personality, emotional distress and coronary heart disease

Personality, Emotional Distress andCoronary Heart Disease

JOHAN DENOLLET*

Department of Medicine, University of Antwerp, Antwerp, andDepartment of Psychology, University of Ghent, Ghent, Belgium

Abstract

Hostility, depression, and anxiety have been associated with coronary heart disease(CHD), but the role of emotional distress in the development of CHD is still acontroversial issue. Evidence shows, however, that emotional distress plays a key role inthe progression of CHD: (i) emotional distress is associated with pathophysiologicalmechanisms and cardiac events in coronary patients, (ii) psychosocial treatments ofemotional stress may reduce mortality and morbidity in these patients, and (iii)inhibition of negative emotions may accelerate CHD. Evidence also shows thatemotional stress as a risk factor for CHD is a chronic characteristic; research has,however, largely ignored the role of personality in this context. The approach topersonality and CHD that is presented in this paper revisits the tradition of globalpersonality traits, and is based on the notion that the interaction between negativeaffectivity (the tendency to experience negative emotions) and social inhibition (thetendency to inhibit self-expression in social interaction) has potential explanatorypower in coronary patients. The construct of type-D personality is introduced todesignate those coronary patients who experience difficulties in the areas of negativeemotions and self-expression. Type-D patients typically report high levels of depressivesymptoms and poor levels of social support. Evidence is presented which suggests that,eventually, the emotional difficulties of type-D patients may result in hard endpointssuch as increased risk for long-term mortality. It is concluded that, in addition toassessing specific psychosocial factors, it is equally important to assess the effect ofglobal traits and their interaction on prognosis in patients with CHD. & 1997 JohnWiley & Sons, Ltd.

Eur. J. Pers. 11, 343±357, 1997.

No. of Figures: 0. No. of Tables: 0. No. of References: 94.

CCC 0890±2070/97/050343±15$17.50 Received 14 March 1997& 1997 John Wiley & Sons, Ltd. Accepted 10 June 1997

European Journal of Personality, Vol. 11, 343±357 (1997)

*Correspondence to: Johan Denollet, University Hospital of Antwerp, Wilrijkstraat 10, B-2650 Edegem,Belgium. Tel: +32 3 821 3973. Fax: +32 3 829 0520.

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, manynew diagnostic and treatment strategies for patients with CHD have been developed,including coronary angiography, cardiac echography, bypass surgery, coronaryangioplasty, beta-blocker therapy, ACE inhibition and thrombolytic therapy. Inpatients with myocardial infarction, short-term prognosis has in fact improved since1960 due to these new developments, but there are still some unknown factors thatappear to play a role in both the development and progression of CHD. The presentpaper focuses on the proposition that emotional distress is such a factor that may bedeleterious to the ischaemic myocardium, and that personality factors, to a largeextent, may account for the relation between emotional distress and CHD.

EMOTIONAL DISTRESS AND DEVELOPMENT OF CHD

In the 20th century, medicine has found cures for most diseases where there is asingle overwhelming obvious cause, such as the infectious diseases. Many healthproblems today, however, are caused by chronic disorders, such as CHD, thatcannot be explained by a classical monocausal model (Cunningham, 1981; Depueand Monroe, 1986). As a consequence, health care professionals are increasinglyconfronted with chronic ailments in which different factors can probably contributeto the development of disease. That is, the human body is a complex organization ofsubsystems where many factors maintain a balance. It follows that disease can beviewed as any persistent harmful disturbance of its equilibrium or homeostasis(Cunningham, 1981). Apart from biological factors, psychosocial and environmentalfactors may adversely affect bodily homeostasis, thereby increasing the vulnerabilityto chronic disease and the likelihood of decrements in emotional well-being (see e.g.Friedman, 1991).

With reference to CHD, evidence indicates that 50 per cent of the new casescannot be identified on the basis of standard risk factors such as hypertension,hyperlipidaemia, and smoking (Krantz, Schneiderman, Chesney, McCann, Reading,Roskies, Stoney and Williams, 1989). Psychosocial research on CHD has receivedimpetus from this inability to explain a large portion of variance in the incidence ofCHD. Among the more controversial risk factors, psychosocial factors are of primeimportance. Initially, research in this area mainly focused on the Type A behaviourpattern (see e.g. Rosenman, Brand, Jenkins, Friedman, Straus and Wurm, 1975), aconstruct that has prompted much research on psychosocial risk factors for thedevelopment of CHD. Although evidence indicates that the Structured Interviewassessment of Type A behaviour predicts actual CHD (Matthews, 1988), the natureof that association is, however, far more complex than is conveyed by the simpleassertion that the Type A behaviour pattern is a risk factor for CHD (Dimsdale,1988).

