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Cardiovascular Reactivity to Stress Predicts Future Blood Pressure in Adolescence

From the Departments of Psychiatry (K.A.M., K.S.) and Psychology (S.S.B.), University of Pittsburgh, Pittsburgh, Pennsylvania and the Department of Education and Psychology (M.T.A.), University of Southern Mississippi, Long Beach, Mississippi

Address reprint requests to: Karen A. Matthews, PhD, Department of Psychiatry, 3811 O’Hara Street, Pittsburgh, PA 15213. Email: matthewska{at}msx.upmc.edu

	ABSTRACT

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OBJECTIVE: This study evaluated the prospective relationship between cardiovascular reactivity to psychological stress and increases in resting blood pressure across a 3-year period among a multiethnic pediatric sample (N = 149).

METHODS: Systolic and diastolic blood pressure; EKG heart rate, pre-ejection period, and mean successive difference of R to R intervals; and impedance-derived measures of cardiac output, stroke volume, and total peripheral resistance were collected during performance of four tasks that elicited different hemodynamic response patterns. Changes from baseline to each task were standardized and averaged to form eight composite scores. Analyses adjusted for time 1 baseline blood pressure and age, body mass index at baseline and change to follow-up, and duration of follow-up.

RESULTS: Rises in SBP over the follow-up period were independently predicted by SBP (ß = 0.161, p = .009), DBP (ß = 0.132, p = .02), and CO (ß = 0.144, p = .02) composite measures of reactivity. Rises in DBP over the follow-up period were predicted by DBP (ß = 0.292, p = .003, respectively), and MSD (ß = -0.176, p < .03) composite measures of reactivity. TPR reactivity was not related prospectively to blood pressure rises.

CONCLUSIONS: This study adds to the pediatric literature documenting an association between cardiovascular reactivity to stress and subsequent risk for hypertension. It is the first to show that impedance-derived measures of myocardial function during stress are related to future blood pressure levels.

Key Words: adolescence, • cardiovascular reactivity, • stress, • prospective, • blood pressure, • African American.

Abbreviations: SBP = systolic blood pressure;; DBP = diastolic blood pressure;; BMI = body mass index;; CO = cardiac output;; COP = Cardiac Output Program;; ECG = electrocardiogram;; SV = stroke volume;; IBI = interbeat interval;; MSD = mean successive difference;; PEP = pre-ejection period;; HR = heart rate;; TPR = total peripheral resistance.

	INTRODUCTION

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Excessive cardiovascular reactivity to psychological stress may have a pathophysiological role in essential hypertension (1). This hypothesis has been evaluated in at least seven large-scale studies that have used the cold pressor test to elicit blood pressure changes (2–8). Only four showed that the magnitude of the blood pressure response predicted future hypertension (2–4, 8). The cold pressor test may not be optimal to evaluate the psychological stress response because it is a thermal pain test and does not elicit a beta-adrenergically mediated myocardial response thought to be important to early neurogenic hypertension (9).

Studies that have used other stressors to elicit blood pressure changes, eg, video games and mental arithmetic, also show associations between blood pressure changes during stressors and subsequent rises in resting blood pressure over 1 to 10 years later (10–14). One study demonstrated an association between blood pressure reactivity in anticipation of exercise and development of hypertension 4 years later in middle-aged men (15). Some of these studies report that the effects are specific to men and are not apparent in women (10, 11). Many of the studies examined adolescents and young adults at a time when they are gaining rapidly in body size and weight (11–13), with few adjusting statistically for increase in weight or change in body size between study entry and evaluation of blood pressure rises. It is possible that cardiovascular reactivity to stress is associated with rises in future resting blood pressure because of associated increases in body mass index (BMI) or changes in body shape (16).

Borderline hypertension is characterized by increased SV and cardiac output CO and normal peripheral resistance, whereas essential hypertension is characterized by normal CO and increased peripheral resistance (9). Blood pressure reactivity can result from increased CO or increased peripheral resistance. None of the available studies has evaluated CO or resistance changes during psychological stress as predictors of rises in resting blood pressure. Cardiac output change during stress may predict blood pressure rises in adolescence and young adults, given the natural history of hypertension.

