Anger expression, hostility, anxiety, and patterns of cardiac reactivity to stress.

The majority of studies investigating the relationships between psychological characteristics and cardiovascular reactivity to stress use a research strategy in which discrete traits are evaluated in isolation. The present study examined the effects of additive and/or interactive relationships among traits on cardiac reactivity to a mental arithmetic task. In addition, impedance cardiographic techniques were employed to examine potential relationships between such psychological traits and a specific measure--pre-ejection period (PEP)--of sympathic influence on the heart. Forty-nine undergraduate men performed a mental arithmetic task while continuous measures of PEP and interbeat interval (IBI) were collected. The subjects then completed questionnaires measuring anger expression, hostility, and trait anxiety. Analyses of variance (ANOVAs) showed a significant main effect for anger-out on PEP change from baseline, but not for IBI. Results also showed that anger-in interacted with anger-out and hostility to affect both PEP and IBI changes significantly. Other results indicated that subjects in the high anger-in/low anger-out and high anger-in/low hostility groups did not show significant PEP change, although they nevertheless showed significant IBI change. These results highlight the importance of the consideration of interactions among traits in predicting cardiac reactivity and of the importance of measuring specific indexes of sympathetic arousal.     

The clinical anger scale: Preliminary reliability and validity

This article reports preliminary evidence for the development and validation of the Clinical Anger Scale (CAS), an objective self-report instrument designed to measure the syndrome of clinical anger. Factor analysis of the CAS confirmed a unidimensional item structure; reliability analyses also demonstrated adequate internal consistency and test-retest stability for the CAS; other results indicated that the CAS was unrelated to social desirability influences. Additional findings indicated that clinical anger was associated positively with several anger-related concepts (e.g., trait anger, state anger, anger-in, anger-out, anger-control) and that the CAS was related in predictable ways to people's psychopathological symptoms, personality traits, and early family environments. Implications for future research and therapeutic assessment with the Clinical Anger Scale are discussed.     

状态-特质愤怒表达量表修订版在大学生中的信效度

目的:引进状态-特质愤怒表达量表修订版(STAXI-2)并检验信效度。方法:通过翻译、回译形成STAXI-2中文版。采用方便取样方法抽取782名大学生,施测STAXI-2中文版,并以愤怒失控量表(ANG)和状态-特质焦虑量表(STAI)为校标。间隔3周,选取30人进行重测。结果:STAXI-2中文版共57个条目,分为状态愤怒(SAS)、特质愤怒(TAS)和愤怒表达(AX)3个分量表。SAS、TAS的内部一致性Cronbachα均0.8,重测信度分别为0.18和0.83,验证性因素分析的拟合指数GFI、AG-FI、NFI、CFI和IFI均在0.88～0.96之间,RM SEA分别为0.09和0.08。AX的控制内部表达和外部表达因子的α均0.8,重测信度均0.6;AX的愤怒内部表达和外部表达因子的α在0.60～0.70之间;AX的拟合指数GFI、AGFI、NFI、CFI和IFI均在0.84～0.90之间,RMSEA为0.06。TAS得分与SAS得分及AX的愤怒内部表达和外部表达分均呈正相关(r=0.36、0.13、0.53),而与AX的控制内部表达和外部表达分负相关(r=-0.47、-0.52);SAS得分与AX的愤怒内部表达和外部表达分正相关(r=0.14、0.30),而与AX的控制内部表达和外部表达因子分负相关(r=-0.26和-0.21),均P0.05。男性的TAS、SAS及AX的愤怒外部表达分均高于女性(均P0.05)。结论:状态-特质愤怒表达量表修订版中的状态愤怒和特质愤怒分量表在中国大学生中具有较好的信效度;愤怒表达分量表的结构效度可以接受,但内部表达和外部表达两因子的信度偏低。     

Pain catastrophizing,physiological indexes,and chronic pain severity: tests of mediation and moderation models

Catastrophizing about pain is related to elevated pain severity and poor adjustment among chronic pain patients, but few physiological mechanisms by which pain catastrophizing maintains and exacerbates pain have been explored. We hypothesized that resting levels of lower paraspinal muscle tension and/or lower paraspinal and cardiovascular reactivity to emotional arousal may: (a) mediate links between pain catastrophizing and chronic pain intensity; (b) moderate these links such that only patients described by certain combinations of pain catastrophizing and physiological indexes would report pronounced chronic pain. Chronic low back pain patients (N = 97) participated in anger recall and sadness recall interviews while lower paraspinal and trapezius EMG and systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) were recorded. Mediation models were not supported. However, pain catastrophizing significantly interacted with resting lower paraspinal muscle tension to predict pain severity such that high catastrophizers with high resting lower paraspinal tension reported the greatest pain. Pain catastrophizing also interacted with SBP, DBP and HR reactivity to affect pain such that high catastrophizers who showed low cardiovascular reactivity to the interviews reported the greatest pain. Results support a multi-variable profile approach to identifying pain catastrophizers at greatest risk for pain severity by virtue of resting muscle tension and cardiovascular stress function.     

