Anger Recall Research Articles

The impact of forgiveness on cardiovascular reactivity and recovery

The current study investigated the relationship between trait forgiveness and cardiovascular reactivity (CVR) and recovery in 99 normotensive participants (mean age = 33.8). Cardiovascular parameters were obtained at 2-minute intervals during a 10-minute baseline period and a 20-minute recovery period, and at 1-minute intervals during a 4-minute anger recall task and a 4-minute serial subtraction task without harassment. Participants filled out a self-report measure of forgiveness prior to the laboratory procedure. Although forgiveness was not related to CVR, higher levels of trait forgiveness were predictive of lower diastolic blood pressure (DBP) at baseline ( p < .02) and faster DBP recovery ( p < .003). Findings suggest that forgiveness may be related to overall reductions in blood pressure levels and may aid in cardiovascular recovery from stress. The results also provide preliminary evidence that forgiveness may impact cardiovascular health not through a myocardial or vascular pathway, but through another mechanism.

Anger Management Style and Hostility Among Patients With Chronic Pain: Effects on Symptom-Specific Physiological Reactivity During Anger- and Sadness- Recall Interviews

We examined whether anger-in, anger-out, and hostility predicted symptom-specific muscle tension reactivity during anger induction (but not sadness induction) among patients with chronic low back pain (CLBP). For patients with CLBP, relevant muscles are the lower paraspinals (LPs). Anger-in x hostility and anger-out x hostility interactions were tested to determine whether particularly reactive groups of patients could be identified with a multivariable profile approach. Ninety-four patients with CLBP underwent anger recall (ARI) and sadness recall (SRI) interviews, whereas LP and trapezius electromyography and systolic blood pressure, diastolic blood pressure, and heart rate were recorded. They completed anger-in, anger-out, hostility, and trait anger measures. Hierarchical regressions were used to test anger-in x hostility and anger-out x hostility interactions for physiological changes during the ARI and SRI. A significant anger-in x hostility interaction was found for LP change during the ARI (but not SRI) such that high anger-in/high hostility patients evinced the greatest reactivity. Effects for trapezius reactivity were nonsignificant. Significant anger-in x hostility interactions were also found for systolic blood pressure and diastolic blood pressure changes during the ARI such that high anger-in/low hostility patients showed the smallest changes. The anger-out x hostility interaction for diastolic blood pressure change during ARI was also significant such that high anger-out/low hostility patients showed the smallest changes. All effects remained significant with trait anger controlled. A multivariable profile approach may help identify especially vulnerable patient groups. Patients with CLBP who tend to suppress anger and are cynically hostile may be more likely to experience high levels of muscle tension near the site of pain and injury during anger, but not during sadness, than other groups.

Perceived racism and cardiovascular reactivity and recovery to personally relevant stress.

This study evaluated cardiovascular responses (CVR) to an active speech task with blatantly discriminatory (BRC) versus neutral (NRC) stimuli and an anger recall task in a sample of Black men (N = 73; age 18 to 47). Diastolic blood pressure scores were higher for NRC versus BRC stimuli during anger recall (p = .05). Moreover, persons in the NRC group who perceived high levels of racism (vs. no racism or BRC group) during active speech showed larger increases in blood pressure across postspeech rest, anger recall, and subsequent rest (p = .03). The notable elevation in CVR in response to an ambiguous event extends current models of racism suggesting that subtle racism is a psychosocial stressor that erodes health through chronically elevated CVR.