We report here the results of a prospective analysis of the relationship between cardiovascular reactivity to psychological stressors and the cold pressor test and subsequent blood pressure increases in a multiethnic sample of children and adolescents followed for approximately 3 years. The psychological stressors were chosen to elicit different patterns of cardiovascular responses. Impedance cardiography evaluated the effects of changes in CO, SV, and TPR during the tasks as possible predictors of rises in blood pressure. Analyses took into account the effects of age, gender, race, BMI, and change in BMI. We examined whether the effects were only apparent among men.

	METHOD

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Participants
A total of 100 children initially 8 to 10 years old and prepubertal (24 black girls, 25 white girls, 22 black boys, 29 white boys) and 49 adolescents aged 15 to 17 and postpubertal (9 black and 15 white girls, 10 black and 15 white boys) participated in two sessions approximately 3 years apart (range 1.4–6.2 years). Of the additional 29 participants eligible for follow-up testing, 15 could not be located, 13 declined follow-up participation, and 1 was deceased. There were no significant differences in resting blood pressure at study entry between participants and eligible nonparticipants. All children were healthy and not on medications that would interfere with cardiovascular assessment. Detailed description of the study protocol and recruitment is available elsewhere (17).

Physiological Recording Apparatus
SBP and DBP blood pressure were monitored using an IBS Model SD-700A automated blood pressure monitor (IBS Corp, Waltham, MA) with a standard occluding cuff placed on the participant’s nondominant arm. Impedance cardiography (Minnesota #304B) and the ECG were used for the measurement of SV, PEP, and HR. Processing of the impedance signals and ECG was accomplished using the COP, an online computerized video graphics system for impedance cardiography analysis (Microtronics Corp, Chapel Hill, NC). The COP program calculates SV using the Kubicek equation (18) and ensemble-averaged waveforms over the designated time periods (19) and TPR from CO and blood pressure readings. Customized software extracted continuous interbeat interval data from files created by the COP program. These IBI files were screened artifactual values, and the MSD statistic was computed for each data series as a measure of vagally mediated heart rate variability (20).

Experimental Tasks
During the 3-minute mirror tracing task, participants traced around a copper star with a metal stylus while only being allowed to see the mirror image of the star. Going off of the star produced a loud beep through the headphones. This task produced increases in vascular resistance thought to be due to increased alpha-adrenergic activation (21). The 3-minute choice reaction time task required the participant to respond as quickly as possible to randomly presented 1000 Hz tones by pressing a joystick button, but to refrain from responding to a 2000 Hz tone. This task elicited a cardiac pattern in many participants (22). During the cold pressor task, a 2-quart bag of two parts crushed ice and one part water was placed on the participant’s head for 1 minute. Only one participant was unable to complete the entire minute. This task evoked strong vasoconstriction activation in many participants (22). Participants were given a 10-minute interview about a recent interpersonal situation that was the most stressful for them (23).

Experimental Protocol
Participants were recruited through school districts by letters describing the study to parents and their children. Adolescents and their parents were required to sign a consent form before participation in the protocol; the younger children signed an assent form and their parents signed a separate consent form before their participation. All consent and assent forms were approved by the Institutional Review Board of the University of Pittsburgh Medical Center.

During both Time 1 and Time 2, participants arrived at the laboratory at about 8:30 AM after an overnight fast and fluid restriction. Height, weight, and skin folds were measured. After a venous blood draw was performed, participants were fed a light breakfast, followed by the application of electrodes for impedance cardiography and the ECG. The blood pressure cuff was placed on the upper part of the nondominant arm with the microphone placed above an area where the brachial artery could be palpated. Children were then given instructions for an initial 10-minute rest period. The reaction time, mirror tracing, and cold forehead tasks were given in a counterbalanced order with 8-minute rest periods after each task. The stress interview was administered only at Time 1 and was always given last because of the variable length of the task. A 10-minute rest period followed the final task. Participants were paid for completing the protocol.

