Tilburg University
Personality, emotional distress and coronary heart disease
Denollet, J.
Published in:
European Journal of Personality
Publication date:
1997
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Peer reviewed version
Link to publication in Tilburg University Research Portal
Citation for published version (APA):
Denollet, J. (1997). Personality, emotional distress and coronary heart disease. European Journal of Personality, 11(5), 343-358.
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Personality, Emotional Distress and Coronary Heart Disease
Johan Denollet
Department of Medicine, University of Antwerp, Antwerp & Department of Psychology, University of Ghent, Ghent
Belgium
Running head: Type-D and CHD
Abstract
Personality, emotional distress and coronary heart disease INTRODUCTION
Coronary heart disease (CHD) is still the leading cause of death in western society, despite a recent decline in cardiovascular mortality (De Vreede, Gorgels, Verstraaten, Vermeer, Dassen and Wellens, 1991). During the last decades, many new diagnostic and treatment strategies for patients with CHD have been developed, including coronary angiography, cardiac echography, bypass surgery, coronary angioplasty, beta-blocker therapy, ACE-inhibition and thrombolytic therapy. In patients with myocardial infarction, short-term prognosis has in fact improved since 1960 due to these new developments, but there are still some unknown factors that appear to play a role in both the development and progression of CHD. The present paper focuses on the proposition that emotional distress is such a factor that may be deleterious to the ischemic myocardium, and that personality factors, to a large extent, may account for the relation between emotional distress and CHD.
EMOTIONAL DISTRESS AND DEVELOPMENT OF CHD
likelihood of decrements in emotional well-being (e.g., Friedman, 1991).
With reference to CHD, evidence indicates that 50 per cent of the new cases cannot be identified on the basis of standard risk factors such as hypertension, hyperlipidemia, and smoking (Krantz, Schneiderman, Chesney, McCann, Reading, Roskies, Stoney and Williams, 1989). Psychosocial research on CHD has received impetus from this inability to explain a large portion of variance in the incidence of CHD. Among the more controversial risk factors, psychosocial factors are of prime importance. Initially, research in this area mainly focused on the Type A behavior pattern (e.g., Rosenman, Brand, Jenkins, Friedman, Straus and Wurm, 1975), a construct that has prompted much research on psychosocial risk factors for the development of CHD. Although evidence indicates that the Structured Interview assessment of Type A behavior predicts actual CHD (Matthews, 1988), the nature of that association is, however, far more complex than is conveyed by the simple assertion that the Type A behavior pattern is a risk factor for CHD (Dimsdale, 1988).
In more recent years, there has been a shift from Type A behavior to specific emotional factors in research on CHD (e.g., Booth-Kewley and Friedman, 1987). Reanalyses of data from the Western Collaborative Group Study (i.e., the first prospective study that identified Type A as a risk factor) and the Multiple Risk Factor Intervention Trial (i.e., a frequently cited study questioning the role of behavioral risk factors in CHD) indicated that interview ratings of hostility were associated with the incidence of CHD (Dembroski, MacDougall, Costa and Grandits, 1989; Hecker, Chesney, Black and Frautschi, 1988).
Dahlstrom and Williams, 1983), but other studies failed to replicate this association between scores on the Cook-Medley Hostility Scale and CHD (Hearn, Murray and Luepker, 1989; Leon, Finn, Murray and Bailey, 1988; McCranie, Watkins, Brandsma and Sisson, 1986). More recently, anger was associated with the development of CHD in a prospective follow-up study (Kawachi, Sparrow, Spiro, Vokonas and Weis, 1996). It is obvious that hostility (Miller, Smith, Turner, Guijarro and Hallet, 1996) and anger (Chesney and Rosenman, 1985) may act as a potential cardiotoxic agent, but that evidence is mixed and more research is needed to elucidate the relationship between hostility/anger and the development of CHD.
