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Objectives: Social isolation has been linked to poor survival in patients with coronary artery disease (CAD). Few studies have closely examined the psychosocial characteristics of CAD patients who lack social contact.Methods: Social isolation was examined as a predictor of mortality in 430 patients with significant CAD. More isolated patients were compared with their less isolated counterparts on factors that might help explain the association between isolation and survival.Results: The mortality rate was higher among isolated individuals. Those with three or fewer people in their social support network had a relative risk of 2.43 (p = .001) for cardiac mortality and 2.11 (p = .001) for all-cause mortality, controlling for age and disease severity. Adjustments for income, hostility, and smoking status did not alter the risk due to social isolation. With the exception of lower income, higher hostility ratings, and higher smoking rates, isolated patients did not differ from nonisolated patients on demographic indicators, disease severity, physical functioning, or psychological distress. Isolated patients reported less social support and were less pleased with the way they got along with network members, but they did not report less satisfaction with the amount of social contact received.Conclusions: Patients with small social networks had an elevated risk of mortality, but this greater risk was not attributable to confounding with disease severity, demographics, or psychological distress. These findings have implications for mechanisms linking social isolation to mortality and for the application of psychosocial interventions. [ABSTRACT FROM AUTHOR]

Objective: Hospitalization for cardiac disease is associated with an increased risk for depression, which itself confers a poorer prognosis. Few prospective studies have examined the determinants of depression after hospitalization in cardiac patients, and even fewer have examined depression within the weeks after hospital discharge. The present study assessed the prospective relations among perceptions of social support and trait hostility in predicting symptoms of depressive symptoms at 1 month after hospitalization for a diagnostic angiography in 506 coronary artery disease (CAD) patients.Method: A series of structural equation models 1) estimated the predictive relations of social support, hostility, and depressive symptoms while in the hospital to symptoms of depression 1 month after hospitalization, and 2) compared these relations across gender, predicted risk classification, and age.Results: Social support assessed during hospitalization was independently negatively associated with depressive symptoms 1 month after hospitalization, after controlling for baseline symptoms of depression, gender, disease severity, and age. Hostility was an indirect predictor of postdischarge depressive symptomology by way of its negative relation with social support. This pattern of relations did not differ across gender, predicted risk classification, and age.Conclusions: Our findings suggest that a patient's perceived social support during hospitalization is a determinant of depressive symptoms 1 month later. The relation of social support and hostility to subsequent depressive symptoms was similar across a variety of populations. [ABSTRACT FROM AUTHOR]

Discusses the clinical and experimental evidence for unresponsive cardiac standstill secondary to toxicity of tricyclic antidepressants. Effects of tricyclic antidepressants on catecholamine uptake in heart muscle and adrenergic nerve endings; Measurement of fluid balance and oxygen by mask; Occurrence of the catecholamine blocking and depleting effects of the antidepressants.

We examined the effects of dietary cholesterol on cardiac and hepatic beta-adrenergic receptor functioning. Age-matched adult desert rodents (Psammomys obesus) were randomized to either a 5% cholesterol diet (CD, n = 20), or normal rabbit chow (RC, n = 18). After a 2-month exposure to the diets, animals were sacrificed and tissue from both heart and liver were retained for radioligand bindings studies. In heart tissue, cholesterol fed animals, relative to controls, showed an increased production of adenosine 3,5>-cyclic monophosphate (cAMP) in response to isoproterenol. Cholesterol supplementation was not associated with an increase in heart beta-adrenergic receptor number. Animals fed the 5% cholesterol diet showed significant increases in the number of beta-adrenergic receptor sites in hepatic tissue (M = 13.2 vs. 10.4 pmol/mg protein, CD and RC, respectively). The increased number of receptor sites in the liver was accompanied by a significant increase in isoproterenol-stimulated cAMP production. Results are supportive of the hypothesis that dietary cholesterol contributes to an upregulation of beta-adrenergic receptor function in cardiac, as well as hepatic tissue. These findings may be relevant to the observations of excessive stress-induced cardiovascular reactivity in persons with high cholesterol levels.

