American Journal of Cardiology
Volume 105, Issue 11 , Pages 1555-1560, 1 June 2010

Anger, Suppressed Anger, and Risk of Adverse Events in Patients With Coronary Artery Disease

  • Johan Denollet, PhD

      Affiliations

    • Center of Research on Psychology in Somatic diseases, Tilburg University, Tilburg, The Netherlands
    • Department of Cardiology, University Hospital, Antwerp, Antwerp, Belgium
    • Corresponding Author InformationCorresponding author: Tel: (+31) 13-466-2390; fax: (+31) 13-466-2067
    • ,
  • Yori Gidron, PhD

      Affiliations

    • University of Brussels, Brussels, Belgium
    • ,
  • Christiaan J. Vrints, MD, PhD

      Affiliations

    • Department of Cardiology, University Hospital, Antwerp, Antwerp, Belgium
    • ,
  • Viviane M. Conraads, MD, PhD

      Affiliations

    • Department of Cardiology, University Hospital, Antwerp, Antwerp, Belgium

Received 7 December 2009; received in revised form 13 January 2010; accepted 13 January 2010. published online 12 April 2010.

Article Outline

Anger is associated with cardiovascular stress reactivity; however, little is known about the effect of suppressed anger in patients with coronary artery disease (CAD). We examined whether patients with CAD who suppress their anger are at risk of adverse events. At baseline, 644 patients with CAD completed measures of anger, anger-in (reluctance to express anger), and Type D personality (tendency to experience distress and to be inhibited). The combination of high anger and anger-in scores was used to identify the presence of suppressed anger. The end points were major adverse cardiac events (a composite of death, myocardial infarction, and revascularization) and cardiac death/myocardial infarction. After an average follow-up of 6.3 years (range 5 to 10), 126 patients (20%) had experienced a major adverse cardiac event, and 59 (9%) had experienced cardiac death or myocardial infarction. Anger (p = 0.009) and suppressed anger (p = 0.011) were associated with future major adverse cardiac events, but these associations were no longer significant after adjustment for clinical characteristics. However, suppressed anger remained associated with the more rigorous end point of cardiac death or myocardial infarction (odds ratio 2.87, 95% confidence interval 1.15 to 7.15, p = 0.024) after controlling for decreased systolic function, poor exercise tolerance, extent of CAD, and revascularization. Anger alone was not independently associated with this end point. Patients with a Type D personality had a fourfold rate of suppressed anger, and an adjustment for a Type D personality attenuated the observed association between suppressed anger and adverse cardiac events. In conclusion, patients with CAD who suppress their anger were at increased risk of adverse cardiac events, and this was accounted for by individual differences in Type D personality.

 

Anger has been related to a poor prognosis in patients with coronary artery disease (CAD)1 and should be considered a potential risk factor for CAD.2 Anger can induce myocardial ischemia and ventricular arrhythmias3, 4, 5 and predicts adverse cardiac events.6 However, negative findings have also been shown for anger and cardiac prognosis,7 suggesting that individual differences exist in anger-related risk,8 possibly related to emotion regulation. Anger suppression is a form of emotion regulation that involves inhibiting the expression of angry feelings and has been related to an increased risk of CAD,9 increased cardiovascular reactivity,10 decreased heart rate variability,11 and cardiac mortality.12 Psychological risk is not uniform across all patients with CAD, and some patients might be particularly vulnerable to suppressing anger. “Negative affectivity” refers to the tendency to experience negative emotions6 and “social inhibition” to the tendency to inhibit self-expression.13 Patients with CAD who simultaneously tend to experience negative emotions and inhibit self-expression have a “distressed” or Type D personality14 and are at an increased risk of adverse events.14, 15, 16 Hence, Type D patients might be a vulnerable group in terms of suppressed anger, and the Type D personality might explain the associations between suppressed anger and cardiac events. However, this has never been tested. The aims of the present study were (1) to investigate the association between suppressed anger and future cardiac events in patients with CAD, and (2) to test the hypothesis that a Type D personality might account for any associations between suppressed anger and prognosis in patients with CAD.