Interestingly, research suggests that the development of CHD may be associated with other negative emotions as well. An important study that provided evidence for the role of various negative affective conditions in the deterioration of health is the meta-analytic survey of Friedman and Booth-Kewley (1987). These authors found that not only anger, but also depression and anxiety may be associated with the incidence of chronic diseases, including cardiovascular disorders. Further analyses of their findings suggested that depression may be a potential risk factor for the development of CHD (Booth-Kewley and Friedman, 1987). This proposition was supported by a clinical follow-up study which demonstrated that interview-ratings of depression in a sample of patients undergoing coronary angiography were associated with the long-term incidence of major coronary events (Carney, Rich, Freedland, Saini, TeVelde, Simeone and Clark, 1988). Recent evidence further supported the notion that the development of CHD is related to symptoms of depression (Barefoot and Schroll, 1996).
complaints that are often related to emotional distress, such as undue fatigue (Appels and Mulder, 1988) and sleeping problems (Wingard and Berkman, 1983), are associated with the incidence of and mortality from CHD. These findings suggest that it is not the occurrence of one specific negative emotion per se, but rather the occurrence of emotional distress in general that may be associated with the development of CHD.
Unfortunately, self-reports of emotional distress are not specific of a cardiac disease. Emotional distress may, for example, be associated with the perception and reporting of cardiologic complaints (e.g., chest pain) but not actual cardiac disease (Costa and McCrae, 1987; Watson and Pennebaker, 1989). Although self-reported emotional distress is in fact not synonymous with the development of organic disease, this phenomenon does not mean that emotional distress cannot also play a true causal role in CHD. Rather, evidence suggests that emotional distress is associated with both invalid health complaints and actual coronary proneness (Friedman, 1990). As pointed out by Alonzo (1975), the overall response of individuals and the medical community to symptoms of emotional distress and general malaise, however, is that they are 'manageable' or that a period of 'wait and see' is appropriate. In contrast to this attitude, the evidence reviewed above suggests that individuals who chronically experience high levels of emotional distress may actually be at risk for CHD. Anyway, the role of emotional distress in the development of CHD still is a controversial issue (see for example Friedman, 1990; Stone and Costa, 1990). Abundant evidence indicates, however, that emotional distress does play a key role in the progression of CHD.
EMOTIONAL DISTRESS AND PROGRESSION OF CHD
recovery from, CHD. Evidence for the role of emotional distress in this area comes from (i) long-term follow-up studies of emotional distress in patients with CHD, (ii) long-term follow-up studies of somatic distress in patients with CHD, (iii) trials of psychosocial interventions in coronary patients, and (iv) studies of pathophysiological processes in CHD. First, follow-up studies indicated that emotional distress is related to progression of CHD. Nowadays, one generally assumes that symptoms of depression are associated with an increased long-term risk for cardiac mortality and reinfarction among patients who survived a myocardial infarction (e.g., Ahern, Gorkin, Anderson, Tierney, Hallstrom, Ewart, Capone, Schron, Kornfeld, Herd, Richardson and Follick, 1990; Frasure-Smith, Lespérance and Talajic, 1995; Ladwig, Kieser, König, Breithardt and Borggrefe, 1991). Depression has also been associated with increased risk for coronary events and mortality in arrhythmia patients (Kennedy, Hofer, Cohen, Shindledecker and Fisher, 1987) and in patients with angiographically documented CHD (Carney, Rich, Freedland, Saini, TeVelde, Simeone, and Clark, 1988).
Fatal and non-fatal cardiac events in coronary patients are, however, not only related to depression but also to anger (Mendes de Leon, Kop, de Swart, Bär and Appels, 1996), anxiety (Julkunen, Idänpään-Heikkilä and Saarinen, 1990; Moser and Dracup, 1996), feelings of vital exhaustion (Kop, Appels, Mendes de Leon, de Swart and Bär, 1994) and symptoms of psychological stress (Frasure-Smith, 1991). In addition, high levels of life stress (Ruberman, Weinblatt, Goldberg and Chaudhary, 1984) and use of sedatives (Wiklund, Oden, Sanne, Ulvenstam, Wilhelmsson and Wilhelmsen, 1988) have been associated with cardiac death and reinfarction in post-myocardial infarction patients. Hence, follow-up research suggests that it is not the occurrence of one specific negative emotion per se, but rather negative emotions in general that may promote progression of CHD. Importantly, associations between emotional distress and CHD progression are independent of disease severity.
coronary death or recurrent myocardial infarction in men who have survived an initial myocardial infarction (Frasure-Smith and Prince, 1985; Shekelle, Vernon and Ostfeld, 1991). As pointed out by Shekelle (1991), symptom reporting in patients with CHD may be related to increased susceptibility to acute emotional stressors that can be deleterious to an ischemic myocardium. Physical discomfort is in fact often accompanied by psychological distress, and the term somatopsychic distress has been proposed by Watson and Pennebaker (1989) to reflect the tendency of some individuals to report high levels of both somatic and emotional distress. That is, the awareness and reporting of somatic symptoms not only reflect physiological manifestations of actual disease, but are also influenced by psychological processes such as the general tendency to experience emotional distress. In general, the similarity of results of follow-up research suggests that, whether psychological stress is inferred from symptoms of emotional distress or somatic distress, the negative emotions involved may have an adverse effect on health in patients with CHD (Frasure-Smith, 1991).