The relation of hostility and harassment to cardiovascular and emotional responses was examined by having 51 women (ages 18-26) high and low in hostility complete a task with or without harassment. Harassed high hostile Ss showed greater systolic blood pressure (SBP) increases during task and recovery periods than did harassed low hostile Ss and nonharassed Ss. Harassed low hostile Ss evidenced greater SBP increases during task and recovery periods than did nonharassed Ss. Among high hostile women, cardiovascular elevations during the task were associated with self-reported levels of negative affect. Antagonistic hostility, relative to neurotic hostility, was positively associated with harassment-induced SBP changes. These results support the hypothesis that hostile people exhibit excessive behaviorally induced cardiovascular responses to interpersonally challenging tasks that evoke anger-related emotional states.

The UNC Alumni Heart Study (UNCAHS) is a prospective study of the role of psychosocial factors, in particular hostility, in the development of coronary heart disease. The target population is composed of persons who completed the Minnesota Multiphasic Personality Inventory while attending the University of North Carolina in the mid-1960s. Logistic regression analyses were used to determine whether hostility, demographic and other variables were significant determinants of the subjects' locatability and participation. It was found that MMPI hostility scores at initial testing were unrelated to either potential or actual locatability or participation. Thus there is no evidence that hostility is the source of selection bias in the UNCAHS. Selection into the study was predicted by age, sex, degree status and variables concerned with the conditions under which the MMPI was administered. It is concluded that follow-up studies of college cohorts may have study-specific sources of selection bias.

Background: Prior research has suggested a weaker parasympathetic antagonism of sympathetic effects on the heart in type A (coronary-prone) men. To confirm this phenomenon and extend our understanding of it, we investigated the effects of prior muscarinic blockade on the electrocardiogram T wave and other cardiovascular and neuroendocrine responses to isoproterenol in type A and type B (non-coronary-prone) men., Methods and Results: Responses to two 5-minute intravenous isoproterenol infusions (0.01 micrograms/kg/min and 0.02 micrograms/kg/min) were evaluated in six type A and six type B men after pretreatment with either dextrose placebo or atropine (1.2 mg). Atropine significantly potentiated T wave attenuation in the recovery period after isoproterenol infusion (0.30 +/- 0.07 mV) compared with placebo (0.54 +/- 0.09 mV, p less than 0.001). Atropine also potentiated the heart rate increase to isoproterenol (39 +/- 3 beats per minute versus 20 +/- 2 beats per minute after placebo). Atropine enhanced decreases in systolic, diastolic, and mean arterial pressures as well as pulse pressure to isoproterenol. Atropine enhancement of many of these responses was increased among subjects with high scores on various hostility/anger scales. Isoproterenol alone produced greater T wave attenuation in type A than in type B men. However, atropine enhancement of T wave attenuation and blood pressure falls by isoproterenol was present only in type B men., Conclusions: These findings indicate that there is accentuated parasympathetic antagonism of T wave attenuation and blood pressure responses induced by beta-adrenergic stimulation. Relative weakness of this antagonism of sympathetic effects on the heart in hostile type A individuals may contribute to their higher coronary disease risk.

A high percentage of patients who undergo diagnostic angiography because they have chest pain are found to be free of significant coronary artery disease. To examine the psychological characteristics of these patients, we used several Minnesota Multiphasic Personality Inventory (MMPI; Hathaway & McKinley, 1943) measures to assess the relationships between different aspects of neuroticism and coronary artery disease severity (CADSEV) in a sample of 1,462 angiography patients. The Conversion V profile was inversely and most strongly related to CADSEV. Single high scores on hypochondriasis or hysteria were also inversely related to CADSEV, but psychasthenia and Taylor Manifest Anxiety Scale (TMA; Taylor, 1953) scores were not. Using measures derived by a factor analysis of the MMPI, items relating somatic complaints were inversely related to CADSEV, but a measure of general neuroticism was not. These results support the hypothesis that the association between neuroticism and angiographic findings may be specific to a particular aspect of neuroticism, somatic preoccupation. The implications for neuroticism measurement and clinical practice are discussed.