Anger Management Style,Opioid Analgesic Use,and Chronic Pain Severity: A Test of the Opioid-Deficit Hypothesis

Anger management style is related to both acute and chronic pain. Recent research suggests that individuals who predominantly express anger (anger-out) may report heightened chronic pain severity due in part to endogenous opioid antinociceptive dysfunction. If exogenous opioids serve to remediate opioid deficits, we predicted that regular use of opioid analgesics by chronic pain patients would alter these relationships such that anger-out would be related to chronic pain severity only among opioid-free patients. For 136 chronic pain patients, anger management style, depression, anxiety, pain severity, and use of opioid and antidepressant medication was assessed. Results of hierarchical multiple regressions to predict chronic pain severity showed: (a) a significant Anger-out × Opioid use interaction such that high Anger-out was associated with high pain severity only among patients not taking opioids; (b) controlling for depressed affect and anxiety did not affect this association; (c) the Anger-out × Antidepressant use interaction was nonsignificant; (d) Anger-in did not interact with use of any medication to affect pain severity. Results are consistent with an opioid-deficit hypothesis and suggest that regular use of opioid medications by patients high in anger expression may compensate for an endogenous opioid deficit, and mitigate the effects of elevated anger expression on chronic pain intensity.     

Anger,adiposity, and glucose control in nondiabetic adults: findings from MIDUS II

Anger has been linked to cardiovascular disease, but few studies have examined the relationship between anger and type 2 diabetes. The aim was to investigate associations among different indicators of anger expression, adiposity, and nondiabetic glucose metabolism in a national survey of adults. Participants were 939 adults without diabetes in the Midlife in the US study (MIDUS II). Glucose metabolism was characterized by fasting glucose, insulin, insulin resistance, and glycosylated hemoglobin (HbA_1c). Spielberger’s Anger Expression inventory was used to measure suppressed anger (anger-in), expressed anger (anger-out), and controlled anger (anger-control). We investigated the relationship between anger and glucose metabolism, and whether anger amplified the adverse relationship between body weight distribution (body mass index = BMI and waist-to-hip ratio = WHR) and glucose metabolism. Multivariate-adjusted analyses revealed an association between anger-out and both insulin and insulin resistance. As predicted, anger-in amplified the relationships between BMI and insulin and insulin resistance, while anger-out amplified the association between WHR and insulin and insulin resistance. Low anger-control was associated with higher glucose. None of the three anger measures was significantly associated with HbA_1c. Our findings extend previous research on anger as a potential risk factor for type 2 diabetes by demonstrating that anger expression is associated with clinical indicators of glycemic control, especially among those with pre-existing risk due to obesity and high central adiposity.     

Hostility and anger expression in African American and European American men is associated with cardiovascular and lipid reactivity

Physiological stress reactivity has been examined with respect to cynical hostility and anger expression, but primarily among Caucasians. Investigations of African Americans are far fewer and have focused only on the cardiovascular system. This study compared the relationships between hostility and anger expression on the one hand, and both cardiovascular and lipid reactivity on the other, among African Americans and European Americans. Forty-six men participated in a study examining cardiovascular and lipid reactivity to a speech stressor. African American men low in cynical hostility had greater blood pressure reactivity to the stressor; this effect appeared to be due primarily to low cynical men with high Anger In. Independent of ethnicity, those with a general tendency to either always express or always inhibit the expression of anger had higher triglyceride reactivity, relative to those with a more flexible style of anger expression. These results suggest that it is important to examine ethnicity in relationship to measures of hostility and anger expression, to uncover vulnerable individuals.     

Gender, anger expression style, and opportunity for anger release determine cardiovascular reaction to and recovery from anger provocation.

