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To examine whether reactions of blood pressure to psychological stress predict future blood pressure. Blood pressure was recorded at a medical screening examination after which pressor reactions to a psychological stress task were determined. Follow up measurement of blood pressure was undertaken, on average, 4.9 years later. 20 civil service departments in London. 1003 male civil servants aged between 35 and 55 years at entry to the study. Blood pressure at follow up screening. Reactions of systolic blood pressure to stress correlated positively with systolic blood pressure at follow up screening (r = 0.22, P < 0.01). The dominant correlate of follow up blood pressure was blood pressure at initial screening (r = 0.60; P < 0.01 between initial and follow up systolic blood pressure; r = 0.59, P < 0.01 between initial and follow up diastolic blood pressure). Stepwise multiple regression analysis indicated that reactions to the stressor provided minimal prediction of follow up blood pressure over and above that afforded by blood pressure at initial screening. In the case of follow up systolic blood pressure, systolic reactions to stress accounted for only 1% of follow up variance; systolic blood pressure at initial screening accounted for 34%. With regard to diastolic blood pressure at follow up, the independent contribution from diastolic reactions to stress was less than 1%. Pressor reactions to psychological stress provide minimal independent prediction of blood pressure at follow up. Measurement of reactivity is not a useful clinical index of the course of future blood pressure.
The prognostic significance of the cold pressor test in hypertension remains a matter of controversy. Following determination at an initial screening session, blood pressure (BP) was recorded at baseline rest and in reaction to a cold pressor test. Follow-up screening BP was determined 5 years later. The effective sample was 1039 men, with an average age of 56.6 years at initial screening. Step-wise multiple regression indicated that BP reactions to the cold pressor test provided minimal independent prediction of follow-up BP over and above that afforded by BP at initial screening. In the case of follow-up systolic pressure, a model including only age and initial screening systolic BP (SBP) accounted for 38% of the variance; SBP reactions to the cold pressor did not enter the regression equation. In the case of follow-up diastolic BP (DBP), diastolic pressure at initial screening accounted for 21% of the variance, and while DBP reaction to the cold pressor test entered the equation, it accounted for only an additional 1% of the variance. These results suggest that the cold pressor test may be of limited clinical use in older populations.
Ischemia during laboratory mental stress tests has been linked to significantly higher rates of adverse cardiac events. Previous studies have not been designed to detect differences in mortality rates. To determine whether mental stress-induced ischemia predicts death, we evaluated 196 patients from the Psychophysiological Investigations of Myocardial Ischemia (PIMI) study who had documented coronary artery disease and exercise-induced ischemia. Participants underwent bicycle exercise and psychological stress testing with radionuclide imaging. Cardiac function data and psychological test results were collected. Vital status was ascertained by telephone and by querying Social Security records 3.5+/-0.4 years and 5.2+/-0.4 years later. Of the 17 participants who had died, new or worsened wall motion abnormalities during the speech test were present in 40% compared with 19% of survivors (P=0.04) and significantly predicted death (rate ratio=3.0; 95% CI, 1.04 to 8.36; P=0.04). Ejection fraction changes during the speech test were similar in patients who died and in survivors (P=0.9) and did not predict death even after adjusting for resting ejection fraction (P=0.63), which was similar in both groups (mean, 56.4 versus 59.7; P=0.24). Other indicators of ischemia during the speech test (ST-segment depression, chest pain) did not predict death, nor did psychological traits, hemodynamic responses to the speech test, or markers of the presence and severity of ischemia during daily life and exercise. In patients with coronary artery disease and exercise-induced ischemia, the presence of mental stress-induced ischemia predicts subsequent death.
Background~Ischemia during laboratory mental stress tests has been linked to significantly higher rates of adverse cardiac events. Previous studies have not been designed to detect differences in mortality rates.