In more recent years, there has been a shift from Type A behaviour to specificemotional factors in research on CHD (see e.g. Booth-Kewley and Friedman, 1987).Reanalyses of data from the Western Collaborative Group Study (the first

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& 1997 John Wiley & Sons, Ltd. Eur. J. Pers. Vol. 11, 343±357 (1997)

prospective study that identified Type A as a risk factor) and the Multiple RiskFactor Intervention Trial (a frequently cited study questioning the role ofbehavioural risk factors in CHD) indicated that interview ratings of hostility wereassociated with the incidence of CHD (Dembroski, MacDougall, Costa andGrandits, 1989; Hecker, Chesney, Black and Frautschi, 1988).

However, studies of associations between self-ratings of hostility as measured bythe Cook±Medley Hostility Scale (Cook and Medley, 1954) and the incidence ofCHD have produced inconsistent findings. High scores on this hostility scale havebeen associated with degree of angiographically documented narrowing of thecoronaries (Williams, Haney, Lee, Kong, Blumenthal and Whalen, 1980) andincreased risk for CHD incidence (Barefoot, Dahlstrom and Williams, 1983), butother studies failed to replicate this association between scores on the Cook±MedleyHostility Scale and CHD (Hearn, Murray and Luepker, 1989; Leon, Finn, Murrayand 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 andRosenman, 1985) may act as a potential cardiotoxic agent, but that evidence is mixedand more research is needed to elucidate the relationship between hostility/anger andthe development of CHD.

Interestingly, research suggests that the development of CHD may be associatedwith other negative emotions as well. An important study that provided evidence forthe role of various negative affective conditions in the deterioration of health is themeta-analytic survey of Friedman and Booth-Kewley (1987). These authors foundthat not only anger, but also depression and anxiety may be associated with theincidence of chronic diseases, including cardiovascular disorders. Further analyses oftheir findings suggested that depression may be a potential risk factor for thedevelopment of CHD (Booth-Kewley and Friedman, 1987). This proposition wassupported by a clinical follow-up study which demonstrated that interview ratings ofdepression in a sample of patients undergoing coronary angiography were associatedwith the long-term incidence of major coronary events (Carney, Rich, Freedland,Saini, TeVelde, Simeone and Clark, 1988). Recent evidence further supported thenotion that the development of CHD is related to symptoms of depression (Barefootand Schroll, 1996).

The development of CHD is, however, not only related to hostility/anger anddepressive symptomatology, but also to anxiety (Haines, Imeson and Meade, 1987;Kawachi, Colditz, Ascherio, Rimm, Giovannucci, Stampfer and Willett, 1994). Inaddition, global ratings of general emotional distress have been associated with theincidence of CHD (Crisp, Queenan and D'Souza, 1984; Rosengren, Tibblin andWilhelmsen, 1991). Research also suggests that health complaints that are oftenrelated to emotional distress, such as undue fatigue (Appels and Mulder, 1988) andsleeping problems (Wingard and Berkman, 1983), are associated with the incidenceof and mortality from CHD. These findings suggest that it is not the occurrence ofone specific negative emotion per se, but rather the occurrence of emotional distressin general that may be associated with the development of CHD.

Unfortunately, self-reports of emotional distress are not specific of a cardiacdisease. Emotional distress may, for example, be associated with the perception andreporting of cardiologic complaints (e.g., chest pain) but not actual cardiac disease

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(Costa and McCrae, 1987; Watson and Pennebaker, 1989). Although self-reportedemotional distress is in fact not synonymous with the development of organicdisease, this phenomenon does not mean that emotional distress cannot also play atrue causal role in CHD. Rather, evidence suggests that emotional distress isassociated with both invalid health complaints and actual coronary proneness(Friedman, 1990). As pointed out by Alonzo, Simon and Feinleib (1975), the overallresponse of individuals and the medical community to symptoms of emotionaldistress and general malaise, however, is that they are `manageable' or that a periodof `wait and see' is appropriate. In contrast to this attitude, the evidence reviewedabove suggests that individuals who chronically experience high levels of emotionaldistress may actually be at risk for CHD. In any case, the role of emotional distressin the development of CHD still is a controversial issue (see for example Friedman,1990; Stone and Costa, 1990). Abundant evidence indicates, however, that emotionaldistress does play a key role in the progression of CHD.