Increases in stimulated secretion of proinflammatory cytokines by blood monocytes following arousal of negative affect: The role of insulin resistance as moderator

We examined the effect of negative affect on changes in stimulated secretion of cytokines by blood monocytes and determined whether insulin resistance (IR), as indexed by the Homeostasis Model Assessment (HOMA), moderated these associations in 58 healthy men (aged 18–65 years). Blood samples and ratings of negative affect were collected at rest and 15 min following subjects’ participation in the Anger Recall Interview (ARI). Assessment of lipopolysaccharide (LPS)-stimulated secretion of IL-1β, IL-6, and TNF-α was accomplished by ELISA of supernatant. Regression models controlling for age, body mass index, and race/ethnicity revealed that higher HOMA-IR values were associated with larger stress-induced increases in IL-1β and TNF-α ( p < .05). Furthermore, arousal of negative affect during the ARI was differentially associated with stress-induced changes in stimulated secretion of TNF-α and IL-6 as a function of HOMA-IR ( p < .05). Increases in stimulated cytokine secretion were associated with arousal of negative affect, but only among men with higher HOMA-IR values. Among men with lower HOMA-IR values, arousal of negative affect was associated with diminished cytokine secretion. Collectively, these data suggest that the HOMA-IR moderates the impact that arousal of negative affect has on the ability of blood monocytes to secrete inflammatory cytokines in response to LPS. Stress-induced increases in cytokine secretion among high HOMA-IR men are consistent with the role of inflammation in cardiovascular disease, hypertension, type 2 diabetes as well as the metabolic syndrome and underscore the relevance of negative affect in the etiology of these inflammatory conditions.

Effects of Psychologic Stress on Repolarization and Relationship to Autonomic and Hemodynamic Factors

Psychological stress can precipitate ventricular arrhythmias in patients with ICDs, as well as sudden death. However, the physiologic pathways remain unknown. We sought to determine whether psychological stress induced in the laboratory setting alters indices of repolarization associated with arrhythmogenesis. Patients with ICDs and a history of ventricular arrhythmia underwent ambulatory ECG monitoring during a laboratory mental stress protocol (anger recall and mental arithmetic). Continuous changes in repolarization indices which have correlated with temporal and spatial myocardial heterogeneity of repolarization, including T-wave alternans (TWA), T-wave amplitude (Tamp), and T-wave area (Tarea) were analyzed in the time domain. In the 33 patients (85% male, 88% with coronary artery disease, mean ejection fraction 30%), norepinephrine, epinephrine, BP, and HR increased during mental stress. TWA increased from 22 (interquartile range 16-27) at baseline to 29 (21-38) uV during mental stress (P < 0.001). Changes in TWA correlated with changes in HR, systolic BP, and catecholamines. Tamp and Tarea also increased with mental stress (P < 0.01) but did not correlate with changes in other variables. Psychological stress increased TWA, Tamp, and Tarea. Autonomically mediated repolarization changes may be a pathophysiologic link between emotion and arrhythmia in susceptible patients.

Alexithymia predicts attenuated autonomic reactivity, but prolonged recovery to anger recall in young women

Alexithymia has been prospectively associated with all-cause mortality and with cardiovascular morbidity. Here, stress-induced autonomic reactivity and recovery were examined as potential pathways linking alexithymia to cardiovascular disease. The relation of alexithymia to blood pressure, heart rate, and other cardiovascular parameters derived from impedance cardiography ( N=80) and heart rate variability ( N=40) was evaluated during rest, an anger recall task and recovery in women (ages 18–30). During anger recall, alexithymia was associated with significantly attenuated heart rate and stroke index reactivity, greater low frequency power, and with marginally dampened blood pressure and high frequency power reactivity. Overall, this response pattern suggests blunted sympathetic activation and diminished vagal withdrawal. Alexithymia was also related to slower diastolic blood pressure and quicker preejection period recovery implying abbreviated sympathetic arousal and possibly greater vagal modulation. These results impart some evidence for the hypoarousal model of alexithymia during reactivity, but the hyperarousal model during recovery. Autonomic dysregulation during and following acute emotional stress is suggested as a possible physiological pathway connecting alexithymia to cardiovascular disease.

Hostility and Distraction Have Differential Influences on Cardiovascular Recovery From Anger Recall in Women.

This study investigated the relation of dispositional hostility to cardiovascular reactivity during an anger-recall task and of hostility and distraction to posttask recovery in 80 healthy women (ages 18-30). Half were randomly assigned to distraction during recovery. Hostility predicted slower systolic blood pressure and preejection period during recovery. Distraction was related to faster cardiac recovery, higher high-frequency (HF) power, lower low-frequency (LF) power and LF:HF ratios, and lower state anger and rumination during recovery. These results indicate deleterious influences of hostility on cardiovascular recovery but not during anger recall. The findings also show beneficial effects of distraction in expediting cardiovascular recovery, possibly through reducing rumination and anger.