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Methods 

The present study included 644 patients with CAD (581 men and 63 women, mean age 55.8 ± 7.9 years) from the University Hospital of Antwerp, Belgium. Patients were recruited to 2 studies; the design of both studies was similar and has been previously described.14, 15 The first study included 303 patients with CAD,14 who had undergone screening for decreased left ventricular ejection fraction using ventricular angiography and 19 patients who had undergone echocardiographic screening of left ventricular ejection fraction. The second study included a new sample of 322 patients with CAD.15 The present study included 347 patients (54%) after myocardial infarction (MI) and 475 patients (74%) after coronary artery bypass graft surgery (CABG) or percutaneous coronary intervention (PCI). Of these 475 patients, 178 had undergone CABG/PCI after MI. Patients with other life-threatening diseases, such as cancer, were excluded. At baseline, all patients underwent an exercise stress test, completed measures of anger and personality, and provided informed consent. The local hospital ethics committee approved the study.

The Spielberger State-Trait Anger Scale17 is a widely used inventory that assesses the frequency and intensity of anger. This scale has also been used to examine the role of anger in the cardiac prognosis of patients with CAD.6 In the present study, tertiles were used to classify patients as being low, intermediate, or high on trait-anger; thus, patients with a score of ≥20 were likely to respond with feelings of anger to negative or frustrating situations.

Patients who frequently experienced anger but, at the same time, tended to inhibit the expression of these angry feelings, were considered to suppress their anger. Anger-in was defined as an inability or unwillingness to express one's anger against people held responsible for one's frustration, to avoid any interpersonal conflict.9 As previously described,18, 19 we used a 4-item scale (“When you get angry, do people around you know about it?,” “If you are angry, do you generally hold it in?,” “When you are being kept waiting for an appointment, would you say anything about it?,” “Do you let people know if you are angry?”). To assess the tendency to inhibit the expression of anger,9 a 4-point rating scale (from 0 to 3) was used, resulting in an anger-in score of 0 to 12. This scale was internally consistent (Cronbach's α = 0.73; mean inter-item correlation 0.40). Tertiles were used to classify patients as being low, intermediate, or high in anger-in. Thus, patients with CAD were considered to suppress their anger if they had a score of ≥20 on trait-anger (upper tertile) combined with a score of ≥7 on anger-in (upper tertile).

Patients with a Type D personality simultaneously tend to experience anger and other negative emotions across time and situations (negative affectivity)6 and to inhibit self-expression in social interaction (social inhibition).13 According to the initial publications on this personality construct,14, 19 the cutoff scores on the Trait Anxiety and Heart Patients' Psychological Questionnaire Social Inhibition scales were used to assess negative affectivity14, 20 and social inhibition.14 In the present study, 174 patients (27%) had a Type D personality (i.e., trait-anxiety ≥43 and social inhibition ≥12). We have previously shown that Type D patients from the present sample14, 15 and other CAD samples16 are at an increased risk of adverse events.

The clinical risk factors included severity of cardiac disorder, functional disability, and CAD as assessed using 3 different markers. Decreased systolic function was defined as a left ventricular ejection fraction of ≤50%, and decreased functional status as poor exercise tolerance, defined by the peak workload on a symptom-limited exercise stress test (ie, ≤140 and ≤120 W for younger and older men and ≤100 and ≤80 W for younger and older women, respectively). Severe CAD was defined as 3-vessel disease (≥70% reduction in internal diameter of the coronary arteries). Other clinical covariates included anterior MI at baseline, a history of MI, invasive treatment with CABG/PCI, β-blocker therapy, angiotensin-converting enzyme inhibitor therapy, smoking, hyperlipidemia (total cholesterol level >240 mg/dl or taking lipid-lowering medication), and hypertension treatment. Age and gender were entered as covariates in all multivariate models.

The first end point was major adverse cardiac events (MACE), defined as a composite of death, MI, and revascularization (CABG/PCI) after an average follow-up period of 6.3 ± 1.5 years (range 5 to 10). The second end point was a composite of cardiac death and MI as a more rigorous measure of clinical outcome during follow-up.13, 16 As previously described,14, 15 follow-up data were derived from the hospital records, and the patient's attending physician was involved in the classification of the cause of death.

Multivariate logistic regression analyses were used to examine the independent associations of age, gender, disease severity, and other clinical variables with future MACE and cardiac death or MI. Cross tabulation and univariate regression analyses were used to analyze the associations between anger and suppressed anger and future MACE or cardiac death/MI. Multivariate logistic regression analyses were used to examine whether the adjustment for demographic and clinical variables would attenuate the effect of anger or suppressed anger on the occurrence adverse events. Next, cross tabulation and univariate regression analyses were used to test the hypothesis that patients with a Type D personality might be at particularly high risk of suppressing their anger. Finally, multivariate regression models were constructed to investigate whether the adjustment for Type D personality would explain the association between suppressed anger and the risk of future adverse events. All variables were entered simultaneously in the multivariate regression models of MACE and cardiac death or MI. The analyses were performed using the Statistical Package for Social Sciences for Windows, version 17.0 (SPSS, Chicago, Illinois).