EMOTIONAL DISTRESS AND PROGRESSION OF CHD

Recent studies demonstrated that, apart from biomedical correlates of diseaseseverity, emotional distress is closely related to cardiac mortality and morbidityamong patients with well established CHD. That is, emotional distress has beenassociated with progression of, and recovery from, CHD. Evidence for the role ofemotional distress in this area comes from (i) long-term follow-up studies ofemotional distress in patients with CHD, (ii) long-term follow-up studies of somaticdistress in patients with CHD, (iii) trials of psychosocial interventions in coronarypatients, and (iv) studies of pathophysiological processes in CHD.

First, follow-up studies indicated that emotional distress is related to progressionof CHD. Nowadays, one generally assumes that symptoms of depression areassociated with an increased long-term risk for cardiac mortality and reinfarctionamong patients who have survived a myocardial infarction (see e.g. Ahern, Gorkin,Anderson, Tierney, Hallstrom, Ewart, Capone, Schron, Kornfeld, Herd, Richardsonand Follick, 1990; Frasure-Smith, LespeÂ rance and Talajic, 1995; Ladwig, Kieser,KoÈ nig, Breithardt and Borggrefe, 1991). Depression has also been associated withincreased risk for coronary events and mortality in arrhythmia patients (Kennedy,Hofer, Cohen, Shindledecker and Fisher, 1987) and in patients with angiographicallydocumented CHD (Carney et al., 1988).

Fatal and non-fatal cardiac events in coronary patients are, however, related notonly to depression but also to anger (Mendes de Leon, Kop, de Swart, BaÈ r andAppels, 1996), anxiety (Julkunen, IdaÈ npaÈ aÈ n-HeikkilaÈ and Saarinen, 1990; Moser andDracup, 1996), feelings of vital exhaustion (Kop, Appels, Mendes de Leon, de Swartand BaÈ r, 1994) and symptoms of psychological stress (Frasure-Smith, 1991). Inaddition, high levels of life stress (Ruberman, Weinblatt, Goldberg and Chaudhary,1984) and use of sedatives (Wiklund, Oden, Sanne, Ulvenstam, Wilhelmsson andWilhelmsen, 1988) have been associated with cardiac death and reinfarction in post-myocardial infarction patients. Hence, follow-up research suggests that it is not theoccurrence of one specific negative emotion per se, but rather negative emotions ingeneral that may promote progression of CHD. Importantly, associations betweenemotional distress and CHD progression are independent of disease severity.

346 J. Denollet


Second, follow-up studies suggest that somatic distress as well is associated withrisk for coronary death or recurrent myocardial infarction in men who have survivedan initial myocardial infarction (Frasure-Smith and Prince, 1985; Shekelle, Vernonand Ostfeld, 1991). As pointed out by Shekelle et al. (1991), symptom reporting inpatients with CHD may be related to increased susceptibility to acute emotionalstressors that can be deleterious to an ischaemic myocardium. Physical discomfort isin fact often accompanied by psychological distress, and the term somatopsychicdistress has been proposed by Watson and Pennebaker (1989) to reflect the tendencyof some individuals to report high levels of both somatic and emotional distress.That is, the awareness and reporting of somatic symptoms not only reflectphysiological manifestations of actual disease, but are also influenced bypsychological processes such as the general tendency to experience emotionaldistress. In general, the similarity of results of follow-up research suggests that,whether psychological stress is inferred from symptoms of emotional distress orsomatic distress, the negative emotions involved may have an adverse effect onhealth in patients with CHD (Frasure-Smith, 1991).

Third, findings from trials of psychosocial interventions suggest that help indealing with emotional distress may significantly reduce mortality among post-myocardial infarction patients. In the USA, post hoc analyses of findings from theRecurrent Coronary Prevention Project (an intervention trial that originally aimedat the modification of Type A behaviour per se) indicated that this trial not onlyproduced significant reductions in Type A behaviour, but also in depression andanger, as well as a significant improvement in self-efficacy and well-being (Mendesde Leon, Powell and Kaplan, 1991). In Canada, findings from the Ischemic HeartDisease Life Stress Monitoring Program suggested that modification of emotionaldistress may slow down progression of CHD in post-myocardial infarction patientswho report high levels of stress (Frasure-Smith and Prince, 1985; 1989). Reductionsin mortality associated with this stress monitoring program and cardiovascularmedication trials, in fact, appear to fall within the same range (Frasure-Smith, 1991).A recent meta-analytic review of intervention trials concluded that there is now goodevidence that psychosocial treatments may reduce mortality and morbidity in CHD(Linden, Stossel and Maurice, 1996). Hence, the similarity of results of these studiessuggests that the accurate monitoring and treatment of emotional distress mayimprove health in patients with CHD.