concluded that there is now good evidence that psychosocial treatments may reduce mortality and morbidity in CHD (Linden, Stossel and Maurice, 1996). Hence, the similarity of results of these studies suggests that the accurate monitoring and treatment of emotional distress may improve health in patients with CHD.
Fourth, pathophysiological research suggests that coronary vasospasm (Nobuyoshi, Tanaka, Nosaka, Kimura, Yokoi, Hamasaki, Kim, Shindo and Kimura, 1991), increased platelet activity (Thaulow, Erikssen, Sandvik, Stormorken and Cohn, 1991) and decreased heart rate variability (Bigger, Fleiss, Rolnitzky and Steinman, 1993) may play a key role in the progression of and mortality from CHD. There is evidence that emotional distress may elicit these pathophysiological mechanisms in patients with CHD. Research on the dynamic process of coronary vasomotion demonstrated that mental stress may cause coronary spasm in coronary patients (Yeung, Vekshtein, Krantz, Vita, Ryan, Ganz and Selwyn, 1991), and evidence suggests that emotional stress in these patients may also initiate increased blood platelet reactivity (Grignani, Soffiantino, Zucchella, Pacchiarini, Tacconi, Bonomi, Psatoris, Sbaffi, Fratino and Tavazzi, 1991) and decreased heart rate variability (Carney, Saunders, Freedland, Stein, Rich and Jaffe, 1995).
myocardial infarction (Mittleman, Maclure, Sherwood, Mulry, Tofler, Jacobs, Friedman, Benson and Muller, 1995) and sudden cardiac death (Leor, Poole and Kloner, 1996). The similarity of these findings suggests that emotional distress may promote pathophysiological processes in CHD.
On the whole, converging lines of evidence suggest that emotional distress is intimately linked to mortality and morbidity in patients with well-established CHD. Apart from emotional distress, CHD has also been associated with the inhibition of emotions and behaviors. Suppressed anger, for example, has been associated with hypertension (Jorgensen, Johnson, Kolodziej and Schreer, 1996), incidence of CHD (Haynes, Feinleib and Kannel, 1980), and extent of angiographically documented CHD (MacDougall, Dembroski, Dimsdale and Hackett, 1985). In fact, there is evidence to suggest that long-term inhibition of negative emotions is a form of disease promoting stress (Pennebaker and Traue, 1993). However, an important unsolved issue is the role of basic personality traits in emotional distress and emotional inhibition among patients with established CHD (Denollet, 1993).
PERSONALITY AND EMOTIONAL DISTRESS
replicable across instruments and observers, and have substantial
predictive power over longer periods of time (Weinberger and Schwartz, 1990). Inotherwords, global traits reflect the general approach to life and summarize the tendencies of individuals.
Negative affectivity and social inhibition are two global personality traits that are relevant to emotion and behavior in a large number of situations. That is, negative affectivity is a basic personality trait that refers to the tendency to experience negative emotions across time and situations (Watson and Pennebaker, 1989). There is evidence to suggest that, in patients with documented CHD, emotional stress is not related to the severity of cardiac disorder but rather reflects individual differences in negative affectivity (Denollet, 1991).
By analogy, the inhibition of self-expression is largely a function of individual differences in normal personality. That is, social inhibition is a basic personality trait that refers to the tendency to inhibit the expression of emotions and behaviors in social interaction (Asendorpf, 1993). Individuals who are high in social inhibition may perceive the outside world as threatening in the sense that they anticipate unsatisfactory reactions from others such as disapproval or nonreward. Inhibited individuals try to avoid these reactions in an active way, which implies that they may adopt self-enhancing strategies such as withdrawal.
