Type A Coronary-Prone Behavior Research Paper

1. Rebirth Of A Mind–Body Hypothesis

The notion that characteristic patterns of emotion and behavior could confer risk for the development of CHD was not novel at the time of Friedman and Rosenman’s initial description of the Type A pattern. Over 100 years ago, Sir William Osler, one of the pioneers in the clinical description of CHD, observed that this illness befell, ‘not the neurotic, delicate person … but the robust, the vigorous in mind and body, the keen and ambitious man, the indicator of whose engine is always at full speed ahead.’ Prior to the 1950s, psychoanalytically oriented clinicians had also suggested that personality traits such as excessive ambition and aggressiveness seemed to characterize coronary patients and hence might indicate that personality traits somehow contributed to the development of the disease. However, these observations were not subjected to thorough scientific investigation, and as a result had limited impact on behavioral or medical science and even less on the clinical care of coronary patients.

Early in their program of research, Friedman and Rosenman reported controlled studies in which patients with and without CHD differed in the behavioral characteristics included in their description of the Type A pattern. Further, they found that Type A and B individuals differed in physiological characteristics that could be involved in the development of the disease. For example, Type A persons displayed greater daily levels of excretion of catecholamines and other stress hormones compared to Type B individuals. In this early work, Friedman and Rosenman intentionally avoided framing their research as an investigation of personality characteristics because of the limited impact and skepticism surrounding the previous, psychoanalytic speculations about the role of personality in CHD. Most importantly, in the late 1960s they launched a large prospective, longitudinal study of the association between the Type A pattern and subsequent CHD. The prospective design pro-vided a more rigorous test of the hypothesis that Type A behavior somehow influenced the development of CHD when compared to the cross-sectional research they had conducted up to that point. The Western Collaborative Group Study (WCGS: Rosenman et al. 1975) demonstrated that among initially healthy men, Type A’s were about twice as likely to develop CHD over an eight-year follow-up period than were Type B’s. This relationship remained significant even when established CHD risk factors (e.g., smoking) were statistically controlled. This study provided the first prospective evidence that the Type A pattern was an independent risk factor for cardiovascular disease, at least in a sample of predominately white, North American, middle-class males.

The results of the WCGS prompted a variety of other investigations, and evidence regarding the health implications of the Type A pattern accumulated rapidly. In 1978, the National Heart Lung and Blood Institute sponsored a panel of neutral experts and charged them with the task of reviewing this evidence. The panel’s report concluded that the Type A pattern was indeed a reliable, independent risk factor, and that it was about as important in the development of CHD as were the established risk factors such as smoking and high blood levels of cholesterol (Review Panel 1981). This represented a unique development in the study of CHD, as it was the first time a psychological construct had been endorsed as a risk factor by a panel of biomedical experts. The Type A pattern quickly became a central focus of a rapidly emerging emphasis on psychological aspects of cardiovascular disease (Steptoe 1981). However, as discussed below, sub-sequent years witnessed the accumulation of a more mixed body of evidence concerning the association between Type A behavior and CHD, and a re-formulation of what are the key aspects of the Type A syndrome related to CHD and other health outcomes.

2. Assessment And Underlying Mechanisms

A variety of methods have been developed to assess Type A, coronary prone behavior. The ‘gold standard’ of these assessment procedures is the Type A Structured Interview. This approximately 10-minute interview consists of a series of questions concerning the individual’s work habits, daily routines, and aspects of the Type A pattern. A semistructured set of prompts and follow-up questions are also included, and many questions are presented in such a way as to evoke Type A responses from predisposed persons. For example, the interviewer is occasionally somewhat challenging and even provocative, or hesitates and delays the completion of a rather obvious question. The content of the individual’s answers is not the primary source of information in making a judgement about the presence and degree of Type A characteristics. Rather, the assessment is based primarily on the style of response. A loud, rapid, and vigorous vocal style, interruptions and ‘talking over’ the interviewer, and subtle or nonverbal expressions of impatience (e.g., an exasperated sigh), hostility or irritation toward the inter-viewer (e.g., sarcasm or condescension) are weighted heavily in the classification of an individual as Type A or B, although self-reports of competitiveness, impatience, over-involvement in work, and easily provoked anger are considered as well. This emphasis on displayed rather than self-reported characteristics is consistent with Friedman and Rosenman’s prior clinical observations that Type A individuals were often unable or unwilling to give accurate descriptions of their emotions and actions, perhaps reflecting a lack of insight or a defensive, uncooperative, or mistrusting nature. Although the Structured Interview procedure can produce quite reliable ratings, it has obvious limitations stemming from the need for expert inter-viewers and raters. Hence, several self-report questionnaires have been developed as alternatives to the Structured Interview. The most widely used of these in the history of Type A research is the Jenkins Activity Survey (JAS: Jenkins et al. 1974). This instrument consists of several multiple-choice questions about the various components of the Type A pattern. Factor analyses have indicated that the primary dimensions of the JAS are hard-driving competitiveness, impatience and speed of activity, and job involvement. Importantly, the JAS does not thoroughly sample the aggressive verbal style, anger, and easily evoked hostility that are weighted heavily in the ratings derived from the Type A Structured Interview. Like many other self-report measures of the Type A pattern, the JAS scores are not closely correlated with the Structured Interview ratings, and are not consistently related to CHD in prospective studies. Further, the various self-report scales are typically only modestly correlated with one another, and in many instances have unique correlates with other psychological characteristics. This suggests that although often grouped together as Type A research, studies using different assessment procedures are likely to be examining what are actually only weakly related personality and behavioral characteristics. These important differences across measures of the construct have contributed to inconsistency in the body of research on the Type A pattern, in part because they identify possibly quite distinct persons as Type A. For example, the self-described competitive, achievement striving, over-extended, hurried, and impatient person who scores high on the JAS may or may not have the emphatic, rapid, dominant, and unfriendly vocal and interactional style that would warrant a classification of Type A in The Structured Interview.

