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Anger and Incident Heart Disease in the Caerphilly Study

From the MRC Epidemiology Unit (South Wales), Llandough Hospital, Penarth, Vale of Glamorgan, United Kingdom (J.E.J.G., P.M.S., P.C.E.); Department of Epidemiology and Public Health, Queen’s University of Belfast, Belfast, Northern Ireland (J.W.G.Y.); Department of Epidemiology and Public Health, University College of London Medical School, London, United Kingdom (S.A.S.).

Address reprint requests to: John E. J. Gallacher, PhD, School of Psychology, Cardiff University, Tower Bldg., Park Place, P.O. Box 901, Cardiff CF1 3YG, United Kingdom. Email: j.gallacher@ glenwood.cix.co.uk

	ABSTRACT

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION APPENDIX ACKNOWLEDGMENTS REFERENCES

 
OBJECTIVE: The idea that anger may predict ischemic heart disease (IHD) is more than 30 years old. Some, but not all, prospective studies have supported this suggestion. Attention has focused on hostility as the critical component of anger for IHD risk. This idea is explored using prospective data from the Caerphilly study.

METHODS: A sample of 2890 men aged 49 to 65 years living in and around Caerphilly, South Wales, was identified. Anger was assessed using the Framingham scales comprising "anger symptoms," "anger in," "anger out," and "anger discuss." A new "suppressed anger" scale was also constructed. Cardiovascular risk factors assessed included baseline blood pressure, total and high-density lipoprotein cholesterol, fibrinogen, white cell count, psychiatric caseness as assessed by the General Health Questionnaire, social support, smoking habit, alcohol consumption, leisure exercise, body mass index, and calorie intake. Prediction of IHD, measured as the occurrence of a major event over a follow-up period of 9 years, was assessed using multiple logistic regression analysis.

RESULTS: A low anger out score predicted increased risk of a major IHD event (relative odds (RO) = 1.70; 95% confidence interval = 1.26–2.29 for all RO). This association was unchanged on controlling for physiological risk factors (RO = 1.74), psychosocial risk factors (RO = 1.72), and behavioral risk factors (RO = 1.69). Suppressed anger showed associations with incident IHD similar to those of anger out but identified the population at risk more closely.

CONCLUSIONS: Anger out and suppressed anger were predictive of incident IHD. Neither of these constructs are overtly similar to hostility. These findings suggest there may be mechanisms other than hostility by which anger predicts IHD risk and that a conceptually varied approach to anger is currently appropriate.

Key Words: anger • hostility • heart disease

Abbreviations: CI = confidence interval; ECG = electrocardiogram; GHQ30 = 30-item General Health Questionnaire; HDL =high-density lipoprotein; ICD = International Classification ofDiseases; IHD = ischemic heart disease; MI = myocardialinfarction; r_sp = Spearman correlationcoefficient; RO = relative odds; SD = standard deviation.

	INTRODUCTION

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The idea that anger may predict IHD is more than 30 years old (1). Prospective studies have supported this suggestion (2–4), although negative findings have also been reported (5–7). Overall, reviews conclude there is an increased risk of IHD for high levels of anger (8–10), with the risk estimated at between 1.5 and 2.6 times that of low levels of anger (11, 12).

Closer scrutiny of the anger construct has focused on hostility, an emphasis on cynical, suspicious, and denigrating beliefs held toward others, as being the vehicle of increased IHD risk (13). In terms of mechanisms, hostility is considered to cause increased exposure to anger-related processes by increasing either the frequency, intensity, or duration of anger episodes (14).

For several reasons, exclusive focus on hostility as the mechanism relating anger to IHD may be premature. From a psychometric perspective, more opinion than evidence appears to have been used in the interpretation of what anger scales measure. Relatively little effort has been expended to validate the reinterpretation of existing anger scales as measures of hostility or to develop specific tests of hostility (14). Also, associations of IHD with measures of anger that do not overtly assess a cynical or distrustful response style have been reported. Julius et al. (15) report higher risk of IHD for those who suppress anger, whereas Kawachi et al. (12) report increased risk of incident IHD for anger but not for cynicism, one of the characteristics of hostility. Lastly, Mittleman et al. (16) have demonstrated the importance of anger episodes as triggers for coronary events regardless of their attitudinal origins. This is supported by Gelernt and Hochman (17), who demonstrated the increased risk of infarction attached to an intense emotional episode.