Effects of mental stress on flow-mediated brachial arterial dilation and influence of behavioral factors and hypercholesterolemia in subjects without cardiovascular disease

Mental and emotional arousal are known to trigger coronary events. The relation between hypercholesterolemia, behavioral factors, and mental stress-induced alterations in endothelial function are not well defined. Flow-mediated brachial arterial vasodilation has been established as a measure of arterial endothelial function. High-resolution ultrasound was used to measure mental stress-mediated, flow-mediated, and the combination of mental stress- and flow-mediated brachial artery dilation in 38 subjects, 20 of whom had total cholesterol levels ≥200 mg/dl. Mental stress was provoked by anger recall and mental arithmetic and trait hostility were assessed using the Cook-Medley scale. Under mental stress, participants with hypercholesterolemia showed less vasodilation than participants without hypercholesterolemia, even after adjustment for age and the magnitude of blood pressure response to mental stress. Mental stress attenuated flow-mediated brachial arterial vasodilation. There was an inverse relation between hostile affect and percent change in brachial artery diameter after mental stress combined with hyperemia (r = −0.57, p <0.001). Thus, hypercholesterolemia is associated with impaired vasodilation in response to mental stress. Mental stress inhibits flow-mediated vasodilation in normal subjects and those with hypercholesterolemia. The magnitude of this inhibition is associated with hostility.

Cardiovascular reactivity of Singaporean male police officers as a function of task, ethnicity and hostility

Objective: This research examined hemodynamic processes in cardiovascular reactivity (CVR) as a function of task, ethnicity and trait hostility. Method: One hundred and fourteen male patrol officers from the Singapore Police Force participated in this experimental study. Trait hostility was measured using the interpersonal hostility assessment technique to derive a hostile behavior index (HBI). Heart rate, blood pressure and hemodynamic measures were taken while participants performed three tasks: mental arithmetic, number reading and anger recall (AR). Results: AR elicited the greatest blood pressure, vascular and cardiac output reactivity. HBI scores were positively related to systolic blood pressure reactivity during AR for Malays whereas this was not true for Indians and Chinese. Across tasks Indians with high HBI scores appeared to be cardiac reactors whereas the reactivity patterns for Malays and Chinese were undifferentiated. Self-report of negative mood was not related to CVR. Conclusion: These results are consistent with the higher rates of coronary heart disease deaths among Indians as well as the higher rates for hypertension among Malays in Singapore.

Psychological and physical stress-induced cardiovascular reactivity and diurnal blood pressure variation in women with different work shifts.

There is increasing evidence that diurnal blood pressure (BP) variation, in addition to high BP per se, is related to target organ damage and the incidence of cardiovascular events. However, the determinants of diurnal BP variation are not adequately understood. This paper tests the hypothesis that cardiovascular reactivity to acute stress and/or delayed recovery predicts greater diurnal BP variation (i.e., a lower sleep/awake BP ratio). We studied the relationship of diurnal BP variation (assessed by ambulatory BP monitoring) to mental stress (mental arithmetic and anger recall tasks) and physical stress (treadmill)-induced cardiovascular reactivity and recovery in 87 female nurses who worked different shifts. The sleep/awake systolic BP (SBP) ratio was negatively correlated with relative SBP reactivity (maximum SBP increase/baseline SBP: r = -0.21, p = 0.06) and relative stress response (average of SBP during stress/baseline SBP:r = -0.23, p = 0.04) induced by anger recall, while the correlations of the sleep/awake SBP ratio with other parameters of reactivity or recovery in the anger recall or mental arithmetic task were not significant. When subjects were divided into day-shift workers (n=54) and night-shift workers (n = 33), the sleep/awake SBP ratio was negatively correlated with relative SBP reactivity (r = -0.41, p = 0.02) and relative stress response of SBP (r = -0.48, p = 0.006) induced by anger recall, and positively correlated with recovery rate (r = 0.34, p = 0.06) in the latter group, while these correlations were not significant in the former group. The sleep/awake SBP ratio was inversely correlated with the exercise-induced SBP increase in the day-shift workers (r = -0.30, p = 0.03), while this association was not found in the night-shift workers. In conclusion, cardiovascular reactivity triggered by psychological and physical stress in the laboratory may be a weak, but significant, determinant of diurnal BP variation; in addition, work shift (day or night) appears to moderate the relationship between these two pressor mechanisms.