Correlated Cook-Medley Hostility Scale (Ho) scores with sociodemographic variables in a national survey of 2,536 adults. Multiple regression models revealed that Ho scores were associated with race (p less than .0001), years of education (p less than .001), sex (p less than .001), occupation (p = .0002), and income (p = .0025). Higher scores were found in non-Whites, men, and those of lower socioeconomic status. There was a Race x Income interaction (p less than .005), such that the greatest Ho score differences between the races occurred among those with the lowest incomes. Age was related to Ho scores in a curvilinear fashion: higher scores in the youngest and oldest age groups than in the middle-aged groups (p = .025). Marital status was unrelated to Ho scores. These patterns of hostility are similar to the patterns of health indicators in the population. Because hostility has been found to be associated with adverse health outcomes, hostility may account for some of the demographic variations in health status. However, it is argued that research must first establish the generality of the hostility-health relationship across subgroups of the population.

The outcome of the diagnostic exercise test depends on such patient-related factors as age, maximum exercise heart rate, exercise time and severity of the underlying coronary artery disease (CAD). This study examined the hypothesis that type A behavior would affect the amount of effort expended, as indicated by the exercise time and the maximum heart rate achieved, thereby resulting in differences in exercise test outcome. A total of 1,260 patients with suspected CAD, all of whom had coronary angiography, a structured interview to assess type A behavior and a treadmill exercise test, participated. Of these patients, 818 (65%) had significant CAD, and 852 (68%) were type A. There were no differences between type A and B patients in either maximum heart rate or total exercise time. Among both type A and B subjects, 36% of treadmill tests were positive. Exercise test sensitivity was similar for both groups (69% for type A vs 72% for type B, p = 0.39). Similarly, specificity was similar for both groups (87% for type A vs 80% for type B, p = 0.09). Results did not change after using logistic regression to control for potential confounding factors. Thus, type A behavior does not need to be taken into account when interpreting exercise test outcome.

Increased coronary disease rates, as well as increased all-cause mortality, in persons with high levels of hostility/anger and in persons suffering from panic disorder or phobic anxiety suggest that biological concomitants of these traits/conditions lead to major medical illnesses. Benzodiazepines have effects, e.g. blunting of stress hormone responses, that could prevent disease in persons so predisposed. It will be necessary to identify subgroups with sufficiently high absolute rates of disease risk to justify pharmacological interventions, and then to carry out controlled prevention trials to document the benefits, before such approaches can be recommended for the general population. This approach (use of drugs when other measures fail) is now standard for more traditional risk factors, such as hyperlipidemia and hypertension. In contrast to primary prevention, a stronger case can be made for the use of benzodiazepines in secondary prevention. Research has shown benzodiazepine treatment to improve control of angina and to reduce "silent ischemia", directly suggesting clinical benefits to be gained from the effects of benzodiazepines to reduce stress hormone responses. While benzodiazepines have long been prescribed for the postmyocardial infarction patient, there are no controlled clinical trials documenting such benefits. These are now clearly in order so that the use of benzodiazepines in coronary patients can be advised on a rational basis.