A variety of models of the underpinnings of the Type A pattern have been proposed. Among the more influential of these views is that of Glass (1977). He suggested that Type A characteristics reflected a strong desire to exercise control over the people and events of one’s life, and a low threshold for perceiving threats to control. From this perspective, the overt Type A characteristics themselves represent a well-developed aggressive style of asserting control in response to perceived threats of loss of control. In another influential model, Price (1982) suggested that a set of beliefs comprise the psychological core of the Type A pattern. She argued that Type A’s believe that one must continuously demonstrate self-worth through achievement, that the resources and opportunities for such achievement are limited and often scarce, and that there is no universal moral principle to ensure that other people will be fair in their pursuit of these valued achievements. As a result, in contrast to the more relaxed and trusting Type B, Type A individuals are engaged in a continuous struggle to demonstrate their self-worth, through competitive and adversarial interactions with unprincipled others. Hence, the overt Type A characteristics are the manifestations of this continuous struggle to sustain externally-referenced self-esteem or value, in real or imagined competition with adversaries. These conceptual models have stimulated a great deal of research on the psychological basis of Type A persons, and have served as guides to the development of interventions for the reduction of Type A behavior (Rhodewalt and Smith 1991).

In most models of Type A behavior, the impact of this psychological variable on the development of CHD is seen as occurring through the mechanism of physiological responses to psychological stress. Briefly, Type A’s are believed to respond to challenges, threats, and demands with larger, sympathetically-mediated increases in heart rate, blood pressure, and various stress hormones. Over long periods of time, the repetition of this physiological reactivity can initiate and hasten the development of coronary artery disease (CAD) or coronary atherosclerosis, the under-lying condition common to the various clinical manifestations of CHD. CAD begins with microscopic injuries to the inner lining, or endothelium of the coronary arteries, and continues through the progressive buildup of fatty deposits at these injury sites. In later stages, a hard, fibrous cover forms, and these advanced plaques can rupture or bleed. At the location of these coronary artery lesions, the passage through which blood would otherwise pass becomes narrowed and oxygen supply to the heart muscle is consequently impeded. Once CAD has advanced to a sufficient degree, exaggerated psychophysiological reactivity can increase the heart’s need for oxygen as it beats more rapidly and forcefully during sympathetic activation. Further, this reactivity can contribute de-creased blood and oxygen supply to the heart through the transient narrowing of the coronary artery at plaque sites. Through either or both increased demand/or decreased supply of oxygen, psychological stress can evoke an insufficient supply of oxygen to the heart muscle. The resulting myocardial ischemia can provide the clinical manifestations of CHD, such as angina pectoris (chest pain), myocardial infarction (death of heart muscle), or sudden coronary death. A large body of evidence suggests that compared to Type B’s, Type A persons do respond to potential stressors with more pronounced psychophysiological responses (Houston 1988). Further, other evidence indicates that such responses can contribute to the initial development of CAD and to myocardial ischemia in individuals with advanced CAD (Rozanski et al. 1999).

In an extension of these models of the connection between Type A behavior and CHD, Smith and Anderson (1986) suggested that Type A individuals not only respond to everyday stressors with heightened physiological reactivity; relative to Type Bs, they are also exposed to more frequent, severe, and pro-longed stressors. This greater exposure to challenges, demands, and hassles in everyday life reflects a stress-engendering process, in which the ambitious, competitive, controlling, and hostile style of Type A’s leads to more tasks, commitments, and obligations, and to competition, opposition, and antagonism in interactions with others. Hence, the exaggerated psychophysiological reactivity that links Type A behavior to disease comes from two sources—the stressors all individuals face and the additional challenges, threats, and demands Type A’s create for themselves.

