A prospective study of dominance and coronary heart disease in the Normative Aging Study.

The purpose of this study was to examine the prospective relation between dominance, as assessed by a Minnesota Multiphasic Personality Inventory (MMPI-2)-derived dominance scale, and incidence of coronary heart disease (CHD), independent of participants' anger level. The study was performed in the VA Normative Aging Study, an ongoing cohort of older (mean age 61 years) men. A total of 1,225 men who were free of CHD in 1986 completed the MMPI-2. A factor analysis of selected MMPI items provided the basis for the construction of a dominance scale and an anger scale. During an average of 8 years of follow-up, 158 cases of incident CHD occurred, including 29 cases of fatal CHD, 69 cases of nonfatal myocardial infarction (MI), and 60 cases of angina pectoris (AP). Compared with men reporting the lowest levels of dominance (lower tertile), the multivariate-adjusted relative risk among men reporting the highest levels of dominance (upper tertile) was 1.80 (95% confidence interval [CI] 1.21 to 3.24) for combined nonfatal MI and fatal CHD. Additional adjustment for anger scores did not significantly alter this relation. There was no significant relation between dominance and AP. Our data suggest that dominance is an independent risk factor for CHD in older men.

Antagonistic behavior, dominance, hostility, and coronary heart disease.

PURPOSE: This study investigated the relationship between antagonistic behavior, dominance, attitudinal hostility, and coronary heart disease (CHD). METHODS: One hundred one men and 95 women referred for thallium stress testing were administered the Structured Interview and the Cook-Medley Hostility Scale. The Hostile Behavior Index, derived from the Structured Interview and developed by Haney et al., served as an index of antagonism, and the frequency with which interviewees interrupted their interviewer served as a measure of dominance. On the basis of their medical history and thallium stress test results, patients were classified as having (N = 44) or not having (N = 99) CHD. RESULTS AND CONCLUSIONS: Multivariate logistic regressions (with age, gender, disease, and lifestyle risk factors in the model) revealed that both the Hostile Behavior Index and dominance were significant independent risk factors for CHD (relative risk [RR] = 1.22 and 1.47, p < .03). Of the two Hostile Behavior Index component scores, indirect challenge and irritability, only the latter correlated significantly with CHD (RR = 1.27, p < .03). Separate logistic regressions for men and women suggest that subtle, indirect manifestations of antagonism confer CHD risk in women and that more overt expressions of anger confer risk in men. A significant univariate correlation between hostility scale scores and CHD became not significant when we adjusted for socioeconomic status.

Dimensions of anger and CHD in men and women: self-ratings versus spouse ratings.

One hundred one males and 95 females referred for thallium stress testing were administered Spielberger's State-Trait Anger Expression Inventory (STAXI), the Ho scale cynicism items, the Cynical Beliefs Scale, and Bendig's Manifest Anxiety Scale. A subset of 53 males and 43 females was rated by their spouses by means of STAXI. Based on the thallium findings and their medical history, patients were classified either as healthy, or as having documented CHD, or as questionable. Patients' STAXI and cynicism measures were submitted to a principal-components analysis which yielded three factors: Impulsive Anger-out. Inwardly experienced anger, and Cynicism. The relationships between factor scores and documented CHD was determined by means of logistic regression analyses. Only Impulsive Anger-out correlated (positively) with CHD, but only when based on spouses' ratings and only in males (p < .01, RR = 3.13). Covarying traditional risk factors and cynicism did not attenuate this relationship. However, a significant relationship between Ho scale cynicism and CHD did not survive adjustment for traditional risk factors. Anxiety was not a risk factor for CHD.

The outward expression of anger, the inward experience of anger and CVR: the role of vocal expression.

Two hypotheses were tested: (1) that only the outward expression of anger, not its mere experience, is associated with heightened cardiovascular reactivity; and (2) that the discussion of anger-arousing experiences in a mood incongruent speech style (soft and slow) attenuates the subjective experience of anger and its cardiovascular correlates. Each of 24 subjects participated in three experimental conditions: (1) Anger-out, in which previously experienced anger-arousing events were described loudly and quickly; (2) Anger-in, in which anger-arousing events were relived inwardly, in subject's imagination; and (3) mood-incongruent speech, in which anger-arousing events were described softly and slowly. Only the Anger-out condition was associated with high cardiovascular reactivity levels. The Anger-in and the mood-incongruent conditions were associated with near-zero and very low reactivity levels, respectively. Subjective anger ratings were highest in the Anger-out condition, moderate in the Anger-in condition, and lowest (not angry) in the mood-incongruent condition. All differences were significant. These findings suggest that the full-blown expression of anger, in all of its paraverbal intensity, is pathogenic and that the mere inner experience of anger is not.

Cardiovascular consequences of expressing, experiencing, and repressing anger.