This study represents an extension of Hokanson's research, which showed that for men anger release after provocation tends to accelerate cardiovascular recovery. The objective of this study was to investigate how gender and habitual style for anger-in or anger-out behavior modulate the effect of anger provocation and release. Male and female subjects (N = 105) were classified as anger-in/anger-out only when a double criterion (i.e., self-report and peer evaluation) was satisfied. Following a state anger rating at pre-test, subjects were harassed during the performance of a 12-minute math task. After task completion, subjects were randomly assigned to one of two 10-minute recovery protocols a) having an opportunity to release negative affect, and b) not not having such an opportunity. All groups (including the anger-ins) that had an opportunity to express negative affect did in fact express similar levels of anger. Men reacted more strongly to the math task performed under anger provocation on all cardiovascular indices. Anger expression style as a trait-type disposition was important for the recovery process in women whereas the situational manipulation (i.e., the opportunity to release anger) had specific effects on the recovery process of men. Opportunity to release anger facilitated heart rate recovery (and to a lesser degree diastolic pressure recovery) in men but not in women. Women with anger-in tendencies on the other hand displayed better systolic pressure recovery than female anger-outs whereas no such effects were observed in men.     

Suppression of anger and subsequent pain intensity and behavior among chronic low back pain patients: the role of symptom-specific physiological reactivity

Suppression of anger may be linked to heightened pain report and pain behavior during a subsequent painful event among chronic low back patients, but it is not clear whether these effects are partly accounted for by increased physiological reactivity during suppression. Chronic low back pain patients (N = 58) were assigned to Suppression or No Suppression conditions for a “cooperative” computer maze task during which a confederate harassed them. During baseline and maze task, patients’ lower paraspinal and trapezius muscle tension, blood pressure and heart rate were recorded. After the maze task, patients underwent a structured pain behavior task (behaviors were videotaped and coded). Results showed that: (a) Suppression condition patients revealed greater lower paraspinal muscle tension and systolic blood pressure (SBP) increases during maze task than No Suppression patients (previously published results showed that Suppression condition patients exhibited more pain behaviors than No Suppression patients); (b) residualized lower paraspinal and SBP change scores were related significantly to pain behaviors; (c) both lower paraspinal and SBP reactivity significantly mediated the relationship between Condition and frequency of pain behaviors. Results suggest that suppression-induced lower paraspinal muscle tension and SBP increases may link the actual suppression of anger during provocation to signs of clinically relevant pain among chronic low back pain patients.     

Anger Cognitions and Cardiovascular Recovery Following Provocation

The current study describes the creation and validation of the Anger Cognitions Inventory (ACI) to assess the cognitive appraisals associated with resentful and reflective anger. The ACI was created based on a content analysis of self-reports of participants' thoughts and feelings following anger provocation in the laboratory. Exploratory and confirmatory factor analyses on two separate college student samples (N = 267 and N = 276, respectively) revealed five subscales which could validly be grouped into resentful and reflective anger. Convergent and divergent validity data showed that resentful anger correlated positively with anger-out/trait anger and reflective anger correlated positively with anger-in/brooding. A second study showed positive correlations between rumination and delayed cardiovascular recovery following anger provocation. Limitations of both studies include restricted samples which limit generalizability of results and cardiovascular recovery data collected in Study II which does not include assessment of autonomic balance between vagal and sympathetic responsivity.     

Anger inhibition and pain: conceptualizations, evidence and new directions

Anger and how anger is regulated appear to affect acute and chronic pain intensity. The inhibition of anger (anger-in), in particular, has received much attention, and it is widely believed that suppressing or inhibiting the verbal or physical expression of anger is related to increased pain severity. We examine theoretical accounts for expecting that anger inhibition should affect pain, and review evidence for this claim. We suggest that the evidence for a link between trait anger-in (the self-reported tendency to inhibit anger expression when angry) and acute and chronic pain severity is quite limited owing to a number of factors including a inadequate definition of trait anger-in embodied in the popular anger-in subscale of Spielberger's Anger Expression Inventory, and a strong overlap between trait anger-in scores and measures of general negative affect (NA). We argue that in order to determine whether something unique to the process of anger inhibition exerts direct effects on subsequent pain intensity, new conceptualizations and approaches are needed that go beyond self-report assessments of trait anger-in. We present one model of anger inhibition and pain that adopts elements of Wegner's ironic process theory of thought suppression. Findings from this emerging research paradigm indicate that state anger suppression (suppression manipulated in the laboratory) may indeed affect sensitivity to subsequent painful stimuli, and we outline potentially productive avenues of future inquiry that build on this model. We conclude that although studies employing correlational designs and self-reports of trait anger-in have not upheld the claim that anger inhibition affects pain severity, evidence from studies using new models suggests that actually inhibiting anger expression during a provocative event may increase perceived pain at a later time.     