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Results 

During follow-up, 126 patients (20%) experienced MACE and 59 (9%) a fatal or nonfatal cardiac event (29 cardiac deaths and 30 MIs). All deaths were attributable to natural causes. A left ventricular ejection fraction of ≤50% and poor exercise tolerance are markers of disease severity that were independently associated with future MACE (Table 1) and cardiac death or MI (Table 1). No revascularization at baseline was also independently associated with both end points. Age was associated with future MACE, and a trend was seen for 3-vessel disease to be associated with cardiac death/MI. The other clinical variables were not associated with the outcome.

Table 1. Demographic and clinical predictors of cardiac events⁎
Baseline CharacteristicOdds Ratio95% Confidence Intervalp Value
Major adverse cardiac events (n = 126)
Demographic variables
Age0.950.93–0.980.001†
Gender (men)0.990.49–1.980.97
Disease severity
Left ventricular ejection fraction ≤50%1.841.07–3.180.029†
Poor exercise tolerance‡1.861.22–2.830.004†
Three-vessel disease1.340.84–2.130.22
Anterior myocardial infarction at baseline1.010.61–1.660.99
Previous myocardial infarction1.070.54–2.110.85
Clinical variables
No coronary artery bypass grafting/percutaneous coronary intervention at baseline1.641.03–2.610.039†
β-Blocker therapy1.350.89–2.040.15
Angiotensin-converting enzyme inhibitors0.770.29–1.970.58
Hyperlipidemia§1.200.77–1.860.42
Hypertension0.870.53–1.430.58
Smoking0.980.59–1.630.45
Cardiac death/myocardial infarction (n = 59)
Demographic variables
Age0.980.94–1.010.22
Gender (men)1.670.55–5.030.37
Disease severity
Left ventricular ejection fraction ≤50%2.531.29–4.960.007†
Poor exercise tolerance†2.801.56–5.000.001†
Three-vessel disease1.820.96–3.420.065
Anterior myocardial infarction at baseline1.190.61–2.300.62
Previous myocardial infarction1.440.63–3.290.39
Clinical variables
No coronary artery bypass grafting/percutaneous coronary intervention at baseline2.051.08–3.900.029†
β-Blocker therapy1.140.64–2.020.66
Angiotensin-converting enzyme inhibitors0.400.10–1.590.19
Hyperlipidemia‡0.710.37–1.350.29
Hypertension§1.230.44–1.790.74
Smoking1.260.64–2.450.51

⁎Multivariable analyses.

†Statistically significant.

‡For younger and older men, ≤140 and ≤120 W; for younger and older women, ≤100 and ≤80 W, respectively.

§Total cholesterol level >240 mg/dl or taking lipid-lowering medication.

Treatment of high blood pressure.

On univariate analysis, both anger and suppressed anger were associated with future MACE (Figure 1) and with the more rigorous end point of cardiac death and MI (Figure 1). No significant associations between anger or suppressed anger and MACE remained after adjustment for the clinical and demographic characteristics (Table 2). However, suppressed anger remained associated with cardiac death or MI after controlling for decreased systolic function, poor exercise tolerance, extent of CAD, and revascularization (Table 2). In contrast, anger was not independently associated with this end point.

Table 2. Anger, suppressed anger, and odds of future adverse event and cardiac death/myocardial infarction (MI)⁎
Baseline CharacteristicOdds Ratio95% Confidence Intervalp Value
Major adverse cardiac events (n = 126)
Anger variables
Anger1.280.80–2.050.31
Suppressed anger1.470.71–3.050.30
Covariates
Age0.950.93–0.980.0001†
Gender (men)0.960.48–1.900.90
Left ventricular ejection fraction ≤50%1.630.98–2.720.060
Poor exercise tolerance‡1.861.23–2.830.004†
Three-vessel disease1.390.89–2.190.15
No coronary artery bypass grafting/percutaneous coronary intervention at baseline1.550.98–2.450.059
Cardiac death/myocardial infarction (n = 59)
Anger variables
Anger0.980.49–1.950.96
Suppressed anger2.871.15–7.150.024†
Covariates
Age0.970.94–1.010.17
Gender (men)1.580.52–4.750.42
Left ventricular ejection fraction ≤50%2.351.25–4.430.008†
Poor exercise tolerance‡2.761.55–4.930.001†
Three-vessel disease1.911.02–3.550.042†
No coronary artery bypass grafting/percutaneous coronary intervention at baseline2.081.11–3.890.022†

⁎Multivariable analyses.

