Oral contraceptive use is associated with increased cardiovascular reactivity in nonsmokers.

Women who smoke and take oral contraceptives (OCs) have significantly increased risk of cardiovascular disease, but the exact mechanismsfor the increased risk are not known. Cardiovascular reactivity to psychological stress may be one mechanism for the enhanced risk, but the small number of studies examining whether OC users who smoke have greater reactivity have produced mixed results. The purpose of this study was to examine the effect of chronic cigarette smoking, acute nicotine administration, and OC use on cardiovascular and lipid reactivity. Sixty healthy women, half of whom had been using OCs for at least the previous 6 months, participated in the study. Approximately two thirds were smokers and were randomized to be tested after either a 12-hr nicotine deprivation or administration of nicotine gum. One third were nonsmokers. Heart rate, blood pressure, and lipid measures were taken at rest, during a videotaped speech task, and during recovery from the task. Results indicated that, among OC nonusers, there was no effect of smoking status or nicotine administration on cardiovascular reactivity. However, among OC users, nonsmokers had significantly greater heart rate and diastolic blood pressure reactivity to stress. These data show that acute nicotine administration, in the form of nicotine gum, has no effect on cardiovascular or lipid stress reactivity in women. However OC use among nonsmoking women is associated with greater cardiovascular reactivity to stress.

Catecholamine stress responses in arterialized blood.

Arterialized and venous blood was compared to determine if the arterialization procedure enhances the detection of stress-related changes in catecholamines. Lipid and hematologic measures were also compared for possible distortion by arterialization. Fifteen men completed two stressors. Indwelling venous catheters were placed retrograde in each hand, and the right hand was warmed to a constant temperature. Blood samples were taken simultaneously from both hands, and plasma catecholamines were determined. Arterialization increased baseline epinephrine; there were no effects of arterialization on catecholamines during stress, nor in lipid or hematologic measures during baseline or stress. Thus, arterialization of blood results in small increases in resting epinephrine levels, but does not obscure lipid measures. More importantly, arterialization of venous blood does not enhance the detection of stress-related changes in catecholamines.

Plasma homocysteine concentrations are positively associated with hostility and anger.

Homocysteine is a sulphur amino acid that is positively associated with risk of vascular disease. Very few behavioral or psychological factors have been studied in relationship to homocysteine levels, despite the fact that several psychological factors have also been linked with risk for cardiovascular disease. One psychological attribute showing a strong association with risk is hostility, which is prospectively predictive of future cardiovascular disease endpoints. Another related psychological factor is anger expression; coronary heart disease risk is associated with both heightened expression and inhibition of anger. The purpose of this study was to test the relationship of hostility and anger expression with homocysteine concentrations in a sample of healthy, middle-aged men and women. Participants completed the Cook-Medley hostility questionnaire, the Speilberger Anger Expression questionnaire, and had blood taken for the assessment of plasma homocysteine concentrations. Results indicated positive and significant associations between hostility and homocysteine levels for all participants, and positive and significant correlations between anger-in and homocysteine levels for men only. These data are among the first to test the relationship between homocysteine and psychological risk factors for cardiovascular diseases, and suggest one potential mechanism for the increased cardiovascular risk associated with hostility and anger expression.

Hostility and the metabolic syndrome in older males: the normative aging study.

OBJECTIVE: Several studies have shown that hostility, as measured by the Minnesota Multiphasic Personality Inventory-derived Cook-Medley Hostility Scale (Ho), is positively associated with several cardiovascular risk factors, possibly accounting for the relationship between Ho scores and cardiovascular mortality. This study was undertaken to examine associations between hostility and cardiovascular risk factors representing the metabolic syndrome in 1,081 older men who participated in the Normative Aging Study. METHODS: Subjects included men who completed the Minnesota Multiphasic Personality Inventory in 1986 and who participated in a subsequent laboratory examination within 1 to 4 years. Total and subscale Ho scores were computed, and associations with anthropometric data, cigarette smoking, dietary information, serum lipids, blood pressure, and fasting glucose and insulin levels were examined. RESULTS: The total Ho score was positively associated with waist/hip ratio, body mass index, total caloric intake, fasting insulin level, and serum triglycerides. The Ho score was inversely related to education and high-density lipoprotein cholesterol concentration. Path analysis also suggested that the effects of hostility on insulin, triglycerides, and high-density lipoprotein cholesterol were mediated by its effects on body mass index and waist/hip ratio, which, in turn, exerted their effects on lipids and blood pressure through insulin. CONCLUSIONS: The results are consistent with those of prior research and also suggest that, in older men, hostility may be associated with a pattern of obesity, central adiposity, and insulin resistance, which can exert effects on blood pressure and serum lipids. Furthermore, effects of hostility on the metabolic syndrome appear to be mediated by body mass index and waist/hip ratio.