Data Reduction and Analyses
BMI was calculated as weight in kilograms divided by height in meters squared (kg/m²). Data for heart rate and impedance-derived variables were collected on a minute-by-minute basis during the last 3 minutes of the initial and final rest periods, during the last minute of the intertask rest periods, during all 3 minutes of reaction time and mirror tracing, and during the first 10 minutes of the stress interview. For impedance cardiography calculations, 55 seconds of each minute were used for ensemble averaging. These minute-by-minute values were averaged to form means for each period. Data were collected in 10-second blocks during the minute of cold forehead and for the 2 minutes of recovery after the ice bag application (7 seconds of each 10-second block were ensemble averaged). The six 10-second blocks during the cold stimulus were averaged to form a mean for that task.

Blood pressures were taken at the 5, 7, and 9 minute mark of the initial and final rest periods, and the last two readings were averaged to form SBP and DBP means for those periods, coincident with impedance cardiography sampling. One blood pressure reading was taken at the 7-minute mark of each intertask rest period. Three readings were taken during the reaction time and mirror tracing tasks, and these readings were averaged to form task means. Readings were taken every other minute during the stress interview, and the five readings taken during the first 10 minutes of the interview were averaged. Finally, one blood pressure reading was taken during the cold forehead task, the reading being initiated 15 seconds into the ice bag application.

Change scores were computed by subtracting baseline mean levels of a variable from the task means. Repeated measures ANOVAs were used to examine the differences in task-induced change scores. To create a composite reactivity score, each task-induced change score was standardized and averaged across four tasks, except for MSD change that was averaged across three tasks. Composite scores were developed because of their higher reliability than individual task scores (24).

A series of multiple regression analyses were conducted predicting Time 2 resting BP with Time 1 resting BP or HR, Time 1 BMI, age group, gender, race, duration between laboratory visits, and change in BMI over time entered at the first step and the composite reactivity measure entered at the second step. Follow-up regression analyses evaluated which individual task reactivity contributed to the overall composite results. To test if the effects of composite reactivity scores were stronger in some demographic groups than others, we conducted additional analyses testing for the interactions of each composite score with age group, gender, and race by adding a third step to the above regression analyses. P values (two-tailed) .05 were considered statistically significant.

	RESULTS

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A comparison of the Time 1 session’s 8 baseline and 31 reactivity scores (8 for each of 4 tasks, except for MSD) between the 149 who participated and the 29 eligible nonparticipants showed no significant differences, P values > .05, except for the following: nonparticipants had smaller declines in MSD during reaction time and smaller declines in PEP during the mirror tracing task, relative to participants. Table 1 contains the mean age, resting blood pressure, heart rate, and BMI of the total sample and each age group at each session. BMI increased in both age groups, HR declined in the younger age group, and DBP increased in the older age group.

Time 2 SBP levels were associated with composite measures of task-induced changes in SBP, DBP, and CO, after adjusting for covariates (Table 3). Examination of the individual task-induced changes showed that Time 2 resting SBP was predicted by SBP change during mirror tracing task (ß = 0.184, p = .002), reaction time (b = 0.171, p = .005), and stress interview (ß = 0.139, p < .05); by DBP change during reaction time (ß = 0.118, p < .05); by CO change during reaction time (ß = 0.187, p = .008); and by SV change during reaction time (ß = 0.142, p < .008) and cold forehead tasks (ß = 0.124, p = .04).

Time 2 DBP levels were associated with composite measures of task-induced changes in DBP and MSD, after adjusting for all covariates (Table 3). Examination of the individual task-induced changes showed that Time 2 resting DBP was predicted by DBP change during the mirror tracing (b = 0.300, p = .001) and cold forehead (ß = 0.195, p < .03) tasks; by MSD change during reaction time (ß = -0.164, p < .05) and the stress interview (ß = -0.173, p < .03). The only other significant association was for CO change during the stress interview (ß = 0.172, p = .04).

TPR, HR, and PEP change during any task did not predict Time 2 SBP or DBP levels.

Each of the composite reactivity scores was tested for interaction with gender, age group, and race. Of the 54 interactions tested, none was statistically significant at p < .05. Among the significant single task interactions, only one interaction approached significance: Age by CO reactivity during the stress interview predicted resting DBP (p < .05), with the relationship apparent in the younger group (ß = 0.291, p = .005) but not in the older group (p = .84).