Fourth, pathophysiological research suggests that coronary vasospasm(Nobuyoshi, Tanaka, Nosaka, Kimura, Yokoi, Hamasaki, Kim, Shindo andKimura, 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 andmortality from CHD. There is evidence that emotional distress may elicit thesepathophysiological mechanisms in patients with CHD. Research on the dynamicprocess of coronary vasomotion demonstrated that mental stress may causecoronary spasm in coronary patients (Yeung, Vekshtein, Krantz, Vita, Ryan,Ganz and Selwyn, 1991), and evidence suggests that emotional stress in thesepatients 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, Richand Jaffe, 1995).

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These pathophysiological mechanisms may cause emotion-related cardiacdysfunctions such as myocardial ischaemia (Blumenthal, Jiang, Waugh, Frid,Morris, Coleman, Hanson, Babyak, Thyrum, Krantz and O'Connor, 1995; Gabbay,Krantz, Kop, Hedges, Klein, Gottdiener and Rozanski, 1996; Krantz, Helmers,Bairey, Nebel, Hedges and Rozanski, 1991), reductions in left ventricular ejectionfraction (Ironson, Barr Taylor, Boltwood, Bartzokis, Dennis, Chesney, Spitzer andSegall, 1992), and cardiac arrhythmias (Carney, Freedland, Rich, Smith and Jaffe,1993). Accordingly, mental and emotional stress has been associated with theincidence of fatal and non-fatal cardiac events (Jiang, Babyak, Krantz, Waugh,Coleman, Hanson, Frid, McNulty, Morris, O'Connor and Blumenthal, 1996) andthe triggering of 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 thatemotional distress may promote pathophysiological processes in CHD.

On the whole, converging lines of evidence suggest that emotional distress isintimately linked to mortality and morbidity in patients with well established CHD.Apart from emotional distress, CHD has also been associated with the inhibition ofemotions and behaviours. Suppressed anger, for example, has been associated withhypertension (Jorgensen, Johnson, Kolodziej and Schreer, 1996), incidence of CHD(Haynes, Feinleib and Kannel, 1980), and extent of angiographically documentedCHD (MacDougall, Dembroski, Dimsdale and Hackett, 1985). In fact, there isevidence to suggest that long-term inhibition of negative emotions is a form ofdisease promoting stress (Pennebaker and Traue, 1993). However, an importantunsolved issue is the role of basic personality traits in emotional distress andemotional inhibition among patients with established CHD (Denollet, 1993).

PERSONALITY AND EMOTIONAL DISTRESS

Although emotional distress as a risk factor for CHD is a chronic characteristic thatis stable over time (see e.g. Barefoot and Schroll, 1996), biobehavioural research onCHD has largely ignored the role of broad, general personality traits in this context(Denollet, 1993). Therefore, the approach to personality and CHD that I would liketo propose in the present paper revisits the older tradition of global personalitytraits; this neo-Allportian approach to personality has been advocated by others aswell (Funder, 1991; Ouellette Kobasa, 1990). The number of traits that one regardsas basic depends on the level at which one chooses to describe personality. A viewwhich regards behaviour as highly specific to situations may be limited to narrowertraits. Conversely, at the highest level of analysis, the focus is on global personalitytraits that are replicable across instruments and observers, and have substantialpredictive power over longer periods of time (Weinberger and Schwartz, 1990). Inother words, global traits reflect the general approach to life and summarize thetendencies of individuals.

Negative affectivity and social inhibition are two global personality traits that arerelevant to emotion and behaviour in a large number of situations. That is, negativeaffectivity is a basic personality trait that refers to the tendency to experiencenegative emotions across time and situations (Watson and Pennebaker, 1989). Thereis evidence to suggest that, in patients with documented CHD, emotional stress is not

348 J. Denollet


related to the severity of cardiac disorder but rather reflects individual differences innegative affectivity (Denollet, 1991).