Previous research has demonstrated an increased rate of clinical coronary heart disease (CHD) events among people who exhibit a "coronary prone" (Type A) behavior pattern. This study was undertaken to determine whether the association between behavior pattern Type A and CHD might be extended beyond clinical CHD events to include also the coronary atherosclerotic process. In addition to usual clinical evaluation, 156 consecutive patients referred for diagnostic coronary angiography were independently assessed on the basis of a structured interview and assigned a rating of Type A, Type B, or Type X (indeterminate). Traditional physiologic factors--age, sex, cholesterol and cigarette smoking--were found to correlate with atherosclerotic disease. Type A patients were found in increasing proportions among groups of patients with coronary occlusions of moderate to severe degree compared with patients with only mild occlusions. This increasing proportion of Type A patients with increasing disease severity remained significant, even when age, sex, blood pressure, serum cholesterol level and cigarette smoking history were all simultaneously covaried. These findings suggest that, independently of traditional risk factors, behavior pattern Type A may contribute to the risk of clinical CHD events via effects on the atherosclerotic process.

This article reviews the epidemiologic evidence linking psychological factors and various indexes of coronary heart disease (CHD) that has been gathered since the Amelia Island Conference in 1978. In general, studies of populations not selected according to CHD risk support the conclusion that the global type A construct is predictive of increased risk of coronary events. In high-risk groups, including patients undergoing coronary angiography, the evidence with respect to global type A is much less clear. This stems from the fact that most of these studies, although generally failing to find statistically significant relationships between coronary events and type A behavior, are flawed in a number of ways, including inadequate statistical power of results, use of less than adequate instruments, and failure to take an apparent interaction between type A behavior and age into account. Nevertheless, taken together, these findings suggest that it may be possible to identify measures of coronary-prone behavior that are more powerful than the global type A measure. Extensive evidence suggests that such measures may be found in the domain of hostility and anger. Measures of hostility and anger coping styles have been found to be associated with coronary atherosclerosis in populations in which global type A was not related to disease, and measures of hostility have predicted increased coronary events and total mortality in prospective population samples followed for from 20 to 25 years. Preliminary evidence suggests that hostility/anger characteristics may account for the increased coronary risk associated with global type A behavior.(ABSTRACT TRUNCATED AT 250 WORDS)

This study examined the interaction of race and parental history of hypertension on patterns of cardiovascular responses among women. Two stressors were used that produce different patterns of cardiovascular reactivity: mental arithmetic, primarily a beta-adrenergic stimulus, and the cold face stimulus, which evokes alpha-adrenergic (i.e. vascular) activity. Systolic and diastolic blood pressure, heart rate, forearm blood flow, and forearm vascular resistance were assessed before, during, and after arithmetic and cold face stimulus. Both tasks produced the expected patterns of cardiovascular adjustment, although no Black-White differences occurred during arithmetic. However, Black subjects did show a slower recovery of diastolic blood pressure following arithmetic. The cold face stimulus produced significantly greater changes in systolic blood pressure in the Black than in the White women. Parental history of hypertension did not relate significantly to reactivity. The results provide limited support for the idea that Black females exhibit a greater pressor response than White females to a stimulus that produces primarily vascular rather than cardiac changes. These findings are discussed in relation to previous findings with males and with respect to their implications for the role of reactivity in Black-White differences in hypertension prevalence.

The Type A behavior pattern and the inhibited power motive have been implicated in the development of coronary heart disease (CHD). Since it is widely believed that enhanced cardiovascular responsivity may be one mechanism by which individuals develop CHD, the present study examined the relationship of Type A behavior and the inhibited power motive to different patterns of cardiovascular response during two behavioral tasks. Forty-one (24 Type A's, 17 Type B's) male undergraduates underwent the Type A structured interview (SI) and the Thematic Apperception Test (TAT) while a broad range of cardiovascular functions were simultaneously recorded. Different patterns of cardiovascular response were observed during the SI and TAT, and Type A's showed a greater tendency than Type B's to exhibit increased heart rate (HR), systolic blood pressure (SBP), and forearm blood flow (FBF) during the SI and the preparatory phase (but not the story-telling phase) of the TAT. The inhibited power motive was not related to enhanced cardiovascular responsivity during the SI or TAT. The implications of these findings for the development of CHD are discussed.

