Rosenman RH. Excretion of catecholamines 17-ketosteroids, 17-hydroxy-corticolds and 5-hydroxy-indole in men exhibiting a particular behavior pattern (A), associated with high incidence of clinical coronary heart disease. J Clin Invest 1960;39:758. 5. Friedman M, Byers SO, Dimnont J, Rosenman RH. Plasma cateCholaInine response of coronary-prone subjects (.Type A) to a special challenge. Metabolism 1975;25:205. 6. Friedman M, Byers SO, Rosenman RH. Plasma ACTH and cortisol concentration of coronary prone subjects. Proc Soc Exp Biol Med 1972;140:681. 7. Zumoff B, Rosenfeld RS, Friedman M, Byers SO, Rosenman RH, Hellman L. Elevated daytime urinary excretion of testosterone glucuromide in men with the Type A behavior pattern. Psychosom Med 1984;40:223. 8. Grundy SM, Griffin AC. Effects of periodic medical stress on serum cholesterol levels. Circulation 1959;19:490. 9. Williams RB, Lane JD, Kuhn CM, Meosh W, White AD, Shanberg SM. Type A behavior and elevated physiological and neuroendocrine responses to cognitive tasks. Science 1982;218:483. 10. Rosenman RH, Friedman M, Straus R, et al. A predictive study of coronary heart disease. The Western Collaborative Group Study. JAMA 1964;189:15. 11. Rosenman RH, Brand RJ, Jenkins CD, Friedman M, Straus R, Wurm M. Coronary heart disease in the Western Collaborative Group Study: final follow-up experience of 81/2 years. JAMA 1975;233:872. 12. Haynes SG, Feinleib M, Levine S, Scotch N, Kannel WB. The relationship of psychosocial factors to coronary heart disease in the Framingham Study. III. Eight year incidence of coronary heart disease. Am J Epidemiol 1980;111:37. 13. Friedman M, Thoresan CE, Gill JJ, et al: Feasibility of altering Type A behavior pattern after myocardial ;nfarction. Recurrent Coronary Prevention Project study: methods, baseline results and preliminary findings. Circulation 1982; 66:83. 14. Friedman M, Thoresen CE, Gill JJ, et al. Alteration of Type
April 1988 American Heart Journal
A behavior and reduction in cardiac recurrences in post myocardial infarction patients. AM HEARTJ 1984;108:237. 15. Friedman M, Thoresen CE, Gill JJ, et al. Alteration of Type A behavior and its effect on cardiac recurrences in post myocardial infarction patients: summary results of the Recurrent Coronary Prevention Project. AM HEARTJ 1986; 112:653. 16. Gill JJ, Price VA, Friedman M, et al. Reduction of Type A behavior in healthy middle-aged American military officers. AM HEARTJ 1985;!10:503. 17. Shekelle R, Hully SB, Neaton J, et al. The MRFIT behavior pattern study. II. Type A behavior and incidence of coronary heart disease. Am J Epidemiol 1985;122:555. 18. Case RH, Hiller SS, Case NB, Moss AJ, Multicenter Post Infarction Research Group. Type A behavior and survival after acute myocardial infarction. N Engl J Med 1985; 312:737. 19. Williams RB, Barefoot JC, Shekelle RB. The health consequences of hostility. In: Chesney MA, Rosenman RH, eds. Anger, hostility and behavioral medicine. New York: McGraw-Hill, 1985:173. 20. Dembroski TM, MacDougall JM, Williams RB, Harley TL, Blumenthal JA. Components of Type A, hostility and anger in; relationship to angiographic findings. Psychosom Med 1985;47:219. 21. Friedman M. The pathogenesis of coronary artery disease. New York: McGraw-Hill, 1969. 22. Friedman M, Rosenman RH. Type A behavior and your heart. New York: Alfred A. Knopf, 1974. 23. Scherwitz L. Interviewer stylistics and Type A predictiveness for CHD incidence: clues for an engagement hypothesis. Presented to Kansas Series in Clinical Psychology, May 10-11, 1986, Lawrence, Kansas. 24. Rosenman RH. As quoted in Psychology Today. "Type A on trial." 1987;Feb:46. 25. Jenkins CD, Rosenman RH, Zyzonski SJ. Prediction of clinical coronary heart disease by a test for the coronary prone behavior pattern. N Engl J Med 1974;290:1271. 26. Halperin PJ, Littman AB. Letter to the Editor. N Engl J Med 1985;310:431. 27. Abbott AV, Peters BK, Vogel ME. Letter to the Editor. N Engl J Med 1985;310:431. 28. Ragland DR, Brand RJ, Rosenman RH, Newmann R. Coronary heart disease mortality in the Western Collaborative Group Study: follow-up experience of 22 years. A m J Epidemiol (In press). 29. McCramie EW, Watkins LO, Brandsma JM, Sisson BD. Hostility, coronary heart disease (CHD) incidence and total mortality: lack of association in a 25-year follow-up study of 478 physicians. J Behav M e d 1986;9(2):119. 30. Friedman M, Byers SO, Rosenman RH, Newmann R. Coronary prone individuals (Type A behavior pattern). Growth hormone responses. J A M A 1971;217:929. 31. Conference on behavioral medicine and cardiovascular disease [Monograph 6]. Circulation 1987;76: 32. Ragland DR, Brand RJ. Type A behavior and mortailityfrom coronary heart disease. N Engl J Med 1988;318:65.