By analogy, the inhibition of self-expression is largely a function of individualdifferences in normal personality. That is, social inhibition is a basic personality traitthat refers to the tendency to inhibit the expression of emotions and behaviours insocial interaction (Asendorpf, 1993). Individuals who are high in social inhibitionmay perceive the outside world as threatening in the sense that they anticipateunsatisfactory reactions from others such as disapproval or nonreward. Inhibitedindividuals try to avoid these reactions in an active way, which implies that they mayadopt 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 interpersonaldimension of introversion. In other words, socially inhibited individuals are not onlylow in self-expression but also tend to decrease the availability of social support in anactive 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 arelevant personality trait in the context of CHD.

More specifically, what I would like to point out here is that the interactionbetween these personality traits has potential explanatory power in coronarypatients. This implies that social inhibition moderates the role of negative affectivityin emotional stress-related CHD. Research in students has provided some indirectevidence to support this proposition; introversion was associated with less positiveobjective life events in undergraduate students as a whole (Magnus, Diener, Fujitaand Pavot, 1993), and with poor emotional well-being in the subgroup of studentswho are also high in neuroticism (McFatter, 1994). In addition, psychopathologicalresearch suggests that individuals who are high in neuroticism as well as introversionare more prone to depression (Phillips, Gunderson, Hirschfeld and Smith, 1990).

The identification of personality subtypes in the population of coronary patientswould make it possible to examine the effect of interactions between global traits onhealth outcomes. Deductive strategies rely on specific theoretical assumptions aboutthe personality characteristics forming the basis for the classification of individualsinto personality subtypes. Inductive strategies rely on statistical procedures wherebyindividuals are grouped quantitatively into subtypes according to the personalitycharacteristics that they share. Cluster analysis is a multivariate procedure that wasspecifically designed to find natural subtypes that are discrete (Lorr and Suziedelis,1982). This inductive approach has been used, for example, to delineate distinctlydifferent personality subtypes in patients with chronic pain and alcoholism (Costello,Hulsey, Schoenfeld and Ramamurthy, 1987; Kline and Snyder, 1985).

PERSONALITY AND PROGRESSION OF CHD

In contrast, biobehavioural research on CHD has largely overlooked the possibilitythat interactive relations among personality traits may affect the course of thedisease process (Denollet, 1993). Cluster analytic research showed, however, that a`negative affectivity6social inhibition' interaction model can also be applied topatients with CHD (Denollet and De Potter, 1992). More specifically, this research

type-D and CHD 349


yielded the existence of a discrete subtype of coronary patients who displayed highlevels of negative affectivity and social inhibition. This personality subtype wascharacterized by high levels of anxiety, anger, and chronic tension, and a low level ofemotional well-being; follow-up assessment demonstrated that these patients stillexperienced much emotional distress at 15 months after the initial assessment.

By analogy with this empirically generated model, a median split on measures ofnegative affectivity and social inhibition was used to introduce the construct of theDistressed 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 ata time but rather on the way these traits interact; i.e., coronary patients with type-Dtend simultaneously to experience negative emotions and inhibit the expression ofemotions in social interaction. By contrast, (i) coronary patients who tend toexperience negative emotions but are likely to express themselves openly to othersare less likely to become depressed, and (ii) coronary patients who tend to bereserved in social interaction but are less likely to experience negative emotions maylead an emotionally stable life. Hence, the construct of type-D designates thosecoronary patients who, given their tendency to experience negative emotions andinhibit the expression of these emotions, are likely to be the victims of emotionaldistress over time.

Coronary patients with a type-D personality, through their liability to difficultiesin the areas of emotional distress and emotional inhibition, may be at risk foradverse health outcomes. Type-D patients are prone to symptoms of anxiety,depression, and psychological stress, and these symptoms are accompanied by therelative absence of positive emotions. These patients may be lacking in self-esteem,are less satisfied with life in general, and tend to report low levels of subjective well-being. Type-D patients also tend to anticipate negative reactions from others;therefore, they are likely to decrease the availability of social support in an activeway. In keeping with this proposition, research showed that introversion measuredat college entry was associated with low perceived social support at midlife (VonDras and Siegler, 1997), and that individuals who were judged to be less competentleaders reported low levels of perceived social support (Sarason, Sarason andShearin, 1986). In fact, poor social support and symptoms of emotional distress werefound to be more prevalent in coronary patients with type-D than in non-type-Dpatients (Denollet et al., 1996). These difficulties may result in poor recovery fromCHD, including persistent chest pain complaints, failure to return to work, and useof tranquilizers (Denollet and De Potter, 1992).