Twenty-six healthy young Caucasian males were defined into high hostile (Hi-Ho) group and low hostile (Lo-Ho) group assessed by Cook-Madley's Hostility (Ho) scale. Mental arithmetic task (MA) and forehead cold stimulus task (FCS) were loaded to both Hi-Ho and Lo-Ho groups. Electrocardiographic T-wave amplitude (TWA), heart rate (HR) and coefficient of variance of 100 R-R intervals (CVR-R) were measured continuously during MA and FCS task periods. Greater TWA attenuation was found in Hi-Ho group (p less than 0.05). Although no significant intergroup difference was represented in HR and CVR-R, HR increased significantly (p less than 0.01) in whole subjects and CVR-R was tend to be suppressed during MA period. In addition, comparison of these physiological responses were performed between Type-A and Type-B groups classified by Jenkins' Activity Survey Form-T (JAS-T). There was no significant difference in reactivity of TWA, HR and CVR-R to both two tasks between high and low Type-A scored groups. Previous data suggested that the TWA reactivity in Hi-Ho subjects to cognitive stress showed similar pattern in Type-A individuals. However, autonomic nervous interaction could not be clarified in Hi-Ho subjects. The differentiation of method for assessment of behavioral pattern was also discussed.

To determine whether there are basic biological differences between Type A and Type B men, we compared hemodynamic, electrophysiologic and neuroendocrine responses to equipotent doses of isoproterenol (ISO) and norepinephrine (NE) in 10 Type A and 10 Type B men ages 18 to 29. Results showed equal hemodynamic and neuroendocrine responses to graded ISO doses in Type A and Type B individuals. In contrast, Type A men showed a more prolonged decrease in electrocardiographic T-wave amplitude (TWA) than did Type B men. Post hoc analyses of the correlates of TWA recovery during high-dose ISO infusion provide preliminary evidence for a more robust parasympathetic antagonism of sympathetic nervous system effects in Type B men, especially those with low scores on the Cook-Medley Ho scale. These findings suggest that, in addition to cognitively mediated increases in sympathetic nervous system reactivity, Type As may also be placed at increased risk of developing coronary heart disease by reduced levels of parasympathetic antagonism of sympathetic effects.

Type A patients with coronary artery disease (CAD) tend to ignore or underreport symptoms, especially during challenging tasks such as the treadmill exercise test. To determine whether type A CAD patients might be more likely than type B patients to have silent ischemia during exercise and consequently a worse prognosis, 403 patients with stable CAD who had significant coronary disease on angiography, a positive Bruce protocol treadmill test and a structured interview to assess type A behavior were studied. Median follow-up time was 6 years. Type A patients were more likely to experience silent ischemia during exercise than were type B patients (35 vs 25%, p = 0.05). Patients with silent ischemia during exercise had a history of fewer anginal episodes/week, and type A patients with silent ischemia were less likely to have had a history of typical angina. However, using the Cox model, there were no significant differences in survival between type A patients and B patients with silent ischemia (4-year survival 86 vs 79%, p = 0.44) and no significant differences in survival between type A patients with silent ischemia and type A patients with symptomatic ischemia (6-year survival 86 vs 80%, p = 0.59). Similar results were obtained for infarction-free survival. Type A patients are more likely than type B patients to have silent ischemia during exercise, but long-term survival is not affected.

Beta-adrenergic sympathetic nervous system (SNS) hyperresponsivity to behavioral stress may play a role in the onset of sustained high blood pressure--particularly in persons with a parental history of hypertension. Although hypertension is extremely prevalent among blacks, the association between parental history of hypertension and cardiovascular hyperresponsivity has not been explored in this group. The present study examined the influence of parental history of hypertension on cardiovascular stress reactivity in a group of young black females. Contrary to previous findings with whites, black subjects with a parental history of hypertension exhibited significantly smaller systolic blood pressure and forearm blood flow increases, and moderately smaller diastolic blood pressure increases to the task. Parental history subjects also exhibited slower heart rates throughout each experimental condition. The results suggest that blacks at risk from hypertension may not exhibit the beta-adrenergic hyperresponsivity to behavioral stress observed in whites. These results may suggest that beta-adrenergically mediated hyperresponsivity may be less involved in the development of hypertension among blacks.