The stability of cardiovascular reactivity: Effects of task-type and family history over a 3-year interval

Although there are now more than one-half dozen published studies examining the longitudinal stability of cardiovascular reactivity, methodological limitations leave several important issues unexplored. In this investigation, 126 disease-free participants completed a laboratory protocol containing physical (hand-grip), cognitive (mental arithmetic), and speech (anger recall interview) tasks at the beginning and end of a 3-year interval. In addition, we collected information regarding family history of hypertension. As expected, blood pressure and heart rate reactivity was statistically reproducible across the 3-year time interval, but coefficients were moderate at best (rs =.37 diastolic blood pressure [DBP], .25 systolic blood pressure [SBP], & .22 heart rate [HR]). In addition, participants with a positive family history of hypertension showed greater stability of systolic reactivity. We conclude that (a) the long-term reproducibility of reactivity is strongly affected by the number of measurements, and (b) family history and task-type may have modest effectson the reproducibility ofcardiovascular reactivity.

Day-to-day reproducibility of mental stress-induced abnormal left ventricular function response in patients with coronary artery disease and its relationship to autonomic activation

Background. Mental stress (MS) results in left ventricular (LV) dysfunction in approximately half of the patients with symptomatic coronary artery disease (CAD) and is an adverse prognostic sign. The reproducibility of various MS tasks in inducing LV dysfunction and its relationship to autonomic activation in patients with CAD are not known. We studied the reproducibility on different days of 3 commonly used MS tasks on LV ejection fraction (LVEF), heart rate, blood pressure, and rate-pressure product and the relationship of reproducibility to autonomic activation as determined by heart rate variability in patients with chronic stable angina.Methods and Results. Ten patients with CAD and exercise-induced ischemia who had abnormal LVEF responses to at least one MS task from a battery of MS tasks (mental arithmetic, anger recall, and color Stroop test) while undergoing continuous ambulatory Holter and LV function monitoring underwent a second MS testing 4 to 8 weeks later, with no change in clinical status or cardiac medications in the interim. Autonomic tone was determined from indexes of heart rate variability (high frequency [HF] for parasympathetic activity and low frequency [LF] and low frequency/high frequency ratio [LF/HF] for sympathetic activity). MS tasks resulted in a small increase in heart rate (P < .0001), a modest increase in systolic blood pressure (P < .0001) and the rate-pressure product (P < .0001), and a small but statistically significant increase in LF (P < .002) and LF/HF (P < .0001), but no change in HF compared with baseline. These changes were highly reproducible over the 2 studies. With a fall in LVEF of 5% or greater considered as indicative of an MS-positive task, anger recall was the most effective and reproducible MS task in inducing LV dysfunction. MS-positive tasks were associated with a greater increase in systolic blood pressure (P = .005). Anger recall resulted in a trend toward a higher increase in systolic blood pressure (P = .08) than the other MS tasks. In MS tasks with inconsistent LVEF responses in the 2 studies (LV dysfunction present in one study but not in the other), there was significant parasympathetic withdrawal (P = .02) in MS-negative tasks but no difference in sympathetic activation. On the other hand, in MS tasks with consistent LV dysfunction on both occasions, there was no difference in parasympathetic or sympathetic activation. MS-positive tasks were not accompanied by chest pain or ST depression.Conclusions. Of the commonly used MS tasks, anger recall produces LV dysfunction with the highest frequency and is the most reproducible task when retested 4 to 8 weeks later in patients with CAD. These data are relevant for planning studies of the effects of therapeutic interventions on MS-induced LV dysfunction. (J Nucl Cardiol 2001;8:347-55.)