Depressed mood is related to high-frequency heart rate variability during stressors.

OBJECTIVE: The purpose of this study was to examine the relationships between depressed mood and parasympathetic control of the heart in healthy men and women at rest and during two stressors. METHODS: Fifty-three healthy college students completed a laboratory stress protocol that included a baseline resting period, a challenging speech task, and a forehead cold pressor task. Depressed mood was assessed using the Beck Depression Inventory (BDI). Parasympathetic cardiac control was measured as the high-frequency (0.12-0.40 Hz) component (HF) of heart rate variability using power spectrum analysis. Blood pressure, respiration rate, and respiration amplitude were measured simultaneously. RESULTS: Participants were categorized as having a high or low depressed mood on the basis of median splits of their BDI scores. Those in the high depressed mood group had significantly greater reductions in HF during the speech task and significantly smaller increases in HF during the forehead cold pressor task than those in the low depressed mood group. Women had significantly greater reductions in HF during the speech task and smaller increases in HF during the forehead cold pressor task than men. However, gender and depressed mood did not interact to predict changes in HF. CONCLUSIONS: Depressed mood is related to the magnitude of decrease in parasympathetic cardiac control during stressors in healthy men and women. These findings extend those of previous studies, in which a similar phenomenon was observed among patients with cardiac disease. Because the participants in this study were healthy, the relationship between depressed mood and parasympathetic cardiac control does not seem to be secondary to cardiovascular disease.

Lipid reactivity among men with a parental history of myocardial infarction.

In the current study, we examined lipid and cardiovascular responses to an acute stressor among men with and without a parental history of myocardial infarction. 37 men were selected from a large group who completed medical history questionnaires and interviews. Twenty-two men who denied parental history of heart disease (negative parental history) were compared with 15 men with one or both parents who had suffered a myocardial infarction (positive parental history). Total cholesterol, high- and low-density lipoprotein cholesterol, triglycerides, heart rate, and blood pressure were measured at rest and during a videotaped speech stressor. Positive parental history men had significantly higher low-density lipoprotein cholesterol levels and blood pressure at baseline, significantly lower high-density lipoprotein cholesterol levels at baseline, and significantly larger total cholesterol and low-density lipoprotein cholesterol reactivity, relative to negative parental history men. Because parental history is a risk factor for subsequent cardiovascular morbidity and mortality, these data suggest that lipid reactivity to stress may be biologically important.

Lipid reactivity to stress: I. Comparison of chronic and acute stress responses in middle-aged airline pilots.

Lipids increase during psychological stress, but no studies have compared the effects of acute and chronic stressors on lipid responsivity in the same individuals. One hundred middle-aged men (n = 92) and women (n = 8) were examined during high chronic occupational stress, low chronic stress, and acute laboratory stressors. In addition to measures of perceived stress and affect, an extensive battery of lipid and lipoprotein measures was undertaken at each time point. Most lipid parameters were significantly increased during the chronic and acute stressors, although the responses to the different stressors were not consistently associated. For example, significant correlations among the chronic and acute stress responses were apparent for the apoproteins, but not for total, low density lipoprotein, or high density lipoprotein cholesterol. The factors and processes regulating these variables during stress may be different during acute and chronic stressors.

Lipid reactivity to stress: II. Biological and behavioral influences.