Psychoanalytic theory's pathogenic view of repression gave rise to the widely held belief that the expression of anger is beneficial to mental and physical health. The present paper reviews a number of experimental and correlational studies which demonstrate that the full expression of anger, with its vocal manifestations, is associated with significant cardiovascular hyperreactivity. Furthermore, epidemiological studies indicate that such expression of anger are also related to coronary heart disease (CHD) and to some physiological and hormonal changes that have been implicated in the pathophysiology of CHD. On the other hand, neither the mere experience of anger nor its repression has any of the above negative cardiovascular consequences, although the repression of anger seems to have other untoward health consequences.

Voices of fear and anxiety and sadness and depression: the effects of speech rate and loudness on fear and anxiety and sadness and depression.

Two studies investigated the role of expressive vocal behavior (specifically, speech rate and loudness) in fear and anxiety and in sadness and depression. In the first study, participants spoke about personally experienced fear and anxiety-arousing and neutral events using 3 different voice styles: fast and loud, normal, and slow and soft. In the second study, participants spoke about personally experienced sad or depressing and neutral events using the same 3 voice styles. In both studies, the participants' highest levels of subjective affective and cardiovascular (CV) arousal occurred when they spoke about the emotional events in a mood-congruent voice style: fast and loud in the case of fear and anxiety, and slow and soft in the case of sadness or depression. Mood-incongruent voice styles canceled the heightened levels of CV arousal normally associated with these negative emotions. The voice-style manipulation had no significant effect on the participants' levels of CV arousal during the neutral discussions.

Speech rate, loudness, and cardiovascular reactivity.

This paper reports the results of two studies that investigated the relationship between speech rate, loudness, and cardiovascular reactivity (CVR). One study involved the separate manipulation of speech rate and loudness and assessed its effects on CVR during a routine reading task. The second study involved the simultaneous manipulation of both loudness and speech rate and studied its effects on CVR within the context of a personal interview. In both studies, the reduction of speech rate and/or loudness was associated with a significant reduction in CVR. On the other hand, increasing speech rate and/or loudness had no, or only a very minimal, effect on CVR. It is suggested that in the absence of emotional arousal, especially anger-arousal, rapid and loud speech per se is not associated with significant cardiovascular hyperreactivity. On the other hand, our findings suggest that training people to speak slowly and softly may be an effective approach for the control of cardiovascular hyperreactivity.

Dimensions of anger-hostility and cardiovascular reactivity in provoked and angered men.

This study investigated the relationship between two dimensions of anger-hostility--the expression of anger-hostility and the experience of anger-hostility--and cardiovascular reactivity in provoked and angered men. A serial subtraction task was administered to 41 male undergraduates who were provoked and angered. A measure of the expression of anger-hostility correlated positively and significantly with systolic and diastolic blood pressure (BP) reactivity. There were no significant correlations between a measure of the experience of anger-hostility and cardiovascular reactivity. The two types of anger-hostility were also found to relate differentially to life-style variables that have been identified as risk factors for coronary heart disease (CHD), with only the expression of anger-hostility showing positive relationships with these life-style CHD risk factors. These findings are discussed within the context of a similar differential relationship between the two dimensions of anger-hostility and CAD and CHD. Finally, significant negative relationships were obtained between the experience of anger-hostility and resting BP and heart rate levels. These findings are discussed within the context of other data suggesting that trait anxiety-neuroticism may have protective properties.

The angry voice: its effects on the experience of anger and cardiovascular reactivity.

The results of two studies show that expressive vocal behavior, specifically, speech rate and loudness, influences the experience of anger and cardiovascular reactivity. In both studies, participants spoke about anger-arousing and neutral events using three different voice styles: fast and loud, slow and soft, and normal (personal rate and loudness level). In describing the anger-arousing events, both male and female participants reported feeling significantly more angry and showed significantly greater blood pressure and heart rate reactivity in the fast-loud compared with the normal speaking condition. They also reported feeling significantly less angry and showed significantly lower blood pressure reactivity in the slow-soft compared with the normal voice condition. For males only, the voice manipulation also had significant effects on the participants' anger self-ratings and cardiovascular responses during the neutral communications, but these effects were clearly weaker and less pervasive than those occurring during the angry communications. The results are discussed in terms of their implications for (1) the role of expressive vocal behavior in emotions, and (2) the modification of coronary-prone behavior.

[Type A personality and its relations: the significance of hostility, neuroticism and verbal behavior for coronary heart diseases]. / Typ A und danach: die Bedeutung von Feindseligkeit, Neurotizismus und Sprechstil für koronare Herzerkrankungen.