Psychophysiological correlates of individual differences in patterns of hemodynamic reactivity

The present study delineates a method for the quantification of six hemodynamic reactivity patterns, in response to a laboratory stressor, and examines the psychophysiological correlates of individual differences in these patterns. One hundred and ninety-four young adult men and women participated in rest periods and two laboratory stressors, mental arithmetic and an anger recall interview. Measures were taken of blood pressure, heart rate, and cardiac output, from which total peripheral resistance was derived, as well as state reports of feelings during the tasks. Six hemodynamic reactor patterns were identified: Non-reactors, Mild Myocardials, Mild Vasculars, Myocardials, Vasculars, and Dual Reactors, each associated with a unique profile of cardiac output and total peripheral resistance change. Myocardial reactors to the interview had the highest resting levels of blood pressure and total peripheral resistance. Dual reactors had the largest increases in diastolic reactivity; Dual and Myocardial reactors had the largest increases in systolic reactivity. The extreme reactor groups (Dual, Myocardial, Vascular) all reported greater task invigoration than the Non-reactors, who reported greater efforts to relax. Reactor groups were similar on anger-related trait affect. Based on both resting blood pressure and magnitude of task-induced reactivity, Myocardial and Dual reactors may be at the greatest risk for subsequent hypertension.

Frontal electrocortical and cardiovascular reactivity during happiness and anger

The present study investigated electrocortical and cardiovascular reactivity during positive and negative emotion, and examined the relation of asymmetric frontal lobe activation to cardiovascular responses. Participants were 30 healthy, right-handed university students (mean age, 23.9; 60% female; 76% Caucasian). Electroencephalographic (EEG), blood pressure (BP), and heart rate (HR) responses were assessed while subjects engaged in laboratory tasks (personally-relevant recall tasks and film clips) designed to elicit happiness or anger. Happiness-inducing tasks evoked more prominent left than right frontal EEG activation, and greater left frontal EEG activation than anger-inducing tasks. However, anger-inducing tasks were, on average, associated with comparable left and right frontal EEG activation. Irrespective of emotional valence, cardiovascular activation was more pronounced during personally-relevant recall tasks than during the viewing of film clips. During anger recall, both greater left frontal EEG response ( r=−0.46, P<0.02) and greater right frontal EEG response ( r=−0.45, P<0.02) were correlated significantly with increased HR reactivity during the task. In addition, a right lateralized frontal EEG response during anger-inducing tasks was associated with greater concomitant systolic BP ( P<0.03) and diastolic BP ( P<0.008) reactivity. Exploratory analyses also indicated that men who displayed a left lateralized frontal EEG response during happiness-inducing tasks showed the greatest concomitant systolic BP and HR reactivity ( P's<0.03). These findings suggest that asymmetric frontal EEG responses to emotional arousal may elicit different patterns of cardiovascular reactivity in healthy adults.

Effects of Exercise and Weight Loss on Mental Stress–Induced Cardiovascular Responses in Individuals With High Blood Pressure

The purpose of this study was to determine the effects of exercise and weight loss on cardiovascular responses during mental stress in mildly to moderately overweight patients with elevated blood pressure. Ninety-nine men and women with high normal or unmedicated stage 1 to stage 2 hypertension (systolic blood pressure 130 to 179 mm Hg, diastolic blood pressure 85 to 109 mm Hg) underwent a battery of mental stress tests, including simulated public speaking, anger recall interview, mirror trace, and cold pressor, before and after a 6-month treatment program. Subjects were randomly assigned to 1 of 3 treatments: (1) aerobic exercise, (2) weight management combining aerobic exercise with a behavioral weight loss program, or (3) waiting list control group. After 6 months, compared with control subjects, participants in both active treatment groups had lower levels of systolic blood pressure, diastolic blood pressure, total peripheral resistance, and heart rate at rest and during mental stress. Compared with subjects in the control group, subjects in the exercise and weight management groups also had greater resting stroke volume and cardiac output. Diastolic blood pressure was lower for the weight management group than for the exercise-only group during all mental stress tasks. These results demonstrate that exercise, particularly when combined with a weight loss program, can lower both resting and stress-induced blood pressure levels and produce a favorable hemodynamic pattern resembling that targeted for antihypertensive therapy.