The present study looks at evidence for the critical components of the anger construct. Anger was measured using items taken from the Framingham study. In the Framingham study, these items were organized into four scales comprising "anger symptoms," which describes the severity of somatic symptoms experienced during an extreme anger episode; "anger in," which describes the likelihood of anger being repressed and so not expressed during an extreme anger episode; "anger out," which describes the likelihood of anger being expressed toward someone else during an extreme anger episode; and "anger discuss," which describes the likelihood of talking about feelings during an extreme anger episode. IHD risk was measured as the occurrence of a major IHD event over a follow-up period of nearly 9 years.

	METHODS

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Study Population and Survey Methods
The general design of the Caerphilly study has been described elsewhere (18, 19). The original cohort of 2512 men aged 45 to 59 years was recruited between 1979 and 1983. Since then, the participants have been reexamined at roughly 5-year intervals. The men who are the subject of this report are those seen at the first reexamination between 1984 and 1988, when they were aged 49 to 65 years. Men of the same age who had moved into the geographically defined area since the original recruitment were also considered eligible. A total sample, therefore, of 2890 men was identified.

At each examination, men were invited to attend an afternoon or evening clinic, where a detailed medical and lifestyle history was obtained. At the first reexamination, this included smoking habit and alcohol consumption, social class and employment status, the GHQ30 (20), three questions on social support taken from the Whitehall study (21), the Minnesota leisure exercise questionnaire (22), and a dietary questionnaire (23). The London School of Hygiene and Tropical Medicine chest pain questionnaire was administered (24), a full 12-lead ECG was recorded, and weight and blood pressure were measured. The men were then invited to return, fasting, to an early morning clinic, where a blood sample was taken. Cardiovascular risk factors measured included baseline blood pressure, fibrinogen, and white cell count. Total and HDL cholesterol were estimated using enzymatic procedures (25).

Eleven items from the Framingham study were used to assess anger. These items assess the expression of anger "when really angry or annoyed" (26). A twelfth item (from the anger symptoms scale) was omitted in error. Answers for each item were recorded using a three-point Likert response format of "very likely," "somewhat likely," and "not too likely.. Responses were scored as 2, 1, or 0, respectively, and the scales were calculated by summing these response scores. The items are given in Appendix 1.

Follow-Up and Incident IHD
The incidence of IHD was measured up to the third reexamination (1994–1997), which occurred at a nearly constant interval of 105 (SD = 6) months after the first reexamination. All men had a marker placed against their records in the National Health Service Central Registry for the purpose of identifying cause of death. ICD codes 410 to 414 on death certificates defined fatal IHD. The chest pain questionnaire and hospital activity analysis of all men admitted to local hospitals with a diagnosis of ICD 410 to 414 were used as a basis for a search of the hospital notes for events meeting standard World Health Organization criteria for acute MI (27). Finally, the appearance on any follow-up ECG of major or moderate Q waves (Minnesota codes 1–1–any, or 1–2-1 to 1–2-5, or 1–2-7) when there were no Q waves (1–1–any, 1–2—any, or 1–3–any) on the baseline ECG was taken as evidence that a nonfatal MI had occurred during the follow-up period. Major incident IHD was defined as the occurrence of any of these three events.

Statistical Methods
For statistical analysis, the anger scales were treated as continuous distributions in relation to associations with IHD risk factors, and no transformations were applied. For analyses on incident IHD, the scales were dichotomized using, as nearly as possible, a median split. Risk of IHD was assessed using multiple logistic regression analysis, and the convention has been that the lower risk group has been taken as the baseline group, so that RO are always given as greater than 1.0. For the logistic regression analyses, age and blood pressure were treated as continuous variables. Social class was entered as a two-level factor (manual/nonmanual), as was employment status (employed/unemployed). Evidence of previous IHD was entered as three factors comprising history of angina pectoris (yes/no), history of MI (yes/no), and evidence of ECG ischemia (probable/possible/no).

All physiological variables were used as continuous variables. For psychosocial variables, the GHQ30 was entered as a six-level factor because of its marked J-shaped distribution. Two social support scores were calculated. The first was an estimate of social support network in terms of the number of social contacts and was used as a continuous variable. The second was an estimate of social support access in terms of the frequency of contact with a confidant and was entered as a three-level factor because of the use of an ordinal scale scoring system. Of the behavioral variables, smoking was entered as a three-level factor and alcohol consumption as a four-level factor, whereas exercise, body mass index, and total calorie intake were entered as continuous variables.

Men with evidence of ischemia at baseline were not excluded. Thirty-one percent of this general population sample had some evidence of ischemia as judged by the chest pain questionnaire and the ECG. Exclusion of such a group, among whom 50% of the incident events occurred, does not seem satisfactory. Instead, measures of angina, history of severe chest pain, and ECG ischemia were included as three covariates in the analysis. As a check, some analyses were performed separately for men with and without evidence of ischemia at baseline.