This study examined behavioral and physiological influences on lipid concentrations during acute and chronic stressors. One hundred men (n = 92) and women (n = 8) were tested during a chronic stressor and during 2 acute stressors. During chronic stress, diet, physical activity, exercise, and sleep were examined. During the acute stressors, catecholamines, cortisol, plasma volume, and cardiovascular responses were examined. None of the behavioral influences could explain the lipid response to chronic stress. Responses of the atherogenic lipids to acute stressors were not solely reflecting hemoconcentration of the plasma but were moderately correlated with cardiovascular, epinephrine, and cortisol reactivity. Diastolic blood pressure reactors to the acute stressors had larger lipid responses to the chronic stressor than did nonreactors. Elevations in blood lipids during stress are not artifacts and may be clinically significant.

Plasma homocysteine levels increase in women during psychological stress.

Homocysteine is an amino acid that has been strongly associated with vascular disease. Plasma homocysteine concentrations are known to vary with dietary patterns and to decrease with exogenous estrogen use, but no other behavioral factors have been examined as potential modifiers of this risk factor. Because psychological stress has also been implicated in the development of cardiovascular disease, the purpose of this study was to test the hypothesis that acute psychological stress induces elevations in plasma homocysteine concentrations. A secondary aim was to test potential differences in response between premenopausal and postmenopausal women. Thirty-four healthy women, one-half of whom were naturally postmenopausal with no hormone replacement, participated in this study. The psychological stressors included standard mental arithmetic and speech stressors. Blood samples were taken prior to, during, and after the stressors, and heart rate and blood pressure were also monitored. Results indicated significant elevations in plasma homocysteine during acute psychological stress, with a return to baseline concentrations during recovery. The pattern of findings for blood pressure and heart rate was similar, suggesting that the rise in homocysteine concentrations may have been sympathetically-mediated. No effects of menopausal status or endogenous estrogens were found. The findings provide preliminary evidence that plasma homocysteine may be an important factor in the relationship between psychological stress and risk for heart disease.

Environmental tobacco smoke: association with cardiovascular function at rest and during stress.

Chronic exposure to environmental tobacco smoke (ETS) contributes to cardiovascular disease morbidity and mortality, and ETS alters cardiovascular performance during exercise stress. However, no study has examined whether those with ETS exposure have altered cardiovascular functioning during psychological stress, relative to those with no substantial ETS exposure. Seventy-eight healthy, nonsmoking adult men with either high levels of current ETS exposure at home and work or no current or significant lifetime ETS exposure were tested in a stress reactivity protocol. Blood pressure and heart rate were monitored during rest and during two psychological stressors. Those with high ETS exposure had significantly elevated heart rate and blood pressure at baseline, relative to those with no exposure. The groups did not differ on their cardiovascular stress responses. These data suggest that chronic ETS exposure is associated with altered cardiovascular functioning at rest, but not during stress. Results are discussed with regard to the role of ETS on the development of heart disease among nonsmokers.

A natural experiment on the effects of ovarian hormones on cardiovascular risk factors and stress reactivity: bilateral salpingo oophorectomy versus hysterectomy only.

To test the effects of declining ovarian hormone levels on cardiovascular risk factors, blood pressure, lipids, weight, and physiological responses to stress were evaluated in 29 middle-aged premenopausal women prior to and following elective hysterectomy and/or bilateral salpingo oophorectomy (BSO). Prior to surgery, there were no group differences in standard or putative risk factors, with the exceptions of body composition measures and total cholesterol level. After surgery, women who had undergone BSO (n = 10) had higher levels of atherogenic lipids and stress-induced lipids and tended to have higher circulating levels of epinephrine and stress-induced systolic and diastolic blood pressure than women who had undergone hysterectomy only (n = 19). This study is consistent with the hypothesis that presence of ovarian hormones plays a key role in determining women's risk factor status.

Temporal stability of lipid responses to acute psychological stress in middle-aged men.