Destabilizing effects of mental stress on ventricular arrhythmias in patients with implantable cardioverter-defibrillators.

The incidence of sudden cardiac death increases in populations who experience disasters such as earthquakes. The physiological link between psychological stress and sudden death is unknown; one mechanism may be the direct effects of sympathetic arousal on arrhythmias. To determine whether mental stress alters the induction, rate, or termination of ventricular arrhythmias, we performed noninvasive programmed stimulation (NIPS) in patients with defibrillators and ventricular tachycardia (VT), which is known to be inducible and terminated by antitachycardia pacing, at rest and during varying states of mental arousal. Eighteen patients underwent NIPS in the resting-awake state (nonsedated). Ten underwent repeat testing during mental stress (mental arithmetic and anger recall). Induced VT was faster in 5 patients (P=0.03). VT became more difficult to terminate in 5 patients during mental stress; 4 required a shock (P=0.03). There was no change in ease of induction with mental stress. There was no evidence of ischemia on ECG or continuous ejection fraction monitoring. Eight patients received a shock in the resting-awake state and did not perform mental stress. Four underwent repeat NIPS after sedation; 3 then had induced VT terminated with antitachycardia pacing. All patients with an increase in norepinephrine of >50% had alterations in VT that required shock for termination (P<0.01). Mental stress alters VT cycle length and termination without evidence of ischemia. This suggests that mental stress may lead to sudden death through the facilitation of lethal ventricular arrhythmias.

Defensive hostility and cardiovascular responses to stress in young men

The relationship between hostility, defensiveness and cardiovascular reactivity to stress was evaluated in a laboratory study. A total of 46 men aged 18-45 years with extreme scores on the Cook–Medley Hostility (Ho) and the Marlowe–Crowne Social Desirability (MC) scales, were recruited to create four groups: Defensive Hostile (DH: high Ho, high MC), Nondefensive Hostile (NDH: high Ho, low MC), Nonhostile Defensive (NHD: low Ho, high MC) and Nonhostile Nondefensive (NHND: low Ho, low MC). After a resting baseline, three stressors were administered: the cold pressor task, a public speech task and an anger recall task. Both DHs and NDHs displayed elevated baseline systolic blood pressures in comparison to others. DH and NHND men in comparison to NDH men exhibited increased diastolic blood pressure reactivity on the cold pressor task. There were no significant differences in reactivity between groups during the mental stressors. To summarize, the positive association between hostility and resting blood pressure supports previous research on the association between hostility and the development of coronary artery disease. Further, the current laboratory study and other laboratory studies (in contrast to field studies) do not provide strong evidence to suggest that DHs in comparison to others may be at increased risk for developing coronary artery disease.

414 Psychometric and neurophysiological approaches to latent hepatic encephalopathy in cirrhotics patients

Alexithymia has been prospectively associated with all-cause mortality and with cardiovascular morbidity. Here, stress-induced autonomic reactivity and recovery were examined as potential pathways linking alexithymia to cardiovascular disease. The relation of alexithymia to blood pressure, heart rate, and other cardiovascular parameters derived from impedance cardiography (N=80) and heart rate variability (N=40) was evaluated during rest, an anger recall task and recovery in women (ages 18–30). During anger recall, alexithymia was associated with significantly attenuated heart rate and stroke index reactivity, greater low frequency power, and with marginally dampened blood pressure and high frequency power reactivity. Overall, this response pattern suggests blunted sympathetic activation and diminished vagal withdrawal. Alexithymia was also related to slower diastolic blood pressure and quicker preejection period recovery implying abbreviated sympathetic arousal and possibly greater vagal modulation. These results impart some evidence for the hypoarousal model of alexithymia during reactivity, but the hyperarousal model during recovery. Autonomic dysregulation during and following acute emotional stress is suggested as a possible physiological pathway connecting alexithymia to cardiovascular disease.