	RESULTS

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Of the total cohort, 2398 (83%) attended the clinic, and of these, 2388 (99.5%) completed the anger questionnaire. Over the average follow-up interval of 105 months, 282 (11.8%) men developed major IHD.

Preliminary investigations included factor analysis of the anger data. Four scales were identified corresponding to the four original scales constructed for the Framingham study. Items 1 to 4 loaded to form the anger symptoms scale, items 5 to 7 loaded to form the anger in scale, items 8 and 9 loaded to form the anger out scale, and items 10 and 11 loaded to form the anger discuss scale. These factors explained 56% of the total variance between the anger items.

None of the Framingham anger scales showed a Gaussian distribution (Figure 1). Spearman correlations showed the anger scales to be largely independent of each other, with the strongest association being between anger symptoms and anger out (r = 0.21). The smallest association was between anger out and anger discuss (r = 0.01). All other associations between anger scales were around r = 0.1. Over our narrow age range, mean anger in scores were higher (p < .001), whereas mean anger out scores were lower in older men (p < .001). This might suggest a reduction in the expression of anger with increasing age. Anger symptoms and anger in scores were found to be lower in the nonmanual social class relative to manual social class and among employed men relative to unemployed men.

View larger version (23K): [in this window] [in a new window]   Fig. 1. Distribution of scores for the Framingham anger scales.

View larger version (16K): [in this window] [in a new window]   Fig. 2. Distribution of scores for the suppressed anger scale.

The interaction of suppressed anger with social support was investigated more closely. For the purposes of this analysis, both social support scores were entered as three- factors. The social support network score showed no interaction with suppressed anger. The social support access score showed a suggestion of an interaction with suppressed anger such that the RO of IHD associated with suppressed anger decrease as the frequency of contact with a close person increases; from 2.60 if the frequency of contact is less than weekly, through 1.76 if frequency of contact is weekly, to 1.45 if frequency of contact is daily. However, a formal test for the presence of an interaction does not achieve statistical significance (2 = 2.71, df = 2, p = .26).

	DISCUSSION

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A starting point for interpreting these data are that three relatively crude questions can be used to identify men at increased risk from IHD. Arising from this observation are issues of whether the association is trustworthy and, if so, what is being measured.

Evidence for the trustworthiness of the associations includes the completeness of the population sample, the varied pattern of association that was found, and the consistency of findings among men with and without any evidence of ischemia at baseline. High response rates in terms of both clinic attendance and questionnaire completion make it unlikely that the associations are unrepresentative of the population concerned. Wider extrapolation is encouraged in that present findings confirm those of the Framingham study in showing, for white collar workers, an association of anger out, but not the other anger scales, with incident IHD (4). That only three of the anger items were associated with incident IHD argues against the presence of an unmeasured factor driving the associations that were found. This possibility cannot be wholly discounted, however, because associations of both anger out and suppressed anger scales with IHD were impervious to subsequent statistical control.

The inclusion or exclusion of men with evidence of ischemia at baseline remains controversial. Inclusion provides a more representative sample but offers opportunity for IHD to affect anger scores. Exclusion removes the opportunity for confounding but reduces greatly the representativeness of the sample and the power of the study. In the present study, for example, an exclusion policy would have required losing more than 30% of the sample who would in turn provide around 50% of incident events. This level of baseline ischemia is typical for a British male population of this age range. Nevertheless, if an inclusion policy is adopted, the issue of confounding needs to be addressed. In the present study, men with ischemia at baseline were included, and the issue of confounding was addressed both by including three different measures of ischemia as covariates in the logistic regression analyses and by repeating the main analyses separately for men with and without any evidence of ischemia at baseline.

The robustness of association between anger scores and IHD regardless of statistical control bears some comment. Psychophysiological, psychosocial, and behavioral mechanisms have been proposed as linking anger scores to IHD (14). The statistical analysis tested these models. That no evidence was found to support these mechanisms is not uninformative. Although the physiological tests were all associated with IHD and covered a broad range of physiological mechanisms, this was a test of resting levels. The present findings do not explain associations of anger with physiological variable in studies that have involved a provoked physiological response (28). It is unlikely that associations of aggressive behavior with indicators of sympathetic arousal in both animal and human studies is unrelated to anger (29, 30). The negative findings reported here reflect more the inadequacy of the observational study design for testing the physiological model rather than on the model’s potential explanatory power. Nevertheless, that suppressed anger rather than anger out is predictive of IHD suggests that IHD risk is not directly related to the expression of aggression.