There is some evidence to suggest that, eventually, the emotional difficulties oftype-D patients may result in hard medical endpoints such as increased risk formortality. Preliminary evidence was found in a follow-up study of 105 men who hadsurvived a recent myocardial infarction (Denollet et al., 1995). At baseline, theycompleted the Trait Anxiety Scale (Van Der Ploeg, Defares and Spielberger, 1980) asa measure of negative affectivity and the Inhibition Scale of the Heart PatientsPsychological 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 540 and inhibition 512) and 77 men as not type D. After 2±5 yearsfollow-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.

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Standard risk factorsÐe.g., low exercise tolerance, previous myocardial infarction,smoking, and ageÐwere also associated with mortality, but could not explain awaythis association.

A second study of 268 men and 35 women with CHD confirmed these initialfindings and demonstrated that social inhibition moderated the relation betweendistress and mortality (Denollet et al., 1996). A median split on the SpielbergerAnxiety and the Erdman Inhibition scales was used to classify 85 patients as type-D(trait anxiety 543 and inhibition 512) and 218 patients as not type-D. After 6±10years follow-up (mean=7.9), the rate of death was significantly higher for type-D(23/85=27 per cent) than for non-type-D (15/218=7 per cent) patients, p<0.00001.After controlling for disease severity and other standard risk factors, the impact oftype-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 negativeaffectivity but low on inhibition did not differ significantly from that for low-negative-affectivity patients (seven per cent). Hence, it was the negativeaffectivity6social inhibition interaction that had an adverse effect on prognosis.This implies that the role of normal personality traits in CHD is not limited tonegative emotions but also includes the (non)expression of emotions and behavioursin social interaction.

Although these findings are encouraging, they only are the beginning of a new lineof research on the role of psychosocial factors in the context of CHD. In otherwords, the construct of type-D is presented here as an adjunct to the lines of researchfocusing on specific psychosocial factors such as, for example, depression, anger, orvital exhaustion. Up to now, many important questions remain unanswered. Can thefindings of epidemiological research on type-D and CHD be replicated in othersettings and other countries? What are the pathways that could explain the effect ofpersonality on adverse health outcomes in coronary patients? What are the optionsfor intervention in type-D patients? These and many other questions need to beaddressed in future research on the role of personality in CHD.

CONCLUDING REMARKS

An obvious limitation of the personality perspective on CHD presented in this paperis the fact that it is largely based on research in men with CHD. Althoughcardiovascular disease is the leading cause of death in women (Kuhn and Rackley,1993), little is known about the role of psychosocial factors in the development/progression of CHD in women. Findings from the Framingham Heart Studyindicated that suppressed hostility was significantly associated with the incidence ofCHD among women holding clerical jobs (Haynes and Feinleib, 1980). Accordingly,it has been suggested that suppressed emotions may be associated with long-termmortality in women who have been diagnosed with a myocardial infarction (Powell,Shaker, Jones, Vaccarino, Thoresen and Pattillo, 1993). These findings support thehypothesis that suppressed emotions may be a risk factor for CHD in women, butadditional research is needed to document the role of type-D personality in thiscontext.

Biobehavioural research on CHD is replete with related concepts such as angerand hostility, depression, anxiety, vital exhaustion, and psychological stress

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(LespeÂ rance and Frasure-Smith, 1996). However, inclusion of negative affectivity inthe definition of type-D summarizes this field; negative affectivity is a trait thatpredisposes to experiencing these negative emotions. In addition, inclusion of socialinhibition 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 addsto the predictive power of negative emotions in CHD.

In other words, the construct of type-D is different from previously studiedpsychosocial variables associated with CHD for a number of reasons. First, type-Dis 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 ofnegative emotions, the expression of emotions and behaviours in social interactionalso 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) tothe role of normal personality dispositions in the context of CHD. Type A behaviouris often mistaken for a personality type (see e.g. LespeÂ rance and Frasure-Smith,1996) but this construct was specifically designed to avoid association with basicpersonality traits (Friedman, 1990). The main purpose of the present paper was topoint out that, in addition to assessing specific psychosocial factors in the context ofCHD, it is equally important to assess broad and stable personality traits (Friedman,Tucker and Reise, 1995).

The evidence reviewed in this paper suggests (i) that emotional distress plays animportant role in the progression of CHD, (ii) that emotional distress in coronarypatients largely reflects individual differences in negative affectivity, and (iii) thatsocial inhibition moderates the association between negative affectivity and CHD.Does this mean that the association between emotional distress and CHD is based onthe solid grounds of personality? Only inclusion of personality traits in futureresearch may provide an appropriate answer to this question. There is good evidencethat type-D may benefit this line of research on CHD.

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