	DISCUSSION

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This study tested the hypothesis that cardiovascular reactivity to psychological stress would predict subsequent blood pressure levels across a 3-year period during adolescence. Our findings suggest that blood pressure reactivity to stress based on summed responses to reaction time, cold forehead, mirror image tracing, and a stress interview did predict subsequent resting levels of blood pressure. This association was apparent when statistical adjustments were made for Time 1 resting measures and BMI, age group, gender, race, change in BMI, and duration between evaluations. Furthermore, our analyses showed that the effects were similar among blacks and whites, boys and girls, and children initially 8 to 10 years old and adolescents initially 15 to 17 years old. Thus, these data add to a growing pediatric literature suggesting that cardiovascular responses to psychological challenges are useful markers of those who subsequently increase in blood pressure during adolescence (11–13).

A second hypothesis was that impedance-derived measures of myocardial function would also predict future rises in blood pressure. Indeed, our study showed that the composite task-induced changes in CO predicted subsequent resting SBP, whereas stressful interview CO predicted resting DBP. None of the TPR changes during the tasks was related to subsequent measures of BP. The effect size of the CO reactivity associations was small, however, and may be too small, to be useful clinically considering the technical demands of impedance cardiography. On the other hand, from a mechanistic point of view, these impedance findings do suggest that the early rise of blood pressure is indeed characterized by myocardial rather than resistance responsivity to stress. This is the first study to show that impedance-derived measures of stress responsivity predict subsequent rises in resting blood pressure.

Also noteworthy is that larger decreases in MSD, especially during the reaction time and stress interview, predicted higher follow-up DBP. MSD reflects cardiac vagal activity (20) thought to be a primary mechanism by which baroreceptors affect changes in heart rate (25). The association of larger decreases in MSD during tasks, a sign of vagal withdrawal, with future higher DBP suggests that vagal increases during stress may protect against vascularly mediated BP rises.

As anticipated, the tasks did not elicit a uniform response. The reaction time task elicited a pattern of responses consistent with beta-adrenergic activation. On the other hand, the cold forehead task elicited a pattern of responses consistent with alpha-adrenergic activation. In this sample, the mirror tracing task and stress interview elicited somewhat similar responses. Perhaps with young people, tasks that elicit a strong myocardial response, like reaction time, predict rises in blood pressure, whereas tasks that elicit a strong resistance response, like cold forehead, do not. Indeed, in our analyses, four change scores during reaction time predicted subsequent SBP, compared with one change score during each of the other tasks. On the other hand, in middle-aged adults, tasks that elicit a strong resistance response may be more informative. This formulation is consistent with the natural history of hypertension.

Limitations of the study include a short follow-up period of 3 years, the healthy nature of the population as it was screened to be free of chronic conditions that might affect blood pressure change with adolescent development, and the small changes in blood pressure over the follow-up period. It should be noted that adolescents in top 15% of distributions of changes in resting blood pressure increased at least 8 mm Hg SBP and 11 mm Hg DBP over the 3-year period. Mechanisms underlying potential relationships between blood pressure reactivity and risk for hypertension are not established. Reactivity may be a marker for total blood pressure burden as estimated by ambulatory blood pressure, impaired arterial compliance, and thickening of the vessel wall (vascular remodeling) from frequent blood pressure surges (26, 27). The positive features of the study include the gender and race composition of the sample, the assessment of stress responses with multiple tasks and with impedance cardiography, and statistical controls for factors affecting aging effects on blood pressure.

In summary, consistent with the hypothesis that cardiovascular responses to stress predict risk of hypertension, blood pressure responses to psychological stress predicted subsequent levels of blood pressure in a multiethnic pediatric sample. Impedance-derived measures of CO responses were also predictive (in contrast to TPR), suggesting myocardial involvement in the early hypertensive risk. The effect size for reactivity was small. It is important to evaluate the reactivity hypothesis in pediatric samples for a sufficient length of time so that early hypertension can be observed.

	ACKNOWLEDGMENTS

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This research was supported by National Institutes of Health Grant HL 25767 and the Pittsburgh Mind-Body Center (HL 65111 and HL 65112).

Received for publication November 2, 2001.

	REFERENCES

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