Limitations in testing the psychosocial model focus on the small numbers of measures that were available rather than on study design. The GHQ30, an established measure for psychiatric caseness, assesses both depression and anxiety and is related to IHD (31). GHQ30 scores were related to anger, but not in the direction accounting for an association of anger with IHD.

A richer literature is available on social support, relating it to both psychosocial and psychophysiological mechanisms. Social support did not remove the association of suppressed anger with IHD, findings that do not support the psychosocial model. Social support has been implicated in the psychophysiological model, however, in terms of moderating the relationship of anger and cardiovascular reactivity to acute stress (32). The interaction of social contact and suppressed anger with IHD did not achieve statistical significance. However, a trend toward smaller association of suppressed anger with incident IHD according to greater social contact was suggested. If this suggestion of an association is not dismissed, it provides epidemiological evidence of a moderating effect of social support. It also extends the evidence of a moderating effect, from laboratory stressors to incident disease.

In contrast, all the major behavioral variables that have been proposed as mediating the anger IHD association were included in this study (33). Smoking, alcohol consumption, exercise, calorie intake, and body mass index all reflect habitual aspects of lifestyle with chronic effects. None of these modified the association of anger with incident IHD. It may be concluded with reasonable confidence that, in and of themselves, the behavioral lifestyle factors considered in this study are not the means by which anger increases IHD risk.

The suppressed anger scale may be viewed as an improvement of the anger out scale, but it is also the result of a post hoc analysis. At issue, however, is the use of three items rather than two in identifying more closely the population at risk rather than the presence or absence of a predictive association. Rather than overinterpret very general questions, it seems that these questions may indicate a chronic process. All three questions refer to habitual ways of coping with anger that emphasize containment rather than expression. This is in contrast to reports showing increased risk of IHD due to specific episodes of anger (16, 17). Chronic and acute mechanisms may not be in conflict, however, if a chronic process sustains the duration of an acute event.

None of these analyses, however, can be considered definitive. The anger questions were framed in the context of what happens when one is really angry or annoyed. No account was taken of frequency or duration of anger episodes or of the level of anger being experienced while being assessed. Furthermore, only white, middle-aged men were included in the sample. In the Framingham study, higher anger in, anger out, and anger discuss scores were found in female incident IHD cases than in noncases (4). This suggests different patterns of association might have been expected for women had they been included in the present study. Although a small negative association (r_sp = -0.09; p < .001) was found between age and suppressed anger, the statistical significance was due to the large numbers available for analysis rather than indicating any great clinical effect. This conclusion is supported by the lack of an age effect in the multivariate analysis (Table 3). Nevertheless, the possibility of greater anger suppression causing greater IHD risk in a more elderly population cannot be discounted.

In relation to the hostility hypothesis, some cautious speculation may be helpful. According to the authors of the Framingham anger scales, the item "keeping anger to oneself" is an expression of suppressed hostility (34). However, none of the items used in this study seem to overtly measure cynicism or denigrating beliefs, which are thought to be characteristic of hostility. This suggests these anger questions may be assessing aspects of anger other than hostility. A broader approach as to why anger seems to increase IHD risk may be a more reasonable way to proceed. Caution is advised, however, and more evidence is required on the construct validity of all the items in the suppressed anger scale before conclusions may be drawn with confidence.

A major problem in taking the anger/hostility debate forward is the lack of an agreed upon coherent framework. If we define anger as an emotional response to a perceived wrong (13), then we allow for a number of response parameters within, and associated with, the anger phenomenon. These include the environmental triggers and constellation of cognitions that provoke the emotion; the intensity, frequency, and duration of the emotion; the physiological and behavioral response to the emotion; and associations of each of these with disease. From within this perspective, hostility is one expression of anger. Hostility, characterized by cynical and denigrating cognitions, may serve to increase IHD risk by increasing the expectation and interpretation of event as requiring an anger response. This would likely increase exposure of the subject to an anger-generated IHD risk.

It may be that hostility is one of the better defined and understood expressions of anger. Hostility may also be a relatively sensitive predictor of heart disease. But it is unlikely that hostility is the only expression of anger that increases IHD risk.

	APPENDIX

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION APPENDIX ACKNOWLEDGMENTS REFERENCES

 
Anger Questionnaire Items

	ACKNOWLEDGMENTS

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION APPENDIX ACKNOWLEDGMENTS REFERENCES

Received for publication September 9, 1998.

Revision received February 24, 1999.

	REFERENCES

TOP ABSTRACT INTRODUCTION METHODS RESULTS DISCUSSION APPENDIX ACKNOWLEDGMENTS REFERENCES

 

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