The objective of this review is to evaluate the evidence for the hypothesis that cardiovascular reactivity can predict the development of preclinical (elevated blood pressure, ventricular remodeling, carotid atherosclerosis) and/or clinical cardiovascular disease states. A review of the literature was conducted examining prospective studies. Three large epidemiological studies with long-term follow-up periods (20 years or more) have found blood pressure responses to the cold pressor task to be predictive of subsequent essential hypertension in initially normotensive samples. Studies showing less consistent results have tended to use shorter-term follow-up periods. A larger body of literature demonstrates consistent associations between stress-related cardiovascular reactivity and blood pressure elevations in youth over the course of 1 to 6 years; such relationships have not been consistently shown among adult samples. Moderately consistent evidence points to a positive relationship between reactivity and other measures of subclinical disease (increased left ventricular mass and carotid atherosclerosis) among the few prospective studies that have examined these issues to date. A number of additional factors, however, such as baseline levels of disease risk and exposure to psychosocial stress, seem to moderate these relationships. Health status at baseline also seems to moderate the association between reactivity and clinical coronary heart disease in recent reports: two of three existing studies in initially healthy samples show no evidence of a relationship between reactivity and clinical outcomes, whereas three of four studies in samples with preexisting coronary heart disease or essential hypertension show a positive relationship between reactivity and subsequent disease states. There is reasonable evidence to suggest that cardiovascular reactivity can predict the development of some preclinical states (eg, increased left ventricular mass and blood pressure) states and perhaps even new clinical events in some patients with essential hypertension or coronary heart disease. However, much more information is needed concerning moderating and potentially confounding variables before the robustness of the positive relationships can become clinically useful.
The purpose of this study was to determine whether (1) there is a menstrual phase effect on blood pressure (BP) and heart rate (HR), and (2) the effects of physical effort, posture, or moods on BP and HR is mediated by the menstrual phase. Twelve normotensive women, aged between 28 and 50, with normal menstrual cycles were studied. BP was measured at 30- to 60-min intervals during a 24-hr period using an ambulatory BP monitor on Days 1, 8, 15, and 22 of the menstrual cycle. Participants were asked to report their posture, physical effort, and mood ("annoyed," "tense," and "happy") on 5-point Likert-type scales each time the ambulatory BP monitor took measurements. Systolic BP (SBP) was lower on Day 8 of the cycle. Diastolic BP (DBP) and HR were lower on Days 1 and 8. Daytime SBP was affected by the time of the day and posture, but not by moods, whereas daytime DBP was affected by posture and levels of tenseness. The level of physical effort only affected HR, not BP. The average daytime physical and emotional variables had little influence over the average daytime BP. In 12 normotensive women with a normal menstrual cycle, SBP was lower during the follicular phase and DBP and HR were lower during the follicular phase and menstruation even after controlling the effects of other factors. Physical activity or moods had only momentary effects on BP or HR. A cross-validation statistical method used is suggested to study how individuals are affected by various factors. With the use of this method, the inclusion of menstrual phase in the model improved the prediction of SBP for 5 out of the 12 women studied.
The study examined whether cardiovascular responses to active or passive coping tasks and single or multiple tasks predicted changes in resting blood pressure (BP) over a ten-month period. Heart rate (HR), BP, cardiac output (CO), and total peripheral resistance (TPR) were measured at rest, and during mental stress tests (mental arithmetic, speech, and cold pressor tasks). A total of 104 eligible participants participated in the initial study, and 77 (74.04%) normotensive adult participants’ resting BP were re-evaluated at ten-month follow-up. Regression analyses indicated that after adjustment for baseline BP, initial age, gender, body mass index, family history of cardiovascular disease, and current cigarette smoking, heighted systolic blood pressure (SBP) and HR responses to an active coping task (mental arithmetic) were associated with increased future SBP (Δ R 2 = .060, Δ R 2 = .045, respectively). Further, aggregated SBP responsivity (over the three tasks) to the predictor models resulted in significant, but smaller increases in Δ R 2 accounting for .040 of the variance of follow-up SBP. These findings suggest that cardiovascular responses to active coping tasks predict future SBP. Further, compared with single tasks, the findings revealed that SBP responses to three tasks were less predictive compared to an individual task (i.e., mental arithmetic). Of importance, hemodynamic reactivity (namely CO and TPR) did not predict future BP suggesting that more general psychophysiological processes (e.g., inflammation, platelet aggregation) may be implicated, or that BP, but not hemodynamic reactivity may be a marker of hypertension.