In fact, introversion has been associated with less seeking of social support (Amirkhan, Risinger and Swickert, 1995) and a poor quality of social interactions (Berry and Hansen, 1996). Social inhibition is closely related to the interpersonal dimension of introversion. In other words, socially inhibited individuals are not only low in self-expression but also tend to decrease the availability of social support in an active way, are likely to feel insecure among others, and may lack in assertiveness. Hence, it appears that, in addition to negative affectivity, social inhibition is a relevant personality trait in the context of CHD.
social inhibition moderates the role of negative affectivity in emotional stress-related CHD. Research in students has provided some indirect evidence to support this proposition; introversion was associated with less positive objective life events in undergraduate students as a whole (Magnus, Diener, Fujita and Pavot, 1993), and with poor emotional well-being in the subgroup of students who are also high in neuroticism (McFatter, 1994). In addition, psychopathological research suggests that individuals who are high in neuroticism as well as introversion are more prone to depression (Phillips, Gunderson, Hirschfeld and Smith, 1990).
The identification of personality subtypes in the population of coronary patients would make it possible to examine the effect of interactions between global traits on health outcomes. Deductive strategies rely on specific theoretical assumptions about the personality characteristics forming the basis for the classification of individuals into personality subtypes. Inductive strategies rely on statistical procedures whereby individuals are grouped quantitatively into subtypes according to the personality characteristics that they share. Cluster analysis is a multivariate procedure that was specifically designed to find natural subtypes that are discrete (Lorr and Suziedelis, 1982). This inductive approach has been used, for example, to delineate distinctly different personality subtypes in patients with chronic pain and alcoholism (Costello, Hulsey, Schoenfeld and Ramamurthy, 1987; Kline and Snyder, 1985).
PERSONALITY AND PROGRESSION OF CHD
subtype was characterized by high levels of anxiety, anger and chronic tension, and a low level of emotional well-being; follow-up assessment demonstrated that these patients still experienced much emotional distress at 15 months after the initial assessment.
By analogy with this empirically generated model, a median split on measures of negative affectivity and social inhibition was used to introduce the construct of the Distressed personality type (Denollet, Sys and Brutsaert, 1995) or type-D (Denollet, Sys, Stroobant, Rombouts, Gillebert and Brutsaert, 1996) in patients with CHD. This implies that the construct of type-D does not focus on only one of these traits at a time but rather on the way these traits interact; i.e., coronary patients with type-D tend simultaneously to experience negative emotions and inhibit the expression of emotions in social interaction. By contrast, (i) coronary patients who tend to experience negative emotions but are likely to express themselves openly to others are less likely to become depressed, and (ii) coronary patients who tend to be reserved in social interaction but are less likely to experience negative emotions may lead an emotionally stable life. Hence, the construct of type-D designates those coronary patients who, given their tendency to experience negative emotions and inhibit the expression of these emotions, are likely to be the victim of emotional distress over time.
individuals who were judged to be less competent leaders reported low levels of perceived social support (Sarason, Sarason and Shearin, 1986). In fact, poor social support and symptoms of emotional distress were found to be more prevalent in coronary patients with type-D than in non-type-D patients (Denollet, Sys, Stroobant, Rombouts, Gillebert and Brutsaert, 1996). These difficulties may result in poor recovery from CHD, including persistent chest pain complaints, failure to return to work, and use of tranquilizers (Denollet and De Potter, 1992).
There is some evidence to suggest that, eventually, the emotional difficulties of type-D patients may result in hard medical endpoints such as increased risk for mortality. Preliminary evidence was found in a follow-up study of 105 men who had survived a recent myocardial infarction (Denollet, Sys and Brutsaert, 1995). At baseline, they completed the Trait Anxiety Scale (Van Der Ploeg, Defares and Spielberger, 1980) as a measure of negative affectivity and the Inhibition Scale of the Heart Patients Psychological Questionnaire (Erdman, 1982) as a measure of social inhibition, respectively. A median split on both scales was used to classify 28 men as type-D (trait-anxiety ≥40 and inhibition ≥12) and 77 men as not type-D. After two to five years follow-up (mean= 3.8 years), the rate of death was significantly higher for type-D (11/28= 39 per cent) than for non-type-D (4/77=5 per cent) patients, p<0.0001. Standard risk factors -e.g., low exercise tolerance, previous myocardial infarction, smoking, and age- were also associated with mortality, but could not explain away this association.
the impact of type-D on prognosis remained significant (odds ratio 4.1 [95 per cent CI 1.9-8.8]; p=0.0004). The rate of death (six per cent) of patients scoring high on negative affectivity but low on inhibition did not differ significantly from that for low-negative affectivity patients (seven per cent). Hence, it was the negative affectivity x social inhibition interaction that had an adverse effect on prognosis. This implies that the role of normal personality traits in CHD is not limited to negative emotions but also includes the (non)expression of emotions and behaviors in socialinteraction.