The purpose of this study was to determine the effects of Type A behavior and family history of hypertension on cardiovascular reactivity to mental stress in a group of employed black women. Measures of heart rate and of systolic blood pressure (SBP) and diastolic blood pressure (DBP) were taken at rest, during a mental arithmetic task, and during the Type A Structured Interview (SI). Results indicated that the Type A behavior pattern was associated with SBP and DBP hyperresponsivity during the SI but not during mental arithmetic. Additionally, certain speech components of the Type A pattern, as well as features of the potential-for-hostility component, were also related to cardiovascular responses during the SI. Family history of hypertension did not influence the cardiovascular parameters either alone or in combination with Type A behavior. The results suggest that many of the cardiovascular response characteristics of the Type A pattern that have been observed in predominantly white samples also hold true for blacks. Replication of these findings with other subgroups of blacks, such as young females and middle-aged males, will help document the generality of these findings within the black population.

Patients with documented coronary artery disease, admitted to Duke Medical Center between 1974 and 1980, were assessed for type A behavior pattern and were followed until 1984. The relation of type A behavior to survival was tested using data from coronary angiography to control for disease severity. Cox model regression analyses demonstrated an interaction (p less than 0.01) between type A behavior and an index of disease severity in the prediction of cardiovascular death. Among those with relatively poor left ventricular function, type A patients had better survival than type B. This difference was not present among patients with better prognoses. Type A behavior did not predict the subsequent incidence of nonfatal myocardial infarctions. Differential risk modification and differential selection into postinfarction status are possible explanations for the findings. These results need not conflict with the proposition that type A behavior plays a role in the pathogenesis of coronary artery disease.

Recent negative research findings have raised questions regarding the robustness of the Type A hypothesis. A growing body of evidence suggests that not all aspects of the global Type A behavior pattern are pathogenic, but only those concerned with hostility and anger. Biologic mechanisms responsible for increased risk of coronary disease in persons with high levels of hostility and anger appear to involve increased cardiovascular and neuroendocrine responses to behavioral challenge, and, possibly, inadequate parasympathetic antagonism of sympathetic nervous system effects. Future research should concentrate on further refining our understanding of the hostility complex and its pathophysiologic mechanisms.

This study reports the development of a brief self-report measure of the Type A behavior pattern based upon a set of adjectives derived from the Gough Adjective Checklist (ACL). Previous work from our laboratory established a set of adjectives identified by experts as being relevant to the Type A construct that subsequently was found to successfully distinguish Type A individuals from their Type B counterparts. In the present study, a Type A self-rating scale based on these adjectives was found to be significantly related to an established Type A self-report instrument, the Jenkins Activity Survey (JAS), and to an independent behavioral rating based upon a standard structured interview (SI). However, no measure of Type A was related to the severity of coronary artery disease (CAD) as documented by coronary angiography. The advantages and disadvantages of the various Type A measures are discussed in the context of their ability to identify individuals at risk for the development of CAD.

beta-Adrenergic hyperreactivity has been proposed as a pathogenic mechanism of increased coronary risk in Type A individuals. This study compared the effects of propranolol, diazepam, and placebo on cardiovascular and neuroendocrine responses to a stressful cognitive task in six young Type A males. Although diazepam did not differ from placebo, propranolol attenuated heart rate and norepinephrine responses and enhanced cortisol responses to the task. Findings suggest that propranolol has reciprocal effects on the norepinephrine and cortisol components of the "fight-flight" response. Possible central nervous system mechanisms are described.