Effects of mental stress on left ventricular and peripheral vascular performance in patients with coronary artery disease.

We sought to investigate the mechanism of a mental stress-induced fall in left ventricular ejection fraction (LVEF) in patients with coronary artery disease. Mental stress induces a fall in LVEF in a significant proportion of patients with coronary artery disease. This is accompanied by an increase in heart rate, blood pressure and rate-pressure product. Whether the mental stress-induced fall in LVEF is due to myocardial ischemia, altered loading conditions or a combination of both is not clear. Left ventricular (LV) function was studied noninvasively by serial equilibrium radionuclide angiocardiography and simultaneous measurement of peak power, a relatively afterload-independent index of LV contractility, in 21 patients with coronary artery disease (17 men, 4 women) and 9 normal subjects (6 men, 3 women) at baseline, during mental stress and during exercise. Peripheral vascular resistance (PVR), cardiac output (CO), arterial and end-systolic ventricular elastance (Ea, Ees,) and ventriculoarterial coupling (V/AC) were also calculated. Patients underwent two types of mental stress-mental arithmetic and anger recall-as well as symptom-limited semisupine bicycle exercise. Nine patients (43%) had an absolute fall in LVEF of > or = 5% (Group I) in response to at least one of the mental stressors, whereas the remaining patients did not (Group II). Group I and Group II patients were similar in terms of baseline characteristics. Both groups showed a significant but comparable increase in systolic blood pressure (15+/-7 vs. 9+/-10 mm Hg, p=0.12) and a slight increase in heart rate (7+/-4 vs. 8+/-7 beats/min, p=0.6) and a comparable increase in rate-pressure product (2.2+/-0.9 vs. 1.9+/-1.2 beats/min x mm Hg, p=0.6) with mental stress. However, PVR increased in Group I and decreased in Group II (252+/-205 vs. -42+/-230 dynes x s x cm(-5), p=0.006), and CO decreased in Group I and increased in Group II (-0.2+/-0.4 vs. 0.6+/-0.7 liters/min, p=0.02) with mental stress. There was no difference in the change in peak power (p=0.4) with mental stress. With exercise, an increase in systolic blood pressure, heart rate, rate-pressure product and CO and a fall in PVR were similar in both groups. Of the two mental stressors, anger recall resulted in a greater fall in LVEF and a greater increase in diastolic blood pressure. Exercise resulted in a fall in LVEF in 7 patients (33%). However, exercise-induced changes in LVEF and hemodynamic variables were not predictive of mental stress-induced changes in LVEF and hemodynamic variables. Conclusions. Abnormal PVR and Ea responses to mental stress and exercise are observed in patients with a mental stress-induced fall in LVEF. Peripheral vasoconstrictive responses to mental stress contribute significantly toward a mental stress-induced fall in LVEF.

Family history of hypertension: a psychophysiological analysis

Family history of hypertension (positive and negative) and gender groups were compared on cardiovascular responses at rest, during stressors and during recovery. Two tasks were employed, mental arithmetic and an anger recall interview. Both levels and reactivity measures of blood pressure, heart rate, cardiac output and total peripheral resistance were included. In addition, participants filled out several questionnaires measuring state feelings during the task and recovery periods, trait anger/hostility and emotions. Both men and women with a positive family history of hypertension exhibited higher tonic levels of blood pressure and heart rate at rest, recovery and during both tasks. They also exhibited greater heart rate reactivity during the mental arithmetic task and greater blood pressure reactivity to both tasks when post-math recovery, but not initial rest, was used as a covariate. Positive family history individuals reported less trust and gregariousness, more depression and aggression, less awareness of somatic responses to the tasks and less effort to relax during the post-task rest periods. Finally, significant correlations were found between low anger expression, low anger experience and high anger control and task SBP levels in positive family history individuals.