Another important view of the association between Type A behavior and CHD was suggested by Krantz (Krantz and Durel 1983). He argued that the overt manifestations of Type A behavior are the con-sequence rather than the cause of the psycho-physiological reactivity associated with this pattern. In this constitutional vulnerability model, Type A behaviors are produced by an underlying biologic predisposition to heightened sympathetic nervous system (SNS) responsivity. This underlying responsivity, in turn, also fosters the development of CAD and CHD. Consistent with this view, twin studies have indicated that the Type A pattern is at least partially heritable, and pharmacological studies suggest that the pattern is related to an underlying SNS responsivity (Smith and Gallo 2001).

3. Evolution Of Type A Research

Shortly after the initial conclusion that the Type A pattern was a reliable, independent risk factor for CHD, several large prospective studies failed to replicate this effect. This led to skepticism in the scientific community about the actual importance of the construct. However, a careful analysis of the evidence revealed possible explanations for the inconsistencies in this literature. In a quantitative review of the available evidence, Miller et al. (1991) found that the Structured Interview was a much more reliable predictor of subsequent CHD than the JAS and other self-report measures of Type A, and that the association between Type A and CHD was larger in initially healthy samples than it was among high-risk samples and among samples with established CHD. The apparent temporal trend of increasing failures to replicate the association between Type A behavior and CHD apparently reflected a growing use of high-risk samples and self-report measures of the behavior pattern. When defined by the Structured Interview, the combined evidence still indicated that Type A behavior was a reliable risk factor for the development of CHD among initially healthy individuals, and that the weaker association in high-risk individuals and clinical samples of CHD patients could be attributed to methodological problems inherent in such study designs. Hence, although the emergence of inconsistent evidence led many researchers and clinicians to lose interest in the Type A concept, this waning importance seems to have been unwarranted.

Inconsistent findings and growing skepticism also had a very positive consequence for the study of coronary-prone behavior. Following earlier seminal work by Matthews et al. (1977), many investigators began to examine the predictive utility not of the global Type A pattern but of its individual components. In these more specific and refined analyses, hostility quickly emerged at the most ‘toxic’ component among the array of individual Type A characteristics, confirming a centuries-old hypothesis about the negative health effects of anger (Siegman 1994). As an umbrella term, hostility refers to individual differences in the tendency to experience anger, negative beliefs and attributions concerning the motives and intentions of others (e.g., cynicism and mistrust), and overtly aggressive verbal and physical behavior. Achievement striving, competitiveness, and impatience, in contrast, did not seem to be reliable risk factors for cardiovascular disease.

Because measures of hostility existed in several large studies in which individuals had completed personality tests decades earlier and were followed over many years, independent tests of the health consequences of hostility could be conducted without the need to begin additional long-term, prospective studies. For ex-ample, hostility scales could be derived from the true–false item pool comprising the Minnesota Multi-phasic Personality Inventory (MMPI), and this psychological test had been in wide use for many several decades, nearly throughout the world. Hence, a literature on this element of the Type A pattern grew rapidly. As with the global Type A pattern, these prospective studies of hostility and subsequent health included mostly positive or confirmatory findings regarding the negative health consequences of hostility, but some failures to replicate the effect as well. However, in a recent quantitative review of this literature, behavioral ratings of hostility and self-report measures of the construct were found to be reliable predictors of the later development of CHD and premature mortality (Miller et al. 1996).

As in the case of the global Type A pattern, research on the mechanisms linking hostility and CHD has focused on psychophysiologic responses to potential stressors (Williams et al. 1985). In response to potential social stressors administered in the laboratory such as disagreements, conflicts, debates, and harassment, hostile persons respond with larger increases in heart rate, blood pressure, and stress hormones (e.g., circulating catecholamines) than their less hostile counterparts. Further, ambulatory studies indicate that this exaggerated psychophysiological reactivity is also characteristic of the responses of hostile persons to their natural, daily environments (Smith and Gallo 2001). Other research has indicated that among persons with CAD, episodes of anger can precipitate myocardial ischemia and even infarction (Rozanski et al. 1999), and that hostile persons with CAD may be particularly prone to such responses. Hence, the psychophysiological responsiveness of hostile persons may be the key mechanism through which they are at increased risk of disease.

Hostility is also associated with greater exposure to interpersonal stressors such as heightened levels of conflict with and reduced levels of social support from friends, family members, and co-workers (Smith and Gallo 2001). Further, much of this ‘psychosocial vulnerability’ associated with hostility may stem from the impact of the hostile person’s thoughts and actions on his or her social environment. Given their mistrusting, cold, and antagonistic interpersonal style, hostile persons may undermine sources of social support and create conflicts, thereby creating more frequent, prolonged, and extreme social stressors to which they react with heightened reactivity. This discordant, unsupportive social environment would also tend to maintain and perhaps even exacerbate the hostile personality style.