Although these findings are encouraging, they only are the beginning of a new line of research on the role of psychosocial factors in the context of CHD. In other words, the construct of type-D is presented here as an adjunct to the lines of research focusing on specific psychosocial factors such as, for example, depression, anger, or vital exhaustion. Up to now, many important questions remain unanswered. Can the findings of epidemiological research on type-D and CHD be replicated in other settings and other countries? What are the pathways that could explain the effect of personality on adverse health outcomes in coronary patients? What are the options for intervention in type-D patients? These and many other questions need to be addressed in future research on the role of personality in CHD.
CONCLUDING REMARKS
mortality in women who had been diagnosed with a myocardial infarction (Powell, Shaker, Jones, Vaccarino, Thoresen and Pattillo, 1993). These findings support the hypothesis that suppressed emotions may be a risk factor for CHD in women, but additional research is needed to document the role of type-D personality in this context.
Biobehavioral research on CHD is replete with related concepts such as anger and hostility, depression, anxiety, vital exhaustion, and psychological stress (Lespérance and Frasure-Smith, 1996). However, inclusion of negative affectivity in the definition of type-D summarizes this field; i.e., negative affectivity is a trait that predisposes to experiencing these negative emotions. In addition, inclusion of social inhibition in the definition of type-D may add a new dimension to this field; i.e., evidence suggests that the tendency to inhibit self-expression in social relations adds to the predictive power of negative emotions in CHD.
In other words, the construct of type-D is different from previously studied psychosocial variables associated with CHD for a number of reasons. First, type-D is based on the notion that negative emotions in general (including depressive affect, anxiety, and anger) are associated with adverse health outcomes in CHD. Second, type-D is based on the notion that, apart from the clinically prominent dimension of negative emotions, the expression of emotions and behaviors in social interaction also accounts for a substantial amount of variance in the progression of CHD. Third, type-D aims to shift focus from psychopathology (e.g., major depression) to the role of normal personality dispositions in the context of CHD. Type A behavior is often mistaken for a personality type (e.g., Lespérance and Frasure-Smith, 1996) but this construct was specifically designed to avoid association with basic personality traits (Fried-man, 1990). The main purpose of the present paper was to point out that, in addition to assessing specific psychosocial factors in the context of CHD, it is equally important to assess broad and stable personality traits (Friedman, Tucker and Reise, 1995).
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Prof. Dr. Sarah Hampson May 28, 1997 Co-Editor, EJP Special Issue
Department of Psychology University of Surrey Guildford
Surrey GU2 5XH, England
Re: Personality, Emotional Distress and Coronary Heart Disease submitted to EJP Special Issue
Dear Dr. Hampson,
Thank you very much for your decision to accept my paper for publication in the special issue of the European Journal of Personality on personality and disease. Please find enclosed two copies of the revised manuscript.
I am in complete agreement with your comments on the paper. In order to deal with these comments, I have added a number of paragraphs to discuss the type-D construct somewhat more in detail. [1] The relation between type-D personality and emotional distress is now discussed in the second paragraph on page 13 (lines 9-18: "This implies that the construct of type-D ... "). The last paragraph on page 13 states that "Coronary patients with a type-D personality, through their liability to difficulties in the areas of emotional distress and emotional inhibition, may be at risk for adverse health outcomes". This paragraph also mentions the social processes linked to type-D (page 13, last line: "Type-D patients also tend to anticipate negative reactions from others ... "). [2] The issue of gender differences is now discussed in the first paragraph of the Concluding Remarks section (page 15, last paragraph: "An obvious limitation of the personality perspective on CHD presented in this paper is the fact that it is largely based on research in men with CHD ... "). [3] The extent to which type-D is different from previously studied psychosocial variables associated with CHD is now discussed in the second paragraph (page 16: "Biobehavioral research on CHD is congested with related concepts such as anger and hostility, ... ") and the third paragraph (page 16: "In other words, the construct of type-D is different from previously studied psychosocial variables associated with CHD for a number of reasons ... ") of the Concluding Remarks section.
I look forward to the EJP special issue. Sincerely yours,
University Hospital of Antwerp
Wilrijkstraat 10 Tel: +-32-3-821 3973