†Statistically significant.

‡For younger and older men, ≤140 and ≤120 W; for younger and older women, ≤100 and ≤80 W, respectively.

Analyses that included the Type D personality indicated that appreciable interindividual variability was present for suppressed anger. Type D patients had a fourfold rate of suppressed anger (31 [18%] of 174) compared to non–Type D patients (20 [4%] of 470; p <0.0001; Figure 2). We have previously reported in 2 separate studies14, 15 that Type D patients from the present sample were at increased risk of adverse events. Accordingly, a Type D personality was also significantly associated with future MACE (Figure 2) and cardiac death or MI (Figure 2) in the present study, with a univariate odds ratio of 2.59 and 3.99, respectively (p <0.0001).

  • View full-size image.
  • Figure 2. 

    Suppressed anger (a), MACE (b) and cardiac death/MI (c) as function of Type D personality. Number of patients with cardiac event/number of patients in subgroup presented below each bar. * 95% Confidence interval 2.70 to 8.82, p <0.0001; † 95% confidence interval 1.73 to 3.90, p <0.0001; ‡ 95% confidence interval 2.32 to 6.91, p <0.0001.

After adjustment for disease severity and age, a Type D personality remained independently associated with a more than twofold increased rate of MACE (Table 3). After adjustment for clinical variables, suppressed anger predicted cardiac death or MI (Table 2), but additional adjustment for Type D attenuated this association. In the final multivariate model (Table 3), a Type D personality, left ventricular ejection fraction of ≤50%, poor exercise tolerance, and no CABG/PCI at baseline predicted cardiac death and MI, but suppressed anger was no longer significant.

Table 3. Multivariate models of adverse events and cardiac death/myocardial infarction (MI) including suppressed anger and Type D personality⁎
Baseline CharacteristicOdds Ratio95% Confidence Intervalp Value
Major adverse cardiac events (n = 126)
Psychological variables
Suppressed anger1.280.64–2.550.48
Type D personality2.341.52–3.620.0001†
Covariates
Age0.950.93–0.980.0001†
Gender (men)1.070.54–2.120.80
Left ventricular ejection fraction ≤50%1.681.00–2.830.05†
Poor exercise tolerance‡1.761.15–2.700.009†
Three-vessel disease1.370.87–2.170.18
No coronary artery bypass grafting/percutaneous coronary intervention at baseline1.560.99–2.480.058
Cardiac death/myocardial infarction (n = 59)
Psychological variables
Suppressed anger1.860.82–4.210.14
Type D personality3.400.88–6.140.0001†
Covariates
Age0.980.94–1.010.22
Gender (men)1.910.63–5.850.26
Left ventricular ejection fraction ≤50%2.441.28–4.670.007†
Poor exercise tolerance‡2.591.44–4.670.002†
Three-vessel disease1.860.99–3.520.056
No coronary artery bypass grafting/percutaneous coronary intervention at baseline2.141.13–4.070.02†

⁎All variables entered at same time.

†Statistically significant.

‡For younger and older men, ≤140 and ≤120 W; for younger and older women, ≤100 and ≤80 W, respectively.

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Discussion 

In the present study, anger was associated with the occurrence of adverse events, but this association was attenuated after adjustment for age and disease severity. Previous research has indicated that anger and hostility might be associated with a poor prognosis in patients with CAD.1, 2, 6 However, the present results have extended these earlier findings by showing that, beyond the propensity to become angry, a failure to express such habitual anger might be of particular importance. Patients with CAD who suppressed their anger had a threefold increased risk of a poor outcome, and this association was confirmed after adjustment for disease severity and anger per se. This finding was not driven by the use of revascularization; suppressed anger was not associated with the broader end point of MACE but was significantly associated with the more rigorous end points of cardiac death and MI.