Hostility may not be the only ‘toxic’ element within the global Type A pattern. In a reanalysis of the original Structured Interviews from the WCGS, Houston et al. (1997) found that behavioral ratings of hostility and a vigorous, dominant interactional style were separate predictors of later CHD and premature death. These authors suggested that hostility and social dominance are separate coronary-prone characteristics. The possible health consequences of social dominance have a clear parallel with one of the best-developed animal models of stress and individual differences in social behavior as risk factors for cardiovascular disease. Kaplan et al. (1994) demonstrated that socially dominant, male cynomolgus monkeys develop more severe coronary artery disease in response to chronic social stress (i.e., recurrent exposure to novel cage mates) than socially sub-ordinate males. Further, this differential impact of social stress among dominant males on vulnerability to coronary disease is apparently mediated by sympathetic nervous system activity. When dominant male animals receive pharmacologic blockade of beta-adrenergic input to the heart, they no longer display vulnerability to coronary atherosclerosis even when under chronic social stress. Hence, chronic sympathetic nervous system activation of the heart and vasculature, as dominant males recurrently assert their status and respond to related challenges and threats, may underlie this psychosocial effect on atherosclerosis. In humans, efforts to assert dominance or control over others is also associated with increases in blood pressure and heart rate (Smith et al. 2000), again suggesting that psychophysiological reactivity could connect a second ‘toxic’ component of Type A behavior—social dominance—to the later development of CHD.

4. Application Of Type A Research

The most obvious benefit of research identifying risk factors for the development and progression of CHD is the design of related, risk reducing interventions. In the case of Type A, coronary-prone behavior, this actually raises two questions. First, can Type A behavior be changed? Second, if so, do such changes reduce the risk of CHD? These questions were the focus of a large, controlled clinical trial conducted by Friedman et al. (1984)—the Recurrent Coronary Prevention Project (RCPP). Compared to a control group receiving typical information and counseling to make appropriate changes in health habits to reduce cardiac risk (e.g., smoking cessation, diet, exercise), postmyocardial infarction patients who had under-gone group therapy designed to identify and reduce Type A behavior were indeed able to change these characteristics, as measured by Structured Interview ratings. Further, patients receiving this psychological intervention were much less likely to experience a recurrence of their coronary disease such as a second myocardial infarction. Among patients with mild initial coronary disease, the intervention also reduced the incidence of subsequent coronary deaths (Powell and Thoresen 1988). Based on the conceptual model of Price described above, this intervention consisted of cognitive restructuring directed toward altering the beliefs underlying the Type A pattern, reducing exposure to environmental cues that activate Type A tendencies, rehearsing alternative, Type B responses to such situations, and instruction and practice of re-laxation exercises and other stress management skills.

A variety of other programs have been developed to modify the Type A pattern, but few have been evaluated in large controlled trials with definitive medical outcomes as in the RCPP. However, the general approach of stress management and related psychological interventions for coronary patients has been found to be successful in reducing recurrent events in this population (Linden et al. 1996). For example, Blumenthal et al. (1997) found that a stress management intervention reduced the frequency of episodes of myocardial ischemia occurring during the daily activities of patients with advanced CAD. Although not specifically targeted at Type A behavior, such interventions are designed to reduce complications from heart disease by altering emotional and physiological stress responses.

5. The Future Of Research On Coronary Prone Behavior

Since the height of scientific and popular attention in the 1970s and 1980s, the number of research studies published each year on Type A behavior has steadily decreased. However, this reflects an evolution rather than growing neglect. The focus on hostility as the toxic component within the global Type A pattern continues in epidemiological, psychophysiological, and intervention research. Further, other individual differences have emerged as reliable risk factors as the search for coronary prone behavior continues and broadens. For example, symptoms of anxiety and depression appear to be reliable risk factors for the initial development of CHD, and are associated with poor prognosis among patients with established dis-ease (Januzzi et al. 2000). These other coronary-prone behaviors will also be the focus of additional studies of their predictive utility, the psychobiological mechanisms through which they impact the development and course of CHD, and the effectiveness of related interventions. The addition to the specific research discussed above, the seminal work of Friedman and Rosenman represents a cornerstone of the study of behavioral aspects of cardiovascular disease. In fact, despite an inconsistent reputation in the scientific community and the popular press, the Type A concept played a central role in the rapid development of the broader fields of health psychology and behavioral medicine. It also has been influential in the expanded attention to psychological factors in the clinical care of patients with CHD.

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