Development of a Russian state–trait anger expression inventory

We examined the possible universality of Spielberger's (1988) model of anger by validating a Russian State–Trait Anger Expression Inventory (STAXI). In Eckhardt, Kassinove, Tsytsarev, and Sukhodolsky (1995), support was found for all STAXI factors except anger-in, using students from St. Petersburg State University. In the present study, 346 students from Russian high schools and the Pavlov Medical School served as subjects. Using new items, we found strong support for the factor structure hypothesized by Spielberger. All scales showed good to excellent alphas, and there was substantial similarity of the current means with results from the earlier study. The Russian samples, however, showed a lower level of state anger. The data support the possibility that state anger consists of two subscales, a simple experience and an experience combined with an action tendency. Trait anger occurs as a general temperament or as a reaction to specific triggers. It is positively related to anger-out and negatively related to anger control. Future studies can use this instrument to evaluate the stability of anger in Russian speaking populations, and to assess anger experiences and expression in response to specific triggers. © 1997 John Wiley & Sons, Inc. J Clin Psychol 53 : 543–557, 1997     

Anger Expression and Pain: An Overview of Findings and Possible Mechanisms

A tendency to manage anger via direct expression (anger-out) is increasingly recognized as influencing responses to pain. Elevated trait anger-out is associated with increased responsiveness to acute experimental and clinical pain stimuli, and is generally related to elevated chronic pain intensity in individuals with diverse pain conditions. Possible mechanisms for these links are explored, including negative affect, psychodynamics, central adipose tissue, symptom specific muscle reactivity, endogenous opioid dysfunction, and genetics. The opioid dysfunction hypothesis has some experimental support, and simultaneously can account for anger-out’s effects on both acute and chronic pain. Factors which may moderate the anger-out/pain link are described, including narcotic use, gender, and genetic polymorphisms. Pain exacerbating effects of trait anger-out are contrasted with the apparent pain inhibitory effects of behavioral anger expression exhibited in anger-provoking contexts. Conceptual issues related to the state versus trait effects of expressive anger regulation are discussed.     

Anger, and Plasma Lipid, Lipoprotein, and Glucose Levels in Healthy Women: The Mediating Role of Physical Fitness

The association between anger, lipid profiles, and glucose levels were examined in this study of 103 middle aged, healthy women. A principal component factor analysis of Spielberger's Trait Anger and Anger Expression scales yielded two anger factors: Impulsive Anger-Out and Neurotic Anger. Impulsive anger-out significantly predicted a negative lipid profile (high total serum cholesterol (TSC), low density lipoproteins (LDL), TSC/HDL (high density lipids), and triglyceride levels) and heightened glucose levels, but only in physically unfit women. Neurotic anger did not predict lipid and glucose levels. These findings parallel previous findings regarding the two anger dimensions and CHD, with only impulsive anger-out predicting CHD. Furthermore, our findings indicate that the protective effect of physical fitness, previously documented for men, also occurs in women.     

Defensive hostility and anger expression: Relationship to additional heart rate reactivity during active coping

The main purpose of the present study was twofold: (a) to assess the relationship between defensive hostility (high hostility/high defensiveness) and additional heart rate reactivity during active coping and (b) to determine if the construct of anger-out might lend additional, sensitivity to the predictive power of the defensive hostility model. Forty individuals were randomly assigned to complete a mental arithmetic task with or without the threat of shock. Participants also completed the Cook-Medley Hostility Inventory (Ho), the Marlowe-Crowne Social Desirability Scale (MC), and the Spielberger Anger Expression Scale. Defensive hostile subjects (high Ho/high MC) were significantly more reactive than any other subgroup. In addition, the combination of low Ho/high anger-out scores yielded a subgroup significantly less reactive than any other subgroup. These findings clarify the complex relationship of hostility and cardiovascular reactivity.     

Cynicism, anger and cardiovascular reactivity during anger recall and human–computer interaction

Cynicism moderated by interpersonal anger has been found to be related to cardiovascular reactivity. This paper reports two studies; Study 1 used an Anger Recall task, which aroused interpersonal anger, while participants in Study 2 engaged in a multitasking computer task, which aroused non-interpersonal anger via systematic manipulation of the functioning of the computer mouse. The Cynicism by State Anger interaction was significant for blood pressure arousal in Study 2 but not for Study 1: in Study 2, when State Anger was high, cynicism was positively related to blood pressure arousal but when State Anger was low, cynicism was negatively related to blood pressure arousal. For both studies, when State Anger was low, cynicism was positively related to cardiac output arousal and negatively related to vascular arousal. The results suggest that Cynicism–State Anger interaction can be generalised to non-social anger-arousing situations for hemodynamic processes but blood pressure reactivity is task-dependent. The implication for the role of job control and cardiovascular health during human–computer interactions is discussed.     