After adjusting for Type D personality, the observed association between suppressed anger and prognosis was no longer significant. This implies that the regulation of emotions clearly occurs within a broader framework of stable personality traits. A Type D personality might explain individual differences in suppressed anger, because it involves the tendency to experience negative emotions and to inhibit self-expression.6 Anger suppression was more prevalent in Type D patients (18%) than in non–Type D patients (4%). Hence, a Type D personality not only involves social withdrawal, but also suppression of negative emotions.21 We have previously reported that a Type D personality accounted for the association between anger and a poor prognosis;6 however, the latter study was conducted in a selected sample of patients with systolic heart failure and did not include a measure of suppressed anger. Therefore, the present study has provided new information by showing that individual differences in Type D personality accounted for the relation between suppressed anger and cardiac prognosis.

Regarding the previously reported association between anger and cardiac prognosis,1 it appears that emotional inhibition might modulate this association.9 Inhibited persons perceive the social world as threatening and inhibit the outward signs of inner feelings as a strategy to avoid negative reactions from others.13 This inhibition decreases overt angry behavior but not anger-provoked arousal.10 Under conditions of social engagement, inhibited persons react with an increase in catecholamines, heart rate, and blood pressure.21 Hence, the accumulation of suppressed anger might have a negative effect on cardiovascular health.10 In healthy persons, suppressed anger has been related to adverse cardiovascular effects11 and cardiovascular death;12 however, evidence on its health effects in patients with CAD has largely been lacking. In the present study, we found clinical evidence that patients with CAD who suppress their anger might be susceptible to MACE. These findings could have important implications for clinical research and intervention.

First, our findings might help to explain why some patients with CAD are particularly vulnerable to stress-related events. Anger induces endothelial dysfunction, myocardial ischemia, and cardiac electrical instability4, 5 and, eventually, might trigger the onset of ventricular arrhythmias3, 4 or acute coronary syndrome.22 Recent evidence has also shown that the Type D personality is associated with an increased risk of ventricular arrhythmia.23 Suppression only decreases the outward signs of anger, not its physiologic impact such as decreased heart rate variability.11 Patients with CAD who suppress their anger might display additional risk factors such as poor sleep24 and a greater immune response.25 It has been suggested that patients who have decreased heart rate variability might have a poorer prognosis owing to insufficient vagal modulation of CAD-related inflammation.26

Second, clinicians might consider referring patients with high levels of suppressed anger for behavioral interventions that would teach them how to use adaptive ways of downregulating their anger. How one thinks about an anger-provoking situation shapes the emotional response one has and learning to reappraise this situation could decrease its effect.27 Evidence has shown that such an intervention can decrease the blood pressure in patients with CAD.28 Dysfunctional venting of anger can have adverse cardiovascular effects; however, this does not imply that cardiologists should advise their patients to inhibit their expression of anger.

The suppression of anger might be adaptive in a large number of situations in daily life. However, rumination about an anger-provoking situation and the inability to relieve anger by talking to others or by solving the anger-provoking problem can also cause increased sympathetic nervous system activation27 and decreased heart rate variability.11 Expressing anger in a proportionate and constructive way29—rather than suppressing or exploding—is often likely to lead to a faster resolution of the anger-provoking situation. Regarding this issue, clinical research has shown that constructive anger expression can also mediate the blood pressure-lowering effects of a hostility reduction intervention.29

These findings should be interpreted with some caution. These findings might not be generalizable to women, because the patients included in the present study only included a minority of women. Furthermore, anger and suppressed anger were only assessed at baseline, and repeated measurements might have improved the accuracy of the assessment of these variables. Finally, we did not include a measure of hostility, which has been conceptualized as a broader construct that also includes antagonistic behavior and cynical cognitions and attributions.1

Anger is a natural emotion that can be very adaptive (e.g., as a warning signal), provided that this negative emotion is regulated and used in a socially meaningful and adaptive way. Although patients who deliberately and habitually inhibit the outward expression of anger might appear unaggressive, they might actually experience high levels of anger. In these patients, emotional suppression could also impede effective cardiac care.13 Inhibited patients are less likely to exhibit signs of emotional distress during a medical consultation and might refrain from discussing their medical and emotional problems with their attending physician or nurse,30 thus running the risk of being underdiagnosed. The findings of the present study have clearly indicated that patients with CAD who tend to suppress their anger represent a vulnerable group that should be closely monitored and, when needed, offered additional clinical care.

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 This study was supported by Vici grant 453-04-004 from The Netherlands Organization for Scientific Research (The Hague, The Netherlands) to Dr. Denollet.

PII: S0002-9149(10)00101-3

doi:10.1016/j.amjcard.2010.01.015

American Journal of Cardiology
Volume 105, Issue 11 , Pages 1555-1560, 1 June 2010

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