Despite the growing body of evidence against Type-A behavior pattern as a risk factor for coronary heart disease, there remains much interest in the relationship between some of the Type-A components, especially hostility, and coronary heart disease. However, the construct of hostility too needs further refinement into overt-expressive hostility which correlated positively with the severity of coronary occlusion and the covert experience of hostility, or neurotic hostility, which is negatively correlated. Loud speech and the frequency of simultaneous interruptive speech are other attributes associated with coronary disease. The paper concludes with a biobehavioral model that assumes a synergistic interaction between hostility, speech style and cardiovascular reactivity.

Expressive vocal behavior and the severity of coronary artery disease.

This study sought to ascertain the relationship of expressive vocal behavior in a structured interview and the severity of coronary artery disease in a group of 79 patients referred for coronary angiography. One half of the structured interview was administered in a nonchallenging manner, the other half in a moderately challenging manner. In patients age 60 and younger, two speech measures derived from the nonchallenging interview, a computer-scored index of the frequency of simultaneous speech and judged loudness level, accounted for 38% of the variance in the patients' severity of stenosis scores, when the latter was indexed by the Gensini method. The same speech indices derived from the challenging interview segment accounted for only 18% of the variance on the patients' Gensini scores. In the older patient group, only one speech variable, speech rate in the nonchallenging interview segment, contributed to the patients' Gensini scores. The findings suggest a) that in younger patients objective, computer-scorable, speech variables correlate significantly with severity of coronary occlusion, and b) that is not essential that these speech indices be derived from a structured interview that is administered in a challenging and provocative manner. In the present study, there were no significant correlations between the participants' global TABP scores and their occlusion scores.

Components of hostility and the severity of coronary artery disease.

Previous research has linked various measures of hostility to the prevalence and incidence of coronary heart disease (CHD). The present study sought to determine whether some dimensions of hostility are differentially related to angiographically documented severity of coronary artery disease (CAD). Specifically, a hostility measure that correlates with indices of neuroticism was compared with a hostility measure unrelated to neurotic tendencies. For patients 60 years and younger, results were significant, revealing that neurotic hostility was inversely associated with severity of CAD whereas nonneurotic hostility scores were positively related to extent of disease. Overall hostility scores derived from the combination of the two kinds of hostility measures were unrelated to CAD severity. Results suggest that the multidimensional nature of the hostility construct should be appreciated in attempts to associate measures of hostility with manifestations of CHD.

Speaking without seeing, or the effect of interviewer absence on interviewee disclosure time.

The results of the present study confirmed earlier findings that the elimination of the usual face-to-face confrontation between interviewer and interviewee enhances disclosure time in relation to intimate questions. By unconfounding speaking time and pausing time, the present research demonstrated that the facilitating effect of an interviewer's absence is not simply an artifact of increased latencies and silent pauses within responses. The earlier findings were extended by manipulating the intimacy level of questions asked of subjects in the context of a gender-balanced design.

Effects of mutual invisibility and topical intimacy on verbal fluency in dyadic communication.

The mutual reduction of visual feedback, which in this study did not interfere with the synchronization of turns, reduced the productivity levels and increased the silent pauses of female speakers, even though it had no effect on their subjective discomfort, anxiety, and ease of communication self-ratings. The same reduction of visual feedback, which was achieved by seating the participants back-to-back rather than face-to-face, caused male speakers to feel anxious and uncomfortable and reduced the duration of their silent pauses, but only in same-gender dyads. These findings are explained in terms of previously noted gender differences in the need for visual feedback and in the anxiety-arousing effects of back-to-back interactions. Intimate communications, on the part of both male and female speakers, were associated with a slow pacing of speech but not with a decrease in productivity level, independently of the seating arrangement. These findings are interpreted in terms of the self-monitoring and self-censoring that is usually associated with the communication of intimate messages.

Toward the automated measurement of the type-A behavior pattern.

Sixty-six structured interviews that were rated by Rosenman on a 5-point Type A/B behavior pattern scale, were scored by means of a semi-automated system for verbosity, voice volume and the temporal pacing of speech. A significant negative correlation obtained between interviewees' A/B ratings and their reaction-time scores; significant positive correlations obtained between their behavior type ratings and their voice volume and duration of vocalization scores. A regression equation consisting of reaction-time and voice volume scores correctly classified the A/B ratings of 89 percent of the interviewees. The significant correlations that were obtained between the interviewer's and the interviewees' speech patterns emphasize the need for standardizing the interviewer's style. Finally, the findings suggest that anxiety-arousal is a mediating variable in the relationship between Type-A behavior and coronary heart disease.

The meaning of silent pauses in the initial interview.

It is usually assumed that anxiety arousal has a disruptive effect on speech and that it is associated with an increase in the frequency and the duration of silent pauses. Evidence is presented that anxiety arousal per se is associated with a reduction in silent pauses and an acceleration of speech rate, unless the speech task involves complex decision making. It is proposed that silent pauses in speech, including those pauses which are a result of anxiety-related defensiveness, are most parsimoniously explained in terms of information processing which is taking place at the time of the pauses.