The purpose of this study was to establish the temporal stability of lipid responses to acute psychological stress. Eighteen men were tested twice an average of 16.2 months apart in identical laboratory reactivity protocols. Total cholesterol, triglycerides, high- and low-density lipoprotein-cholesterol, plasma volume, heart rate, and blood pressure were assessed during rest, serial subtraction, and speech. After correction for changes in plasma volume, significant elevations were recorded for all variables during the speech task, but fewer variables showed changes during the serial subtraction task. Strong intersession associations were found when considering levels of the variables during baseline and stress (rs > or = .58). Correlations for the change scores ranged from .36 to .52 for the atherogenic lipids and from .39 to .87 for the cardiovascular variables. Little evidence was found for stability of plasma volume changes. There is moderate to high temporal stability of the atherogenic lipids when considering rest and stress levels and small to moderate temporal stability when considering change scores.

Anger expression and lipid concentrations.

We used 2 different strategies to examine the relation between anger expression and lipid concentrations in 116 middle-aged men. Using the common analytic method used in the literature, the group crossing approach, we examined whether Anger-In. Anger-Out, and their interaction were related to lipids. Regression analyses revealed that Anger-In and Anger-Out were marginally related to total cholesterol. These associations disappeared after controlling for hostility, anger, and anxiety. Using a new intraindividual difference approach, we determined individuals' relative dominance of Anger-In and Anger-Out and examined linear and quadratic associations with lipids. Regression analyses revealed the quadratic was related to both total cholesterol and low-density lipoprotein-cholesterol (LDL-c), indicating that individuals who almost always express their anger or almost never express their anger had both elevated total cholesterol and LDL-c. The curvilinear association with total cholesterol persisted even after controlling for hostility, anger, and anxiety.

Gender and ethnicity in children's cardiovascular reactivity: 7 years of study.

A total of 295 children (127 White boys, 15 Black boys, 133 White girls, and 20 Black girls) participated in reactivity examinations in 1987 (all were in 3rd grade; age, M = 9.1 years), 1988, 1989, 1991, 1992 and 1993 (all were in 9th grade; age, M = 15.1 years). An analysis of residualized reactivity change values indicated consistent and significant ethnicity effects (Blacks greater than Whites) for systolic and diastolic blood pressure and for heart rate. Gender effects were also apparent for both systolic and diastolic blood pressure (boys greater than girls). These data suggest that the transition from childhood to adolescence is associated with a significant pattern of ethnic differences in reactivity, although the association of this pattern with the development of cardiovascular risk and disease remains to be ascertained.

Are cardiovascular reactors to asocial stress also reactors to social stress?

The authors tested the generalizability of measures of cardiovascular reactivity to asocial and social stress among fathers, mothers, and their adolescent sons. Results showed significant associations between reactivity to individual psychomotor tasks and to conflict resolution only for mothers, suggesting that laboratory measures of reactivity obtained during asocial tasks are of limited value in predicting reactivity during social tasks. Given that interpersonal constructs are important to risk for cardiovascular diseases, these findings point to the importance of measuring cardiovascular reactivity during social stress, not only during asocial achievement stress.

Menopausal status influences ambulatory blood pressure levels and blood pressure changes during mental stress.

BACKGROUND: Frequent and large cardiovascular and neuroendocrine responses to psychological stress are thought to enhance an individual's risk for cardiovascular diseases. Preliminary data suggest that levels of reproductive hormones affect the magnitude of stress responses, perhaps contributing to the protective effect of ovarian hormones on premenopausal women's rates of coronary heart disease. METHODS AND RESULTS: Healthy middle-aged men and premenopausal and postmenopausal women performed a series of standardized mental and physical challenges while blood pressure, heart rate, plasma catecholamines, lipids, and lipoproteins were measured. Subjects then wore an ambulatory blood pressure monitor during two consecutive workdays. Results showed that postmenopausal women had larger mean +/- SEM stress-induced increases in systolic blood pressure (24.7 +/- 2.2 mm Hg) and diastolic blood pressure (14.3 +/- 1.0 mm Hg) compared with either premenopausal women (16.9 +/- 1.3 and 10.2 +/- 0.9 mm Hg) or men (17.7 +/- 1.5 and 10.9 +/- 1.1 mm Hg, respectively). Postmenopausal women and men had higher mean +/- SEM ambulatory diastolic blood pressure levels (75.5 +/- 3.2 and 76.4 +/- 1.8 mm Hg) than did premenopausal women (69.9 +/- 2.2 mm Hg). Large blood pressure responses during public speaking were associated with high cholesterol levels and low educational attainment. CONCLUSIONS: Menopause is associated with enhanced stress-induced cardiovascular responses and elevated ambulatory blood pressure during the workday. These effects may contribute to the risk of cardiovascular morbidity and mortality after the menopause.