Anger Management Style and Endogenous Opioid Function: Is Gender a Moderator?

This study explored possible gender moderation of previously reported associations between elevated trait anger-out and reduced endogenous opioid analgesia. One hundred forty-five healthy participants underwent acute electrocutaneous pain stimulation after placebo and oral opioid blockade in separate sessions. Blockade effects were derived reflecting changes in pain responses induced by opioid blockade. Hierarchical regressions revealed that elevated anger-out was associated with smaller pain threshold blockade effects (less opioid analgesia) in females, with opposite findings in males (interaction p < .001). Similar marginally significant interactions were noted for blockade effects derived for nociceptive flexion reflex threshold, pain tolerance, and pain ratings (p < .10). Anger-in was also associated negatively with pain threshold blockade effects in females but not males (interaction p < .05). Across genders, elevated anger-in was related to smaller pain tolerance blockade effects (p < .01). Overlap with negative affect did not account for these opioid effects. The anger-in/opioid association was partially due to overlap with anger-out, but the converse was not true. These findings provide additional evidence of an association between trait anger-out and endogenous opioid analgesia, but further suggest that gender may moderate these effects. In contrast to past work, anger-in was related to reduced opioid analgesia, although overlap with anger-out may contribute to this finding.     

Interactive effects of traits,states, and gender on cardiovascular reactivity during different situations

Interactive effects of anger and anxiety traits, negative affect state, different situations, and gender on cardiovascular reactivity (CVR) to stress were examined. Subjects (91 men, 92 women) performed a reaction time task under either a Social Evaluation, a Harassment, or a Control condition; SBP, DBP, and HR were recorded continuously. Hierarchical multiple regressions revealed intricate interactions. The interaction of anger expression style and anger experience was significant only among men, such that anger suppressors with high trait anger showed the largest CVR of any group during Harassment; anger expressors exhibited generally high CVR across conditions. However, anger expression style and state negative affect interacted to affect CVR in both men and women. Finally, the fear of negative evaluation predicted elevated DBP responses only among men in the Social Evaluation condition. Results imply that the extent to which traits of anger and anxiety contribute to coronary risk may depend on interactions with other traits, gender, and the environment.     

Harassment,hostility, and Type A as determinants of cardiovascular reactivity during competition

Anger/hostility and Type A behavior have been implicated in elevated cardiovascular reactivity and disease. In the present experiment systolic blood pressure (SBP), diastolic blood pressure (DBP), and heart rate (HR) were monitored during conditions of competition alone or in conjunction with goal blocking or harassment. Cardiovascular reactivity was examined as a function of conditions, Type A or B pattern, and various measures of anger/hostility. Harassment elicited significantly elevated SBP and HR changes relative to goal-blocking and control conditions. Type As reliably exceeded Type Bs in magnitude of SBP change during the harassment condition only. However, exploratory analyses correlating anger/hostility measures and cardiovascular reactivity indicated that only subjects scoring high on the Buss-Durkee Hostility Inventory showed significantly elevated SBP reactivity as a function of Type A behavior pattern, rated hostility during the A-B interview, or outward expression of anger assessed by the Framingham Anger-In vs Anger-Out Scale.This study was supported in part by National Heart, Lung and Blood Institute (NHLBI) Training Grant HL07426 to the University of Miami. We thank Professor T. Dembroski for his overall consultation during the study and for providing training in the administration and scoring of the Type A structured interview and components.     

The relationship of anger expression and alexithymia with coronary artery stenosis in patients with coronary artery diseases

This study examined the relationship between anger expression or alexithymia and coronary artery stenosis in patients with coronary artery diseases. 143 patients with coronary artery diseases (104 males and 39 females) were enrolled in this study. The severity of their coronary artery stenosis was measured by angiography. The Anger Expression Scale and the Toronto Alexithymia Scale were used to assess the level of anger expression and alexithymia. The more stenotic group (occluded by 75% or more) exhibited a significantly higher level of alexithymia than the less stenotic group (occluded by less than 25%). Multiple regression analysis on the extent of stenosis also revealed that regardless of gender and age, the coronary artery disease patients with higher alexithymia were likely to show a greater level of stenosis. However, no significant differences were found on either the anger-in or anger-out subscale scores between the two groups. These results suggest that alexithymia is associated with the severity of coronary artery stenosis in patients with coronary artery disease. However, both anger expression and anger suppression were not shown to be associated with the severity of coronary artery stenosis.