Hemodynamic adjustments to laboratory stress: the influence of gender and personality.

Exaggerated cardiovascular reactivity to psychological stress is a potential pathophysiological mechanism linking behavior and cardiovascular disease. Because of the recognized gender differences in incidence of cardiovascular disease, potential gender differences in cardiovascular reactivity to laboratory stressors have been evaluated. The current study examined the cardiovascular responses of a total of 42 young women (N = 22) and men (N = 20) undergoing a laboratory protocol including the following: a nonverbal math task, a mirror tracing task, the Stroop Color-Word interference task, and an isometric handgrip task. In addition to the assessment of heart rate and blood pressure, cardiac output, stroke volume, total peripheral resistance and preejection period were assessed by impedance cardiography. A number of personality characteristics that vary in prevalence by gender were also measured to evaluate their ability to explain potential gender differences in cardiovascular responses. Results indicated that men responded with greater total peripheral resistance and systolic and diastolic blood pressure responses than did women on a subset of tasks, whereas women exhibited larger increases in heart rate on a subset of tasks. Thus, men were more likely to be "vascular" reactors, with women being more likely to be "cardiac" reactors. Personality characteristics did differ between men and women, but did not explain significant variance in the gender differences in cardiovascular responses. We conclude that additional studies should focus on experimental manipulations of potential physiological mechanisms responsible for these differences, such as reproductive hormones.

Do cardiovascular responses to laboratory stress relate to ambulatory blood pressure levels?: Yes, in some of the people, some of the time.

Because the correspondence between laboratory measures of blood pressure and heart rate responses to stress and ambulatory measures is less than optimal, this study tested two hypotheses: Are ambulatory measures of blood pressure elevated during periods of perceived stress, relative to no stress? Are ambulatory blood pressures elevated during perceived stress among those individuals who exhibit elevated blood pressure and heart rate responses to laboratory stress? These questions were addressed in a sample of employed, middle-aged men and premenopausal and postmenopausal women, who vary in reproductive hormone status, and in risk for coronary heart disease. All participants performed a series of laboratory studies while their physiological parameters were monitored and then wore an ambulatory blood pressure monitor for a day and a half. This monitor recorded blood pressure every half hour during the waking hours and at the same time the participants assessed their mood states. After excluding participants who reported no variability in stress levels, those who were cardiovascular reactors to a laboratory speech task exhibited elevated ambulatory blood pressure levels during periods of perceived stress. Furthermore, in general, periods of perceived stress were associated on a within subject basis with elevated ambulatory blood pressure. These results suggest that the correspondence between laboratory and field measures of blood pressure would be improved by taking into account the environmental circumstances during the ambulatory assessments and the person characteristics of reactor-nonreactor to laboratory stress.

Lipids in psychological research: the last decade.

We review the recent literature examining lipid changes during stressful experiences, and the psychological and constitutional differences that influence lipid levels at rest and that may modulate lipid response to stress. Mild forms of chronic or episodic stress are apparently not associated with alterations in lipids and lipoproteins, but severe forms of real or perceived stress do appear to alter lipid levels. Acute laboratory stress is frequently associated with short-term alterations in lipids and lipoproteins, but the significance of these changes is unclear. Several individual characteristics, such as heightened neuroendocrine or autonomic reactivity to stressors, Type A component behavior, and other aspects of personality, appear to be associated with an atherogenic lipid profile. Stress may influence lipid concentrations and metabolism through a variety of physiological and behavioral mechanisms, but none have been clearly elucidated. Future research should concentrate on understanding these mechanisms.